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A 66-year-old female is admitted to the hospital with atrial fibrillation. Her past medical history has hypertension, diabetes mellitus type II, hypercholesterolemia, and rheumatoid arthritis. During her evaluation for work up it is noted that the patient has had recurring symptomatic episodes of atrial fibrillation for the last year, some resulting in the patient not being able to ambulate due to hypotensive events. Her current blood pressure is 146/83, and her heart rate is 87. Given this clinical scenario, what is the most appropriate procedure for this patient?
A Ablation therapy
B Cardiac catheterization
C Synchronized cardioversion
D Permanent pacemaker insertion
E Pacemaker and defibrillator insertion
Ablation therapy
the clinical scenario for patients who have recurrent symptomatic episodes related to atrial fibrillation is ablation therapy (A). Cardiac catheterization (B) is sometimes performed based on suspicion of coronary artery disease, but does not address the electrophysiological reasons for the patient's episodes. Cardioversion (C) would not address a patient who is having recurrent episodes, and there is no clinical indication for pacing or defibrillation needs (D and E).
A female patient presents with a history of hypertension and low plasma HDL. She is asking you if she has metabolic syndrome. She does not have diabetes and she is not obese. Which of the following NCEP ATP III criteria would be needed to confirm that diagnosis?
A LDL > 70 mg/dL
B LDL > 90 mg/dL
C Triglycerides > 100 mg/dL
D Triglycerides ≥ 150 mg/dL
E Triglycerides > 300 mg/dL
The correct choice is D, triglycerides ≥ 150 mg/dL. The NCEP ATP III criteria for metabolic syndrome include three or more of the following:
Central obesity with waist circumference > 102 cm in men and > 88 cm in women Hypertriglyceridemia with serum triglycerides ≥ 150 mg/dL, or the patient is taking medication for hypertriglyceridemia Low HDL level < 40 mg/dL in men and < 50 mg/dL in women, or the patient is taking medication for low HDL Hypertension with blood pressure ≥ 130 mm systolic or ≥ 85 mm diastolic, or the patient is taking medication for high blood pressure Fasting plasma glucose ≥ 100 mg/dL, or a positive diagnosis for diabetes mellitus, or the patient is taking medication for hyperglycemia
According to the ATP III revised guidelines, which of the following should be your primary focus of treatment in patients with dyslipidemia?

A lowering apolipoprotein B
B lowering LDL cholesterol
C Lowering non-HDL cholesterol
D lowering triglycerides
E raising HDL cholesterol
lowering LDL cholesterol
Given their proven efficacy, ease of administration, and enhanced patient compliance over other classes of medications, statin agents are the drugs of first choice for most patients. In particular, patients with diabetes or those in the highest risk category derive special benefits from their use due to their innate anti-inflammatory effects. Myopathy and elevated liver enzymes are the main potential side effects from statin agents. An increase of serum aminotransferase levels to more than three times normal occurs in 1% of patients taking high doses of statins. Monitoring of liver function tests at six weeks, 12 weeks, six months, and annually thereafter can help identify patients with hepatic side effects and facilitate prompt discontinuation of the agents. Rhabdomyolysis occurs in less than 0.1% of cases. It can be prevented by the prompt discontinuation of the agent when muscle pain and elevated muscle enzymes occur. Unexplained pain in large muscle groups should prompt investigation for myopathy; however, routine monitoring of muscle enzymes is not supported by any evidence. Side effects from statins may not be class specific. Therefore, a side effect with one agent should not prevent a trial with another statin agent. Prior concerns about statins causing cataracts or cancer have been alleviated by the release of two large meta-analyses in 2001.
You are a physician assistant working in family practice. A 54-year-old male with a history of hypertension comes to your office complaining of fatigue. Which of the following medications is the most likely cause of the complaint and the EKG findings below?

A hydralazine
B losartan
C metoprolol
D captopril
E terazosin
Metoprolol
The correct answer is (C). This patient has a sinus bradycardia with a heat rate of about 38 bpm. Metoprolol is a beta blocker known to cause bradycardia. ARBs (such as losartan) and ACE inhibitors (such as captopril) are unlikely to cause bradycardia. Hydralazine an alpha blocker that may cause symptomatic hypotension, but it is unlikely to cause bradycardia. Hydralazine, a direct vasodilator, is more likely to cause tachycardia. Terazosin does not have an effect on rate.
A father brings his son to the family practice clinic for a concern for coarctation of the aorta. The father was recently diagnosed with this disease, and he is concerned that his 5-year-old son may have it as well. What is the cardinal physical finding in coarctation of the aorta?

A Decreased or absent femoral pulses
B Systolic machinery-type murmur
C Holosystolic murmur at the lower left sternal border
D Thrill in the carotid arteries
E Cyanosis at birth
Decreased or absent femoral pulses
Decreased or absent femoral pulses is the correct answer. A systolic machinery-type murmur is classic for a patent ductus arteriosus. A holosystolic murmur at the lower left sternal border is most commonly seen with a ventricular septal defect. A thrill in the carotid arteries is associated with aortic stenosis. Cyanosis at birth can occur with many different congenital anomalies, but is not seen with coarctation of the aorta.
A 64-year-old African American female presents to the clinic for evaluation of her hypertension, which she has had for several years. In the past she had been taking hydrochlorothiazide and lisinopril, with little effect on her blood pressure management. At today's visit, she has no complaints and feels well. Her vitals show T m 96.6, P 85, R 18, BP 191/99. She has no jugular venous distention seen on the neck exam, her lungs are clear, and cardiac exam has a regular rate and rhythm without murmur or gallop. Her abdomen is soft, non-tender, and a bruit is appreciated at the mid-abdomen just a few centimeters below the epigastric region. There is no fullness or enlargement of the abdominal aorta on palpation. Based on the history and clinical findings, what is the most appropriate procedure for this patient?

A Hepatic venous angiography
B Renal artery angiography
C Cardiac catheterization
D Lower extremity arteriography
E Venous duplex ultrasound of lower extremities
B Renal artery angiography
To appreciate the extent of this patient's renal artery stenosis by history and physical exam, the patient would benefit the best by renal artery angiography (B). This test will help determine the extent of stenosis, as well as map the surrounding arterial supply. Hepatic venous arteriography (A) and cardiac catheterization (C), and lower extremity arteriography (D) would not be indicated given the physical exam findings. Venous duplex ultrasounds would not yield the appropriate information given this clinical scenario.
A 64-year-old African American female presents to the clinic for evaluation of her hypertension, which she has had for several years. In the past she had been taking hydrochlorothiazide and lisinopril, with little effect on her blood pressure management. At today's visit, she has no complaints and feels well. Her vitals show T m 96.6, P 85, R 18, BP 191/99. She has no jugular venous distention seen on the neck exam, her lungs are clear, and cardiac exam has a regular rate and rhythm without murmur or gallop. Her abdomen is soft, non-tender, and a bruit is appreciated at the mid-abdomen just a few centimeters below the epigastric region. There is no fullness or enlargement of the abdominal aorta on palpation. Based on the history and clinical findings, what is the most likely diagnosis?

A Renal artery stenosis
B Abdominal aortic aneurysm
C Mitral stenosis radiating murmur
D Tricuspid stenosis
E Coarctation of the aorta
Renal Artery Stenosis
A This patient is exhibiting hypertension that appears to be quite high, along with evidence of a bruit on abdominal exam. Because there are no appreciable murmurs on cardiac exam, it would be less likely that a cardiac valvular murmur (C) is the reason. The abdominal aorta is of normal size, and most coarctation murmurs (E) are better appreciated in the back of the chest than on abdominal exam. Because the patient has uncontrolled hypertension despite being on two antihypertensive medications, the most likely reason for the bruit is renal artery stenosis (A). An abdominal aortic aneurysm (B) is less likely given the normal size of the aorta on exam, and tricuspid stenosis (D) would not present with these symptoms.
Patients with suspected familial hypercholesterolemia have serum cholesterol levels > 300 mg/dL and are at increased risk of atherosclerosis. Which of the following physical exam findings are nearly pathognomonic for familial hypercholesterolemia?

A Tendon xanthomas
B Lipomas
C Bouchard's nodes
D Carotid bruits
E Visceral obesity
Tendon Xanthomas
The correct choice is A, tendon xanthomas. These are depositions of cholesterol rich substances that can present in any tendon as a mass-like lesion. They are most commonly found in the Achilles, patellar, and hand extensor tendons. Choice B, lipomas, are benign, soft, moveable subcutaneous tumors made from fat cells. Choice C, Bouchard's nodes, are painless nodules on the PIP joints, commonly seen in patients with osteoarthritis. Choice D, carotid bruits, may be heard with auscultation of the neck during the physical exam in patients with artherosclerosis of the carotid arteries. Choice E, visceral obesity, is a risk factor for diabetes and atherosclerosis, but is not pathognomonic of familial hypercholesterolemia.
A 22-year-old African American male presents to the emergency department with shortness of breath, which started 2 hours prior to arrival. He does not have a history of pulmonary disease that he is aware of, and he states that in the past at random events he has had similar episodes. He does nothing to get the episodes to stop, and he also states that he feels his chest pounding at the same time of the shortness of breath. He has no medical history that he is aware of, and he takes no medications or any illicit drugs. On examination he is alert, awake, and oriented. His vital signs show T 99.0, P 142, R 18, and BP 132/82. His chest x-ray is negative for any acute cardiopulmonary disease, and his electrocardiogram has an irregularly irregular rhythm and a rate of 142 with visible delta waves.
Based on the information provided, what is the most likely diagnosis for this patient?

A Torsade de pointes
B Atrial fibrillation with Wolff-Parkinson-White syndrome
C Atrial fibrillation with re-entrant tachycardia
D Junctional tachycardia
E Atrio-ventricular re-entrant tachycardia
B This patient most likely has Wolff-Parkinson-White (WPW) syndrome (B), based on the explanation of the delta wave findings on EKG. In addition, the patient is also having atrial fibrillation with a rapid ventricular response. Patients that present with a new finding of WPW can often present with atrial fibrillation, along with symptoms such as those described above. There is nothing noted that gives the history of ventricular tachycardia (D), or re-entrant tachycardia (C and E). Torsade de points (A) is an ventricular tachycardia without evidence of a noticeable rhythm.
A 30-year-old healthy female's labs return showing an HDL of 28 mg/dl, LDL of 132 mg/dl, and total cholesterol of 185mg/dl. She is concerned due to a family history of coronary artery disease (CAD) on her father's side in his 60s. She denies tobacco use. Her blood pressure is 108/50, P-64. She requests advice on what she can due to increase her HDL. What do you advise her?

A atorvastatin
B cholestyramine
C ezetimibe
D gemfibrozil
E exercise
Exercise
E The correct answer is (E). This patient is at very low risk of CAD based on the 10-year Framingham projections. Based on her < 1%, 10-year risk drug therapy is not indicated. Exercise has been shown to increase HDL. HDL is lower in patients who have a sedentary lifestyle or are obese. Her LDL may also be reduced with exercise, weight loss, and dietary modifications.
An 84-year-old male is admitted to the hospital for the chief complaint of syncope. The history provided states that the patient was in his normal state of health and feeling well when he had fallen, with an apparent loss of consciousness for 25-30 seconds. He has a history of hypertension and arthritis, and is well managed on medications that include lisinopril and acetaminophen. During his time on the telemetry unit it's noted that the patient has periods of sinus bradycardia in the 30s, followed by normal sinus rhythms that fluctuate in the 60 to 120 range. During several of the bradycardia episodes the patient becomes symptomatic with shortness of breath, lightheadedness, and dizziness. His blood pressure during these episodes is measured at 88/56.
Given this clinical scenario, what is the most appropriate treatment for this patient?

A Observation
B Increase in lisinopril
C Cardiac catheterization
D Permanent pacemaker insertion
E Beta blocker therapy
Permanent Pacemaker Insertion
D This patient is having sick sinus syndrome, in which the patient has developed an aberrancy wherein the heart is not able to regulate a steady rate and maintain an adequate blood pressure. Because of the patient having syncope, observation only (A) is not advised. Increasing the ACE inhibitor (B) is contraindicated given the patient experiencing hypotension. This is also true with beta-blocker therapy (E). The best treatment for this clinical situation would be permanent pacemaker insertion (D). Cardiac catheterization (C) is not indicated in this situation, and does not address the electrophysiological issue.
A 30-year-old healthy female's labs return showing an HDL of 28 mg/dl, LDL of 132 mg/dl, and total cholesterol of 185mg/dl. She is concerned due to a family history of coronary artery disease (CAD) on her father's side in his 60s. She denies tobacco use. Her blood pressure is 108/50, P-64. She requests advice on what she can due to increase her HDL. What do you advise her?

A atorvastatin
B cholestyramine
C ezetimibe
D gemfibrozil
E exercise
Exercise
A 73-year-old, male with a 30 pack-year smoking history presents to the clinic with complaints of headache and dizziness. Labs reveal a hemoglobin of 21.3 g/dl, hematocrit of 63%, and platelet count of 498,000. He tests positive for the JAK2 mutation.
Which of the following should be recommended to this patient to prevent secondary complications from his diagnosis?

A Aspirin 81 mg daily
B Ferrous Sulfate 325 mg twice daily
C Eat a diet rich in vitamin B12
D Eat a diet rich in folate
E Maintain stable consumption of foods that contain vitamin K
Aspirin 81 mg daily
A The patient most likely has polycythemia vera and is at risk for thrombotic events that can be reduced through the use of daily aspirin. In addition, he should be counseled on smoking cessation if he is still currently smoking.
The patient should not take iron supplements (B) as they compete with phlebotomy therapy that seeks to reduce iron stores. Patient's with PCV similarly do not require vitamin B 12 (C) or folate (D) supplementation, and are not impacted by fluctuations in vitamin K consumption (E) unless they are being treated with warfarin for a current/recent thrombotic event.
A 17-year-old female presents to your family practice office for the annual physical examination required by her cheerleading coach. Upon examination you note that her joints are more flexible than anticipated. You also note her long thin fingers. You listen to her heart and hear no murmurs. Her blood pressure is 105/65 mmHg, pulse 60 beats/min and regular, respirations of 15 breaths/min, and temperature 98.7˚F. As you are examining her she tells you that her "joints sprain and strain easily." Furthermore, you obtain family history and she tells you that some connective tissue disorder runs in her family. Before you can medically clear her you should do which of the following?

A This patient does not require any further evaluation.
B Obtain an echocardiogram.
C Perform and EKG.
D Perform a chest radiograph.
E Refer her to a rheumatologist.
Obtain an echocardiogram
B This patient has clear signs and symptoms that are suspicious for Marfan syndrome. The complications of Marfan syndrome include cardiovascular issues, especially valvular and aortic disease. An echocardiogram is an appropriate, non-invasive initial first-step to begin your investigation to rule out significant valvular and/or aortic root abnormalities.
Which of the following is the most common cause of sudden death in young athletes under 35 years of age?

A sthelosclerotic heart disease
B Brugada syndrome
C commotio cordis
D idiopathic hypertrophic cardiomyopathy
E Marfan syndrome
Idiopathic Hypertrophic Cardiomyopathy
D Undetected idiopathic hypertrophic cardiomyopathy is the most common cause of sudden death in otherwise healthy young athletes. A heart murmur, chest pain, or shortness of breath in this patient population should trigger an escalating level of investigation including consideration of at least both an EKG and an echocardiogram. Commotio cordis, while most common in adolescent athletes, remains extremely rare.
A 22-year-old non-obese female presents to the clinic with sign and symptoms of deep vein thrombosis (DVT). She denies recent trauma, prolonged immobilization, smoking, use of oral contraceptives, or changes in her health. Her last menstrual period was one week ago. Which of the following is the most likely diagnosis that contributed to the development of her DVT?

A Antithrombin deficiency
B Factor V Leiden
C Protein C deficiency
D Protein S deficiency
E Hyperhomocysteinemia
Factor V Leiden
B Factor V Leiden mutation is one of the most common genetically inherited prothrombotic states.
Deficiencies of antithrombin (A), protein C (C) and protein S (D) when homozygous in nature typically present as fetal death or severe thrombosis at birth. When heterozygous, they carry a much lesser risk of developing thrombosis as compared to Factor V Leidin. Hyperhomocysteinemia (E) also carries a much lesser risk of developing thrombosis.
A 57-year-old woman with a history of rheumatic fever is seen complaining of dyspnea while vacuuming her apartment, which has been worsening over the last few months. On physical exam, a possible opening snap, loud S 1 , and a very soft diastolic rumbling murmur is auscultated. When the patient is placed in the left lateral decubitus position, the murmur is accentuated, and heard best at the apex. With inspiration, the murmur does not increase in amplitude. Which of the following is the most appropriate next diagnostic study?

A Chest x-ray
B Transesophageal echocardiogram
C Holter monitor
D Treadmill exercise stress test
E Transthoracic echocardiogram
Transthoracic echocardiogram
Choice E, transthoracic echocardiogram, is a simple, sensitive and non-invasive diagnostic tool, which can evaluate for the presence of valvulopathy in the setting of a patient with a diastolic murmur and a history of rheumatic fever. Mitral Valve stenosis is the MC murmur associated with RF!!
Choice B is also useful for an evaluation for the presence of valvulopathy, but is more invasive than choice E; therefore, choice E is the more appropriate study. Choice A might be able to give evidence of cardiomegaly, but would not be sensitive enough to detect valvulopathy. Choice C is a useful diagnostic tool for the evaluation of patients complaining of palpitations, but incorrect for this patient who has no symptoms. Choice D, although a useful diagnostic tool for the evaluation of exercise tolerance and in patients complaining of chest pain, does not allow direct visualization of the heart valves to evaluate for valvulopathy.
A 45-year-old woman with a no significant past medical history presents with a 4-month history of dull, aching heaviness sensation in her proximal right leg. She notes that this sensation is provoked by extended periods of standing and walking, and is relieved when she lies in a recumbent position. Her past medical history is remarkable for pregnancy 4 times, the most recent being approximately 2 years ago. She denies a history of smoking, trauma, injuries, fever, chills, chest pain, shortness of breath, hemoptysis, cough, skin changes and coolness, and peripheral edema. Her physical exam reveals several dilated, tortuous, elongated veins along the medial right thigh, which are especially pronounced upon standing. The remainder of the physical exam is normal.



Question
What will be the most appropriate therapeutic approach for this patient at this time?

Answer Choices
1 Warfarin (Coumadin)
2 Clopidogrel (Plavix)
3 Sclerotherapy
4 Furosemide (Lasix)
5 Cilostazol (Pletal)
Sclerotherapy
This patient's diagnosis is varicose veins.

Sclerotherapy can be used to treat varicose veins. It involves the injection of an irritating solution into the varicose vein to promote an inflammatory response, scarring, and obliteration of the lumen

Warfarin is indicated for myocardial infarction or cerebrovascular accident prevention and in patients with atrial fibrillation, mechanical heart valves, or deep venous thrombosis.

Diuretics are ineffective for varicose veins.

Cilostazol and clopidogrel both inhibit platelets. Clopidogrel is used in CAD and CVA prevention, as well as post-ST-segment MI. Cilostazol lowers lipid levels and is indicated in peripheral arterial disease.
A 43-year-old woman is interested in getting pregnant; she is being evaluated for a follow-up. She has a history of poorly controlled hypertension, but she is compliant to 3-drug antihypertensive therapy.

Her physical exam reveals hypertension, a cardiac gallop, and a medium-pitched systolic murmur that is best heard posteriorly in the interscapular area; there is radiation to the left axilla, apex, and anterior precordium. The lower extremities demonstrate a 16 mm Hg pressure difference as compared to the upper extremities. Additionally, there are delayed femoral pulsations; her upper extremity pulsations are normal.



Question
What health care recommendation would be considered appropriate regarding this patient?

Answer Choices
1 A high sodium, low potassium diet and restricted physical activity should be encouraged
2 Cardiovascular surgical intervention is contraindicated due to her increased age
3 Following procedural correction, blood pressure should be continuously monitored
4 Conceiving a child can be safely encouraged without risk to a developing fetus
5 Surveillance echocardiograms are not necessary in this patient
Following procedural correction, blood pressure should be continuously monitored
This patient's manifestations suggest a diagnosis of coarctation of the aorta.

Hypertension recurs in about 25 - 33% of patients with repaired coarctation in long-term follow-up; exercise-induced hypertension is even more common, occurring in 25 - 56% of patients. Continued, aggressive hypertension control should be recommended, which includes a low sodium, increased potassium diet, and physical activity.

For patients younger than age 40, surgery is advisable if the patient has refractory hypertension or significant left ventricular hypertrophy. Although the surgical mortality rate is considerable for patients 50 and older, percutaneous stenting is now the procedure of choice in this age demographic.

Coarctation of any significance may be poorly tolerated in pregnancy because of the inability to support the placental flow; in a pregnant patient, coarctation may be associated with fetal underdevelopment because of the diminished uterine blood flow.

Echocardiograms are recommended as the initial test because it can identify about 95% of coarctations through the first 8 cm of the descending aorta; this range covers 99% of cases. A long-term complication from untreated disease includes left ventricular failure, which should also be monitored through echocardiography.
A patient is presenting with substernal crushing chest pain and shortness of breath for just 15 minutes prior to arriving to the emergency department. An EKG is obtained and appears suspicious for an acute myocardial infarction. What would most likely be seen in this patient's EKG?

Answer Choices
1 S-T segment depression
2 T-wave changes
3 Ventricular bigeminy
4 Q-wave elongation
5 Hyperacute T-wave
Hyperacute T waves
The earliest presentation of an acute myocardial infarction is the hyperacute T wave. If found, this is treated the same as an ST segment elevation type of infarction (STEMI). The hyperacute T wave is considered very rare in clinical practice, as it only exists for 2-30 minutes after the onset of an infarction. Hyperacute T waves must also be distinguished from the characteristic peaked T waves, which commonly are seen with hyperkalemia.

A Q-wave elongation may appear hours to as much as 24 hours after the onset of the infarction.

ST-T segment elevation is more than likely due to an acute change, while depression is not as specific.

T-wave changes may have many other causes, and is not likely due to an MI.

Ventricular bigeminy may indicate heart irritability due to an MI, but it is more of a conduction problem.
A 55-year-old man presents with severe central chest pain. Pain started suddenly and it radiates to the back and neck. He is unable to lie flat. He feels sick but has not vomited. He has no major illnesses and knows of none that run in his family. He does not use alcohol, tobacco, or illicit substances. He is allergic to sulfa drugs.

On physical exam he appears in extreme pain and is lying on his side. Temperature - 37.0°C, heart rate 110, blood pressure 180/105 mmHg, respiratory rate 20. Cardiac exam reveals normal S1 and S2 without rubs or gallop. The top of his internal jugular venous column is present at 2 to 3 cm above the sterna notch. Chest auscultation shows normal vesicular breathing. He has normal active bowel sounds tympanic to percussion. Extremity exam is normal and the lower motor and sensory function is intact.

ECG shows left ventricular hypertrophy. Chest X-ray shows widened mediastinum.



Question
What treatment should be given immediately to this patient?

Answer Choices
1 Nitroglycerin spray
2 Intravenous labetalol
3 Streptokinase
4 Angioplasty
5 Surgery
IV Labetolol
Aortic dissection is more common in patients with hypertension, connective tissue disorders, congenital aortic stenosis or bicuspid aortic valve, and in those with first-degree relatives with history of thoracic dissections.

Chest pain is the most common presenting symptom in patients with an aortic dissection. The pain is usually sudden and severe and described as ripping or tearing.

In all individuals with aortic dissections, medication should be used to control high blood pressure, if present. Intravenous beta blockers such as labetolol are effective at reducing blood pressure and heart rate. The target systolic blood pressure should be 100-120 mm Hg. The target heart rate should be 60 - 80 beats per minute.

The choice of definite treatment depends on the location of the dissection. For ascending aortic dissection, surgical management is superior to medical management. On the other hand, in the case of an uncomplicated distal aortic dissection (including abdominal aortic dissection), medical management is preferred over surgical treatment.

Nitroglycerin spray, angioplasty, and streptokinase are the treatment modalities for acute coronary syndrome.
A 75-year-old African American man presents with a 5-month history of gradually-progressive dyspnea that is especially pronounced when climbing stairs. He also has been noticing that his ankles and lower legs have "gotten larger" over roughly the same time period, which does not allow him to fit into his sneakers any longer. He denies fever, chills, chest pain, palpitations, cough, pleurisy, calf pain, abdominal complaints, sick contacts, or travel. His psychosocial history is noteworthy for chronic alcohol use. His physical exam reveals tachycardia, bibasilar rales, JVD of 5 cm, an S3 gallop, and 2+ pitting edema to the level of the mid-calves, bilaterally.



Question
What is the expected echocardiogram finding in this patient?

Answer Choices
1 Asymmetric septal hypertrophy
2 Diffuse increase of ventricular thickness without ventricular chamber dilation
3 4-chamber dilatation with thin left ventricular walls
4 Presence of valvular vegetations
5 Abnormal segmental wall motion during systole or diastole
4-chamber dilatation with thin left ventricular walls

This patient's presentation is significant for dilated cardiomyopathy. Dilated cardiomyopathy occurs more often in African-American populations than in Caucasians, and in men more often than women. Often no cause can be identified, but chronic alcohol abuse, major catecholamine discharge, myocarditis, postpartum, and doxorubicin are frequent causes.

On echocardiography, 4-chamber dilatation is a common, but not uniform, finding. Also present is an increased LV end-diastolic diameter and volume with decreased fractional shortening, thinning LV walls, increased E point-septal separation, LA enlargement, and limited mitral and aortic valve opening (caused by low stroke volume). Intracardiac thrombi are frequently observed and are most often found in the LV apex. M-mode imaging of the mitral leaflets may demonstrate a B bump, or notch, just before systolic valve closure, indicating elevated LV diastolic pressure. Mitral annular dilatation and secondary MR are common.

Asymmetric septal hypertrophy is found in hypertrophic cardiomyopathy.

Typical echocardiographic findings of restrictive cardiomyopathy include a diffuse increase of ventricular thickness in the absence of marked ventricular chamber dilation and marked biatrial enlargement.

Valvular vegetations are indicative of infective endocarditis, while abnormal segmental wall motion during systole or diastole signifies ischemic coronary heart disease.
A 74-year-old Caucasian woman with a history of hypertension, hyperlipidemia, and myocardial infarction presents with shortness of breath upon exertion, lightheadedness, increased fatigue, and palpitations for 3 days. She has found it difficult to walk short distances due to shortness of breath. She denies any orthopnea, nocturnal dyspnea, abdominal pain cough, fever, chills, diaphoresis, anxiety, chest pain, pleurisy, cough, nausea, vomiting, diarrhea, rashes, or syncope.

She is well nourished and afebrile, but tachypnic. Her cardiac exam reveals an irregularly irregular pulse, hypotension, diminished first heart sound, S3 gallop, and laterally displaced PMI. Her lung, peripheral vascular, and abdominal exams are normal.

An echocardiogram is remarkable for a left ventricular ejection fraction of 25% while an electrocardiogram displayed the included results.



Question
What agent would be most appropriate in the management of this patient at this time?

Answer Choices
1 Digoxin
2 Furosemide
3 Isosorbide dinitrate and hydralazine
4 Nifedipine
5 Milrinone
Digoxin
This patient is presenting with signs and symptoms consistent with congestive heart failure. The echocardiogram confirms a reduced left-ventricular ejection fraction, while the electrocardiogram identifies atrial fibrillation.

Overall, digoxin use usually is limited to CHF patients with left-ventricular systolic dysfunction in atrial fibrillation or to patients in sinus rhythm who remain symptomatic despite maximal therapy with ACE inhibitors and β-adrenergic receptor antagonists. Although digoxin does not confer a survival benefit, it has reduced the number of hospitalizations that occur as a result of worsening heart failure.

Diuretics remain central in the pharmacologic management of congestive symptoms in patients with CHF. Diuretics should be administered at minimal doses required to maintain euvolemia in patients symptomatic from hypervolemia. Sustained natriuresis and/or a rapid decline in intravascular volume from diuretic use, however, may induce undesirable Frank-Starling curve dynamics, resulting in an unwanted decrease in cardiac output.

In addition to diuretic therapy, vasodilators are recommended as first-line therapy for patients with acute heart failure in the absence of hypotension, for relief of symptoms; this patient has hypotension. Fixed-dose combinations isosorbide dinitrate and hydralazine (BiDil) is indicated for heart failure in African-American patients, based in part on results from the African-American Heart Failure Trial.

Calcium channel blockers can worsen heart failure and may increase the risk of cardiovascular events; only the vasoselective calcium channel blockers have been shown not to adversely affect survival. Generally, calcium channel blockers (CCBs) should be avoided. CCBs do not play a direct role in the management of heart failure; however, these agents may be used to treat other conditions, such as hypertension or angina in heart failure patients.

Intravenous positive inotropic agents, such as milrinone, dobutamine, or dopamine, should only be used in inpatient settings, and only in patients who manifest signs and symptoms of low cardiac output syndrome (volume overload with evidence of organ hypoperfusion).
A 72-year-old man with a history of poorly-controlled HTN and previous myocardial infarction presents with nocturnal cough, bilateral ankle swelling, and dyspnea on exertion. He denies any fever, chills, URI symptoms, chest pain, headache, N/V, diaphoresis, or syncope. He further denies smoking, alcohol, or drug use. Physical exam reveals bipedal edema and bibasilar crackles. Chest x-ray is remarkable for enlargement of the cardiac silhouette and interstitial infiltrates, while EKG analysis indicates deep S waves in lead V1 and tall R waves in lead V5.



Question
What is the most appropriate next step in the evaluation and management of this patient?

Answer Choices
1 Biopsy of the endocardium
2 Chest CT scan with IV contrast
3 Transthoracic echocardiography
4 Bronchoalveolar lavage
5 Coronary angiography
Transthoracic echocardiography
This patient has clinical manifestations and initial diagnostic test results suggestive of congestive heart failure. The most useful test is an echocardiogram, which is a noninvasive and ionizing-free imaging modality that reveals the size and function of both ventricles and atria. Furthermore, it can be used to evaluate for the presence of pericardial effusions, valvular abnormalities, intracardiac shunts, and segmental wall-motion abnormalities.

Endocardial biopsy may aid in the diagnosis of restrictive cardiomyopathy and constrictive pericarditis, but is invasive.

Chest CT scanning offers the superior delineation of anatomic features to that of plain radiographs; the use of contrast serves to distinguish vascular from nonvascular structures. It does not, however, measure cardiac function.

Coronary angiography measures left ventricle ejection fraction and identifies regional wall motion. However, it is an invasive procedure and should follow an echocardiogram.

Bronchoalveolar lavage is indicated in the bronchoscopic investigation of infiltrative, malignant, occupational, and infectious lung diseases.
A 76-year-old man presents with progressive exertional dyspnea associated with substernal chest pain, easy fatigability, and dizziness. Symptoms are exacerbated with walking short distances, and they are relieved with rest. He denies fever, chills, cough, wheezing, pleurisy, calf pain, abdominal complaints, peripheral edema, cigarette, drug, or alcohol use, sick contacts, and travel. His physical exam reveals hypertension and a rough, harsh, low-pitched crescendo-decrescendo systolic murmur beginning after the first heart sound; it is best heard at the second intercostal space in the right upper sternal border. Its intensity is increased toward midsystole; the murmur radiates to both carotid arteries. It is accentuated upon squatting and reduced during Valsalva strain.



Question
What regarding the management of this patient is correct?

Answer Choices
1 β-adrenergic blocker therapy is contraindicated in this patient
2 An increase in aerobic activity to improve conditioning is recommended
3 Maximum reduction of preload and afterload with ACE inhibitors is necessary
4 Surgical intervention provides the only definitive treatment
5 Bacterial endocarditis prophylaxis is required in patients with this diagnosis
Surgical intervention provides the only definitive treatment
This patient's presentation is significant for aortic stenosis. The only definitive treatment for aortic stenosis is aortic valve replacement. The development of symptoms due to aortic stenosis provides a clear indication for replacement. For patients who are not candidates for aortic replacement, percutaneous aortic balloon valvuloplasty may provide some symptom relief.

In cases of moderate aortic stenosis, moderate-to-severe physical exertion and competitive sports should be avoided.

Beta-blockers might be used if the predominant symptom is angina.

The medical treatment options are limited in symptomatic patients with aortic stenosis who are not candidates for surgery. Those with pulmonary congestion may benefit from cautious use of digitalis, diuretics, and angiotensin-converting enzyme (ACE) inhibitors.

Although vasodilators may be used for heart failure and for hypertension associated with aortic stenosis, they should be used with extreme caution in order to prevent excessive decreases in preload or systemic arterial blood pressure. Reducing the blood pressure to normal levels in patients with hypertension and aortic stenosis is advisable, but hypotension must be avoided.

Antibiotic prophylaxis for the prevention of bacterial endocarditis is no longer recommended in patients with valvular aortic stenosis.
A 48-year-old man is brought to the ER complaining of difficulty breathing, fatigue, and intermittent chest pain for the past month. On further questioning, he states that the breathing seems to worsen when lying down. On physical exam, you note elevated respiratory and heart rates and pale, sweaty skin. On auscultation, rales are noted as well as a 3rd heart sound. Which of the following is the most likely diagnosis?
Answer Choices
1 Right Ventricular failure
2 Pulmonary Embolism
3 Mitral Valve Stenosis
4 Left Ventricular failure
5 Chronic Obstructive Pulmonary Disease (COPD)
Left Ventricular Failure
Explanation The clinical picture is suggestive of left ventricular failure (LVF). Clinical presentation includes dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. The patient may also have hemoptysis, chest pain, fatigue, nocturia, and confusion. On physical exam, the patient may present with cold, pale sweaty skin, tachypnea and tachycardia, rales, and 3rd and 4th heart sounds. This is diagnostically different from right ventricular failure.
Right ventricular failure (RVF) has a clinical picture of shortness of breath, pedal edema, and abdominal pain. On PE, RVF will present with a S3, jugular venous distention (JVD) and may have signs of LVF.

Pulmonary embolism has sudden onset of dyspnea, pleuritic chest pain, and may have hemoptysis. But there is no history of immobilization or the presence of a deep vein thrombosis (DVT), swollen, tender lower extremities, in this patient.

Mitral Valve stenosis can have a clinical presentation of dyspnea/orthopnea, hemoptysis, and fatigue. The patient may complain of palpitations or a rapid heart beat. On auscultation, rales can be heard but also a murmur will be heard which is not present on physical exam in this patient.

COPD needs to be separated into either Chronic Bronchitis or Emphysema. There is no history of smoking and there is no cough indicated. COPD can have some of the same symptoms as LVF or RVF but a CXR would be necessary to determine lung changes.
A 67-year-old man with a prior history of endocarditis and a prosthetic mitral valve presents requesting antibiotic prophylaxis for a dental procedure that entails the extraction of one of his molars. He is able to speak and swallow normally and is presently asymptomatic. His physical exam is remarkable only for a "loudly-clicking S1" in the mitral position. He has a known allergy to penicillin, which results in urticaria and angioedema upon exposure.


Question
What is the best intervention concerning this patient?
Answer Choices
1 Amoxicillin 2 grams PO within 1 hour before the procedure
2 No antibiotic prophylaxis for the dental procedure is necessary
3 Cephalexin 2 grams PO 1 hour before the procedure
4 Clarithromycin 500 mg PO 1 hour before the procedure
5 Clindamycin 600 mg IV or IM 1 hour before the procedure
Clarithromycin 500 mg PO 1 hour before the procedure
The American Heart Association and the European Society of Cardiology currently recommend prophylactic antibiotics only for those patients at highest risk for severe morbidity or death from endocarditis. Cardiac conditions in which prophylactic antibiotics are recommended include high-risk cardiac lesions such as prosthetic heart valves, prior endocarditis, unrepaired cyanotic congenital heart disease including palliative shunts or conduits, completely repaired congenital heart defects during the 6 months after repair, incompletely repaired congenital heart disease with residual defects adjacent to prosthetic material, and valvulopathy developing after cardiac transplantation.

This patient meets 2 of the identified high-risk cardiac lesions and should receive prophylaxis.

His allergic history precludes the use of amoxicillin and cephalexin, while desensitization is unnecessary given available alternatives.

The patient speaks and swallows without difficulty, making Clarithromycin the most suitable agent. Clindamycin would also be appropriate for this patient, but not via IV or IM.
A 52-year-old patient, with a known case of renovascular hypertension, presents in the with poorly-controlled hypertension. He has been treated with both enalapril and nifedipine. He had been diagnosed with unilateral left renal artery stenosis, but recent tests have demonstrated mild changes in the right renal artery also. What should be the next step in management?

Answer Choices
1 Diuretics
2 Reduction of NaCl consumption
3 Percutaneous transluminal angioplasty
4 Add atorvastatin and observe
5 Left nephrectomy
Percutaneous transluminal angioplasty
The correct choice would be percutaneous transluminal angioplasty because the patient is already on 2 antihypertensives, yet his hypertension is poorly controlled. Also, he is gradually developing bilateral renal artery stenosis. This will probably worsen his hypertension. If there are no contraindications for a surgical repair of the arteriosclerotic artery, it is the preferred course of action. It cures the hypertension without the need for medication. Percutaneous transluminal angioplasty is the procedure of choice in symptomatic stenosis. Additional stenting can also be done. This procedure has shown 90% success rates.

It is unliky that adding other antihypertensives, such as diuretics, would be useful. Atorvastatin is used only as adjunctive therapy to lower blood cholesterol in case there is hyperlipidemia. Similarly, a low salt diet to lower BP, cessation of smoking, and low dose aspirin are used as general measures and not as the only line of management.

To remove the affected kidney would definitely cure the hypertension, but is too radical. Leaving the patient with only one kidney would be very hard to justify in a case like this.
A 15-year-old girl presents with a 1-hour history of rapid heartbeat, faintness, sweating, and nervousness. She is also experiencing shortness of breath and chest pain. The patient has no significant past medical history. There is no history of similar episodes. The patient is on no medications, and she denies illicit drug use.

On exam, her vital signs are BP70/60 mm Hg; pulse 200 bpm; RR 22/min, temperature afebrile. She looks pale, and her palms are slightly sweaty. She is not comfortable sitting up, so she prefers lying down. She looks slightly apprehensive. Her heart and lung exam are negative except for the tachycardia; except for cool sweaty hands, a brief abdominal and extremity exam are non-revealing.

The physician quickly places the paddles on the patient's chest to record the rhythm; this shows a narrow-complex regular tachycardia at 210 bpm. He requests oxygen, IV line, and continuous monitoring. An EKG is in the process of being completed.



Question
At this point, what should be done?

Answer Choices
1 Carotid sinus massage
2 Synchronized cardioversion
3 Adenosine 6 mg IV push
4 Diltiazem 10 mg IV push
5 Verapamil 5 mg IV push
Synchronized cardioversion is the correct reponse.

Tachycardia can be classified based on the appearance of the QRS complex on the ECG as narrow and wide complex tachycardia. Narrow complex tachycardia consists of sinus tachycardia, atrial fibrillation, atrial flutter, AV nodal reentry, and atrial tachycardia (ectopic and reentrant). Wide complex tachycardia consists of ventricular tachycardia and supraventricular tachycardia with aberrancy.

The patient presents with a tachycardia and associated serious symptoms of faintness, shortness of breath, chest pain and apprehension, mild hypotension, and peripheral vasoconstriction. Thus, while young patients can tolerate a rapid heartbeat for some time, this patient would be classified as hemodynamically unstable. The treatment of choice for unstable patients with a narrow complex tachycardia would be immediate synchronized cardioversion.

However, whenever possible, it is advisable to provide analgesia and sedation for conscious patients before cardioversion.

In stable patients, vagal maneuvers such as carotid sinus massage or Valsalva maneuver should be the initial approach; it should be followed by administration of adenosine. Performing a carotid sinus massage and asking the patient to perform a Valsalva maneuver are relatively innocuous means of increasing vagal tone, and there is the potential for breaking the narrow-complex tachycardia.

If the vagal maneuvers do not succeed, the physician may wish to give a fluid bolus and try medications such as adenosine (6mg rapid IV push over 3 seconds). Adenosine works in 90% of narrow complex tachycardias, and with vagal maneuvers, it can be viewed as the initial management choice. The adenosine can be repeated twice at doses of 12 mg IV; the doses must be spaced at 1 - 2 minutes apart, and the adenosine must be injected in a vein that is close to the heart (at the very least, a brachial vein with elevation of the arm); it should be followed by a 20cc saline push. If there is still no rate conversion, then diltiazem or verapamil can be administered.
A 64-year-old woman presents with severe chest pain and dyspnea. She has a past medical history of diabetes mellitus, hypertension, and hyperlipidemia. She appears pale, apprehensive, and diaphoretic. She is in a confused state and is agitated; her pulse is weak. In addition, she has a narrow pulse pressure, tachypnea, a weak apical impulse, and significant jugular venous distention. Her lungs are remarkable for bilateral crackles. Her bedside electrocardiogram is notable for the following imaging.



Question
What is the most likely expected clinical manifestation in this case?

Answer Choices
1 Hyperresonance to lung percussion
2 Polyuria
3 Poor skin turgor
4 Hypotension
5 Warm and dry extremities
Hypotension
Explanation
The correct response is hypotension.

This patient exhibits signs and symptoms of cardiogenic shock due to myocardial infarction.

The vast majority of cases of cardiogenic shock in adults are due to acute myocardial ischemia. The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing the presence of hypotension, absence of hypovolemia, and clinical signs of poor tissue perfusion, such as oliguria, cyanosis, cool extremities, and altered mentation.

The lung examination demonstrates rales due to the presence of pulmonary edema. In the case of pulmonary edema, dullness is expected upon percussion. Jugular venous distention and a positive abdominal jugular reflex are usually present. However, with right ventricular (RV) infarction, the lung fields may be clear, despite hypotension and jugular venous distention. Patients are usually ashen or cyanotic, and they may have cool skin and mottled extremities. Peripheral edema suggests preexisting heart failure.

Diaphoresis indicates activation of the sympathetic nervous system.

Patients with hypoperfusion due to cardiogenic shock do not typically have polyuria.

Poor skin turgor suggests dehydration or hypovolemia; cardiogenic shock occurs due to poor cardiac output.
A 20-year-old woman presents for counseling after being diagnosed as a carrier of Emery-Dreifuss muscular dystrophy. She manifests a mild form of the disease, with only contractures of the Achilles' heels and elbows. Both her brother and her father have been diagnosed with the disease.



Question
What test will help to change the course of the disease in this young woman?

Answer Choices
1 Electrocardiography
2 Creatine kinase
3 Electromyography
4 Muscle biopsy
5 Antibodies to emerin
Electrocardiography
An electrocardiogram (ECG) should be obtained in all Emery-Dreifuss muscular dystrophy patients, including female carriers. Conduction defects may occur even with minimal musculoskeletal and joint involvement. It is estimated that 10 - 20% of female carriers have atrial arrhythmias or conduction defects and need to be monitored with yearly ECG to try to prevent sudden cardiac death. Early ECG changes include low amplitude P waves and a prolonged PR interval that progress to bradycardia, absent P waves, irregular atrial rhythm, atrial fibrillation/flutter, AV-conduction defects, and a late cardiomyopathy. There is no electrical and mechanical activity of the atria; the myocardium, not the conduction system, is affected. No specific treatment for Emery-Dreifuss muscular dystrophy exists. Supportive care to preserve muscle activity and functional ability, as well as the treatment of cardiac and/or pulmonary complications, are currently the only options. Early pacemaker implantation can change the course of the disease.

The creatine kinase (CK) level is mildly elevated in Emery-Dreifuss muscular dystrophy. Levels of CK will not influence the course of the disease.

Needle electromyography (EMG) and nerve conduction studies may be obtained to confirm the myopathy and to exclude other neuromuscular syndromes. Myopathic potentials of small amplitude, narrow duration, and the early recruitment are typical for myopathies; nerve conduction studies are normal.

A muscle biopsy should be obtained in all patients with presumed muscular dystrophy for routine histologic staining. Your patient is already diagnosed as a carrier; confirmation of the diagnosis will not affect the course of the disease.

Immunohistochemical studies (antibodies to emerin) can help confirm the diagnosis, but they will not affect the course of the disease.
A 4-year-old boy presents with poor weight gain, small size for his age, and dyspnea upon feeding. His mother notes that the child suffers from frequent upper respiratory tract infections.

On physical exam, the child is underweight for his age. You note a precordial bulge, a prominent right ventricular cardiac impulse, and palpable pulmonary artery pulsations. You also find a widely split and fixed second heart sound as well as a mid-diastolic rumble at the left sternal border.



Question
What pharmacologic agent would be most appropriate in the medical management of this patient at this time?

Answer Choices
1 Lasix (Furosemide)
2 Coumadin (Warfarin)
3 Procardia (Nifedipine)
4 Inderal (Propranolol)
5 Indocin (Indomethacin)
Lasix
This patient's manifestations suggest a diagnosis of an atrial septal defect (ASD). ASD with moderate-to-large left-to-right shunts result in increased right ventricular stroke volume across the pulmonary outflow tract, creating a crescendo-decrescendo systolic ejection murmur. This murmur is heard in the second intercostal space at the upper left sternal border. Patients with large left-to-right shunts often have a rumbling middiastolic murmur at the lower left sternal border because of increased flow across the tricuspid valve.

Definitive therapy for ASD includes closure of the defect, which is achieved surgically or through interventional catheterization. No specific or definitive medical therapy is available; however, patients with significant volume overload or atrial arrhythmias may require specific drug therapy. For patients with large shunts and heart failure, diuretics, digoxin, and ACE inhibitors should be used before surgery.

Although patients are at risk for paradoxical emboli formation, this patient does not present with manifestations consistent with vascular occlusion. For prophylaxis following use of transcatheter occlusion devices, a common practice is aspirin for 6 months.

Propranolol may be used along with morphine sulfate, phenylephrine, oxygen, volume expansion, and knee-chest or squatting positioning to manage Tet spells associated with Tetralogy of Fallot.

Indomethacin is indicated in the closure of patent ductus arteriosus.
A 20-year-old male presents following a syncopal episode during football practice. The patient is conscious and is not in acute distress. He denies abusing alcohol or "street drugs." The patient says he did not have fatigue, dizziness, or palpitations. On auscultation, you identify a systolic murmur in late systole. The murmur increases when you try Valsalva's maneuver. Otherwise, the review of systems is unremarkable. The patient's BP is 125/70 mmHg and HR is 94 bpm. The ECG you obtained shows right bundle branch block with QT interval of 495 ms. You decide to proceed with the study of cardiac anatomy and function with cardiac MRI. Refer to the image. Out of the following, what is the most probable complication that can result from this patient's condition?

Answer Choices
1 Atrial fibrillation
2 Thromboembolism
3 Sudden death
4 Progressive LV failure
5 Pulmonary hypertension
Sudden cardiac death
The patient is an otherwise asymptomatic male who has had a syncopal episode during football practice . The patient also has a systolic murmur, which exacerbates with Valsalva's maneuver. ECG shows an obvious QT prolongation, since RR interval for the heart rate of 94 is 638 ms (60000 ms/94 bpm=638 ms per RR interval). In addition, the patient has a right bundle branch block.

Cardiac MRI study shows a mild hypertrophy, but more importantly it shows systolic anterior motion. This finding can be seen on the image by the anterior leaflet of the mitral valve touching the septum during the systolic phase. These are the common features of hypertrophic cardiomyopathy (HCM). Commonly, patients with HCM are asymptomatic, and as such are generally diagnosed following a syncopal episode or during a routine ECG examination. Quite often, the only presentation of this disease is sudden death, the diagnosis being made at autopsy.

Hypertrophic cardiomyopathy typically features left ventricular hypertrophy, otherwise unexplainable without the presence of the usual factors for it, which include high blood pressure, coronary artery disease, and its presentation in young individuals. In HCM, abnormal ECG is also present in most of the patients, and QT prolongation is one of the distinguishing features. Systolic murmur and its increase, with the decrease of preload and afterload that occur during Valsalva maneuver, together with septal anterior motion on an imaging study, reveal the presence of systolic outflow obstruction with exertion. This patient, therefore, has an obstructive form of HCM. Valsalva's maneuver is very specific for obstructive HCM.

With this clinical picture that features a patient with HCM presenting in young age, the most probable complication is sudden death. The thickness of the left ventricular wall strongly correlates with the risk of sudden death and is being used for risk stratification in these patients. If the myocardium is 30 mm or thicker in end-diastole, the placement of an implantable cardioverter-defibrillator (ICD) is strongly recommended. Less severe cases are treated with medications to prevent sudden arrhythmias.

Most commonly, beta-blockers (atenolol, metoprolol), calcium antagonists (verapamil, diltiazem), and amiodarone are used in settings of HCM for the prevention of sudden death and for the relief of symptoms. It would be advisable to start this specific patient on a low-dose atenolol and reassess the findings to see if there is an improvement in systolic anterior motion. Other complications, such as pulmonary hypertension or progressive LV failure, generally do not occur until late in the course of the disease. Usually, advanced left ventricular hypertrophy (> 25 mm) accompanies such findings.

Thromboembolism is a rather non-specific complication and usually does not present itself unless there is a long-standing course of significant mitral regurgitation, or if atrial fibrillation is present. Atrial fibrillation is not a frequent complication in such patients, and it is mostly seen in patients with the calcification of the mitral valve ring. Once atrial fibrillation sets in, the risk for thromboembolic complications rises to about 6-fold (non-rheumatic form of atrial fibrillation).
A 30-year-old woman with no significant past medical history presents with a history of recurrent palpitations. These episodes occur primarily upon exertion. She recalls periodic bouts of anxiety, panic attacks, and lightheadedness. She denies fever, chills, changes in weight, chest pain, shortness of breath, rashes, diaphoresis, abdominal pain, nausea, and vomiting. She denies any history of cigarette smoking, drug, or alcohol use. Her physical exam revealed normal vital signs. The cardiac exam revealed a high-pitch late systolic click at the apex. The valsalva maneuver and a standing position result in prolongation of the murmur and a movement of the click to earlier in the cardiac cycle. The remainder of her examination is normal.



Question
What is the most likely diagnosis?

Answer Choices
1 Patent ductus arteriosus
2 Mitral regurgitation
3 Mitral valve prolapse
4 Mitral stenosis
5 Hypertrophic cardiomyopathy
Mitral Valve Prolapse
This patient's most likely diagnosis is mitral valve prolapse. The classic auscultatory finding is a mid-to-late systolic click, which is present due to the leaflets prolapsing into the left atrium, resulting in tensing of the mitral valve apparatus. It may or may not be followed by a high-pitched, mid-to-late systolic murmur at the cardiac apex. Activities that reduce end-diastolic volume, such as Valsalva maneuver or a standing position, cause an earlier click and a prolonged murmur. In the supine position, especially with the legs raised for increased venous return, left ventricular diastolic volume is increased, resulting in a click later in systole and a shortened murmur.

Patent ductus arteriosus is characterized by an abnormal patency of the ductus arteriosus, which diverts blood from the right side of the heart to the systemic circulation during fetal life. Blood typically shunts from the higher-pressured left side (systemic circulation) to the lower-pressured right side (pulmonary circulation). This murmur is described as a hollow, machinery-like murmur that is continuous throughout the cardiac cycle.

Mitral regurgitation is a medium to high-pitched apical, holosystolic, harsh murmur, which may radiate to the left axilla or less commonly to the left sternal border. It may be soft or loud and associated with a decreased S1.

The murmur of mitral stenosis is a decrescendo low-pitched rumble usually limited to the apex with an accentuated opening S1 and opening snap that follows S2.

The murmur associated with hypertrophic cardiomyopathy is a loud, harsh systolic murmur present along the left sternal border. The gradient and the murmur may be enhanced by maneuvers that decrease ventricular volume, such as an upright posture, standing, or Valsalva maneuver. It is decreased by increasing ventricular volume or vascular resistance, which occurs with squatting, sustained handgrip, lying down, or straight leg raises.
A 58-year-old woman presents with a 3-month history of postprandial abdominal pain. This crampy pain occurs 30 minutes after eating, every time. Due to these symptoms, the patient has lost 30 pounds and is afraid to eat. Her past medical history includes hypertension treated with enalapril, coronary artery disease for which she has undergone a right coronary artery stent, and she underwent a carotid endarterectomy for symptomatic carotid stenosis. She has smoked 2 packs of cigarettes a day for 30 years.


Question
What is the best initial test for this patient?
Answer Choices
1 Mesenteric angiogram
2 Mesenteric duplex ultrasound
3 Computerized tomography (CT)
4 Magnetic resonance angiography (MRA)
5 Computerized tomography angiography (CTA)
Mesenteric Duplex Ultrasound
The symptoms of chronic mesenteric ischemia have a typical presentation, including a cachectic, middle-aged patient with crampy abdominal pain after eating. The risk factors for chronic mesenteric ischemia are the same as those for atherosclerosis. Treatment aimed at restoration of mesenteric blood flow is required to restore blood supply, prevent bowel necrosis, and restore normal weight. Mesenteric duplex ultrasound is an excellent screening test to detect chronic mesenteric ischemia; however, angiography allows for confirmation of the diagnosis. Combined B-mode and color Doppler ultrasound analyze flow though the mesenteric arteries and identifies stenosis as an elevated velocity. Limiting factors include obesity and intestinal gas, which may obstruct the ability to obtain a good ultrasound image.

Mesenteric angiography remains the 'gold standard' investigation of choice for the diagnosis of arterial mesenteric ischemia. Due to the risks associated with this invasive procedure, CT angiography or magnetic resonance angiography (MRA) are sometimes substituted for angiography. The role of CT angiography and MRA remains undefined when diagnosing chronic mesenteric ischemia and has not yet met their potential as replacements for mesenteric angiography.
A 56-year-old man presents with primary hypertension. His additional medical history includes only nephrolithiasis. Past analysis of his kidney stones has revealed a calcium oxalate composition. What class of antihypertensives might best be avoided due to his history of nephrolithiasis?

Answer Choices
1 Angiotensin-converting enzyme (ACE) inhibitors
2 Beta blockers
3 Calcium channel blockers
4 Loop diuretics
5 Thiazide diuretics
Loop Diuretics
Loop diuretics reduce blood pressure by decreasing fluid retention and normalizing plasma volume. Loop diuretics act on the ascending limp of the loop of Henle and block the Na+/K+/2Cl- cotransporter. They are highly potent because this transporter is responsible for the greatest proportion of renal salt and water absorption. Loop diuretics also increase urinary calcium excretion, which may enhance the formation of calcium oxalate kidney stones.

The thiazide diuretics act in the kidney at the luminal side of the distal convoluted tubule to inhibit the Na+/Cl- cotransporter and therefore increase urinary salt and water excretion. This leads to decreases in extracellular fluid and plasma volumes. Thiazide diuretics also directly reduce peripheral arteriolar resistance, thereby improving both systolic and diastolic blood pressures. In addition to their antihypertensive effect, thiazide diuretics reduce urinary calcium excretion by indirectly increasing the activity of the 2Na+/Ca2+, also in the distal tubule. This occurs because relatively more sodium is delivered to this transporter due to the blockade of the Na+/Cl- cotransporter. Therefore, they can be helpful in controlling kidney stones that occur as a result of hypercalciuria.

Angiotensin-converting enzyme (ACE) inhibitors block the conversion of angiotensin I to angiotensin II. Angiotensin II promotes the production of aldosterone, which causes sodium and water retention. Angiotensin II also stimulates the sympathetic nervous system. ACE is also responsible for the breakdown of the vasodilator bradykinin. Blockade of this enzyme therefore leads to decreased peripheral arterial resistance by a combination of these mechanisms. Because they reduce the secretion of aldosterone, ACE inhibitors can produce hyperkalemia. However, they have no impact on urinary calcium excretion.

Beta-blockers are one of the most commonly prescribed medications to treat hypertension. In the heart, beta-1 receptor blockade has negative inotropic and chronotropic effects, leading to decreased cardiac output. Nonselective beta-blockers such as propranolol also block beta-2-mediated vasodilation. This action, combined with reduced cardiac output, promotes peripheral vasoconstriction. While nonselective beta-blockers still usually lead to net reductions in systolic and diastolic blood pressures, they must be used with caution in patients with peripheral vascular disease because they reduce peripheral circulation. Similarly, since beta-2 activation produces bronchodilation, nonselective beta-blockers may exacerbate respiratory symptoms in patients with reactive airway disease. So-called selective beta-blockers act only upon beta-1 receptors, thereby improving the side effect profile of this class of antihypertensives. Reductions in cardiac output caused by beta-blockers may lead to decreased renal perfusion, promoting aldosterone production and sodium retention. However, beta-blockers do not impact calcium or other electrolyte transport in the kidneys.

Calcium channel blockers reduce intracellular transit of calcium in both cardiac and vascular smooth muscle cells. This causes a reduction in peripheral arterial resistance and coronary artery dilation. Some calcium channel blocks are also used as antiarrhythmics because they block atrial-ventricular conduction. Calcium channel blockers have no impact of renal calcium handling.
A 68-year-old man with a past medical history of diabetes mellitus type II, hypothyroidism, and hypderlipidemia presents with a 1-hour history of constant moderate to severe "squeezing, pressure and tight" left-sided chest pain. Additionally, he admits to shortness of breath and nausea. He notes that he has had a 1-week history of similar, recurrent chest pain of about 10 minutes duration that had been occurring following exposure to the cold weather and consumption of a meal. He denies chills, abdominal pain, diarrhea, cough, and pleurisy.



Question
What physical exam finding is an anticipated finding consistent with this patient's most likely diagnosis?

Answer Choices
1 Grouped, vesicular lesions of the precordium
2 Jugular venous distension
3 Chest wall tenderness
4 Deviated trachea
5 Flushed, warm and dry skin
Jugular Venous Distension
This patient's most likely diagnosis is acute myocardial infarction.

Common general physical exam findings include anxiousness, diaphoresis, and a low-grade fever.

Bradycardia may occur most commonly with inferior infarctions, while tachycardia may be due to increased sympathetic activity, low cardiac output, or arrhythmia. Blood pressures may be high in hypertensive patients or low in patients with shock.

Jugular venous distension reflects right atrial hypertension, which may indicate right ventricular infarction or elevated left ventricular filling pressures.

Atrial gallops (S3) are common, with ventricular gallops (S4) less common and reflecting significant left ventricular dysfunction.

The skin is often pale, cool, and moist, with cyanosis and cold temperatures indicating low output.

A grouped, vesicular rash over the precordium is inconsistent with acute myocardial infarction and most likely represents thoracic herpes zoster.

Chest wall tenderness may be observed in chest wall pain syndromes, such as costochondritis.

A deviated trachea may suggest a pneumothorax, pleural effusion, atelectasis, aneurysm, or lung mass.

Splenomegaly is not a finding common to myocardial infarction.
Your patient is a 78-year-old woman who is an inpatient status post-colectomy for colon cancer. On post-operative day 3, her oral temperature is noted to be elevated to 100.6° F. Chest x-ray and urinalysis are both negative for signs of infection. An infectious disease consult is placed in order to better define the patient's new fever.



Question
What physical examination findings would support a diagnosis of superficial thrombophlebitis?

Answer Choices
1 Abdominal tenderness in the right upper quadrant
2 Positive Homans Sign in left calf
3 Abdominal tenderness in the left lower quadrant
4 Erythema and tenderness along the vein with IV insertion
5 Erythema and tenderness along her incision site
Erythema and tenderness along the vein with IV insertion
Superficial thrombophlebitis is an inflammation of a vein and can be related to a septic condition. One risk factor for superficial thrombophlebitis is presence of an IV catheter, which this patient would have due to being an inpatient and post-operative. 65-78% of cases are caused by Staphylococcus aureus, and about 88 out of 100,000 patients experience a superficial thrombophlebitis while admitted. The physical examination would reveal tenderness, erythema, and edema of the vein where the IV is present. 84% of patients would also have signs of systemic sepsis, including fever in about 70% of cases.

Abdominal tenderness of the right upper quadrant and left lower quadrant would not be indicative of superficial thrombophlebitis because these are not typical sites where this would occur. The definition of thrombophlebitis is inflammation of a vein, and the veins in the abdomen are not as superficial as other regions of the body. Abdominal tenderness in any quadrant is more typically caused by non-superficial disorders related to the organs in the abdomen.

A patient with superficial thrombophlebitis would not have a positive Homans Sign. A positive Homans Sign is defined as pain in the calf with dorsiflexion of the foot while the patient's knee is slightly bent. Although this test only has about 50% sensitivity, when present it is indicative of a deep vein thrombosis.

Erythema and tenderness at the patient's incision site would not indicate superficial thrombophlebitis, as this is not a site where this would occur. Instead, a patient with erythema and tenderness of any incisional site post-operatively could have an infection.
A 74-year-old man presents with a 1-hour history of constant moderate-to-severe "squeezing, pressure, and tight" left-sided chest pain, accompanied by nausea. He has a past medical history of diabetes mellitus type II, hypothyroidism, and hyperlipidemia. He also has a 1-week history of similar, recurrent chest pain of about 10 minutes duration; the pain occurs following exposure to cold weather and consumption of a meal. He denies fever, chills, abdominal pain, diarrhea, cough, pleurisy, and shortness of breath.



Question
What additional findings would be most consistent with his most likely diagnosis?

Answer Choices
1 The chest pain is relieved by sitting forward
2 This pain will be relieved with antacids and belching
3 Movement of the chest, trunk, and arms are provocative factors
4 Vomiting, diaphoresis, and weakness are associated findings
5 There is localized tenderness to the chest wall
Vomiting, diaphoresis, and weakness are associated findings
This patient's most likely diagnosis is acute myocardial infarction. His symptoms prior to this episode represent angina pectoris. Common symptoms associated with myocardial infarction include dyspnea, nausea, vomiting, diaphoresis, and weakness.

Chest pain relieved by a forward-sitting position suggests pericarditis.

Pain relieved with antacids or belching is common to reflux esophagitis.

Provocation factors, such as chest, trunk, and arm movement, as well as localized tenderness, suggest chest wall pain; these may be found in herpes zoster or costochondritis.
A 48-year-old man presents with a log book of home-recorded blood pressure readings between 125-185/75-100 mmHg. His past medical history is significant for hypertension and obesity (BMI 31 kg/m2). He is a non-smoker and does not drink alcohol. He has been adhering to a sodium-restricted diet and tries to walk 2 miles at least twice a week. For the past 2 years, he has been taking hydrochlorothiazide 12.5 mg daily with no apparent side effects. Physical exam is unremarkable, and vital signs reveal a heart rate of 85 beats per minute and blood pressure of 150/85.


Question
Based on this information, what is the most appropriate next step in the management of the patient's hypertension?
Answer Choices
1 Add a calcium channel blocker to his current therapy
2 Change hydrochlorothiazide 12.5 mg daily to chlorothiazide 125 mg daily
3 Continue current management and schedule a follow-up visit in 3 months
4 Discontinue hydrochlorothiazide and begin an angiotensin-converting enzyme (ACE) inhibitor
5 Increase hydrochlorothiazide dose to 25 mg daily
Increase hydrochlorothiazide dose to 25 mg daily
Explanation This patient is on a low dose of hydrochlorothiazide with no reported side effects. In addition, his blood pressure is consistently higher than the target of <140/90. In light of this information, it is most appropriate to increase his daily dose of hydrochlorothiazide in order to optimize blood pressure control.

As the patient presents with clearly documented persistent hypertension from home, it is not advisable to delay further treatment. Although many patients with essential hypertension will require 2 or more medications, it is reasonable to maximize the current drug therapy before adding a second agent. In the absence of intolerable side effects, there is no need to change drug classes.

Thiazide diuretics are widely considered first-line agents in the treatment of patients with essential hypertension. They have a wide safety profile and are associated with minimal side effects. In addition, they have been used extensively in studies demonstrating reduced cardiovascular morbidity and mortality with improved blood pressure control.
A 4-year-old child presents in cardiopulmonary arrest after being found at the bottom of a swimming pool. CPR is administered by paramedics, and an intraosseous needle and endotracheal tube are inserted.

What confirms that an intraosseous needle is correctly inserted into the marrow cavity?

Answer Choices
1 An X-ray showing the needle is in the bone
2 A sudden increase in resistance as the needle passes through the bony cortex and reaches the other side
3 Pulsations of blood can be seen in the hub
4 The needle remains upright without support
5 Insertion of the needle up to the hub
The needle remains upright without support
The needle will remain upright without support; this indicates that it is well-seated within, surrounded by the bony cortex, and advanced far enough to be fully supported. Though it can remain upright without support, it should still be stabilized with tape and a bulky dressing to prevent accidental displacement by staff during patient transport or other procedures.

An X-ray cannot confirm adequate placement because there can be a great deal of distortion; depending on the angle of exposure, an X-ray can falsely give the impression that the needle is correctly situated in the bone.

The tip of the needle would ideally be in the center of the marrow cavity and not touching the other side, so a distinct decrease in resistance should be felt after passing thorough the bony cortex.

Pulsation of blood in the hub indicates cannulation of an artery. This can be used to confirm needle placement within a major artery.

Insertion up to the hub may or may not be necessary. The needle should no longer be advanced once decrease in resistance is felt, the needle remains upright without support, marrow is aspirated (though this does not always occur), and fluid infuses freely without any sign of subcutaneous extravasation.
A 25-year-old African-American man presents with blood pressure issues. He states that he attended a work-sponsored health fair; he had his blood pressure taken, and the health fair representative strongly urged him to make an appointment to be seen by his primary care provider. The fair occurred 3 months ago. He has randomly checked his blood pressure at different times since the health fair in local grocery stores, and although he does not remember the numbers, he knows that "they were above normal". The patient also believes that both his mother and father are taking blood pressure medication, but he is not 100% sure. Vitals at this time reveal a BMI of 30 kg/m2 and a waist circumference of 41 inches; blood pressure in the left arm is 175/95 mm Hg, and in the right arm it is 172/99 mm Hg.



Question
Based upon the diagnosis at this time, what would most likely be seen during the fundoscopic examination of this patient?
Answer Choices
1 Drusen bodies
2 Microaneurysms
3 Deep retinal hemorrhages
4 Cotton-wool patches
5 Macular star
Cotton wool spots
The correct response is cotton-wool patches.

The patient above based on the information provided has the diagnosis of primary essential hypertension. Essential hypertension accounts for 95% of all hypertension diagnosis, with secondary, malignant, and other causes making up the remaining 5%. It is widely known how detrimental hypertension is to cardiovascular health in the United States; 35% of myocardial infarctions and strokes, 49% of episodes of heart failure, and 24% of all premature deaths has some link to hypertension, making this a widespread health concern. It is strongly recommended by the US Preventive Services Task Forces that all people 18 years or older be screened for high blood pressure.

Every patient has risk factors that make him/her more susceptible to having hypertension, even with lifestyle modifications. The patient above has both modifiable as well as non-modifiable risk factors that are most likely contributing to his diagnosis. He is African American and male; in addition, his family history, obesity, increased BMI, and increased waist circumference are all factors. Other well known risk factors for developing essential hypertension include a lack of physical activity, smoking, high cholesterol levels, and the diagnosis of diabetes.

Fundoscopic examination of any patients diagnosed with essential hypertension is a priceless component; it can reveal how severe the high blood pressure has been anatomically and physiologically on the body up to that point in time. Cotton-wool patches usually appear as gray or white ovoid lesions that have soft borders. These occur secondary to infarction of the nerve fibers within the fundus area; hypertension is a common etiology that can lead to the presence of this pathology.

Drusen bodies are fundoscopic findings that are yellowish, round spots; they vary in size, but they are generally small. Edges of these areas may appear soft or hard. Although Drusen bodies may be seen in normal aging patients, it is very commonly related to the diagnosis of age-related macular degeneration.

Microaneurysms are considered a hallmark finding of diabetic retinopathy.

Deep retinal hemorrhages are also commonly seen in patients with diabetes.

A macular star results from punctuate exudates that radiate from the fovea in a star pattern; this is seen is patients who are experiencing malignant hypertension.
A 23-year-old woman gives birth to a healthy male infant in the hospital. On postnatal day 6, she begins to experience some abdominal discomfort as well as cramping lower pelvic pain. Suddenly, she begins to bleed profusely from her vagina. A rapid clinical assessment reveals a boggy sub involuted uterus. Her temperature is 37 degrees centigrade; systolic BP is 70. Heart rate is 130, and she appears pale. Her heart and lungs seem normal.



Question
With secondary post partum hemorrhage as her working diagnosis, what is the next best step in management?

Answer Choices
1 Resuscitation with fluids
2 Examination for undiagnosed laceration to birth canal
3 Administration of uterotonic drugs
4 Bimanual compression of uterus
5 Ultrasonography for retained placenta
Resuscitation with fluids
Resuscitation with fluids is the correct answer. Regardless of the cause of hemorrhage, when a patient is exsanguinating, the 1st priority is to restore a degree of hemodynamic stability before the patient descends into irreversible shock. From the given blood pressure, heart rate, and general appearance, in addition to an obvious source of blood loss, hemorrhagic shock is the diagnosis; therefore, resuscitation should be the 1st step.

Examination for undiagnosed laceration to the birth canal is an incorrect response. While it is a cause of postpartum bleeding, it should only be undertaken after resuscitation.

Administration of uterotonic drugs is an incorrect response. While a cause of post partum bleeding, it should only be undertaken after resuscitation.

Bimanual compression of uterus is an incorrect response. It is a temporary measure, which is usually tried after other methods have failed, and it should only be undertaken after resuscitation.

Ultrasonography for retained placenta is an incorrect response. While a retained placenta can cause postpartum bleeding, ultrasonography should only be undertaken after resuscitation.
A 55-year-old man presents with severe central chest pain. He is a farmer and describes the pain as tearing, saying it started suddenly and is radiating. He is only able to lie comfortably on his side. He denies any previous symptoms. He feels nauseous but has not vomited. He has no major illnesses and knows of none that run in his family. He does not use alcohol, tobacco, or illicit substances. He is allergic to sulfa drugs.

On physical exam he appears to be in extreme pain, despite lying on his side. His temperature is 37.0°C, heart rate is 110 BPM, blood pressure is 180/105 mm Hg, and his respiratory rate is 20/min. Cardiac exam reveals normal S1 and S2 without rubs or gallop. The top of his internal jugular venous column is present at 2 to 3 cm above the sternal notch. Chest auscultation reveals no abnormalities. He has normal active bowel sounds tympanic to percussion. Extremity exam was normal and the lower motor and sensory function is intact.

ECG shows left ventricular hypertrophy and chest X-ray shows widened mediastinum. Labs show:

Hemoglobin 13.5 g/dL
Leukocyte count 5,000 cells/dL
Platelet count 190.000 cells/mL
Urea 70 mg/dL
Creatinine 2.5 mg/dL
Sodium 139 mmol/dL
Potassium 4.8 mmol/dL
Calcium 8.9 mg/dL
Bicarbonate 30 mEq/L
Troponin T <0.03
Creatinine Kinase 150 IU

Question
What is the best test for diagnosing this patient's condition?

Answer Choices
1 CT angiography
2 Magnetic resonance angiography (MRA)
3 Transesophageal echocardiography
4 Troponin
5 Chest X-ray
This patient has an aortic dissection. Aortic dissections are more common in patients with hypertension, connective tissue disorders, congenital aortic stenosis or bicuspid aortic valve, and in those with first-degree relatives with history of thoracic dissections. Chest pain is the most common presenting symptom. The pain is usually sudden and severe and described as ripping or tearing.

Magnetic resonance angiography (MRA) is currently the best test for the detection and assessment of an aortic dissection. It will produce a 3-D reconstruction of the aorta, allowing the physician to determine the location of the intimal tear, the involvement of branch vessels, and locate any secondary tears. It is a non-invasive test, does not require the use of iodinated contrast material, and can detect and quantify the degree of aortic insufficiency.

Computed tomography angiography is a fast, non-invasive test that will give an accurate 3-D view of the aorta. Disadvantages include the need for iodinated contrast material and the inability to diagnose the site of the intimal tear.

Widening of the mediastinum on an X-ray of the chest has moderate sensitivity in the setting of an ascending aortic dissection.

A transesophageal echocardiogram (TEE) is a good test in the diagnosis of aortic dissection. Disadvantages of the TEE include the inability to visualize the distal ascending aorta and the descending abdominal aorta.
A 56-year-old man presents with fatigue following evening walks. The patient has been treated with atorvastatin for hyperlipidemia for about 6 months. Other medications that the patient has been receiving include diltiazem, ciprofloxacin, alpha-tocopherol, aspirin, and actos. What pair of medications can cause this adverse reaction?

Answer Choices
1 Atorvastatin and diltiazem
2 Ciprofloxacin and alpha-tocopherol
3 Atorvastatin and actos
4 Ciprofloxacin and diltiazem
5 Atorvastatin and ciprofloxacin
Atorvastatin and diltiazem
The patient you are seeing has been treated for hyperlipidemia with atorvastatin for about 6 months now. When taking care of the patients with hyperlipidemia correspondently treated with statins, one needs to remember that about 2% of patients may experience rhabdomyolysis. The patient's symptoms are usually decreased ability to walk, muscle pain, and fatigue. Statins are able to induce rhabdomyolysis on their own, but the chances of being clinically relevant rise with the presence of the medications that decrease the metabolism of atorvastatin, thereby increasing its concentration in the plasma.

Atorvastatin is metabolized by the cytochrome P-450 3A4/5 isoenzyme; therefore, an inhibitor of the substrate may be capable of the interaction that would increase the clinical appearance of the side effects of atorvastatin. Out of the choice of medications, diltiazem is a documented inhibitor of the correspondence substrate for the isoenzyme. Therefore, co-administration of atorvastatin and diltiazem may increase side effects of atorvastatin in general and may increase rhabdomyolysis in particular.

Ciprofloxacin is metabolized by the liver and the kidneys. Interactions with alpha-tocopherol or pioglitazone have not been documented. Relevant interactions of ciprofloxacin include those that decrease (Zn, Fe, sucralfate, Mg) its absorption from the stomach, lead to Q-T interval prolongation (hismanal, macrolides), toxicity (alkylxanthines), seizures (foscarnet), and increased ciprofloxacin action (probenecid, etc.).

Actos is partially metabolized by 3 P-450 isoenzymes; therefore, the chances of the classic substrate-inhibitor interactions are less than with an agent that has a mono-metabolism by an isoenzyme. Drug interactions between atorvastatin and ciprofloxacin have not been documented to have relevant clinical significance.
A 35-year-old woman presents with fatigue and yellowish coloration of her eyes and skin that started several weeks after noneventful implantation of the prosthetic mechanical heart valve. Physical examination reveals the presence of regurgitant murmur and subicterus. Laboratory results are: hemoglobin 7.0 g/dL; reticulocytes 21%; white blood cells 11,500/µL; platelets 80,000/µL; and undetected levels of haptoglobin. In lactate dehydrogenase, the direct and indirect bilirubin levels are all elevated (3,100 U/L, 2.1 and 1.2 mg/dL, respectively). Peripheral blood smear shows burr and helmet cells (schistocytes) and polychromasia. Both direct and indirect Coombs' tests are negative. You suspect microangiopathic hemolytic anemia.



Question
What is the next step in management?

Answer Choices
1 Hemoglobin electrophoresis
2 Glucose-6-phosphate dehydrogenase deficiency
3 Echocardiography
4 Hepatitis B panel
5 Direct agglutination test
Echocardiography

Anemia, reticulocytosis, and jaundice are the characteristics of hemolytic anemias. Red blood cells (RBC) survival is shortened; bone marrow increases erythroid production that results in the increased number of reticulocytes; and RBC breakdown manifests as increased unconjugated bilirubin and lactate dehydrogenase and decreased (undetectable) haptoglobin. Microangiopathic hemolytic anemia occurs when the red cell membrane is damaged in circulation, leading to intravascular hemolysis and the appearance of schistocytes (fragmented erythrocytes).

Hemolytic anemia due to mechanical damage is seen with prosthetic mechanical heart valves. Your first and most important next step in the management of this patient will be to find out if there is a dysfunction of the prosthetic valve. Echocardiography will reveal the presence of significant leaking or valve dysfunction.

Hemolytic anemias are generally caused by intrinsic (defects in erythrocytes membranes, enzyme systems, and hemoglobin; mostly hereditary) and extrinsic factors (immune and microangiopathic hemolytic anemias). Hemoglobin electrophoresis will be useful in the diagnosis of thalassemia or sickle cell anemia that is caused by intrinsic hemoglobin defect. Anemias in those disorders are usually hypochromic and microcytic.

Glucose-6-phosphate dehydrogenase deficiency is usually drug-induced. In this case, hemolytic anemia is intrinsic and caused by the defect in the enzyme system. Hemolytic anemia may occur in the course of some viral diseases and is autoimmune (Coombs test will be positive). Hepatitis B rarely causes this sort of anemia. Besides, the probability that she acquired hepatitis B during the surgery is very low these days.

A direct agglutination test is looking for serum antibodies using whole organisms. It has no place in the diagnosis of microangiopathic hemolytic anemia.
A 25-year-old Asian-Indian woman presents with pain, weakness, and increased numbness in her right hand for the last 24 hours. The patient also states that, for the last month, she has not felt very well; she has experienced malaise, night sweats, decreased appetite, and arthralgias. She notes that, for the last week when she washed her hands with cold water, her right hand would turn blue. On clinical examination, the patient has fever, tachycardia, decreased pulse, and decreased blood pressure in the right arm; Babinski's sign is negative. Auscultation on the right supraclavicular space reveals a bruit. Laboratory findings are an elevated ESR and mild anemia. What is the most appropriate next step in the management?

Answer Choices
1 Aortic arteriography
2 Echocardiogram
3 CT scan of the chest
4 Chest X-ray
5 VDRL
Complete aortic arteriography is the investigation of choice for a patient with suspicion of Takayasu's arteritis, an inflammatory and stenotic disease of medium- and large-sized arteries most likely in young Asian women between 15 and 30 years of age. Because of the predilection for aortic arch and its branches involvement, Takayasu's arteritis is often referred as the aortic arch syndrome or pulseless disease. The clinical course may be fulminant, hence the need for arteriography that shows the characteristic lesions with stenosis and post stenotic dilatations, aneurysms, and increased collateral circulation. The most frequent affected site is the subclavian artery manifested as claudication and Raynaud's phenomena. Steroids are used for treatment.

Involvement of the aorta may lead to aortic insufficiency that would indicate echocardiography. X-ray and CT scan of the chest would not reveal lesions of Takayasu's arteritis.

VDRL may be indicated for a patient with aortic insufficiency secondary to tertiary syphilis with luetic aortitis. The clinical picture includes a different history and presentation.
A 56-year-old man with a past medical history of diabetes mellitus type II, hypertension, myocardial infarction 1 year ago, and a 50-pack/year smoking history presents with unilateral leg edema and leg pain for the last 6 hours. His physical exam is remarkable for an elevated systolic blood pressure, obesity, and localized left lower extremity edema, erythema, and tenderness to the left lateral calf.



Question
What additional physical exam finding would be most consistent with a diagnosis of superficial thrombophlebitis in this patient?

Answer Choices
1 Linear induration along the course of a vein
2 Peripheral cyanosis
3 A positive Homan's sign
4 Reduced amplitudes of the dorsalis pedis and tibialis anterior pulses
5 A shallow, well-circumscribed ulcer above the medial malleolus
Linear induration along the course of a vein
Superficial thrombophlebitis is a common inflammatory-thrombotic disorder in which a thrombus develops in a vein located near the surface of the skin. Superficial thrombophlebitis usually presents with pain, swelling, redness, and tenderness of superficial veins. When superficial thrombophlebitis occurs in the short or long saphenous veins, there is usually redness, tenderness, and often linear induration that follows the course of the involved vein (medial calf or thigh).

Peripheral cyanosis and reduced peripheral pulse amplitudes are examination findings common to peripheral arterial occlusive disease.

Homan's sign (calf pain precipitated by dorsal flexion of the foot) is present in fewer than 50% of deep venous thrombosis cases.

Physical examination of chronic venous insufficiency shows orange-brownish skin discoloration at the level of the ankle with hemosiderin deposition, lower extremity edema, superficial varicosities, and ulceration; ulcers usually occur at the medial and lateral malleoli of the ankle.
A 12-year-old girl presents with hypertension, which is not being treated at this time. Although she does not note any symptoms, she is once again found to be hypertensive; there is a cardiac gallop and a medium-pitched systolic murmur, which is best heard posteriorly in the interscapular area, with radiation to the left axilla, apex, and anterior precordium. A prominent anterior chest heave is also observed. The lower extremities demonstrate a 16 mm Hg pressure difference as compared to the upper extremities. Additionally, there are delayed femoral pulsations; her upper extremity pulsations are normal. The remainder of the physical exam is normal. A recent chest X-ray is notable for the following images.



Question
What pharmacotherapeutic agent would be most beneficial to this patient at this time?

Answer Choices
1 Prostaglandin E1
2 Dopamine
3 Enalapril (Vasotec)
4 Lopressor (Metoprolol)
5 Furosemide (Lasix)
Metoprolol
The correct response is Lopressor (Metoprolol). This patient's most likely diagnosis is coarctation of the aorta.

Radiography in patients with late onset of coarctation of the aorta may reveal cardiomegaly. An inverted "3" sign of the barium-filled esophagus or a "3" sign on a highly penetrated chest radiograph (frontal view) may be visualized. Rib notching secondary to collateral vessels may also be seen.

The percutaneous interventional procedure of choice is endovascular stenting when anatomically feasible; self-expanding and balloon-expandable covered stents have been shown to be advantageous over bare metal stents. Otherwise, surgical resection (usually with end-to-end anastomosis) should be performed.

Preoperative hypertension can be effectively treated using beta-blockers. The goal should be to reduce upper extremity hypertension, but vigorous attempts to achieve normal upper extremity blood pressure (BP) may result in inadequate lower-body perfusion. Beta-blocker therapy prior to surgery may reduce the severity of postoperative hypertension, although most patients with preoperative hypertension require at least transient postoperative therapy.

Prostaglandin E1 (0.05 - 0.15 mcg/kg/min) is infused intravenously to open an associated patent ductus arteriosus (pda). Although a patent ductus arteriosus is a commonly associated defect in coarctation of the aorta, prostaglandins are not indicated in the general treatment of coarctation without PDA.

Treatment of patients with congestive heart failure (CHF) includes the use of diuretics and inotropic drugs.

ACE inhibitors or angiotensin II antagonists may be added if hypertension persists despite beta-blocker therapy. Pediatric dosing is not established for angiotensin II antagonists.
A 73-year-old man presents to the local A+E with a 1-hour history of chest pain and shortness of breath. An ECG is obtained and found to have T wave inversion and wide Q waves in leads V1, V2, and V3. What are these ECG findings are most consistent with?
Answer Choices
1 Acute ischemia without myocardial infarction
2 Acute lateral myocardial infarction
3 Acute inferior myocardial infarction
4 Acute posterior myocardial infarction
5 Acute anterior myocardial infarction
Acute anterior MI
Explanation The correct answer is acute anterior myocardial infarction, as ECG findings include T wave inversion and wide Q waves in the anterior leads (V1, V2, V3, and/or V4).

T wave inversion without significant Q waves would suggest ischemia without myocardial infarction (MI). T wave inversion and wide Q waves in leads I and AVL would suggest a lateral MI. T wave inversion and wide Q waves in leads II, III, and AVF would suggest an inferior MI. Large R waves and ST segment depression in leads V1, V2, and/or V3 suggests a posterior MI.
A 30-year-old Japanese woman presents with dizziness and weakness. On examination, her blood pressure is 90/60 mm Hg. Her upper extremities are cold. Both of her radial pulses are very weak. On further questioning, her relative says that she has had such several attacks in the past. The angiography reveals narrowing of the brachiocephalic and subclavian arteries. What is the probable diagnosis?

Answer Choices
1 Takayasu's arteritis
2 Giant cell arteritis
3 Kawasaki disease
4 Microscopic polyangiitis
5 Polyarteritis nodosa
takayasu's arteritis
Takayasu's arteritis is a granulomatous vasculitis of medium sized and larger arteries. Takayasu first described it in 1908 as a clinical syndrome characterized by ocular disturbances and marked weakening of the pulses in the upper extremities (Pulseless disease). This is related to the fibrous thickening of the aortic arch with narrowing, or virtual obliteration, of the origins or more distal portions of the great vessels arising in the arch. Microscopically, there is adventitial mononuclear infiltrate with perivascular cuffing of the vasa vasorum (initially). Later, there is intense mononuclear inflammation in the media, in some cases accompanied by granulomatous changes replete with giant cells and patchy necrosis of the media. In addition, when it heals, the inflammation is replaced by marked collagenous fibrosis involving all the layers of the vessel wall accompanied by lymphocytic infiltration.
A patient presents for routine analysis of cholesterol levels. The results show plasma cholesterol levels of 300-mg/100 ml. You prescribe the drug simvastatin (Zocor). She is reluctant to take drugs to treat her hypercholesterolemia. After further discussion, she agrees to take a vitamin to treat the elevated cholesterol. She also has questions concerning familial hypercholesterolemia.


Question Ico-delete Highlights
Familial hypercholesterolemia is due to what defect??

Answer Choices
1 Cholesterol biosynthesis
2 Low density lipoprotein receptors
3 Cholesterol degradation
4 Lysosomal function
5 Cholesterol esterification
In familial hypercholesterolemia, which is a genetic disorder, the plasma levels of cholesterol and LDL are elevated. In this disease, cholesterol is deposited in many tissues because of the concentrations of cholesterol-LDL in the plasma. The molecular defect results in the absence or deficiency of functional LDL receptors. Therefore, the entry of LDL into the liver and other cells is impaired and all of the deleterious effects of the disease can be attributed to the elevated LDL-cholesterol levels.

High levels of cholesterol have 3 major metabolic effects. Cholesterol inhibits the activity of the enzyme β-Hydroxy-β-methyl-glutaryl-CoA (HMG-CoA) reductase, which catalyzes the rate-limiting step of cholesterol biosynthesis. Cholesterol also inhibits the production of low-density lipoprotein (LDL) receptors by suppressing the transcription of the LDL receptor mRNA. The third point of regulation involves the activation of the enzyme acyl-CoA: cholesterol acyltransferase (ACAT), which esterifies cholesterol for storage.

The LDL receptors are located in specialized regions of the membrane called coated pits. These coated pits contain a protein called clathrin. Clathrin participates in the endocytosis of LDL receptors, as well as other proteins such as transferrin and sialoglycoproteins. Clathrin forms a closed polyhedral lattice around the coated pit forming a coated vesicle. The coated vesicle then loses its clathrin and fuses with an endosome. In the endosome, the ligand is dissociated from the receptor, and sorting of the different components can occur.
A 70-year-old man, with a history of HTN and aortic valve replacement 3 months ago, presents with complaints of arthralgia, myalgia, anorexia, fatigue, and weight loss over the last month, with recent dyspnea on exertion and lower extremity edema. Vital signs are as follows: Temperature 38°C, BP 102/64, P 98, RR 20. On physical exam, a new high-pitched, blowing, decrescendo diastolic murmur is noted along the left lower sternal border. Two separate blood cultures are positive for S. aureus. Which of the following is the most appropriate next diagnostic study?
TEE
A 70-year-old man with a history of hypertension, DM Type 2, and hyperlipidemia is seen for preoperative evaluation prior to left knee replacement. On auscultation, a very soft high-frequency decrescendo early diastolic murmur is heard at the upper left sternal border. Which of the following maneuvers would be the most appropriate to choose to increase the intensity of the murmur for better identification?

A Isometric hand grip exercise
B Listening with the bell at the apex with the patient in the left lateral decubitus position
C Inspiration, followed by the patient holding his/her breath
D The Valsalva maneuver
E Having the patient lie flat with the knees bent
isometric hand grip
A 22-year-old woman with a history of scoliosis presents to the office with complaints of retrosternal chest discomfort, occurring frequently at rest and lasting for several hours at a time. She is currently experiencing this chest discomfort during the office visit, but has never experienced this while working out three days per week. On physical exam, a mid-systolic click is noted. With standing, the click moves closer to S1. An EKG demonstrates normal sinus rhythm at 76 bpm, with no acute ST or T wave changes. A transthoracic echocardiogram reveals mild prolapse of the posterior leaflet of the mitral valve. Which of the following would be the most appropriate next step in the management of this patient?

A Reassurance and monitoring with periodic transthoracic echocardiogram
B Cardiac catheterization
C Infectious endocarditis prophylaxis
D Mitral valve replacement
E Transesophageal echocardiogram
Reassurance and monitoring with periodic transthoracic echocardiogram
Most patients with mitral valve prolapse are asymptomatic, and do not demonstrate significant progression of their valvulopathy over their lifetime. Periodic transthoracic echocardiogram allows a noninvasive, highly sensitive method of monitoring. Choice B, cardiac catheterization, is useful for evaluation of coronary artery anatomy and for evaluation of valvulopathy; however, it is invasive, and usually reserved for investigation of serious valvular dysfunction, and/or following a stress test suggestive of myocardial ischemia. The chest pain experienced by patients with mitral valve prolapse is varied in presentation, and in this setting, with a young patient with no cardiac risk factors, unlikely to be secondary to coronary artery disease. According to the American Heart Association's most recent guidelines, patients with mitral valve prolapse alone do not require infectious endocarditis prophylaxis, so choice C is inappropriate. Choice D, mitral valve replacement, is only indicated with severe mitral valve prolapse, resulting in severe mitral regurgitation. Choice E, transesophageal echocardiogram, while an excellent diagnostic tool for the evaluation of mitral valve disease, would be more invasive than monitoring via transthoracic echocardiogram, and thus would not be an appropriate choice in this patient with only mild mitral valve prolapse.
A 58-year-old female two days status-post coronary artery bypass graft (CABG) surgery is being treated with heparin to prevent thrombosis. Her routine CBC reveals a hemoglobin of 11.2 mg/dL, hematocrit of 35%, WBC count of 5.6, and platelet count of 22,000. In addition to discontinuing heparin, which of the following is the most appropriate intervention?

A Administer prednisone
B Administer warfarin
C Bone marrow aspirate
D CT of the abdomen
E Observation
Administer Warfarin
The patient most likely has developed heparin-induced thrombocytopenia (HIT), which is associated with qualitative platelet function changes that result in increased risk of thrombosis. She should begin warfarin (B) and be evaluated for thrombosis (e.g., lower extremity Dopplers).
Prednisone (A) is not indicated for the treatment of HIT, and a bone marrow aspirate (C) would not aid in establishing the diagnosis. CT of the abdomen (D) would be indicated if she had symptoms consistent with thrombosis in that region, and observation (E) fails to address her increased thrombotic risk.
A 3-month-old baby girl presents after becoming cyanotic post-feeding, and then crying inconsolably. The foster mother reports this is the 2nd episode of this type. The 1st episode was last week after the baby made a bowel movement, but it resolved quickly. She does not know anything about the birth history of the baby, but knows the birth mother received no prenatal care. Upon cardiac exam a loud systolic ejection murmur is ascertained at the left upper sternal border. An EKG reveals normal sinus rhythm and the chest X-ray reveals a "boot shaped" cardiac shadow.
Question
What is the most likely diagnosis?

Answer Choices
1 Atrial septal defect
2 Coarctation of the aorta
3 Pulmonary stenosis
4 Tetralogy of Fallot
5 Ventricular septal defect
The clinical picture is suggestive of Tetralogy of Fallot. It is more common in Down Syndrome children, fetal alcohol syndrome children, as well as children born to women that do not receive pre-natal care. These infants often exhibit slowed growth and development, cyanosis at birth, and clubbing. An older child or adult may experience dyspnea with exertion that improves with squatting. In addition, at approximately 2-4 months of age "hypoxic spells" or "tet spells" are noted. They are described as prolonged crying spells with increasing cyanosis, and with crying there is a decrease in the intensity of the heart murmur. These spells usually occur after crying, feeding, or defecation. The heart murmur is usually audible at birth and described as a harsh systolic ejection murmur at the left upper sternal border. The EKG may reveal right ventricular hypertrophy or right atrial dilatation. The chest x-ray reveals a small heart size or "boot" shaped cardiac shadow.
A 41-year-old woman presents due to worsening symptoms. She was diagnosed with idiopathic pulmonary hypertension about 2 years prior to presentation; she is on home oxygen therapy. She has longstanding fatigue and dyspnea, but she is now experiencing profound dyspnea with exertion; swelling in her ankles; some discomfort in her right, upper abdomen; and the inability to breathe well when lying down. She has always been thin, but her weight has increased by 10 pounds in the last month. She denies fever and chills.

She recently had an electrocardiogram (ECG), but she has not seen a healthcare provider to discuss the results. The ECG report indicates peaked p waves, right axis deviation, and tall R wave in V1.

Question
What is the most appropriate intervention for her current condition?

Answer Choices
1 Prescribe a calcium channel blocker, such as verapamil
2 Prescribe a diuretic, such as furosemide
3 Prescribe a fluoroquinolone, such as levofloxacin
4 Prescribe a lipase inhibitor, such as orlistat
5 Prescribe a thiazolidinedione, such as pioglitazone
This patient is presenting with a progression of a primary pulmonary disease (pulmonary hypertension) into cor pulmonale, which is also known as pulmonary heart disease. Cor pulmonale, when moderate to severe, will present with signs and symptoms of right heart failure, such as the severely fluid overloaded state. In addition to treatment of the underlying pulmonary disorder, cor pulmonale is treated much like right-sided heart failure is treat. It would be most appropriate to prescribe a diuretic, such as furosemide, at this time. If possible, this patient should also be referred to a cardiopulmonary specialist.
A 62-year-old man presents at the coronary care unit following a massive anterolateral myocardial infarction. After coronary stenting and intensive care, he is fit for discharge, which occurs 10 days after initial admission. He is a known hypertensive and diabetic, and his conditions were well controlled prior to the attack. At the time of discharge, his BP is 120/70; pulse is 70/minute. Physical examination reveals no significant findings. An intern suggests placing the patient on spironolactone (Aldactone), quoting a recent study that he had read.
Question
What pathophysiologic mechanism of this disease does the intern aim to combat?

Answer Choices
1 Potassium retention by aldosterone
2 Potassium depletion by renin
3 Cardiac remodelling by aldosterone
4 Fluid retention by ADH
5 Hypertension by Aldosterone
Cardiac remodeling by aldosterone is the correct answer. Aldosterone acts on ventricular fibers both directly and indirectly, causing remodeling and thereby changing the shear stresses on the ventricular wall. The use of spironolactone, an aldosterone receptor blocker, prevents this remodeling.

Potassium retention by aldosterone is incorrect. Aldosterone causes potassium depletion, not retention.

Potassium depletion by renin is incorrect. Although spironolactone helps prevent potassium depletion by blocking the action of aldosterone, this is not the mechanism by which it prevents ventricular remodeling, thereby reducing mortality rates after a myocardial infarction.

Fluid retention by ADH is incorrect. Spironolactone acts on aldosterone receptors, not ADH.

Hypertension by aldosterone is incorrect. Spironolactone is a weak diuretic, and it has minimal antihypertensive efficacy.
A long-standing patient of yours is experiencing acutely worsening symptoms and signs of his dilated cardiomyopathy; symptoms include fatigue, dyspnea with mild exertion, paroxysmal nocturnal dyspnea, severe lower extremity edema, clubbing, an S3 gallop, and jugulovenous distention. Medications this patient is taking daily include a β-blocker, adult dose aspirin, and an ACE inhibitor.

Question
What clinical intervention would be the most logical next step in helping resolve his current symptoms?

Answer Choices
1 Initiation of a calcium channel blocker
2 Initiation of an aldosterone antagonist
3 Initiation of a statin
4 Initiation of a diuretic
5 Initiation of an angiotensin II antagonist
The correct answer at this point in time would be to start this patient on a diuretic agent. Diuretics are the most effective means of providing symptomatic relief to patients with exacerbations of signs and symptoms relating to their significant heart failure. Many of the signs and symptoms being relayed in the original stem point to significant pulmonary edema and/or congestion. This is a key characteristic in the overall pathology of dilated cardiomyopathy, along with other related consequences of ventricular dilation/dysfunction. Dilated cardiomyopathy is the cause in about 25% of all patients suffering from congestive heart failure.
A 69-year-old woman suffered a massive stroke 6 weeks ago. She is now recovering from the stroke, but she has residual paralysis and sensory impairment of her right arm. She is also unable to speak and unable to turn her eyes to the right. The most likely site of her lesion is in the area that is supplied by what artery?

Answer Choices
1 Right anterior cerebral artery
2 Left anterior cerebral artery
3 Right middle cerebral artery
4 Left middle cerebral artery
5 Left posterior cerebral artery
6 Right posterior cerebral artery
Left Middle Cerebral Artery

To determine the vessel involved, the site of the lesion must be determined. The sensory and motor homunculi are both located on the lateral surface of the cerebral hemispheres. Each half supplies the contralateral side of the body. From this, it is possible to determine that the area affected is on the lateral surface of the left cerebral hemisphere.

The motor and sensory homunculus are placed such that the lower half of the body is more medial and superior with the representation of the area below the knee extending on to the medial surface of the hemisphere.

The area that supplies the lateral surface of the cerebral hemisphere is the middle cerebral artery, except for a small band in the superior most aspect, which is supplied by the anterior cerebral artery. Thus, the area that is affected comes under the middle cerebral artery.

The left hemisphere is also the language side where connections exist among Wernicke's area, Broca's area, and the oral motor cortex. Both the Broca's motor area (area # 44) and the Wernicke's area are in the area supplied by the middle cerebral artery on the lateral aspect of the hemispheres.

Involvement of the posterior cerebral artery results in visual deficits.
A 66-year-old man with a past medical history of myocardial infarction 2 years ago, angina pectoris, aortic regurgitation, congestive heart failure, atrial fibrillation, and chronic obstructive pulmonary disease is presently being monitored in the hospital status-post admission for chest pain 1 day ago. Myocardial infarction has been ruled out. An EKG performed upon admission revealed a prolonged Qt interval and significant Q waves in the anterior leads. A diagnostic echocardiogram confirms moderate aortic and mitral valve regurgitation and a left-ventricular ejection fraction of 30%. He denies any complaints upon bedside evaluation. His physical exam reveals a blood pressure of 105/70 and tachycardia. Continuous bedside ECG monitoring notes wide, monomorphic QRS complexes with a heart rate of 160 beats per minute that spontaneously resolve within 20 seconds, reverting to the pattern identified upon admission.


Question
What antiarrhythmic agent is considered to be the pharmacologic treatment of choice in the management of this patient?
Answer Choices
1 Lidocaine
2 Procainamide
3 Verapamil
4 Sotalol
5 Amiodarone
Amiodarone
The bedside electrocardiogram was remarkable for nonsustained, monomorphic ventricular tachycardia. The patient with hemodynamically stable VT in the setting of significant left ventricular dysfunction should be treated with intravenous amiodarone. When antiarrhythmic drug therapy is chosen to prevent recurrence or when VT is accompanied by hemodynamic instability, amiodarone is the treatment of choice. Patients in VT with hemodynamic compromise, congestive heart failure, chest pain, or ischemia should be treated promptly with DC cardioversion.
A 46-year-old man presents for evaluation of his diabetes. He has been erratic with taking his medication. His BMI is 28 and BP is 155/100 mmHg; he exercises regularly. He currently smokes 1 pack of cigarettes per day. His lab values are as follows:

Blood Urea: 32 mg/dl

Creatinine: 1.4 mg/dl

Fasting Blood Sugar: 148 mg/dl

Post Prandial Blood Sugar: 213 mg/dl

HbA1c: 9.6%

HDL: 39 mg/dl

LDL: 131 mg/dl

Triglyderides: 280 mg/dl



Question
What is the best step in the management of his cholesterol levels?

Answer Choices
1 Recommend diet alone
2 Repeat the lipid profile after 6 weeks and reassess
3 Start him on a statin drug at this time
4 Recommend exercise alone
5 Start niacin for high triglycerides and vitamin deficiency
start him on statin
A 12-year-old presents with an injury of his left arm and leg. He states that he felt dizziness during the 2nd mile of the long distance run organized by the school. He fell and lost the consciousness for several seconds, but after that he felt "normal". His father has been diagnosed with Emery-Dreifuss muscular dystrophy type 1. On examination, you find a few superficial excoriations; there is also symmetric humero-peroneal weakness involving the biceps, triceps, and peroneal muscles. There is also atrophy and contractures of Achilles-heel, elbows, and posterior neck.



Question
After taking care of his injuries, what test should you order?

Answer Choices
1 CK
2 LDH
3 EKG
4 EEG
5 CT
EKG
Both family history and clinical presentation in this patient are consistent with Emery-Dreifuss muscular dystrophy. Cardiac disease in Emery-Dreifuss muscular dystrophy is nearly universal. It usually begins after the onset of weakness, and it manifests as syncope in the 2nd or 3rd decade of life; it can also be a cause of sudden cardiac death. Cardiac disease can take form of the bradycardia, atrial arrhythmias (including atrial fibrillation/flutter), AV conduction defect, or even atrial or ventricular cardiomyopathy. Pacemakers are often needed by the age of 30. Minimal follow up requirements in patients are annual cardiac assessment (ECG, Holter, echocardiography) and the monitoring of respiratory function.

In most cases of Emery-Dreifuss muscular dystrophy, CK levels are mildly elevated; however, CK values will not be useful in this case because both mild muscle injury and muscle exertion affect CK values.

The use of the test for lactate dehydrogenase (LDH) as a general indicator of the presence and the severity of the tissue damage (both acute and chronic) will not contribute to the management of Emery-Dreifuss muscular dystrophy.

EEG is most often used to diagnose epilepsy. The symptoms and clinical picture in this patient is however more consistent with a syncopal episode due to abnormal cardiac function.

CT is not indicated after a syncopal episode without head injury.
An 80-year-old man was treated for ventricular arrhythmias. He presents 1 month later with joint pain. He also has an unusual mask-like rash over his face and body. Discontinuation of drug therapy causes the symptoms to abate. What drug was most likely administered to this patient?

Answer Choices
1 Tocainide
2 Quinidine
3 Procainamide
4 Phenytoin
5 Propranolol
The correct response is procainamide.

This question addresses issues related to the treatment of arrhythmias and lupus-like side effects. The initial treatment should control arrhythmias using lidocaine, unload the heart using a balanced vasodilator such as nitroglycerin or nitroprusside, and use aspirin and heparin to prevent further clot formation. Once discharged, patients are frequently placed on atenolol to control catecholamine-induced arrhythmias. Finally, long-term control of arrhythmias is accomplished using drugs such as procainamide or quinidine. Unfortunately, procainamide can cause lupus-like side effects.

The use of thrombolytics has reduced myocardial damage caused by thrombus formation. Streptokinase, urokinase, and tissue plasminogen activator (tPA) all will lyse clots. This leads to coronary reperfusion. If performed within the first several hours post-clot, myocardium will be spared. The use of aspirin and heparin are directed at prevention of platelet aggregation and clot stabilization.
A 70-year-old woman with a history of hypertension, hyperlipidemia, and myocardial infarction presents with a 3-day history of shortness of breath at rest. She has found it difficult to walk short distances due to this shortness of breath. Additionally she complains of orthopnea and nocturnal dyspnea. She denies cough, fever, chills, nausea, abdominal pain, vomiting, diarrhea, rashes, and edema. Upon physical examination, the patient is short of breath and requires numerous pauses during conversation. She is tachycardic and diaphoretic, and her extremities are cool. There is a diminished first heart sound, S3 gallop, laterally displaced PMI, bibasilar rales and dullness to percussion, and expiratory wheezing noted. There is no JVD noted; however, 2+ pitting edema of the lower extremities to the level of the mid calf is evident.



Question
What diagnostic test result would be considered most useful in differentiating a cardiac from noncardiac cause of this patient's presentation?

Answer Choices
1 Hyponatremia on a basic metabolic profile
2 Elevations of T3 and T4 on thyroid assay
3 Sinus arrhythmia and low voltage on EKG
4 Pulmonary congestion pattern on the chest x-ray
5 Elevations of B-type natriuretic peptide
Elevations of B-type natriuretic peptide

This patient's presentation is consistent with congestive heart failure.

Rapid measurement of B-type natriuretic peptide (BNP) or its precursor, N-terminal proBNP (NT-proBNP), can aid clinicians in differentiating between cardiac and noncardiac causes of dyspnea. The major source of plasma BNP is the cardiac ventricles, and the release of BNP appears to be in direct proportion to ventricular volume and pressure overload. BNP levels greater than 80 pg/mL have a specificity greater than 95% and a sensitivity greater than 98% in the diagnosis of heart failure; higher BNP levels correlate with higher sensitivity and specificity of the presence of heart failure.

Electrolyte levels, thyroid assessments, EKG, and chest X-ray findings are important diagnostic modalities useful in the evaluation of CHF, but they cannot readily differentiate cardiac versus noncardiac causes of this patient's presentation to the extent of B-type natriuretic peptide.
A 42-year-old white female delivers her third child while you are on call at a local hospital on the Atlantic coast. She thanks you for your help and mentions that she is grateful that her baby was on time. She states that the family is planning on taking their newest with them to Colorado in 2 weeks. You advise her not to attempt the trip, as the baby will have difficulty adjusting to the high altitudes. Which of the following factors is a major component in closure of the ductus arteriosus?
Answer Choices
1 Increase in pulmonary arterial pressure associated with increase in blood flow to the lungs
2 Reduction of aortic arterial pressure due to reduction in systemic resistance
3 Decrease in carbon dioxide levels in the blood
4 Increase in oxygen tension within the blood
5 Presence of prostaglandin E2 in the wall of the ductus arteriosus
Increase in oxygen tension within the blood

Increase in oxygen tension is thought to be the primary initiator of closure of the ductus arteriosus. The pO2 increases from 15 to 20 mm Hg to around 100 mm Hg in a few hours.
A 50-year-old man presents with chest pain. The pain is substernal, described as sharp, worsens with inspiration, and improves with leaning forward. A pericardial friction rub is appreciated on auscultation.



Question
What EKG finding is expected with this patient's condition?

Answer Choices
1 Diffuse ST elevation
2 S1Q3T3 pattern
3 Delta waves
4 U waves
5 Sine wave pattern
Diffuse ST elevations

Diffuse ST elevation is correct. The history of pleuritic chest pain paired with a pericardial friction rub on examination is suggestive of pericarditis. Pericarditis is associated with diffuse ST elevation on electrocardiogram.
S1Q3T3
S1Q3T3 is associated with pulmonary embolism. While it is not always seen, when present, it is suggestive of pulmonary embolism.
Delta waves
The presence of delta waves indicates an accessory AV pathway, most likely Wolff-Parkinson-White syndrome.
U waves
U waves are associated with hypokalemia and medications such as quinidine and procainamide.
Sine wave
Sine wave pattern is associated with hyperkalemia.
A 68-year-old male presents with the complaint of palpitations in the center of his chest over the last few hours. The symptoms come and go, and last anywhere from 30 seconds to a few minutes. There is some associated lightheadedness with these episodes, and occasionally there is mild shortness of breath. While examining the patient, he has another episode. During this time, the patient's vital signs reveal a pulse of 170 and a blood pressure of 118/69. Based on this history and the findings on the exam and rhythm strip shown, what is the best treatment for this patient?

A Diltiazem
B Digoxin
C Lisinopril
D Metoprolol
E Amiodarone
E Amiodarone
This patient is having non-sustained ventricular tachycardia (NSVT). Based on the clinical presentation, this patient can benefit from an infusion of amiodarone. The dose is normally a 150mg bolus, followed by a drip of 1mg/min for the first 6 hours, then followed by 0.5mg/min for the next 18 to 24 hours.
The other agents would not be able to maintain a rhythm for this type of abnormality.
A 48-year-old African American male presents with dyspnea, 2-pillow orthopnea, and swelling to his lower legs that has developed over the last month. He also complains of fatigue and decreased exercise tolerance, stating that he has trouble climbing one flight of steps. On physical examination, his blood pressure is 178/98, pulse rate is 102, and respiratory rate is 20. There is 5 cm JVD, crackles at the bilateral lung fields, tachycardia, and an S3 is heard on cardiac auscultation. There is 2+ pitting edema to the lower extremities. His electrocardiogram reveals a sinus tachycardia at a rate of 105 and left ventricular hypertrophy. The chest x-ray reveals cardiomegaly with increased interstitial markings in all lung fields. There is a small right pleural effusion that blunts the costophrenic angle. He is on a thiazide diuretic. On repeat examination, the patient's blood pressure remains high. Which medication should be added to better control the patient's blood pressure?

A Lisinopril
B Diltiazem
C Spironolactone
D Amiodarone
E Hydralazine
A Lisinopril
The use of an ACE inhibitor is a logical second order medication for this patient. Along with the diuretic, the ACE will further lower blood pressure. Calcium channel blockers are not an optimal choice, as they can worsen heart failure. ACE inhibitors can also have a protective effect on renal function, as well as improve morbidity and mortality in diabetics. While hydralazine can also be used for pressure control, ACE inhibitors would be a choice above hydralazine.
What is the most common cause of restrictive cardiomyopathy?

A Amyloidosis
B Pericarditis
C Marfans syndrome
D Fatty infiltrative disease
E Sarcoidosis
A Amyloidosis
While restrictive cardiomyopathy is seen in such cases as hemochromatosis, glycogen deposition, endomyocardial fibrosis, sarcoidosis, hypereosinophilic disease, and scleroderma, amyloidosis is the most common cause among the choices provided.
What is the treatment for a patient who has recurrent ventricular tachycardia with no reversible cause, and has failed oral medication therapy?

A Biventricular pacemaker insertion
B Ablation therapy
C Heart transplantation
D Implantable defibrillator
E Single chamber pacemaker
D Implantable Defibrillator
Patients with recurrent symptoms benefit from the implantation of a defibrillator, which will reduce sudden death. Ablation therapy is usually not indicated. In rare cases of patients who do not have any other underlying disease, cardiac transplantation is an option. Pacemakers are options if the underlying rhythm is in need of pacing.
A 66-year-old female has a chief complaint of vision loss in her left eye. She denies pain and states that this occurred over the past few hours. Her past medical history includes hypertension, high cholesterol, and peripheral vascular disease. Upon funduscopic exam, you note marked hemorrhages in all quadrants and disc edema. The contralateral eye shows only mild hypertensive vascular changes. What is your diagnosis?

A Macular degeneration
B Retinal detachment
C Central retinal artery occlusion
D Cerebrovascular accident
E Central retinal vein occlusion
E central retinal vein occlusion
A central retinal vein occlusion is characterized by a "blood and thunder" fundus, with marked hemorrhages, tortuous vessels, and optic disc edema.
A 22-year-old African American male presents to the emergency department with shortness of breath, which started 2 hours prior to arrival. He does not have a history of pulmonary disease that he is aware of, and he states that in the past at random events he has had similar episodes. He does nothing to get the episodes to stop, and he also states that he feels his chest pounding at the same time of the shortness of breath. He has no medical history that he is aware of, and he takes no medications or any illicit drugs. On examination he is alert, awake, and oriented. His vital signs show T 99.0, P 142, R 18, and BP 132/82. His chest x-ray is negative for any acute cardiopulmonary disease, and his electrocardiogram has an irregularly irregular rate of 142 with visible delta waves.
Given the clinical situation above, what is the best medication for managing this patient's condition with a long-term approach?


A Amiodarone
B Atropine
C Hydralazine
D Flecainide
E Digoxin
Flecainide
This patient has Wolff-Parkinson-White (WPW) syndrome along with atrial fibrillation and a rapid ventricular response. Of the choices given in managing this patient's tachycardia, oral flecainide (D) will serve to slow the process within the accessory pathway and prolong the refractory period. Amiodarone (A) has been shown to not be effective in managing the patient's tachycardia with respect to WPW, and the other medications (B, C, and E) would not have an effect on the condition and may actually worsen the patient's symptoms.
WPW ekg
The diagnosis of WPW syndrome is typically made with a 12-lead electrocardiogram (ECG) and sometimes with ambulatory monitoring (eg, telemetry, Holter monitoring). Supraventricular tachycardia (SVT) is best diagnosed by documenting a 12-lead ECG during tachycardia, although it is often diagnosed with a monitoring strip or even recorder. The index of suspicion is based on the history, and rarely, physical examination (Ebstein anomaly or hypertrophic cardiomyopathy [HOCM]). Although the ECG morphology varies widely, the classic ECG features are as follows:

A shortened PR interval (often < 120 ms)
A slurring and slow rise of the initial upstroke of the QRS complex (delta wave)
A widened QRS complex (total duration >0.12 seconds)
ST segment-T wave changes, generally directed opposite the major delta wave and QRS complex
A 62-year-old man with a history of hypertension, diabetes mellitus type 2, hyperlipidemia, and chronic tobacco use presents to the office with complaints of a retrosternal chest pressure radiating down his left arm, associated with diaphoresis, nausea, and dyspnea, for the last 45 minutes after mowing his lawn. The patient's vital signs are stable, and on physical examination a new systolic murmur is appreciated. According to the most recent American College of Cardiology/American Heart Association Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation MI recommendations, an EKG should be performed on patients with a clinical suspicion for acute coronary syndrome within how many minutes of their arrival to the emergency department?

A 1 minute
B 5 minutes
C 10 minutes
D 15 minutes
E 20 minutes.
C 10 minutes
As the 2007 American College of Cardiology/American Heart Association Guidelines for Management of Patients with Unstable Angina/Non-ST-Elevation MI recommend that an ECG "be performed and shown to an experienced emergency physician as soon as possible after ED arrival, with a goal of within 10 minutes of ED arrival for all patients with chest discomfort or other symptoms suggestive of ACS." Although choices A and B would be optimal, the question asks for the goal time for which busy emergency departments should aim for in obtaining an EKG in at-risk patients. Choices D and E are less desirable, as times greater than 10 minutes increase both morbidity and mortality rates.
What is the most common heart sound that is heard in patients with pulmonary hypertension?

A S3 gallop
B S2 Split
C S4
D Normal S1S2
E Regularly irregular rhythm
B S2 split
The splitting on the second heart sound is also accompanied by the louder second sound of a split of the pulmonary component. There should not be a change in the rhythm with the patient due to pure pulmonary hypertension.
A 65-year-old man presents to the emergency department with an acute ischemic stroke. His CT scan is normal. His blood pressure is 180/100 mm Hg. What is the most appropriate treatment for his hypertension?

A labetalol (Normodyne) 20 mg IV
B nifedipine (Procardia) 10 mg po
C nitroprusside (Nipride) drip at 1 mg/kg/min
D clonidine (Catapres) 0.1 mg po
E no antihypertensive at this time
E no anti-hypertensive tx
Blood pressure is typically elevated at the time of presentation in acute ischemic stroke. It will decline without medication in the first few hours to days. Aggressively lowering blood pressure in an acute ischemic stroke may decrease the blood flow to the ischemic but salvageable brain tissue. This potentially salvageable brain tissue is referred to as the penumbra. Decreasing blood flow to the ischemic penumbra by acutely lowering blood pressure may result in eventual infarction of this brain tissue. Treatment of previously undiagnosed hypertension should be deferred for several days. Blood pressure should be treated if there are other indications, such as angina or heart failure. Control of blood pressure is appropriate in patients who are receiving tissue plasminogen activator (t-Pa) for their stroke. Blood pressure should be lowered cautiously to a systolic of less than 185 mm Hg and a diastolic of less than 110 mm Hg. This is thought to decrease the incidence of intracerebral hemorrhage in these patients.
A 54-year-old man presents with chest pain. He has a past medical history of hypertension and diabetes mellitus. The pain is located in the middle of his chest and radiates to his jaw. The pain began about 20 minutes ago, and he rates the pain as a 10 on a 0 - 10 point scale, with 10 being the worst pain he has ever felt. He has had 3 similar episodes, but they have always resolved after 5 minutes or so of rest. He has smoked 1 pack of cigarettes a day for the past 36 years. He drinks 2 or 3 beers on Friday nights. Review of systems (ROS) is positive for diaphoresis, acute dyspnea, and impending doom. ROS negative for fever, chills, and malaise. Physical exam shows an obese, middle-aged man in moderate distress. BP 126/80, pulse 100, respirations 26. Heart and lung exams are normal, except for tachycardia and tachypnea. He has no pedal edema.



Question
What aspect of the patient's history is the largest risk factor for an acute myocardial infarction?

Answer Choices
1 Alcohol use
2 Cigarette smoking
3 Diabetes mellitus
4 Hypertension
5 Obesity
Diabetes Mellitus
Diabetes mellitus (DM) is an independent risk factor for atherosclerosis. The risk of myocardial infarction (MI) in a patient with diabetes is the same risk as someone without diabetes who has had a previous MI. The risk of death from cardiac events is also the same between the 2 groups (1).

Other important contributors to atherosclerosis and ischemic heart disease, including dyslipidemia, cigarette smoking, obesity, and hypertension, contribute to the risk of MI; however, when evaluated independently, DM is a greater risk factor (2).

Alcohol consumption may have a protective effect. People who drink moderate amounts of alcohol reduce their risk of cardiovascular events (2).

Patients with diabetes mellitus should be advised to stop smoking and aggressively control other risk factors, such as glucose, hypertension, and dyslipidemia, in order to reduce the risk of ischemic heart disease.
A 48-year-old man with hypertension and coronary artery disease is evaluated for protracted fever, fatigue, anorexia, weight loss, night sweats, and nonspecific, nonradiating joint pains, which began following a routine dental cleaning. His physical exam is remarkable for a fever of 101.3 ° F, oral mucosa, conjunctival petechiae, palpable purpuric skin rashes, reduced bilateral peripheral pulsations, linear subungual hemorrhages, small, flat, irregular erythematous spots on the palms and soles, and tender, erythematous nodules occurring in the fingers. His funduscopic examination was remarkable for cytoid bodies and hemorrhages while his cardiac exam demonstrated a soft, medium-pitched holosystolic murmur located at the apex with radiation to the axilla. A comparison to the patient's last physical exam reveals no abnormal physical exam findings.
Question
What is the next most appropriate step in the management of this patient?

Answer Choices
1 Begin empiric treatment with IV ceftriaxone and gentamicin
2 Refer the patient for a cardiac MRI
3 Begin unfractionated intravenous heparin
4 Obtain specimen for blood cultures
5
Obtain a throat culture and anti-streptolysin O antibody levels
Obtain specimen for blood cultures
This patient's presentation is most consistent with native valve endocarditis caused by Viridans group streptococci (-hemolytic streptococci). These are a frequent cause of community-acquired native valve endocarditis. Viridans streptococci are normal residents of the oropharynx and easily gain access to the circulation after dental or gingival trauma.

The proper acquisition of blood cultures before initiation of antimicrobial therapy is essential. The importance of obtaining blood cultures by appropriate methods, before the institution of antibiotics, cannot be overemphasized. Three separate sets of blood cultures obtained from different venipuncture sites over 24 hours are recommended. For the most commonly encountered bacterial pathogens (staphylococci, streptococci, enterococci), the first two sets of blood cultures will be positive in the vast majority of cases. Following microbial identification, intravenous aqueous crystalline penicillin G or ceftriaxone and gentamicin is appropriate.

All patients with suspected infective endocarditis should undergo prompt echocardiographic assessment (either trans-thoracic echocardiography or trans-esophageal echocardiography), with the vast majority of patients undergoing initial trans-thoracic imaging because of its immediate availability. Although trans-esophageal echocardiography is invasive and requires conscious sedation, it has excellent specificity and offers better sensitivity for the detection of vegetations and intracardiac abscesses, and has greater spatial resolution than trans-thoracic echocardiography.

Despite their theoretical benefit, there are no human studies that support the use of either antiplatelet or antithrombin agents to prevent embolic complications or hasten antibiotic cure.

Throat cultures and anti-streptolysin antibody levels would be useful in the diagnostic approach of rheumatic fever, not endocarditis.
A 25-year-old woman presents with intermittent palpitations that are associated with lightheadedness; she admits to a past medical history of having a self-described "hole in her heart". These seem to occur upon significant exertion and when she is "stressed out." She denies chest pain, shortness of breath, wheezing, hemoptysis, cough, syncope, abdominal pain, rashes, peripheral edema, diaphoresis, and vomiting.

Her physical exam is remarkable for a mid-to-late systolic click; it is followed by a high-pitched, 'whooping' late systolic crescendo-decrescendo murmur, and it is heard best at the apex. The click occurs earlier with standing and upon Valsalva strain, and it also occurs later in the cardiac cycle with squatting and sustained handgrip.

Question
What is the most likely diagnosis?

Answer Choices
1 Aortic stenosis
2 Mitral valve prolapse
3 Ventricular septal defect
4 Aortic regurgitation
5 Mitral stenosis
Mitral Valve prolapse
This patient's diagnosis is mitral valve prolapse (MVP). It most commonly occurs in young women and in patients with heritable disorders of connective tissue, including Marfan's syndrome, osteogenesis imperfecta, and Ehlers-Danlos syndrome. Rarely, it occurs as a sequel to acute rheumatic fever, in ischemic heart disease, in various cardiomyopathies, as well as in 20% of patients with ostium secundum atrial septal defect.

MVP varies in its clinical expression, ranging from only a systolic click and murmur with mild prolapse of the posterior leaflet to severe mitral regurgitation due to chordal rupture and leaflet flail; in North America, MVP is now the most common cause of isolated severe MR requiring surgical treatment.

The most important finding is the mid- or late- (non-ejection) systolic click following S1, and it is thought to be generated by the sudden tensing of slack, elongated chordae tendineae or by the prolapsing mitral leaflet when it reaches its maximum excursion. Systolic clicks may be multiple, and representing mitral valve regurgitation, they may be followed by a high-pitched, late systolic crescendo-decrescendo murmur, occasionally 'whooping' or 'honking' and heard best at the apex. The click and murmur occur earlier with standing, during the strain phase of the Valsalva maneuver, and with any intervention that decreases LV volume, exaggerating the propensity of mitral leaflet prolapse. Conversely, squatting and isometric exercises, which increase LV volume, diminish MVP; the click-murmur complex is delayed, moves away from S1, and may even disappear.

Patients with MVP most frequently have symptoms of autonomic dysfunction, including easy fatigability, dizziness, and atypical chest pain. Further symptoms include palpitations, light-headedness, and syncope.

The murmur of aortic stenosis is characteristically an ejection (mid) systolic murmur that commences shortly after the S1, increases in intensity to reach a peak toward the middle of ejection, and ends just before aortic valve closure. It is characteristically low-pitched, rough and rasping in character, and loudest at the base of the heart, most commonly in the 2nd right intercostal space. It is transmitted upward along the carotid arteries. Exertional dyspnea, angina pectoris, and syncope are the 3 cardinal symptoms; they become most apparent beginning in the 6th decade.

Ventricular septal defect is the most common congenital cardiac malformation. Blood flows from the left ventricle to the right ventricle and presents as a harsh, blowing holosystolic murmur with a thrill localized to the 4th left intercostal space. This murmur may decrease with Valsalva and handgrip.

Findings consistent with aortic regurgitation consist of tachycardia and widened pulse pressures. The classic auscultatory finding is a decrescendo, diastolic, high-pitched murmur loudest at the left sternal border that is accentuated with the patient leaning forward in full expiration. An Austin-Flint murmur may be evident, characterized by a low-pitched, mid-diastolic rumbling murmur due to blood jets from the murmur striking the anterior leaflet of the mitral valve, which results in premature closure of the mitral leaflets. Corrigan pulse ('water-hammer' pulse) is described as an abrupt distention and quick collapse on palpation of the peripheral arterial pulse; booming systolic and diastolic sounds auscultated over the femoral arteries characterize Traube sign ('pistol-shot' pulse).

Rheumatic fever is the leading cause of mitral stenosis (MS). The first heart sound (S1) is usually accentuated and slightly delayed. The pulmonic component of the second heart sound (P2) also is often accentuated, and the 2 components of the second heart sound (S2) are closely split. The opening snap (OS) of the mitral valve is most readily audible in expiration at, or just medial to, the cardiac apex. It is followed by a low-pitched, rumbling, diastolic murmur; it is heard best at the apex with the patient in the left lateral recumbent position, and it is accentuated by mild exercise carried out just before auscultation.
You are called to the emergency department at 2 P.M. to see a 44-year-old male patient. He is a 3-pack-a-day, unfiltered cigarette smoker with crushing chest pains. He has a wide-complex, rapid, regular tachyarrhythmia at 160 beats per minute. When you reach his examination room, you note his monitor also reveals evidence of "P" waves at 75 beats per minute. What type of rhythm do his symptoms show?
Answer Choices
1 Paroxysmal supraventricular tachycardia
2 Sinus tachycardia
3 Ventricular tachycardia
4 Ventricular fibrillation
5 Asystole
Ventricular Tachycardia
Explanation The observation of a wide-complex tachyarrhythmia at a rate of 160 beats per minute associated with P waves at a rate of 75 beats per minute represents a total dissociation (AV Dissociation) between the atria (upper portions of the heart) and the ventricles (lower portions of the heart). A prudent provider will recognize that, in the presence of a rapid, wide complex tachyarrhythmia, AV Dissociation is the classic criterion of ventricular tachycardia (V.T.).
Having diagnosed ventricular tachycardia, you will endeavor to obtain a more complete history and reasonably complete medical physical examination. It is essential that you provide timely placement of this patient in a medical intensive care unit or a coronary care unit with placement on the critically ill list and advise out-of-town family to travel to visit him. Should the patient survive, then his healthcare providers will need to document his verbalized understanding of their medical professional advice in his chronological record of medical care, which includes the recommenadation that he stop smoking cigarettes immediately and abstains from smoking cigars and pipes as well as from chewing tobacco and dipping snuff.

Paroxysmal supraventricular tachycardia (PSVT) is a narrow-complex tachyarrhythmia. Sinus tachycardia is also a narrow-complex tachyarrhythmia. Ventricular fibrillation (V.F.) is a very chaotic tachyarrhythmia with no readily discernible P waves and no readily discernible QRS complexes. Asystole represents a total absence of cardiac contractions and is seen as a flat line on the monitor. Atrial fibrillation is both irregular and narrow-complex. These answers, therefore, are incorrect.
What is not a common cause of aortic stenosis?

Answer Choices
1 Rheumatic heart disease
2 Chronic intravenous drug abuse
3 Congenital bicuspid aortic valve
4 Monckeberg senile calcific changes
5 Age greater than 60 years
Chronic IVDA
Intravenous drug abuse has not been described as a common cause of aortic stenosis.

Common causes of aortic stenosis are:

Infants, children and adolescents
(a) congenital aortic stenosis
(b) congenital subvalvular aortic stenosis
(c) congenital supraclavicular aortic stenosis

Young adults to middle age:
(a) calcification and fibrosis of congenitally bicuspid aortic valve
(b) rheumatic aortic stenosis

Middle aged to elderly
(a) calcification of bicuspid valve
(b) senile degenerative aortic stenosis
(c) rheumatic aortic stenosis
A 55-year-old man presents with severe central chest pain. Pain started suddenly and it radiates to the back and neck. He is unable to lie flat. He feels sick but has not vomited. He has no major illnesses and knows of none that run in his family. He does not use alcohol, tobacco, or illicit substances. He is allergic to sulfa drugs.

On physical exam he appears in extreme pain and is lying on his side. Temperature - 37.0°C, heart rate 110, blood pressure 180/105 mmHg, respiratory rate 20. Cardiac exam reveals normal S1 and S2 without rubs or gallop. The top of his internal jugular venous column is present at 2 to 3 cm above the sterna notch. Chest auscultation shows normal vesicular breathing. He has normal active bowel sounds tympanic to percussion. Extremity exam is normal and the lower motor and sensory function is intact.

ECG shows left ventricular hypertrophy. Chest X-ray shows widened mediastinum.

Question
What treatment should be given immediately to this patient?

Answer Choices
1 Nitroglycerin spray
2 Intravenous labetalol
3 Streptokinase
4 Angioplasty
5 Surgery
Intravenous Labetolol
Aortic dissection is more common in patients with hypertension, connective tissue disorders, congenital aortic stenosis or bicuspid aortic valve, and in those with first-degree relatives with history of thoracic dissections.

Chest pain is the most common presenting symptom in patients with an aortic dissection. The pain is usually sudden and severe and described as ripping or tearing.

In all individuals with aortic dissections, medication should be used to control high blood pressure, if present. Intravenous beta blockers such as labetolol are effective at reducing blood pressure and heart rate. The target systolic blood pressure should be 100-120 mm Hg. The target heart rate should be 60 - 80 beats per minute.

The choice of definite treatment depends on the location of the dissection. For ascending aortic dissection, surgical management is superior to medical management. On the other hand, in the case of an uncomplicated distal aortic dissection (including abdominal aortic dissection), medical management is preferred over surgical treatment.

Nitroglycerin spray, angioplasty, and streptokinase are the treatment modalities for acute coronary syndrome.
Orthostatic Hypotension is defined as:
Drop in systolic pressure 20 mm Hg, drop in diastolic pressure of 10 mm Hg, increase in pulse of 20 beats per minute
A 65-year-old man presents with a 2-week history of progressive dyspnea, orthopnea, and pedal edema. His history is significant for heavy smoking (30 cigarettes/day for more than 40 years), a 20 pound weight loss over past 3 months, loss of appetite, and weakness. His physical examination reveals pulse - 130 per min., blood pressure - 105/90 mmHg, paradoxic pulse, distant heart sounds, nonpalpable cardiac impulse, slight dullness at both lung bases, and bilateral pedal edema. His chest X-ray shows enlarged cardiac silhouette and a large pericardial effusion; they are confirmed by echocardiography. Acid-fast staining of the pericardial fluid is negative for Acid-Fast Bacilli (AFB). CT scan reports are awaited. What is the most likely etiology of this pericardial effusion?

Answer Choices
1 Pulmonary TB
2 Viral pericarditis
3 Bacterial pericarditis
4 Malignant pericardial effusion
5 Congestive heart failure
Malignant Pericardial Effusion
The most likely etiology is a malignant pericardial effusion. Pericardial effusion is present in 20% of cancer patients. Cancer is the most frequent cause of pericardial tamponade, accounting for 16 to 41% of cases. This patient's smoking history, age, loss of appetite, and weight loss are strong predictors of malignant etiology. Lung and breast cancers are the most common cancers involving the pericardium; they are followed by leukemia, lymphoma, sarcoma, and melanoma. Unlike this case, malignant pericardial effusions are usually asymptomatic. When present, symptoms are nonspecific and can be obscured by symptoms of the malignancy. Only 30% of the effusions are correctly diagnosed ante-mortem. The diagnosis is most often suggested by enlarged cardiac silhouettes on chest X-ray and is confirmed by echocardiography. Cytology of the pericardial fluid for malignant cells can be performed. Pericardial biopsy in cases of malignant pericardial effusion is positive in only 55% of patients. Cardiac tamponade needs prompt treatment with pericardiocentesis to relieve the increased end-diastolic pressure and inadequate ventricular filling.

Pulmonary TB is suspected if the X-ray shows mottled shadows, particularly in the upper lobes. Acid-fast staining will be positive for AFB.

Viral pericarditis and bacterial pericarditis present chest pain over the anterior chest. As the patient inhales, the pain exacerbates and it is usually associated with tachycardia. A low-grade fever may also be present.

Congestive heart failure is characterized by weakness, breathlessness, abdominal discomfort, and edema in lower portions of the body. The chest X-ray may show cardiac enlargement via increased size of the left ventricular shadow. There may be pulmonary congestion with audible rales. Echocardiography confirms the diagnosis.
A 24-year-old woman with no significant past medical history presents for her yearly medical examination. She denies any medical problems. Her cardiac exam is notable for a mid-systolic click. This finding precedes a high-pitched, late systolic crescendo-decrescendo murmur, described as "whooping" or "honking," and was heard best at the apex and is without radiation. The provider noticed that these sounds occurred earlier in the cardiac cycle when the patient was standing and during the Valsalva maneuver, and later when she squatted or during handgrip.



Question
What is the most likely diagnosis?

Answer Choices
1 Aortic regurgitation
2 Aortic stenosis
3 Mitral stenosis
4 Mitral regurgitation
5 Mitral valve prolapse
Mitral Valve prolapse
This patient's diagnosis is mitral valve prolapse (MVP). Most patients are asymptomatic, and it is more common in women and occurs most frequently between the ages of 15 and 30 years. The clinical course is most often benign. The most important finding is the mid- or late (nonejection) systolic click. Systolic clicks may be multiple and may be followed by a high-pitched, late systolic crescendo-decrescendo murmur, which occasionally is "whooping" or "honking" and is heard best at the apex. The click and murmur occur earlier with standing, during the strain phase of the Valsalva maneuver, and with any intervention that decreases left ventricular (LV) volume, exaggerating the propensity of mitral leaflet prolapse. Squatting and isometric exercises (handgrip), which increase LV volume, diminish MVP; the click-murmur complex is delayed, moves away from S1, and may even disappear.

Findings consistent with aortic regurgitation consist of tachycardia and widened pulse pressures. The classic auscultatory finding is a decrescendo, diastolic, high-pitched murmur loudest at the left sternal border that is accentuated with the patient leaning forward in full expiration. An Austin-Flint murmur may be evident, characterized by a low-pitched, mid-diastolic rumbling murmur due to blood jets from the murmur striking the anterior leaflet of the mitral valve, which results in premature closure of the mitral leaflets. Corrigan pulse ("water-hammer" pulse) is described as an abrupt distention and quick collapse on palpation of the peripheral arterial pulse; booming systolic and diastolic sounds auscultated over the femoral arteries represent Traube sign ("pistol-shot" pulse).

The murmur of aortic stenosis is characteristically an ejection (mid) systolic murmur that commences shortly after the S1, increases in intensity to reach a peak toward the middle of ejection and ends just before aortic valve closure. It is characteristically low-pitched, rough, and rasping in character, and loudest at the base of the heart, most commonly in the second right intercostal space. It is transmitted upward along the carotid arteries. Exertional dyspnea, angina pectoris, and syncope are the three cardinal symptoms, which become most apparent beginning in the sixth decade.

Rheumatic fever is the leading cause of mitral stenosis (MS). The first heart sound (S1) is usually accentuated and slightly delayed. The pulmonic component of the second heart sound (P2) also is often accentuated, and the two components of the second heart sound (S2) are closely split. The opening snap (OS) of the mitral valve is most readily audible in expiration at, or just medial to, the cardiac apex. It is followed by a low-pitched, rumbling, diastolic murmur, heard best at the apex with the patient in the left lateral recumbent position; it is accentuated by mild exercise carried out just before auscultation.

Although usually asymptomatic in mild disease, fatigue, exertional dyspnea, and orthopnea are the most prominent complaints in patients with chronic severe mitral regurgitation (MR). On auscultation, S1 is generally absent, soft, or buried in the holosystolic murmur of chronic MR. In patients with severe MR, the aortic valve may close prematurely, resulting in wide but physiologic splitting of S2.

A systolic murmur of at least grade III/VI intensity is the most characteristic auscultatory finding in chronic severe MR. It is usually holosystolic, is decrescendo, and ceases in mid- to late systole in patients with acute severe MR. The systolic murmur of chronic MR is usually most prominent at the apex and radiates to the axilla. The systolic murmur of chronic MR not due to MVP is intensified by isometric exercise (handgrip) but is reduced during the strain phase of the Valsalva maneuver because of the associated decrease in LV preload.
A 50-year-old man presents to your office for a follow up appointment of his hypertension. He has complaints of some non-specific chest discomfort, so you decide to perform an ECG. The ECG demonstrates peaked T waves in several leads without any other abnormality.


Question
Which of the following medications is most likely to cause this ECG finding?
Answer Choices
1 Lisinopril
2 Furosemide
3 Atenolol
4 Hydrocholorothiazide
5 Prazosin
Lisinopril
Explanation The correct answer is lisinopril, as it is an angiotensin converting enzyme inhibitor that blocks the production of aldosterone, leading to possible hyperkalemia. Peaked T waves on ECG are indicative of hyperkalemia.
Furosemide is a loop diuretic and is associated with hypokalemia. Atenolol is a beta-blocker and is not associated with hyperkalemia. Hydrochlorothiazide is a thiazide diuretic and may cause potassium loss. Prazosin is an alpha-blocker antihypertensive and is not associated with hyperkalemia.
A 77-year-old man presents with significant persistent hypotension that has been worsening for 1 hour. Further investigation of this patient reveals a significant increase in the patient's heart rate as well as substantial tachypnea. Urinary output is too minimal to measure, and upon quick physical examination, the patient's extremities are cool to touch. After beginning fluid resuscitation for shock protocol, the patient's symptoms appear to be worsening.



Question
Based on this scenario, what type of shock would this patient be categorized as having?

Answer Choices
1 Obstructive shock
2 Distributive shock
3 Cardiogenic shock
4 Septic shock
5 Hypotensive shock
Cardiogenic shock
Explanation
The correct response is cardiogenic shock.

Early identification of shock is a necessity to help improve any patient's chance of survival and recovery. It is also critical to lead to reversing the cause of the shock and initiating early resuscitation efforts. Early on, patients suffering from shock may have only a few or very subtle symptoms such as tachypnea, tachycardia, hyper or hypothermia, weak or bounding peripheral pulses, delayed capillary refill, or even pale or cool skin. Decreased mental status, weak or absent central pulses, central cyanosis, hypotension or bradycardia are ominous and later signs indicating the shock has progressed.

Shock is generally classified into 4 major categories, depending on the etiology of the hock: cardiogenic, hypovolemic, distributive, or obstructive. Cardiogenicshock occurs as a consequence of cardiac pump failure. Myopathic, mechanical, or arrhythmic issues lead to cardiogenic shock. Whatever the cause there is typically an acute loss of 15 - 20% of circulating blood volume that leads to lack of blood to pump throughout the circulatory system.

The prompt treatment of hypoperfusion and hypotension is essential in the initial management of cardiogenic shock. This is usually initiated by use of vasopressors or inotropic agents. Usually both pharmacologic as well as nonpharmacolgic methods of circulation support are promptly initiated to reverse hypotension, maintain vital organ perfusion, and maintain coronary perfusion pressures as high as possible until intervention of the etiology of the cardiogenic shock can be treated. Administering fluids will worsen the signs and symptoms that a patient is displaying who is has cardiogenic shock.
A 62-year-old woman with past medical history of hyperlipidemia presents due to shortness of breath. She is a nonsmoker and drinks a pint of vodka daily. Chest X-ray reveals severe cardiomegaly. She is ultimately diagnosed with cardiomyopathy.



Question
What type of cardiomyopathy does the patient most likely have?

Answer Choices
1 Dilated cardiomyopathy
2 Hypertrophic cardiomyopathy
3 Restrictive cardiomyopathy
4 Takotsubo cardiomyopathy
5 Postpartum cardiomyopathy
Dilated Cardiomyopathy
Explanation
The above patient is most likely suffering from dilated cardiomyopathy. Dilated cardiomyopathy occurs when the left ventricle dilates and is unable to pump blood effectively. Patients may develop symptoms of congestive heart failure, with dyspnea as the most common presenting complaint. Chest X-ray will reveal cardiomegaly, due to the dilatation of the left ventricle. Alcohol abuse is a risk factor for the development of dilated cardiomyopathy. Patients with dilated cardiomyopathy are encouraged to abstain from alcohol use.

Hypertrophic cardiomyopathy is less likely given the patient's age. Patients with hypertrophic cardiomyopathy typically present in early adulthood and have a familial history of hypertrophic cardiomyopathy. Chest X-ray may reveal cardiomegaly, but it is typically less marked than what would be seen in dilated cardiomyopathy.

Restrictive cardiomyopathy is less likely given the patient's history of alcohol abuse. Restrictive cardiomyopathy is relatively rare and is typically caused by amyloidosis. Chest X-ray may reveal cardiomegaly, but the patient's past medical and social history make dilated cardiomyopathy more likely.

Takotsubo cardiomyopathy is unlikely given the patient's chest X-ray findings. Patients with Takotsubo cardiomyopathy typically do not have cardiomegaly on chest X-ray.

Postpartum cardiomyopathy is an incorrect answer; the patient is not of childbearing age.
A 36-year-old woman presents with chronic dyspnea that is worse while lying prone.
The patient reports progressive worsening of the symptoms. On physical examination, a heart murmur is detected upon cardiac auscultation, heard best with the bell over the apex. The murmur is a non-radiating, low-pitched diastolic rumble. A loud S1 and opening snap can also be heard in addition to an apical thrill and decreased pulse pressure. An EKG is done and shows an arrhythmia. What is the patient's most likely underlying condition?

Answer Choices
1 Aortic regurgitation
2 Pulmonic stenosis
3 Mitral stenosis
4 Hypertrophic subaortic stenosis
5 Mitral valve prolapse
Mitral Stenosis
Explanation This patient has mitral stenosis. Dyspnea and orthopnea are symptoms that can be seen with mitral stenosis. The murmur of mitral stenosis is heard best over the apex area with the bell. It is a non-radiating, low-pitched diastolic rumble. A loud S1 and opening snap is consistent with mitral stenosis. Atrial fibrillation can sometimes be seen because of dilation of the left atrium. Mitral stenosis most often occurs after an episode of rheumatic fever.
Physical findings most consistent with an aortic regurgitation include a diastolic decrescendo murmur and increased pulse pressure.

Patients with pulmonic stenosis usually exhibit harsh, systolic ejection murmurs best heard over the pulmonic area. A wide split S2 and opening click after S1 can also be auscultated.

In patients with mitral valve prolapse, a heart murmur is best auscultated at the apex. There will also be a presence of a late systolic murmur, mud-systolic click, and a widely split S2.

Physical findings of hypertrophic subaortic stenosis include a murmur heard best at apex and left sternal border, and a systolic ejection murmur.
A 56-year-old patient presents to the office with a complaint of a discoloration of her fingertips over the past few months. The symptoms have been recurrent and worsening. Upon clinical exam, the tips of all fingers present with splinter hemorrhages. What is the most likely diagnosis for this finding??

Answer Choices
1 Vasculitis
2 Wilson's disease
3 Argyria
4 CHF
5 Nutritional disorder
Vasculitis

Explanation
Congestive heart failure, right sided, is associated with the finding of a red lunulae.

With a diagnosis of Wilson's disease, blue lunulae of the nails are often found.

1Argyria, (silver poisoning), often shows up in a clinical exam with gray lunulae of the nails. In chronic argyria, a permanent ashen gray appearance of the skin is noted.

Vasculitisis associated with splinter hemorrhages of the finger and toenails.

Nutritional disorders generally associated with changes in the nail itself. Often ridges, longitudinal or horizontal, are indicative of nutritional disorders.
A 58-year-old man who is a long standing patient of yours is experiencing worsening symptoms and signs of his dilated cardiomyopathy; symptoms include fatigue, dyspnea with mild exertion, paroxysmal nocturnal dyspnea, severe lower extremity edema, clubbing, an S3 gallop, and jugulovenous distention. Medications that this patient is taking on a daily basis include a β-blocker, adult dose aspirin, and an ACE inhibitor.



Question
What intervention would be the most logical next step in helping resolve his current symptoms?

Answer Choices
1 Initiation of a calcium channel blocker
2 Initiation of an aldosterone antagonist
3 Initiation of a statin
4 Initiation of a diuretic
5 Initiation of an angiotensin II antagonist
diuretic
the correct answer at this point in time would be to start this patient on a diuretic agent. Diuretics are the most effective means of providing symptomatic relief to patients with significant heart failure. Many of the signs and symptoms being relayed in the original stem point to significant pulmonary edema and/or congestion. This is a key characteristic of the overall pathology of dilated cardiomyopathy, along with other related consequences of ventricular dilation/dysfunction. Dilated cardiomyopathy is the etiology in about 25% of all patients suffering from congestive heart failure.

Calcium channel blockers should be avoided unless they are absolutely necessary for rate control (as in cases of atrial fibrillation). Nothing in the case suggests that the patient is currently in atrial fibrillation.

Evidence is currently lacking in regard to the initiation of angiotensin II receptor blockers improving the morbidity and mortality in patients such as the one described above.

Aldosterone antagonists are used primarily in patients with a history of hypertrophic or fibrotic cardiomyopathy; this patient is suffering from dilated cardiomyopathy.

Statin therapy's main goal is to lower lipid levels; it is seen as part of secondary treatment and the prevention of cardiovascular disease. This factor is most likely not related to the signs and symptoms currently presenting in this patient.
A 3-month-old term infant presents for a wellness exam, and his parents report worsening in his feeding habits and rapid breathing. On exam, there is a grade III/VI harsh heart murmur heard over the left subclavicular region that starts in early systole, peaks at S2, and decrescendos until the next S1. The infant is tachypneic and has bounding pulses of his upper and lower extremities. All other findings are within normal limits. A chest x-ray shows an enlarged left ventricle and atrium and increased pulmonary vasculature markings.



Question
Based on the above findings, what is the most likely diagnosis?

Answer Choices
1 Atrial Septal Defect
2 Congenital Pulmonic Valve Stenosis
3 Ventricular Septal Defect
4 Patent Ductus Arteriosus
5 Congenital Aortic Valve Stenosis
PDA
The correct answer is patent ductus arteriosus (PDA), because this is a continuous murmur heard throughout S1 and S2 with a crescendo decrescendo sound. Patients often experience exercise intolerance, palpitations, tachycardia, dyspnea, and fatigue at an older age. As an infant, they can present with early congestive heart failure symptoms, tachycardia, poor feeding, slow growth, tachypnea, and recurrent lower respiratory tract infections. The murmur is best heard over the left subclavicular region. With a large sized PDA, chest x-ray findings show enlargement of the left ventricle and left atria. There is also an increase in pulmonary vasculature. This is due to the left-to-right shunting, which causes volume overload and enlargement of these areas.

Atrial septal defect (ASD) is incorrect because the murmur is a widened, fixed splitting pattern during S2. The systolic murmur is heard at the upper left sternal border. On chest x-ray, there is enlargement of the right atrial and right ventricle because of the left-to-right shunting that occurs.

Congenital pulmonic valve stenosis is incorrect because this tends to be asymptomatic. If symptoms do occur, they present with right-sided heart failure, abdominal fullness, and pedal edema in advanced disease. On exam, a prominent a wave is present, and a right ventricular heave is palpated. The murmur is a loud, late-peaking crescendo decrescendo systolic ejection murmur heart at the upper left sternal border.

Ventricular septal defect is incorrect because this is a harsh, holosystolic murmur heard best at the left sternal border. Most people remain asymptomatic. A systolic thrill is often palpated on exam.

Congenital aortic valve stenosis is incorrect because this is a harsh, crescendo decrescendo systolic murmur. It is loudest at the base of the heart and radiates to the neck. This is present from birth unlike the murmurs in ASD, VSD, and PDA.
A 1-month-old full term male infant has been diagnosed with Tetralogy of Fallot. His disease is being classified as moderate, and he has been admitted to the neonatal intensive care unit for monitoring. He is now stable and is doing well. During a consultation between the newborn's parents and the pediatric cardiologist, treatment options are being discussed.


Question
What is the pediatric cardiologist likely to recommend as definitive treatment?
Answer Choices
1 Chronic oral β-blocking agents
2 No treatment, as this disease is self-limiting
3 Closure of ventricular septal defect and pulmonary valvulotomy
4 Closure of atrial septal defect and aortic valvulotomy
5 Closure of atrial septal defect and pulmonary valvulotomy
Explanation The correct answer is 'closure of ventricular septal defect and pulmonary valvulotomy.' Tetrology of Fallot (ToF) is the most common cyanotic congenital heart disease and accounts for about 10% of all congenital heart disease. In ToF, a ventricular septal defect is present, as is an obstruction to right ventricular outflow. The other 2 characteristics include right ventricular hypertrophy and an overriding aorta. The degree of right ventricular outflow obstruction determines the severity of symptoms. Most patients experience episodes of cyanosis, and some may have delayed development or retarded growth. Diagnosis is typically made with imaging, such as echocardiogram. Definitive total corrective treatment is usually achieved between birth and age 2. It involves closure of the ventricular septal defect and removal of the obstruction to right ventricular outflow. Since pulmonic stenosis is the etiology, pulmonary valvulotomy will relieve the right ventricular outflow.

'Chronic oral β-blocking agents' is not the correct answer. In cases where infants are markedly symptomatic and surgery has been deemed too dangerous, palliative treatments may be attempted. There are some surgical palliative measures, such as creation of a systemic arterial to pulmonary arterial anastomosis or balloon angioplasty to dilate the pulmonic valve. Another palliative measure that some institutions will use would be chronic oral β-blocking agents. However, this infant is stable, and chronic oral β-blocking agents do not represent "definitive" treatment.

'No treatment, as this disease is self-limiting' is not the correct answer. ToF is not a self-limiting disorder, and all children require open heart surgery as long as they can tolerate surgery. Complete repair usually occurs by age 2, but as long as it occurs by age 5, the results are usually fair to good.

'Closure of atrial septal defect and aortic valvulotomy' is not the correct answer. ToF has a ventricular septal defect, as opposed to an atrial septal defect. The pulmonic valve is stenotic, requiring valvulotomy rather than the aortic valve needing valvulotomy.

'Closure of atrial septal defect and pulmonary valvulotomy' is not the correct answer. While the pulmonic valvulotomy is part of the correct treatment, Tof has a ventricular septal defect, as opposed to an atrial septal defect.
LBBB
Left bundle branch block is often a marker of 1 of 4 underlying conditions associated with increased risk of cardiovascular morbidity and mortality rates. These include coronary heart disease associated with impaired left ventricular function, hypertensive heart disease, aortic valve disease, and cardiomyopathy. Bundle branch blocks may be chronic or intermittent. A bundle branch block may be rate-related; for example, it often occurs when the heart rate exceeds some critical value.
EKG of Mitral Valve Prolapse
Inverted T Waves in leads II, III, and AVF are encountered EKG findings found in mitral valve prolapse.
A 60-year-old man, following up after a recent myocardial infarction, presents with sharp inspiratory chest pain. Other than his recent myocardial infarction, his past medical history is significant for peptic ulcer and renal insufficiency. You suspect Dressler's syndrome after seeing diffuse ST elevations on an electrocardiogram. What is the most appropriate treatment for this patient?
Answer Choices
1 Indomethacin
2 Ibuprofen
3 A corticosteroid taper
4 Hydrocodone
5 Diclofenac sodium
A corticosteroid taper
Explanation Administering a corticosteroid taper in this patient is the safest option given his peptic ulcer history and renal insufficiency.
Indomethacin is incorrect because of the history of peptic ulcer disease and renal insufficiency.

Ibuprofen is incorrect because of the history of peptic ulcer disease and renal insufficiency.

Hydrocodone is incorrect because the patient has pain secondary to inflammation, and an agent with anti-inflammatory properties will best suit him.

Diclofenac sodium is incorrect because of the history of peptic ulcer disease and renal insufficiency.
Dressler's Syndrome
Dressler's syndrome is a type of pericarditis — inflammation of the sac surrounding the heart (pericardium). Dressler's syndrome is believed to be an immune system response after damage to heart tissue or to the pericardium, from events such as a heart attack, surgery or traumatic injury. Symptoms include chest pain, which may be similar to chest pain experienced during a heart attack.

Dressler's syndrome may also be called postpericardiotomy syndrome, post-myocardial infarction syndrome and post-cardiac injury syndrome. With recent improvements in heart attack treatment, Dressler's syndrome is less common than it used to be.
A 76-year-old man presents with progressive exertional dyspnea associated with substernal chest pain, easy fatigability, and dizziness. Symptoms are exacerbated with walking short distances, and they are relieved with rest. He denies fever, chills, cough, wheezing, pleurisy, calf pain, abdominal complaints, peripheral edema, cigarette, drug, or alcohol use, sick contacts, and travel. His physical exam reveals hypertension and a rough, harsh, low-pitched crescendo-decrescendo systolic murmur beginning after the first heart sound; it is best heard at the second intercostal space in the right upper sternal border. Its intensity is increased toward midsystole; the murmur radiates to both carotid arteries. It is accentuated upon squatting and reduced during Valsalva strain.

Question
What regarding the management of this patient is correct?

Answer Choices
1 β-adrenergic blocker therapy is contraindicated in this patient
2 An increase in aerobic activity to improve conditioning is recommended
3 Maximum reduction of preload and afterload with ACE inhibitors is necessary
4 Surgical intervention provides the only definitive treatment
5 Bacterial endocarditis prophylaxis is required in patients with this diagnosis
Surgical intervention provides the only definitive treatment
Explanation-
This patient's presentation is significant for aortic stenosis. The only definitive treatment for aortic stenosis is aortic valve replacement. The development of symptoms due to aortic stenosis provides a clear indication for replacement. For patients who are not candidates for aortic replacement, percutaneous aortic balloon valvuloplasty may provide some symptom relief.

In cases of moderate aortic stenosis, moderate-to-severe physical exertion and competitive sports should be avoided.

Beta-blockers might be used if the predominant symptom is angina.

The medical treatment options are limited in symptomatic patients with aortic stenosis who are not candidates for surgery. Those with pulmonary congestion may benefit from cautious use of digitalis, diuretics, and angiotensin-converting enzyme (ACE) inhibitors.

Although vasodilators may be used for heart failure and for hypertension associated with aortic stenosis, they should be used with extreme caution in order to prevent excessive decreases in preload or systemic arterial blood pressure. Reducing the blood pressure to normal levels in patients with hypertension and aortic stenosis is advisable, but hypotension must be avoided.

Antibiotic prophylaxis for the prevention of bacterial endocarditis is no longer recommended in patients with valvular aortic stenosis.
A 45-year-old man presents to the ER complaining of tearing chest pain that radiates to his back. He has known coronary artery disease and a previous history of myocardial infarction. Vital signs reveal a blood pressure of 150/90 mm Hg and a heart rate of 120/min. After a titration of esmolol was started his blood pressure was 110/70 mm hg and his heart rate was 70/min. An electrocardiogram revealed new ischemic changes. A CT scan reveals a proximal aortic dissection. The patient does not demonstrate any signs of limb malperfusion or renal insufficiency.


Question
What is the next step?
Answer Choices
1 Obtain a cardiac catheterization
2 Proceed immediately to the operating room for repair of the dissection
3 Add a nitroprusside infusion
4 Continue the esmolol infusion and monitor patient closely
5 Obtain an echocardiogram to evaluate for the presence of pericardial effusion
obtain a cardiac catheterization

Explanation Cardiac catheterization is warranted in this patient because of his history of coronary artery disease and myocardial infarction, as well as new ischemic changes on the electrocardiogram.
This patient will most likely proceed to the operating room but there is no evidence of hemodynamic instability and the patient is stable. He should be evaluated by catheterization for the need of concomitant bypass grafting at the time of aortic dissection repair. Therefore proceeding to the OR immediately is incorrect.

Adding a nitroprusside infusion is not necessary at this time as he has adequate heart rate and blood pressure control on esmolol.

Continuing the esmolol infusion and monitoring is also important but this patient also needs further workup, i.e. cardiac catheterization, prior to going to the operating room.

It is not necessary to perform an echocardiogram to evaluate for presence of a pericardial effusion because it would have shown up on the CT scan.
A preterm female infant born to a 32-year-old woman with no known past medical illnesses presents for the infant's 1-week follow-up. The mother reports that the patient is behaving normally and is feeding well. The physical exam is remarkable for a murmur, which is located at the 2nd left intercostal space. The murmur is continuous throughout cardiac systole and diastole, nonradiating, and of a "machinery" quality. Additionally, there is a widened pulse pressure. The skin and mucosa is without cyanosis, and there is no evidence of fluid retention.



Question
Based upon the physical exam finding, what is the most likely diagnosis?

Answer Choices
1 Atrial septal defect
2 Ventricular septal defect
3 Tetralogy of Fallot
4 Patent ductus arteriosus
5 Pulmonary stenosis
PDA
This infant is most likely exhibiting signs consistent with patent ductus arteriosus. Patent ductus occurs more commonly in females and has an incidence rate of up to 50% in infants born with a birth weight of less than 1 kilogram. Patent ductus arteriosus is characterized by an abnormal patency of the ductus arteriosus, which diverts blood from the right side of the heart to the systemic circulation during fetal life. Blood typically shunts from the higher-pressured left side (systemic circulation) to the lower-pressured right side (pulmonary circulation).

Normally, this ductus closes following spontaneous respiration of the newborn, as well as a lowering of endogenous prostaglandin and adenosine levels. The patency is normally sealed with fibrous tissue following a duration of 2 - 3 weeks.

Atrial septal defect is characterized by a shunting of blood from the left atrium to the right atrium, whose murmur is mild in intensity, located in the pulmonic area, and is associated with a widely-split S2 heart sound.

Ventricular septal defect is the most common congenital cardiac malformation. Blood flows from the left ventricle to the right ventricle and presents as a harsh, blowing holosystolic murmur with a thrill localized to the fourth left intercostal space. This murmur may decrease with Valsalva and handgrip.

Tetralogy of Fallot is the most common cyanotic congenital heart defect. There are 4 associated defects, which include: 1) ventricular septal defect; 2) dextroposition or overriding of the aorta upon the right ventricle; 3) pulmonic valve stenosis; and 4) right ventricular hypertrophy. Cyanosis is caused by a right-to-left shunt across the ventricular septal defect. A harsh systolic ejection murmur along the narrowed right ventricular outflow track is typical.

Pulmonary stenosis is crescendo-decrescendo and is characterized by a harsh systolic murmur in the 2nd and 3rd left interspaces, with a medium pitch. It may radiate to the left shoulder and neck, and if severe, be associated with a widely-split S2 with a diminished or inaudible pulmonic component.
A 22-year-old woman presents due to palpitations. She denies chest pain and shortness of breath; she has not had any recent infections. Aside from a tonsillectomy as a child, she has no significant past medical history. Examination reveals a thin woman in no acute distress. Lungs are clear to auscultation bilaterally. Cardiac exam reveals a mid-systolic click.
Question
What is the most likely diagnosis?

Answer Choices
1 Mitral valve prolapse
2 Mitral stenosis
3 Mitral regurgitation
4 Aortic stenosis
5 Aortic regurgitation
The above patient is suffering from mitral valve prolapse. Mitral valve prolapse occurs when the mitral valve protrudes back into the left atrium. It is most frequently found in young, thin women. Patients may be asymptomatic, or they may experience dyspnea, fatigue, palpitations, and chest pain. Mitral valve prolapse will produce a mid-systolic click on auscultation.

Mitral stenosis occurs when the mitral valve becomes narrowed, which is often due to rheumatic fever or congenital heart disease. Patients may also complain of similar symptoms, but they will have an opening snap and diastolic murmur on cardiac auscultation.

Mitral regurgitation may be caused by mitral valve prolapse. However, this patient has only a mid-systolic click on cardiac examination, and if her mitral valve prolapse had progressed to mitral regurgitation, then a pansystolic murmur would be heard.

Aortic stenosis develops due to either congenital narrowing of the aortic valve or calcification of the aortic valve. Patients will have a systolic ejection murmur on examination, which may radiate into the neck.

Aortic regurgitation is associated with rheumatic heart disease, congenital abnormalities, infection, and hypertension. It is associated with a diastolic murmur.
A 79-year-old man with a past medical history of diabetes mellitus, hypertension, and hyperlipidemia presents with severe chest pain and dyspnea. He appears pale, apprehensive, and diaphoretic. He is in a confused state and agitated. His pulse is weak and tachycardic, with a systolic blood pressure of 60 mmHg. He has a narrow pulse pressure, tachypnea, a weak apical impulse, and significant jugular venous distention. His lungs are free of crackles. Bedside electrocardiogram reveals ST-segment elevations in the anterior and septal leads.



Question
What is the preferred initial pharmacologic agent of choice for this patient?

Answer Choices
1 Phenylephrine
2 Norepinephrine
3 Metoprolol
4 Dobutamine
5 Dopamine
dopamine
This patient's exhibits signs and symptoms of cardiogenic shock due to myocardial infarction.

Treatment of cardiogenic shock includes general supportive measures of oxygen, aspirin, heparin, and 'gentle' fluid challenges (250 cc) if there is no overt pulmonary edema.

For more serious hypotension (MAP < 70 mm Hg), dopamine or norepinephrine may be given, with a target systolic pressure of 80 to 90 mm Hg (and not > 110 mm Hg).

Norepinephrine is a potent alpha-adrenergic agonist with minimal beta-adrenergic agonist effects. Norepinephrine can increase blood pressure successfully in patients who remain hypotensive following dopamine.

Dopamine is a precursor of norepinephrine and epinephrine and has varying effects according to the doses infused. A dose of less than 5 mcg/kg/min causes vasodilation of renal, mesenteric, and coronary beds. At a dose of 5 - 10 mcg/kg/min, beta1-adrenergic effects induce an increase in cardiac contractility and heart rate. At doses of approximately 10 mcg/kg/min, alpha-adrenergic effects lead to arterial vasoconstriction and an elevation in blood pressure. The blood pressure increases primarily as a result of the inotropic effect. The undesirable effects are tachycardia, increased pulmonary shunting, as well as the potential for decreased splanchnic perfusion and increased pulmonary arterial wedge pressure.

In the setting of acute myocardial infarction (MI), dobutamine use could increase the size of the infarct because of the increase in myocardial oxygen consumption that may ensue. In general, avoid dobutamine in patients with moderate or severe hypotension (e.g., systolic blood pressure < 80 mm Hg) because of the peripheral vasodilation. If hypotension is moderate (e.g., mean arterial pressure [MAP] 70 to 90 mm Hg), dobutamine infusion may be used to improve cardiac output and reduce left ventricular filling pressure. Tachycardia and arrhythmias occasionally occur during dobutamine administeration, especially at higher doses.

Pure vasoconstrictors/1-adrenergic receptor agonists, such as phenylephrine, are generally contraindicated; they increase cardiac afterload without augmenting cardiac contractility.

If there is pulmonary congestion, crystalloid infusion should not be given.

β-Blockers should not be given to patients with acute ST-elevation MI or non-ST-elevation MI who are in cardiogenic shock; they should also be avoided in those who are at risk for cardiogenic shock. Calcium-channel blockers should also be avoided.
A 2-month-old female infant presents for a well-child visit. Her mother states that she is concerned about the patient's lack of interest in feeding as well as rapid breathing spells. You acknowledge these concerns, and during the physical examination, you note severe tachypnea, bounding peripheral pulses, and a rough, machinery murmur that is auscultated best near the 2nd left intercostal space.
Question
What is the most likely diagnosis?
Answer Choices
1 Atrioventricular septal defect
2 Patent ductus arteriosus
3 Coarctation of the aorta
4 Ventricular septal defect
5 Still murmur
Patent ductus arteriosus (PDA) is the correct answer; the characteristic murmur of PDA is described as a rough, machinery murmur that is best heard at the 2nd left intercostal space. Signs of moderate-to-severe PDA include failure to thrive, tachypnea, diaphoresis with feeding, and bounding pulses.
Still murmur
Still murmur is recognized as the most common innocent murmur of early childhood. It is described as musical, vibratory, short, and high-pitched.
Coarctation of the aorta murmur
Murmurs in patients with coarctation of the aorta are best described as blowing, systolic murmurs that radiate to the left axilla and left back.
Ventricular septal defect
Ventricular septal defects produce a harsh, pansystolic murmur that is heard best at the left sternal border in the 3rd and 4th intercostal spaces.
A 15-year-old girl presents with a 1-hour history of rapid heartbeat, faintness, sweating, and nervousness. She is also experiencing shortness of breath and chest pain. The patient has no significant past medical history. There is no history of similar episodes. The patient is on no medications, and she denies illicit drug use.

On exam, her vital signs are BP70/60 mmHg; pulse 200 bpm; RR 22/min, temperature afebrile. She looks pale, and her palms are slightly sweaty. She is not comfortable sitting up, so she prefers lying down. She looks slightly apprehensive. Her heart and lung exam are negative except for the tachycardia; except for cool sweaty hands, a brief abdominal and extremity exam are non-revealing.

The physician quickly places the paddles on the patient's chest to record the rhythm; this shows a narrow-complex regular tachycardia at 210 bpm. He requests oxygen, IV line, and continuous monitoring. An EKG is in the process of being completed.



Question Ico-delete Highlights
At this point, what should be done?

Answer Choices
1 Carotid sinus massage
2 Synchronized cardioversion
3 Adenosine 6 mg IV push
4 Diltiazem 10 mg IV push
5 Verapamil 5 mg IV push
synchronized cardioversion
Explanation
Tachycardia can be classified based on the appearance of the QRS complex on the ECG as narrow and wide complex tachycardia. Narrow complex tachycardia consists of sinus tachycardia, atrial fibrillation, atrial flutter, AV nodal reentry, and atrial tachycardia (ectopic and reentrant). Wide complex tachycardia consists of ventricular tachycardia and supraventricular tachycardia with aberrancy.

The patient presents with a tachycardia and associated serious symptoms of faintness, shortness of breath, chest pain and apprehension, mild hypotension, and peripheral vasoconstriction. Thus, while young patients can tolerate a rapid heartbeat for some time, this patient would be classified as hemodynamically unstable. The treatment of choice for unstable patients with a narrow complex tachycardia would be immediate synchronized cardioversion.

However, whenever possible, it is advisable to provide analgesia and sedation for conscious patients before cardioversion.
what medication should you use in the case of narrow complex tachycardia
If the vagal maneuvers do not succeed, the physician may wish to give a fluid bolus and try medications such as adenosine (6mg rapid IV push over 3 seconds). Adenosine works in 90% of narrow complex tachycardias, and with vagal maneuvers, it can be viewed as the initial management choice. The adenosine can be repeated twice at doses of 12 mg IV; the doses must be spaced at 1 - 2 minutes apart, and the adenosine must be injected in a vein that is close to the heart (at the very least, a brachial vein with elevation of the arm); it should be followed by a 20cc saline push. If there is still no rate conversion, then diltiazem or verapamil can be administered.
A 54-year-old man presents with a 6-month history of increasing intolerance to exercise. He describes "breathlessness" with exertion, as well as fatigue and 2 pillow orthopnea. He denies tobacco use but does admit to 4 or 5 whisky sours daily for the last 20 years. He is a businessman and often entertains clients, which "involves drinking alcohol." Chest x-ray reveals an enlarged cardiac silhouette, EKG reveals normal sinus rhythm. A surface echocardiogram reveals an ejection fraction or 35%, mild mitral regurgitation, and dilated left ventricle.



Question
Which of the following statements about this patient's illness is true and should be shared with the patient?

Answer Choices
1 His cardiomyopathy is likely familial.
2 There is minimal risk with this disease, so he can be treated symptomatically.
3 Symptoms can significantly improve with alcohol cessation.
4 He is in need of an implantable defibrillator emergently.
5 His cardiomyopathy is the result of his heart murmur.
Symptoms can significantly improve with alcohol cessation

This patient's clinical presentation and diagnostic work-up is consistent with dilated cardiomyopathy, and the likely cause is his excessive alcohol intake, rather than genetics. There is a significant amount of risk associated with this disease, which cannot be ignored, but he can experience a significant improvement in symptoms and reversal of damage within 3-6 months of abstinence from alcohol. It is appropriate to wait for that 6-month period of time before reassessing for the need of an implantable defibrillator, as his disease is not considered severe at this point and the condition may improve to the point where a defibrillator is no longer necessary. His mild mitral regurgitation is the result of annular dilation related to the disease, not the cause of the disease.
A 76-year-old man with a past medical history of hyperlipidemia and diabetes mellitus presents to the emergency room with a 2-hour history of acute, severe, "crushing" left precordial chest pain; it is associated with nausea, vomiting, diaphoresis, and altered mental status. His physical exam is notable for an ashen and cyanotic appearance, hypotension, rapid and weak peripheral pulsations, distant heart sounds, elevated jugular venous distension and pulmonary crackles. A stat bedside chest X-ray reveals the following image.
Question
What is correct regarding the diagnostic work-up of this patient?

Answer Choices
1 Serum lactate levels are expected to be elevated
2 A low brain natriuretic peptide (BNP) confirms cardiogenic shock
3 Coronary angiography is contraindicated
4 A normal electrocardiogram rules out the contributing infarction
5 Pulmonary capillary wedge pressure (PCWP) of less than 15 mm Hg is expected
Serum lactate levels are expected to be elevated

The patient is presenting with signs and symptoms consistent with cardiogenic shock due to myocardial infarction. On chest X-ray, findings of left ventricular failure are visualized. These radiologic features include pulmonary vascular redistribution, interstitial pulmonary edema, enlarged hilar shadows, the presence of Kerley B lines, cardiomegaly, and bilateral pleural effusions. Alveolar edema manifests as bilateral perihilar opacities in a so-called butterfly distribution.

An elevated serum lactate level is an indicator of shock. Serial lactate measurements are useful markers of hypoperfusion and are also used as indicators of prognosis. Elevated lactate values in a patient with signs of hypoperfusion indicate a poor prognosis; rising lactate values during resuscitation portend a very high mortality rate.

A low BNP level may effectively rule out cardiogenic shock in the setting of hypotension.

Coronary angiography is urgently indicated in patients with myocardial ischemia or myocardial infarction (MI) who also develop cardiogenic shock. Angiography is required to help assess the anatomy of the coronary arteries and the need for urgent revascularization.

Electrocardiography should be performed immediately to help diagnose myocardial infarction (MI) and/or myocardial ischemia. A normal ECG, however, does not rule out the possibility of acute MI. Acute myocardial ischemia is diagnosed based on the presence of ST-segment elevation, ST-segment depression, or Q waves. T-wave inversion, although a less sensitive finding, may also be seen in persons with myocardial ischemia.

The hemodynamic measurements of cardiogenic shock are a pulmonary capillary wedge pressure (PCWP) of greater than 15 mm Hg and a cardiac index of less than 2.2 L/min/m2.
A 54-year-old man presents with chest pain. He has a past medical history of hypertension and diabetes mellitus. The pain is located in the middle of his chest and radiates to his jaw. The pain began about 20 minutes ago, and he rates the pain as a 10 on a 0-10 point scale, with 10 being the worst pain he has ever felt. He has had 3 similar episodes, but they have always resolved after 5 minutes or so of rest. He has smoked 1 pack of cigarettes a day for the past 36 years. He drinks 2 or 3 beers on Friday nights. Review of systems (ROS) is positive for diaphoresis, acute dyspnea, and impending doom. ROS is negative for fever, chills, and malaise. Physical exam shows an obese, middle-aged man in moderate distress. BP is 148/80; pulse is 100; and respirations are 26. Heart and lung exams are normal, except for tachycardia and tachypnea. He has no pedal edema. Electrocardiogram (ECG) shows ST elevation in leads II, III, and AVF; this is a new finding when compared to ECG from 3 months ago.

Question
What is the diagnosis?

Answer Choices
1 Pericarditis
2 Stable angina
3 Pulmonary embolism
4 Chostochondritis
5 Acute myocardial infarction
Acute MIExplanation
The patient has several risk factors for coronary heart disease, including diabetes, hypertension, and cigarette smoking. A patient presenting with signs and symptoms of ischemia and new ECG changes meet the criteria for acute myocardial infarction (AMI) (3).

Stable angina, unstable angina, and AMI are a spectrum of diseases related to underlying atherosclerosis. Stable angina causes chest pain that is usually predictable, due to physical exertion, and is relieved by rest. Chest pain that becomes more frequent, occurs more often, or occurs at rest is unstable angina. Unstable angina is differentiated from AMI by ECG and biochemical marker changes (Troponin, CK-MB).

Diabetes mellitus (DM) is an independent risk factor for atherosclerosis. The risk of myocardial infarction (MI) in a patient with diabetes is the same risk as someone without diabetes who has had a previous MI. The risk of death from cardiac events is also the same between the 2 groups (1).

Other important contributors to atherosclerosis and ischemic heart disease, including dyslipidemia, cigarette smoking, obesity, and hypertension, contribute to the risk of MI; however, when evaluated independently, DM is a greater risk factor (2).

Patients with diabetes mellitus should be advised to stop smoking and aggressively control other risk factors, such as glucose, hypertension, and dyslipidemia, in order to reduce the risk of ischemic heart disease.

Patients with pericarditis report that pain is related to position and worse with inspiration. The ECG shows diffuse ST elevation. Patients with pulmonary embolism may present with acute onset chest pain and dyspnea, but will not have the characteristic ECG changes. Chest pain associated with costochondritis is reproducible with palpation of the affected area and is not associated with dyspnea or ECG changes.
A 26-year-old African-American man with no significant past medical history presents with a history of dyspnea on exertion, which occurs after running. The dyspnea is associated with mild substernal chest pain. All symptoms are relieved with rest. He denies fever, chills, cough, wheezing, pleurisy, calf pain, abdominal complaints, peripheral edema, cigarette, drug, or alcohol use, sick contacts, or travel. His physical exam reveals a harsh murmur best heard at the left lower sternal border and an S4 gallop. A bedside electrocardiogram was remarkable for left ventricular hypertrophy and septal Q waves in the inferolateral leads. An echocardiogram noted asymmetric LVH, anterior motion of the mitral valve during systole, a small and hypercontractile LV, and delayed relaxation and filling of the LV during diastole. The septum was 2 times the thickness of the posterior wall.
Question
What is expected to be true regarding the murmur in this patient?

Answer Choices
1 It decreases while in an upright posture.
2 It becomes less intense with the Valsalva maneuver.
3 It decreases with squatting.
4 It increases with sustained handgrip.
5 It increases with lying down.
It decreases with squatting
Explanation
This patient's presentation is significant for hypertrophic cardiomyopathy. The murmur is a loud, harsh systolic murmur present along the left sternal border. The gradient and the murmur may be enhanced by maneuvers that decrease ventricular volume, such as an upright posture, standing, or Valsalva maneuver. It is decreased by increasing ventricular volume or vascular resistance, which occurs with squatting, sustained handgrip, lying down, or straight leg raises. These maneuvers help differentiate the murmur of HOCM from that of aortic stenosis, since in HOCM, reducing the LV volume increases obstruction and the murmur intensity; whereas, in valvular aortic stenosis, reducing the stroke volume across the valve decreases the murmur.
A 42-year-old hypertensive, diabetic Native American woman is scheduled for a follow-up visit today. She says that her father recently passed away after having a heart attack. She is extremely worried and wants to know what she can do to reduce her risk of cardiovascular disease (CAD). You explain to her that that the risk factors for CAD are classified as either non-modifiable or modifiable.

Question
What is the strongest non-modifiable risk factor for CAD in this woman?

Answer Choices
1 Her age
2 Her ethnicity
3 Hypertension
4 Diabetes
5 Her gender
Her ethnicity
A 61-year-old male presents with a recent history of increased fatigue with mildly increased exertional dyspnea. Patient denies any significant past medical history but states that he had some heart problems as a child, though he was never clear as to what was the problem. On cardiac examination, you hear an early diastolic, soft decrescendo murmur with a high pitch quality, especially when patient is sitting and leaning forward. No thrill is felt.


Question
Based on this patient's presentation, you expect the patient to have
Answer Choices
1 Tricuspid stenosis
2 Aortic regurgitation
3 Mitral stenosis
4 Mitral valve prolapse
5 Pulmonic stenosis
AR
Explanation The correct answer is aortic regurgitation, as it presents as a soft, early diastolic, high-pitched murmur heard best when sitting and leaning forward. It is often a result of rheumatic heart disease, which may be inferred by the patient's history.
Tricuspid Stenosis
Tricuspid stenosis presents as a diastolic rumbling murmur typically accompanied by a thrill heard louder on inspiration.
Mitral stenosis
You can hear the opening snap near the cardiac apex, but more easily appreciate it along the lower left sternal border.
A 65-year-old man presents to the office with complaints of 6 months of bilateral buttock and thigh cramping pain that occurs after walking 20 feet and is completely and quickly relieved with resting. His past medical history included hypertension treated with atenolol, and he had a stroke 3 years ago. He also complains of impotence for approximately the same duration of time. What is the patient's physical exam likely to include?

Answer Choices
1 Absent femoral, popliteal, and pedal pulses
2 Absent popliteal and pedal pulses, normal femoral pulses
3 Absent pedal pulses, normal femoral and popliteal pulses
4 Normal femoral, popliteal, and pedal pulses
5 Normal femoral, normal popliteal, and diminished pedal pulses
1 Absent femoral, popliteal, and pedal pulses
Chronic arterial insufficiency is characterized by intermittent claudication, which is a very specific symptom defined as crampy pain consistently reproduced by the same level of exercise and is completely and quickly relieved by rest. The other symptoms of peripheral vascular disease include ischemic ulceration, blackening or gangrene formation, pain at rest, which occurs with worsening of the disease and coldness of the limb. This patient has thigh and buttock claudication with associated impotence, which is consistent with aortoiliac occlusive disease. The location of the pain is dependent on the location of vascular compromise. Thigh and buttock claudication associated with impotence or erectile dysfunction is called Leriche syndrome. Aortoiliac occlusive is characterized by absent femoral, popliteal, and pedal pulses. The classic symptoms, originally described by Leriche, include a triad of claudication, impotence, and absent femoral pulses. This disease often remains stable for years and can actually improve with time as collaterals enlarge. Aortoiliac occlusive disease can be diagnosed via Doppler and confirmed with CT angiography, MRA, or angiography.

Calf claudication is associated with femoral artery occlusive disease. Physical exam is characterized by absent popliteal and pedal pulses with normal femoral pulses.

Foot claudication is rare, but it may exist in the presence of infrapopliteal artery occlusion. Physical examination is characterized by absent pedal pulses, normal femoral, and popliteal pulses.
A 69-year-old man was brought to the Emergency Department by ambulance with sudden onset of severe, described as tearing, chest pain that radiates down the back for the past 25 min. He admits to a long-standing history of hypertension that has not been treated effectively for the past 25 years. He states that he feels short of breath but without dyspnea, is beginning to feel dizzy, his legs are becoming weak, and paralysis is beginning to occur. His vitals are as follows: respirations are 24/min, pulse is 110/min, BP is 208/152 mm Hg in right arm and 212/156 mm Hg in the left arm. He is afebrile.


Question
At this time, based on the above information, the most likely diagnosis is
Answer Choices
1 Myocardial infarction
2 Acute pancreatitis
3 Dissecting aortic aneurysm
4 Pulmonary embolism
5 Inferior vena cava syndrome
Dissecting aortic aneurysm

Explanation The correct answer is dissecting aortic aneurysm because the symptomatology described above as:
-tearing chest pain radiating down the back with long standing history of uncontrolled hypertension, and
-lower extremities becoming weak with progressive paralysis are characteristic of a dissecting aortic aneurysm.

All of the other choices are not likely to present with the constellation of signs and symptoms demonstrated above and are therefore less likely diagnoses.
A 70-year-old male presents with acute onset back pain for one hour. His past medical history includes coronary artery disease, for which he has undergone a coronary artery bypass grafting , 3 times, two years ago. He also has hypertension, and has smoked a pack of cigarettes per day for fifty years. His physical exam includes a BP of 80/76 mm Hg, pulse of 116/min, and has a palpable infraumbilical pulsatile abdominal mass with left lower quadrant fullness. What is the best diagnostic test to use in the diagnosis of this patient's condition?

Answer Choices
1 Computed Tomography(CT)
2 Aortogram
3 Magnetic Resonance Imaging(MRI)
4 Venogram
5 Abdominal x-ray
CT
Explanation This patient has a ruptured abdominal aortic aneurysm, which is defined as a localized dilation of the abdominal aorta greater than or equal to twice the normal diameter, with a disruption which allows blood outside the aortic wall. Abdominal aortic aneurysm is seen in 5-7% of people above age 60 years in the US. The incidence rises sharply after 55 years of age in men and 70 years of age in women. Men outnumber women by a ratio of approximately 4 to 1. Most abdominal aortic aneurysms encountered by primary care physicians are intact, asymptomatic, and found incidentally on routine physical examination, or in radiographic studies performed for other indications. Cigarette smoking, family history and hypertension are all risk factors for abdominal aortic aneurysms. Due to the high death rate from rupture (35-80%), elective surgical repair or implantation of an endovascular stent graft is advisable in appropriate patients. In general, patients with aneurysms 5cm or larger in diameter, symptomatic aneurysms, or rapidly enlarging aneurysms should be considered for repair.

The approximate rupture rate for aneurysms of diameter 4-4.9cm is 0.5-5% per year, while aneurysms 5-6cm in diameter have a rupture rate of 3-15% per year. Those with a diameter of 6-7cm rupture at a rate of 10-20% per year and for aneurisms with a diameter of 7-8 cm, it is 20-40% per year. Ultrasound is often utilized to screen patients at risk for abdominal aortic aneurysm and monitor aneurysms over time. Ultrasounds have also proved useful in the evaluation of the aorta in the emergency room in addition to being a useful screening test. This exam can confirm the presence of an aneurysm, however, it can't identify a rupture. Computed tomography is used following ultrasound identification of an aneurysm to provide definitive size of the aneurysm and for possible endovascular repair. CT is also the most accurate method of diagnosing a ruptured abdominal aortic aneurysm. The presence of retroperitoneal blood was found to be 77% sensitive and 100% specific and is viewed as the "gold standard". Aortogram can be utilized to plan repair but is not utilized to make the diagnosis of a rupture. MRI has little role in this emergency setting as does venography unless rupture is associated with a vena caval or renal vein fistula.

Endovascular repair of abdominal aortic aneurysm have identical criteria for repair as does open repair, namely: size, symptoms or rapid expansion. Well documented short-term benefits of endovascular repair compared to conventional surgical repair include reduced blood loss and shorter hospital stay. Conversion to open repair is approximately 0.7-1.7%. Perioperative mortality was approximately 2.4%. The greatest benefit for endovascular repair of abdominal aortic aneurysm has been found to be in older patients for whom surgery poses a higher risk, whereas in good risk younger patients, open surgery may be the better option. Endovascular repair has also been utilized in several centers to treat ruptured abdominal aortic aneurysms. Overall, the results of endovascular repair of ruptured aneurysm have been positive. As endovascular techniques expand, this technology has the potential to reduce the mortality of ruptured abdominal aortic aneurysms.

Expected mortality rates are 4-8% for elective open surgical repair. Open repair remains the standard for ruptured abdominal aortic aneurysm. Mortality for open repair in the presence of rupture is from 50-70%. The crucial element of open repair in the setting of rupture is rapid and effective proximal control to achieve hemodynamic stability.
A 35-year-old woman presents with fatigue and yellowish coloration of her eyes and skin that started several weeks after noneventful implantation of the prosthetic mechanical heart valve. Physical examination reveals the presence of regurgitant murmur and subicterus. Laboratory results are: hemoglobin 7.0 g/dL; reticulocytes 21%; white blood cells 11,500/µL; platelets 80,000/µL; and undetected levels of haptoglobin. In lactate dehydrogenase, the direct and indirect bilirubin levels are all elevated (3,100 U/L, 2.1 and 1.2 mg/dL, respectively). Peripheral blood smear shows burr and helmet cells (schistocytes) and polychromasia. Both direct and indirect Coombs' tests are negative. You suspect microangiopathic hemolytic anemia.



Question
What is the next step in management?

Answer Choices
1 Hemoglobin electrophoresis
2 Glucose-6-phosphate dehydrogenase deficiency
3 Echocardiography
4 Hepatitis B panel
5 Direct agglutination test
Echocardiography
Explanation
Anemia, reticulocytosis, and jaundice are the characteristics of hemolytic anemias. Red blood cells (RBC) survival is shortened; bone marrow increases erythroid production that results in the increased number of reticulocytes; and RBC breakdown manifests as increased unconjugated bilirubin and lactate dehydrogenase and decreased (undetectable) haptoglobin. Microangiopathic hemolytic anemia occurs when the red cell membrane is damaged in circulation, leading to intravascular hemolysis and the appearance of schistocytes (fragmented erythrocytes).

Hemolytic anemia due to mechanical damage is seen with prosthetic mechanical heart valves. Your first and most important next step in the management of this patient will be to find out if there is a dysfunction of the prosthetic valve. Echocardiography will reveal the presence of significant leaking or valve dysfunction.

Hemolytic anemias are generally caused by intrinsic (defects in erythrocytes membranes, enzyme systems, and hemoglobin; mostly hereditary) and extrinsic factors (immune and microangiopathic hemolytic anemias). Hemoglobin electrophoresis will be useful in the diagnosis of thalassemia or sickle cell anemia that is caused by intrinsic hemoglobin defect. Anemias in those disorders are usually hypochromic and microcytic.

Glucose-6-phosphate dehydrogenase deficiency is usually drug-induced. In this case, hemolytic anemia is intrinsic and caused by the defect in the enzyme system. Hemolytic anemia may occur in the course of some viral diseases and is autoimmune (Coombs test will be positive). Hepatitis B rarely causes this sort of anemia. Besides, the probability that she acquired hepatitis B during the surgery is very low these days.

A direct agglutination test is looking for serum antibodies using whole organisms. It has no place in the diagnosis of microangiopathic hemolytic anemia.
A 65-year-old African-American man presents in your office for a follow-up for hypertension. Three months earlier you prescribed furosemide. He checks his blood pressure daily and states that it is markedly lower since he has been on the medication. However, it feels like his heart is skipping a beat once in a while. What deficiency is most likely?
Answer Choices
1 Sodium
2 Potassium
3 Vitamin C
4 Thiamin
5 Riboflavin
Potassium
Explanation Furosemide is a diuretic that can cause acute dehydration and mineral depletion, especially potassium deficiency. Since potassium regulates nerve conduction, muscle contraction, fluid and acid-base balance, and is necessary for a regular heartbeat, the symptom described above is a sign of hypokalemia. It can be avoided by giving a potassium-sparing diuretic like spironolactone.
In sodium deficiency, expected symptoms could be nausea and vomiting, apathy, abdominal or muscle cramps, and exhaustion.

Vitamin C deficiency would present with easy bruising and sore gums.

Thiamin (vitamin B1) deficiency would present with irritability, anorexia, and fatigue.

Riboflavin (vitamin B2) deficiency would present with anorexia, inflammation of mouth mucosa, sensitivity to light, and dim vision.
A 27-year-old man with Marfan syndrome presents due to exercise intolerance and heart palpitations. On exam, you note a mid-systolic click and late systolic murmur heard at the apex of the heart. The click and murmur are noted later in systole with squatting and earlier in systole with sudden standing.



Question
What is the most likely diagnosis?

Answer Choices
1 Aortic stenosis
2 Aortic regurgitation
3 Mitral stenosis
4 Mitral valve prolapse
MVP
Mitral valve prolapse (MVP) is correct because this is a common finding in people who also have Marfan syndrome or Ehlers-Danlos syndrome. Most commonly, MVP is found on routine physical examination, but it can have non-specific complaints, such as fatigue, dizziness, exercise intolerance, and palpitations. Most adults with MVP have a mitral regurgitation murmur. The click and murmur is mobile, changing timing with different positions. Anything that increases the volume of the left ventricle, such as squatting, delays the prolapse in systole; therefore, the click and murmur occur later in systole. The same is true of the reverse; anything that decreases the volume of the left ventricle, such as standing, causes the prolapse to occur earlier. Therefore, the click and murmur occur earlier in systole. The midsystolic click is thought to be because of the chordae tendineae tensing up as the leaflet is forced back to the left atrium.




Mitral stenosis is incorrect; it is typically a common finding in someone who has had rheumatic fever. Examination reveals a loud S1 in early stages of the disease. There is a high-pitched opening snap that follows S2, which is followed by a diastolic rumble.
Aortic stenosis
it is a more common valvular disease in older people. The murmur associated with aortic stenosis is a coarse, late-peaking systolic ejection murmur. There is also a weakened and delayed upstroke of the carotid artery pulse. Other findings include an S4 heart sound.
Aortic Regurgitation
widened pulse pressure is a typical finding in the disease. A diastolic murmur is noted in aortic regurgitation. Other findings could include a soft S1, variable S2, a soft A2, and an S3 gallop.
Mitral Stenosis
it is typically a common finding in someone who has had rheumatic fever. Examination reveals a loud S1 in early stages of the disease. There is a high-pitched opening snap that follows S2, which is followed by a diastolic rumble.
Aortic Dissection
it is a medical emergency, and the patient would have presented with sudden, severe, 'tearing' pain in the anterior chest or between the scapulae.
Having Marfan syndrome does put a patient at an increased risk of an aortic dissection, but an aortic dissection would be a true emergency, and it would not manifest with vague symptoms.
A 68-year-old man with a past medical history of diabetes mellitus type II, hypothyroidism, and hyperlipidemia presents with a constant moderate to severe "squeezing, pressure, and tight" left-sided chest pain for 1 hour. Additionally, he admits to shortness of breath, nausea, productive cough with a frothy sputum, and profound diaphoresis. He notes that he has had a 1-week history of similar, recurrent chest pain of about 10 minutes duration that has been occurring following exposure to the cold weather and following consumption of a meal. He denies chills, abdominal pain, diarrhea, cough, and pleurisy. His physical exam reveals tachycardia, hypertension, cyanosis, cool and moist skin, diaphoresis, an S3 gallop, and evidence of painful respiratory distress. His lung exam is noteworthy for diffuse crackles. Bedside electrocardiogram demonstrates sinus tachycardia, ST-segment elevations, and occasional premature ventricular contractions.



Question
What is the most appropriate treatment of the pain, hypertension, and suspected pulmonary edema in this patient?

Answer Choices
1 Clopidogrel
2 Nitroglycerin
3 Metoprolol
4 Lisinopril
5 Nifedipine
Nitroglycerin
This patient's most likely diagnosis is acute ST-segment elevation myocardial infarction with pulmonary edema. Control of pain in STEMI is accomplished through a combination of nitrates, analgesics (morphine), oxygen, and β-adrenergic blocking agents.

Nitroglycerin is indicated in the treatment of ongoing ischemic pain, control of hypertension, or management of pulmonary congestion. Due to its vasodilating effect, it is able to relieve coronary pain. It decreases venous return (reducing preload) and arterial blood pressure (reducing afterload), thereby reducing oxygen consumption. It may also limit infarction size.

Clopidogrel reduces platelet aggregation by inhibiting the ADP pathway in platelets.

Metoprolol, a β-adrenergic blocking drug, decreases myocardial oxygen demand by reducing heart rate, cardiac contractility, and systemic arterial blood pressure. Moderate to severe left ventricular failure in myocardial infarction resulting in pulmonary congestion and edema should not be treated with β-adrenergic blocking agents.

ACE inhibitors, such as Lisinopril, are usually started within the first 24 hours of infarction, usually following completion of fibrinolytic therapy. ACE inhibitors do not significantly change cardiac output or heart rate, but are extremely useful in the treatment of heart failure and after myocardial infarction.

In patients with unstable angina or myocardial infarction, short acting calcium channel blockers, such as Nifedipine, can increase the risk of adverse cardiac events and therefore are contraindicated. In patients with non-Q-wave MI, diltiazem can decrease the frequency of post-infarction angina and may be used.
A 61-year-old man presents with chest pain for the last hour. An ECG is obtained and found to have T wave inversion and wide Q waves in leads II, III, and AVF.
Question
What condition are these ECG findings are most consistent with?

Answer Choices
1 Acute ischemia without myocardial infarction
2 Acute lateral myocardial infarction
3 Acute inferior myocardial infarction
4 Acute posterior myocardial infarction
5 Acute anterior myocardial infarction
Acute inferior MI
Explanation The correct answer is acute inferior myocardial infarction, as ECG findings include T wave inversion and wide Q waves in the inferior leads II, III, and AVF.
Acute Ischemia without MI
T wave inversion without significant Q waves would suggest ischemia without myocardial infarction (MI).
Acute Lateral MI
T wave inversion and wide Q waves in leads V1 and AVL would suggest a lateral MI.
Acute Anterior MI
T wave inversion and wide Q waves in leads V1, V2, V3, or V4 suggest an anterior MI.
Acute Posterior MI
Large R waves and ST segment depression in leads V1, V2, and/or V3 suggest a posterior MI.
A 45-year-old woman with a no significant past medical history presents with a 4-month history of dull, aching heaviness sensation in her proximal right leg. She notes that this sensation is provoked by extended periods of standing and walking, and is relieved when she lies in a recumbent position. Her past medical history is remarkable for pregnancy 4 times, the most recent being approximately 2 years ago. She denies a history of smoking, trauma, injuries, fever, chills, chest pain, shortness of breath, hemoptysis, cough, skin changes and coolness, and peripheral edema. Her physical exam reveals several dilated, tortuous, elongated veins along the medial right thigh, which are especially pronounced upon standing. The remainder of the physical exam is normal.

What will be the most appropriate therapeutic approach for this patient at this time?
Answer Choices
1 Warfarin (Coumadin)
2 Clopidogrel (Plavix)
3 Sclerotherapy
4 Furosemide (Lasix)
5 Cilostazol (Pletal)
Sclerotherapy
This patient's diagnosis is varicose veins.

Sclerotherapy can be used to treat varicose veins. It involves the injection of an irritating solution into the varicose vein to promote an inflammatory response, scarring, and obliteration of the lumen

Warfarin is indicated for myocardial infarction or cerebrovascular accident prevention and in patients with atrial fibrillation, mechanical heart valves, or deep venous thrombosis.

Diuretics are ineffective for varicose veins.

Cilostazol and clopidogrel both inhibit platelets. Clopidogrel is used in CAD and CVA prevention, as well as post-ST-segment MI. Cilostazol lowers lipid levels and is indicated in peripheral arterial disease.
A 70-year-old African American man presents to his primary care provider with a complaint of gradual but progressive dyspnea and fatigue on exertion. He notes difficulty in climbing stairs with associated lightheadedness, increased abdominal girth, and swollen bilateral lower extremities. He admits to chronic alcohol use, but denies any heart disease, chest pain or pressure, diaphroesis, palpitations, a history of diabetes, cigarette smoking, or claudication. His physical exam reveals sinus tachycardia, bibasilar rales, a laterally-displaced PMI, an elevated JVP, an S3 gallop, a mitral regurgitation murmur, peripheral edema, and abdominal ascites.

Question
What is the next most appropriate step in the management of this patient?

Answer Choices
1 Obtain an echocardiogram
2 Refer the patient for cardiac catheterization
3 Perform a cardiac biopsy
4 Order coxsackie and adenovirus serological titers
5 Order cardiac troponin levels
Obtain an echo
Chronic alcohol abuse is a major risk factor for the development of congestive cardiomyopathy, accounting for up to 45% of all dilated cardiomyopathies.

For the usual subacute presentation, the diagnosis of cardiomyopathy is confirmed by echocardiography, and further evaluation is directed to ascertain whether myocarditis is present. An echocardiogram is indicated to exclude unsuspected valvular or other lesions and confirm the presence of dilated cardiomyopathy and the reduced systolic function (as opposed to pure diastolic heart failure). Four-chamber dilatation is a common but not uniform finding. Other findings include increased left ventricle end-diastolic diameter and volume with decreased fractional shortening, thinning left ventricle walls, increased E point-septal separation, left atrial enlargement, and limited mitral and aortic valve opening caused by low stroke volume. Intracardiac thrombi may also be observed.

Cardiac catheterization is seldom of specific value unless myocardial ischemia or left ventricular aneurysm is suspected.

Myocardial biopsy is rarely useful in establishing the diagnosis, though occasionally the underlying cause (e.g., sarcoidosis, hemochromatosis) can be discerned. Biopsy is most useful in transplant rejection.

Acute and convalescent viral titers are usually sent but are more likely to be important from the public health standpoint than for the individual.

Following confirmation of cardiomyopathy upon echocardiography, further evaluation is directed to ascertain whether myocarditis is present; mild troponin elevations may be measured, as well as release of creatine kinase with cardiac injury or skeletal muscle involvement.
The mechanism of the anticoagulant effect of low molecular weight heparin is
Answer Choices
1 Degradation of activated coagulation factors
2 Forming a complex with antithrombin III
3 Inhibition of a vital enzyme in the coagulation factor activation
4 Inhibition of coagulation factors synthesis
5 Stimulating the production of anticoagulant proteins
Forms a complex with antithrombin 3
Explanation Both unfractionated heparin and low molecular weight Heparin act by forming a complex with antithrombin III. The formed complex is capable of directly inhibiting the generation of thrombin, as well as accelerating thrombin decay. The complex unfractionated heparin-antithrombin III, is capable of binding both thrombin and factor Xa. The antithrombin activity of unfractionated heparin is dependent on the chain length of the heparin molecule; therefore, this mechanism is negligible with the low molecular weight fraction of heparin. The low molecular weight heparin fraction relies predominantly on the anti-factor Xa for its anticoagulant effect.

Heparin does not destroy coagulation factors, nor does it inhibit their synthesis. Heparin does not have any role in stimulating the production of anticoagulant proteins.

Warfarin exerts its anticoagulant effect, by inhibiting the reductase enzymes involved in restoring the reduced form of vitamin K. The reduced form of vitamin K is needed for the carboxylation reaction involved in the gamma carboxylation of coagulation factors II, VII, IX and X.
A 74-year-old man presents with a 1-hour history of constant moderate-to-severe "squeezing, pressure, and tight" left-sided chest pain, accompanied by nausea. He has a past medical history of diabetes mellitus type II, hypothyroidism, and hyperlipidemia. He also has a 1-week history of similar, recurrent chest pain of about 10 minutes duration; the pain occurs following exposure to cold weather and consumption of a meal. He denies fever, chills, abdominal pain, diarrhea, cough, pleurisy, and shortness of breath.
Question
What additional findings would be most consistent with his most likely diagnosis?

Answer Choices
1 The chest pain is relieved by sitting forward
2 This pain will be relieved with antacids and belching
3 Movement of the chest, trunk, and arms are provocative factors
4 Vomiting, diaphoresis, and weakness are associated findings
5 There is localized tenderness to the chest wall
Vomiting, diaphoresis, and weakness are associated findings

Explanation
This patient's most likely diagnosis is acute myocardial infarction. His symptoms prior to this episode represent angina pectoris. Common symptoms associated with myocardial infarction include dyspnea, nausea, vomiting, diaphoresis, and weakness.

Chest pain relieved by a forward-sitting position suggests pericarditis; pain relieved with antacids or belching is common to reflux esophagitis.

Provocation factors such as chest, trunk, and arm movement, as well as localized tenderness, suggest chest wall pain; these may be found in herpes zoster or costochondritis.
A 74-year-old man with a past medical history of hyperlipidemia, myocardial infarction, rheumatic heart disease, and hypertension presents for a routine evaluation. He states that he has no complaints and feels well. The physical exam reveals an elderly man in no apparent distress whose vital signs are within normal limits. The cardiac exam is noteworthy for a soft S1 to auscultation, a systolic thrill palpable at the cardiac apex, lateral displacement of the point of maximal impulse, and a holosystolic murmur of III/VI intensity, which is loudest at the apex and radiates to the axilla. The remainder of the exam is normal.
Question
What EKG finding would be most likely associated with this patient's presentation?

Answer Choices
1 Wide QRS complexes
2 Diffuse ST elevations
3 Prolonged PR intervals
4 Negative P-wave deflection in V1
5 Large P-wave amplitude in II
Negative P-wave deflection in V1
Explanation
This patient's murmur is identified as mitral regurgitation. In patients with sinus rhythm, there is evidence of LA enlargement. This is characterized by a bimodal P wave in some leads, and lead V1 is characterized by an initial positive component followed by a negative deflection at the wave's terminus. Right atrial hypertrophy is typically accompanied by a large, positive P-wave deflection in lead II.

In left atrial enlargement, left atrial depolarization lasts longer than normal but its amplitude remains unchanged. Therefore, the height of the resultant P wave remains within normal limits but its duration is longer than the normal 120 ms. Additionally, a notched p-wave may be evident.
A 55-year-old man, who has a history of rheumatic fever that occurred when he was 15, presents with a 5-day history of sharp chest pain. Further questioning reveals that the patient has had a high fever along with this chest pain. The pain itself seems to vary with positioning and movement, but it extends into the shoulder; he gains mild relief sitting up but when he is laying down the pain becomes intense. Physical examination reveals a pericardial friction rub. You order an ECG to be performed on this patient.



Question
Considering the likely diagnosis, what findings would confirm your suspicion?

Answer Choices
1 ST segment depression
2 Lengthening PR intervals
3 Diffuse ST-segment elevation
4 P wave missing QRS complex
5 Peaked T waves
diffuse ST segment elevation
Our patient above is most likely suffering from a case of acute inflammatory pericarditis. Causes of pericarditis include autoimmune or inflammatory disorders, uremia, trauma, myocardial infarction, cancer radiation, or even medications. The patient has a history of having rheumatic fever; this is one of the many causes of pericarditis. The most common cause of infectious pericarditis is viral in origin; the most common culprits include echovirus, influenza virus, coxsackie B virus, and HIV). It should be kept in mind that the pericardium and myocardium are innervated similarly; for this reason sometimes chest pain of pericarditis is similar to myocardial issues such as ischemia. There will be dull or sharp precordial or substernal pain that may radiate to the neck, back, or shoulders. Patients will present with complaints of anterior pleuritic chest pain that is worse supine and somewhat relieved by sitting upright and leaning forward; the movement of the thoracic cavity (coughing, motion, or breathing) helps differentiate a pericardial cause of the pain versus a myocardial source. Fever is common and a pericardial friction rub (considered a key finding) is auscultated during the cardiac examination. ECG findings will include diffuse ST-segment elevation with associated PR depression; eventually the ST will return to baseline and then have signs of T wave inversion.

A myocardial infarction typically will result in reciprocal depression in ST segments. Lengthening PR intervals or a P wave missing a QRS complex are more indicative of a type of different types of atrioventricular block. Peaked T waves are characteristically seen in patients who have hyperkalemia.
Hyperkalemia on ekg
Peaked T waves are characteristically seen in patients who have hyperkalemia.
A 25-year-old woman presents the ER after a syncopial episode. She had loss of consciousness 3 times over the past 12 months. Each event occurred during or just after physical exercise. On PE: BP 110/70 mm Hg, HR 75/min, normal S1/S2, and a III/VI systolic ejection murmur is heard best at the left sternal border that decreases with squatting. The EKG shows a normal sinus rhythm with diffuse increased QRS voltage. What is the most likely diagnosis?
Answer Choices
1 Hypertrophic Cardiomyopathy
2 Mild Mitral Valve Insufficiency
3 Moderate Pulmonary Stenosis
4 Severe Aortic Stenosis
5 Moderate Mitral Valve Stenosis
hypertrophic cardiomyopathy
Explanation The clinical picture is suggestive of a Hypertrophic Cardiomyopathy (HCM). The age of presentation is usually in the mid-20's and the most frequent symptom is dyspnea although most patients are asymptomatic with a normal physical examination. Syncope may result from an arrhythmia due to abnormal myofibers. The transient increase in LV size during squatting reduces the LV outflow tract obstruction in HCM and softens the intensity of the murmur. The increase in QRS voltage indicates a hypertrophied heart and, depending on which leads (V1-V6), will tell you right or left heart.
In Aortic stenosis, the murmur will get louder with squatting and in this patient the murmur gets softer.

Mitral valve stenosis produces a diastolic murmur, while there is a systolic murmur in this patient.

Mitral valve insufficiency (MVI) does produce a systolic murmur but it is described as pansystolic and the patient with MVI could have symptoms of shortness of breath, fatigue, palpitations, and orthopnea which is not present in this patient.

Pulmonary stenosis is rare and would produce signs of jugular venous distention (JVD), cyanosis of nail bed, and general symptoms of hypoxia. There is no mention of JVD or cyanosis in this patient.
A 35-year-old Caucasian woman presents with a 5-day history of nervousness and palpitations. She has had diarrhea for most of the previous month and has had a 3 kg weight loss despite an increased appetite. She also reports increased fatigue and sweating. Her vital signs are an irregular pulse of 114 BPM, blood pressure of 125/75 mm Hg, respirations of 18/min, and a temperature of 37.8°C. Physical exam reveals exophthalmos, a mass in the midline of her neck that moves with deglutition, fine resting tremor, and hyperactive reflexes. Her thyroid stimulating hormone (TSH) level is low. An ECG is performed, revealing atrial fibrillation with an atrial rate of 420/min, and a ventricular response ranging between 110 and 130/min.



Question
What would be the most appropriate initial intervention regarding her arrhythmia?

Answer Choices
1 Heparin
2 Electrical cardioversion
3 Esmolol
4 Ibutilide
5 Amiodarone
Esmolol
Explanation
Atrial fibrillation is the most common chronic arrhythmia, frequently developing in the course of hyperthyroidism.

The initial step in the management of atrial fibrillation is to control the ventricular response. A short acting beta-blocker such as Esmolol is generally preferred for emergency use, because of its rapid onset of action. Other drugs used in the management of atrial fibrillation include:

a) Calcium channel blockers like verapamil or diltiazem when the usage of beta-blockers are contraindicated

b) Digoxin when calcium channel blockers and beta-blockers are not suitable

Once rate control has been achieved, the mainstay of treatment for patients with atrial fibrillation and hyperthyroidism involves restoration of euthyroid status, by the use of antithyroid drugs. Restoration of euthyroid status is frequently associated with conversion to sinus rhythm.

Amiodarone may cause thyroid dysfunction in patients with pre-existing thyroid disease. In a patient with unknown duration of atrial fibrillation, Amiodarone and Ibutilide are not indicated due to the potential risk of thromboembolic phenomenon due to sudden conversion into sinus rhythm.

The use of antithrombotic therapy in thyrotoxic atrial fibrillation lacks clear guidelines currently and more evidence-based trials are necessary to clarify the issue. In this case, due to the patient's young age, lack of underlying heart disease, hypertension or other independent risk factors for embolization, the risk of anticoagulant therapy outweighs the benefits.

Electric cardioversion may be considered to revert the patient to sinus rhythm provided the patient has been restored to a euthyroid state. The maintenance of sinus rhythm is unlikely if the patient remains with hyperthyroidism.
A 72-year-old man with known hypertension and high cholesterol presents with acute chest pain. He describes the pain as an excruciating tearing pain radiating to his back. His blood pressure in his right arm is 105/65 mm Hg and in his left arm 140/90 mm Hg. He also has a decreased pulse in his right arm. On auscultation of the chest, a III/VI early diastolic murmur is best heard at the left sternal border, third intercostal space. His EKG shows a sinus tachycardia with no acute changes. What is the most likely diagnosis?
Answer Choices
1 Pericarditis
2 Musculoskeletal pain
3 Aortic dissection
4 Myocarditis
5 Acute myocardial infarction
Aortic dissection
Explanation The clinical picture is suggestive of an aortic dissection. This condition is most common in the 6th and 7th decades and occurs more frequently in men. A history of hypertension is often present. 85% percent of patients report sudden excruciating (ripping) pain in the chest or upper back. On physical examination, peripheral pulses and blood pressures may be diminished or unequal. A diastolic murmur of aortic insufficiency may be heard.

With pericarditis, the patient does present with chest pain but it is usually described as sharp, retrosternal with radiation to the back, and worse with deep breathing or coughing. The pain is position dependent, worse when lying flat and improved while sitting up and leaning forward. On physical examination, the pericardial rub is pathognomonic of pericarditis which is not present in this patient.

Common causes of musculoskeletal pain include injury and joint or muscle strain. If there is any damage to the ribs from injuries or tumors this can cause pain in the chest. This is not present in this patient.

Myocarditis often follows an upper respiratory infection and may present with chest pain, described as pleuritic or non-specific.

An acute myocardial infarction would show ST-segment elevation or depression, evolving Q waves, and/or symmetric inversions of T waves, which are not present in this patient.
Pericarditis
With pericarditis, the patient does present with chest pain but it is usually described as sharp, retrosternal with radiation to the back, and worse with deep breathing or coughing. The pain is position dependent, worse when lying flat and improved while sitting up and leaning forward. On physical examination, the pericardial friction rub is pathognomonic of pericarditis which is not present in this patient.
Treatment- NSAIDS
A 42-year-old man has had systolic blood pressure in the 140's and diastolic blood pressure in the 80's on several occasions despite changing his diet and exercise regimen. His physician decides to start him on hydrochlorothiazide.
Question
What electrolyte abnormality may be associated with hydrochlorothiazide?
Answer Choices
1 Hypokalemia
2 Hypoglycemia
3 Hypernatremia
4 Hypocalcemia
5 Hypermagnesemia
Hypokalemia
Explanation
Hydrochlorothiazide is a thiazide diuretic. It is associated with hypokalemia, hypomagnesemia, hypercalcemia, and hyponatremia. Thiazide diuretics are less likely to cause electrolyte abnormalities than loop diuretics, such as lasix; however, patients should still be monitored for their development.
A 77-year-old man presents with significant persistent hypotension that has been steadily worsening for 1 hour. The patient's history reveals he was originally admitted with the primary diagnosis of a myocardial infarction. Further investigation of this patient reveals a significant increase in the patient's heart rate as well as substantial tachypnea. Urinary output is too minimal to measure, and upon quick physical examination, the patient's extremities are cool to touch. A Swan-Ganz catheter is in place, and it offers the following information: Cardiac Output ↓, Central Venous Pressure ↑, Pulmonary Artery Obstructive Pressure ↑, as well as the Systemic Vascular Resistance being ↑.
Question
Based on this scenario, what type of shock would this patient be categorized as having?

Answer Choices
1 Neurogenic shock
2 Distributive shock
3 Cardiogenic shock
4 Septic shock
5 Anaphylactic shock
Cardiogenic Shock
Explanation
The correct response is cardiogenic shock.

Early identification of shock is a necessity to help improve any patient's chance of survival and recovery. It is also critical to lead to reversing the cause of the shock and initiating early resuscitation efforts. Early on, patients suffering from shock may have only a few or very subtle symptoms such as tachypnea, tachycardia, hyper or hypothermia, weak or bounding peripheral pulses, delayed capillary refill, or even pale or cool skin. Decreased mental status, weak or absent central pulses, central cyanosis, hypotension, and/or bradycardia are ominous and later signs that indicate that the shock has progressed.

Shock is generally classified into 4 major categories, depending on the etiology causing it: cardiogenic, hypovolemic, distributive, or obstructive. Cardiogenicshock occurs as a consequence of cardiac pump failure. Myopathic, mechanical, or arrhythmic issues lead to cardiogenic shock.

A patient with cardiogenic shock will display increased heart rate and systemic vascular resistance; there will also be decreased cardiac output, pulse pressure, and mixed venous oxygen saturation. Distributive shock results in increased heart rate, cardiac output, pulse pressure, and mixed venous oxygen saturation. When looking at the classification of shock, septic, anaphylactic, and neurogenic shock are all categorized as a type of distributive shock, making these incorrect responses.
A 25-year-old African-American man presents with blood pressure issues. He states that he attended a work-sponsored health fair; he had his blood pressure taken, and the health fair representative strongly urged him to make an appointment to be seen by his primary care provider. The fair occurred 3 months ago. He has randomly checked his blood pressure at different times since the health fair in local grocery stores, and although he does not remember the numbers, he knows that "they were above normal". The patient also believes that both his mother and father are taking blood pressure medication, but he is not 100% sure. Vitals at this time reveal a BMI of 30 kg/m2 and a waist circumference of 41 inches; blood pressure in the left arm is 175/95 mm Hg, and in the right arm it is 172/99 mm Hg.



Question
Based upon the diagnosis at this time, what would most likely be seen during the fundoscopic examination of this patient?

Answer Choices
1 Drusen bodies
2 Microaneurysms
3 Deep retinal hemorrhages
4 Cotton-wool patches
5 Macular star
Cotton wool patches
Fundoscopic examination of any patients diagnosed with essential hypertension is a priceless component; it can reveal how severe the high blood pressure has been anatomically and physiologically on the body up to that point in time. Cotton-wool patches usually appear as gray or white ovoid lesions that have soft borders. These occur secondary to infarction of the nerve fibers within the fundus area; hypertension is a common etiology that can lead to the presence of this pathology.

Drusen bodies are fundoscopic findings that are yellowish, round spots; they vary in size, but they are generally small. Edges of these areas may appear soft or hard. Although Drusen bodies may be seen in normal aging patients, it is very commonly related to the diagnosis of age-related macular degeneration.

Microaneurysms are considered a hallmark finding of diabetic retinopathy.

Deep retinal hemorrhages are also commonly seen in patients with diabetes.

A macular star results from punctuate exudates that radiate from the fovea in a star pattern; this is seen is patients who are experiencing malignant hypertension.
A 45-year-old man is admitted to the hospital with fever, weakness, weight loss, muscle and testicular pain, and a rash on his legs. He states that his symptoms began about 1 week ago. The testicular pain began about 1 day ago and has increased significantly over the last 24 hours. He denies recent illness or injury and states that has been in good health for as long as he can remember. On physical exam, the patient was well-developed, well-nourished, and in mild physical distress. His blood pressure was elevated at 152/94mmHg, and a chest radiograph was negative. Laboratory analysis revealed an elevated sedimentation rate and C-reactive protein, elevated BUN, and creatinine. His red blood cell count was decreased, and his ANCA was negative. An arteriogram showed diffuse arterial saccular aneurysms and narrowing of the arteries.



Question
What is the most likely cause of this patient's symptoms?

Answer Choices
1 Systemic lupus erythematosus
2 Polyarteritis nodosa
3 Rheumatoid arthritis
4 Sjögren syndrome
5 Kawasaki disease
polyarteritis nodosa
Polyarteritis nodosa is a rare autoimmune disease that can affect medium-sized arteries in any organ of the body. The cause is unknown. It commonly affects nerves, skin, intestines, muscles, and joints. It is seen more in middle-aged people and results in decreased blood supply to affected body parts. Men and women are affected approximately equally. There has been some association made with hepatitis B. 3 criteria need to be met out a list of possible symptoms before the diagnosis of polyarteritis nodosa can be made. These include: muscle pain, a positive hepatitis B surface antigen or antibody test, elevated BUN or creatinine, livedo reticularis (a mottled purplish skin discoloration over the extremities or torso), an elevated diastolic blood pressure (greater than 90 mmHg), weight loss of 4kg or more, a biopsy positive for vasculitis, dilated arteries or constricted blood vessels (seen by arteriogram), testicular pain or tenderness, or nerve disease.

It is diagnosed by examining the tissues. This is usually achieved through a biopsy. Histological analysis usually shows focal necrotizing arteritis and a mixed cellular infiltrate within the walls of the affected blood vessels. Testing for an elevated sedimentation rate and C-reactive protein will also help with the diagnosis. Patients often have an elevated white blood cell count and a decreased red blood cell count. Urinalysis may show proteinuria and hematuria.

Polyarteritis nodosa is usually treated with high doses of cortisone and immunosuppressive drugs such as cyclophosphamide or azathioprine. If the patient also has hepatitis B, antiviral medications such as interferon-alpha may be included in treatment.

Kawasaki disease is normally found in children. The biopsy results are characteristic of polyarteritis nodosa, but none of the other choices. The negative ANCA also makes SLE unlikely
A 74-year-old man with a past medical history of diabetes mellitus, hypertension, and hyperlipidemia presents with severe chest pain and dyspnea. On examination, he is confused, agitated, pale, apprehensive, and diaphoretic. His pulse is weak and tachycardic, with a systolic blood pressure of 80 mmHg. He has a narrow pulse pressure, tachypnea, a weak apical impulse, significant jugular venous distention, and pulmonary crackles. Bedside electrocardiogram reveals ST-segment elevations in the anterior and septal leads, while a portable chest X-ray notes diffuse pulmonary congestion.



Question
What is the most appropriate step in the management of this patient?

Answer Choices
1 Crystalloid infusion
2 Initiate intravenous β-Blocker therapy
3 Begin phenylephrine
4 Nitrates and morphine
5 Emergent percutaneous coronary intervention
emergent percutaneous coronary intervention
Explanation
This patient's exhibits signs and symptoms of cardiogenic shock due to myocardial infarction with pulmonary edema.

Treatment of cardiogenic shock includes general supportive measures of oxygen, aspirin, heparin, and "gentle" fluid challenges (250 cc) if there is no overt pulmonary edema. In cardiogenic shock, early revascularization with percutaneous coronary intervention (angioplasty) or coronary artery bypass graft is the treatment of choice. Survival from cardiogenic shock is highest with emergency coronary intervention, followed by intra-aortic balloon pump combined with thrombolytic therapy, and with thrombolytic therapy alone being least effective in reducing mortality. The greatest short-term benefit is reported in patients <75 years of age, those without previous MI, and those treated within 6 hours of symptom onset.

β-Blockers should not be given to patients with acute ST-elevation MI or non-ST-elevation MI who are in cardiogenic shock; it also should not be given to those at risk for cardiogenic shock. Calcium-channel blockers should also be avoided.

Pure vasoconstrictors (1-adrenergic receptor agonists), such as phenylephrine, are generally contraindicated; they increase cardiac afterload without augmenting cardiac contractility.

If there is pulmonary congestion, crystalloid infusion should not be given.

If BP is >90 systolic, chest pain may be relieved by careful use of IV nitroglycerin or morphine; however, vasodilators cannot be used in most cases when hypotension is present.
A 30-year-old woman with no significant past medical history presents to the emergency room with severe, retrosternal, and left precordial chest pain; it has occurred over the past 3 days. Pain is sharp in quality; it is referred to the neck, arms and left shoulder. It is pleuritic. It is aggravated by inspiration and coughing as well as lying in a supine position. Her review of systems is remarkable for a low grade fever, myalgias, and arthralgias. It is relieved by sitting up and leaning forward. Upon physical exam, her vital signs are normal, and her skin is warm and dry. Auscultation of the chest wall with the diaphragm at the left lower sternal border reveals a high-pitched, rasping, scratching, and grating sound, most audible at the end of expiration. A bedside electrocardiogram reveals the following imaging.



Question
What is an additional expected diagnostic finding in this patient?

Answer Choices
1 Lobar consolidation on chest radiography
2 Positive urea breath test
3 Evolution of q-waves on electrocardiogram
4 Elevated ESR and CRP levels
5 Bloody pericardial fluid aspirate
Explanation
The correct response is elevated ESR and CRP levels.

This patient is demonstrating manifestations of acute pericarditis, which is most likely of a viral etiology. Viral or idiopathic acute pericarditis occurs at all ages, but it is more common in young adults and is often associated with pleural effusions and pneumonitis. The almost simultaneous development of fever and precordial pain, often occuring 10 to 12 days after a presumed viral illness, constitutes an important feature in the differentiation of acute pericarditis from AMI, in which chest pain precedes fever. Acute pericarditis occurs in association with illnesses of known or presumed viral origin, and it is probably caused by the same agent. Commonly, there is an antecedent infection of the respiratory tract, and viral isolation and serologic studies are negative.

Coxsackievirus A or B, influenza, echovirus, mumps, herpes simplex, chickenpox, adenovirus, cytomegalovirus, Epstein-Barr, and HIV are all viruses capable of causing viral pericarditis.

Erythrocyte sedimentation rate (ESR) and CRP levels are usually elevated in pericarditis. High-sensitivity CRP (hs-CRP) levels are elevated in 78% of cases of acute pericarditis. Therefore, an elevated CRP level may confirm the diagnosis of acute pericarditis.

A lobar consolidation on chest X-ray is usually indicative of a bacterial pneumonia.

A urea breath test suggests H. pylori infection of the gastrointestinal tract.

Unlike MI, acute pericarditis does not cause reciprocal depression in ST segments (except in leads aVR and V1), and there are no pathologic Q waves.

Bloody fluid from a pericardial aspirate is most commonly due to neoplasm in the United States and tuberculosis in developing nations; however, it may also be found in the effusion of acute rheumatic fever, post-cardiac injury, as well as post-myocardial infarction, renal failure, or dialysis.
Austin Flint Murmur
Austin Flint Murmur (low pitched diastolic murmur)
▫ Mid-late diastolic rumble heard at apex - severe Aortic Regurgitation; often confused with the murmur of MS
Aortic regurgitation PE findings- Corrigan Pulse
Corrigan pulse - "water hammer" pulse that is full and then suddenly collapses.
Aortic Regurgitation PE findings- Pulsus Bisferens/Biphasic Pulse
"Pulsus Bisferiens" AKA Bisferiens pulse - carotid/ brachial/femoral arteries
is a sign where, on palpation of the pulse, a double peak per cardiac cycle can be appreciated.
Aortic Regurgitation PE findings-
deMusset's sign
• deMusset's sign — A head bob occurring with each heart beat.
Aortic Regurgitation PE findings-
Traube's sign
• Traube's sign — A pistol shot pulse (systolic and diastolic sounds) heard over the femoral arteries.
Aortic Regurgitation PE findings-
Duroziez's sign
• Duroziez's sign — A systolic and diastolic bruit heard when the femoral artery is partially compressed.
Aortic Regurgitation PE findings-
Quickne's sign
• Quincke's pulses — Capillary pulsations in the fingertips or lips.
Aortic Regurgitation PE findings-
Mueller's sign
• Mueller's sign — Systolic pulsations of the uvula.
Aortic Regurgitation PE findings-
Becker's sign
• Becker's sign — Visible pulsations of the retinal arteries and pupils.
Aortic Regurgitation PE findings-
Hill's sign
• Hill's sign — Popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg.
EKG findings for LVH strain pattern
1) The R waves in any one or more of the leads V4, V5 or V6 exceeds 27 mm.
2) The tallest R wave in any of the leads V4, V5 or V6 plus the deepest S wave in any of the leads V1, V2 or V3 exceeds 40 mm.
3) The S waves in one or more of the leads V1, V2 or V3 exceeds 30 mm.
4) The R wave in aVL exceeds 13 mm.
5) The ventricular activation time (e.g. in V6) = 0.05 s.
6) Abnormal ST segment depression (>1 mm below the isoelectric line) in any lead facing the left ventricle (i.e. V4, V5 or V6 and in leads I and aVL when the heart is horizontal or in leads II and aVF when the heart is vertical).
7) T wave inversion in leads facing the left ventricle (as in point 6 above).
Ortner Syndrome
Ortner syndrome= compression of the left recurrent laryngeal nerve from a severely dilated left atrium may result in hoarseness
Mitral Stenosis symptoms
• Dyspnea
o Progresses insidiously and patients reduce their activity without being aware of it
• Symptoms of Left HF (i.e. - PND, orthopnea, DOE) commonly in fourth decade (later symptoms of Right HF develop)
o precipitated by exertion, excitement, fever, anemia, paroxysmal tachycardia, pregnancy, fluid overload
• Possibly Palpitations or Embolic Stroke if A-fib is present
• Cough & hemoptysis
o Advanced tight mitral stenosis.
o Due to a rupture of a bronchial vein, generally self limited and does not represent an emergency situation.
Blood tinged sputum associated with pulmonary edema
Most common valvular disorder
MVP
Endocarditis Prophylaxis
Endocarditis Prophylaxis is no longer indicated in acquired valvular diseases unless....
▫ Patient has a history of bacterial endocarditis
OR
▫ Patient has had a valve replacement

Amoxicillin (Amoxil)- Prophylactic dose for bacterial endocarditis BEFORE dental or other procedures (2 GRAMS PO 1 hr BEFORE PROCEDURE)
Aortic Stenosis
-Major causes
-Pathophysiology
-Symptoms
- PE findings
-Classifying Severity
-Diagnostic Imaging
-Treatment
Major causes: Calcification of aortic valve and congenital bicuspid aortic valve (born with 2 valves instead of 3)

Pathophysiology: Chronic LV Pressure Overloading and eventually LVH occurs which may cause diastolic dysfunction with the onset of HF symptoms

Symptoms: Heart failure, Angina, Syncope

PE findings: Harsh late-peaking SEM (systolic ejection murmur) radiating to the neck heard best in the RUSB; +/- palpable systolic thrill
- slow rising carotid pulse (pulses pervious et tardus)
- S4 if LVH is present
-Narrow pulse pressure (<30)

Echo classification of AS severity: *Normal Valve is 3 cm
-Mild--> Valve area 1.5-2.0 cm and Mean Pressure Gradient <25 mmHg
-Moderate--> Valve area 1.0-1.5 cm and Mean Pressure Gradient 24-40 mmHg
-Severe--> Valve area 0.6-1.0 cm and Mean Pressure Gradient >40
Critical --> Valve area <0.6 cm

Diagnostic Imaging:
ECG- LVH with strain pattern, LBBB common, chronic ischemia
CXR- calcification of Aortic Valve and LV dilatation
ECHO- Most important diagnostic test

Treatment:
- Non surgical treatment in asymptomatic patients avoid strenuous activity
-Indications for surgery is symptomatic AS-->
cardiac cath indicated before sx to determine if CAD is also present
Exercise Stress test would be CI
Bioprosthetic valve vs Biochemical Valve placement
- treatment for non-surgical candidates that are symptomatic-->
Percutaneous Balloon Valvuloplasty (angioplasty) for temp (~6 mo) relief of symptoms
Systolic Murmurs
AS, PS, TR, MR, MVP
Diastolic Murmurs
AR,PR, TS, MS
Harsh late-peaking SEM (systolic ejection murmur) radiating to the neck heard best in the RUSB; +/- palpable systolic thrill
Aortic Stenosis
Aortic Regurgitation/Insufficiency
-Causes
-Pathophysiology
-Symptoms
-PE findings
-Diagnostics
-Treatment
Causes:
-Aortic Root causes include aortic dissection, age related dilatation, HTN and Marfan's syndrome
-Aortic Valve causes include endocarditis, rheumatic fever, Bicuspid congenital aortic valve, calcific degeneration, myxomatous degeneration, degeneration of the prosthetic valve

Pathophysiology:
-AI causes volume overload of the LV (increased LV EDV)
-LVH occurs but the ejection fraction usually is preserved until the late stages of the disease

Symptoms:
- usually remain asymptomatic for decades (4th or 5th decade)
-DOE, PND, orthopnea after significant LVH and cardiomegaly has occurred
-Angina often at night; Palpitations and Head Pounding especially in supine position

PE findings:
- High frequency, best heard over the LSB with pt sitting up and leaning fwd and holding their breath after expiration
-Duration and intensity increases with severity
Mild AI= early diastole, high pitched blowing
Severe AI= holodiastolic and rough sound
-Aortic root disease heard best over RSB
-Aortic valve disease heard best over 3-4th ICS LSB
-wide pulse pressure
-apical impulse displaced laterally or inferiorly

Diagnostics:
-ECG shows LVH strain
-CXR shows cardiomegaly, dilatation of aorta
-Echo shows LVH
-Cardiac cath confirms diagnosis

Treatment:
- vasodilators (unloads the LV, reduce SBP, improves SV, reduces regurgitant volume) - ACEI, CCB, Hydrazaline, Prazosin
- Treat CHF- diuretics, spironolactone, digoxin
- avoid vigorous exercise
-avoid BETA BLOCKERS!!

Indications for sx:
-severe AI
mild symptoms with vasodilator therapy
EF <55%
-acute AI
MEDICAL EMERGENCY, aortic valve replacement usually caused by aortic dissection, acute dysfunction of prosthetic valve and infective endocarditis
Aortic Regurgitation Murmur
- High frequency, best heard over the LSB with pt sitting up and leaning fwd and holding their breath after expiration
-Duration and intensity increases with severity
Mild AI= early diastole, high pitched blowing
Severe AI= holodiastolic and rough sound
Mitral Stenosis
-Causes
-Symptoms
-PE findings
-Diagnostics
-treatment
Caused mainly by Rheumatic Fever and majority are Female

Symptoms of dyspnea, orthopnea, and Afib are the most (symptoms of L HF and A fib )common

PE findings:
-low pitched early diastolic "rumbling" murmur with an opening snap heard best in the LLDP at the apex
-signs of PHTN (loud S2 and palpable heave) if present

Diagnostics:
-cardiac cath confirms MS
-severe stenosis is a mean pressure gradient >12 mm Hg

Treatment:
- no treatment if asymptomatic
-treat HF symptoms with medications
- treat A fib with heart rate control (b blocker) and anticoagulation (coumadin)
-Surgery for patients with severe stenosis; balloon valvuloplasty, surgical commisurotomy, Mitral valve replacement
What bacteria causes Rheumatic Fever?
Consequence of infection with group A b-hemolytic streptococci
What murmur MC is caused by Rheumatic Fever
MS
Jones Criteria for Acute Rheumatic Fever
• Major Criteria
o Sydenham's Chorea- or chorea minor (historically referred to as Saint Vitus Dance) is a disorder characterized by rapid, uncoordinated jerking movements primarily affecting the face, hands and feet.
o Transient polyarthritis
o Rheumatic subcutaneous nodules
o Erythema marginatum
o Pancarditis (pleuritic chest pain, friction rub, heart failure)
• Minor Criteria
o Fever
o Arthralgia
o Previous rheumatic fever or known rheumatic heart disease
o Elevated ESR
o Prolonged PR interval
Rheumatic Fever
• Acute rheumatic fever (ARF) is a nonsuppurative sequela that occurs two to four weeks following group A streptococcus pharyngitis and may consist of arthritis, carditis, chorea, erythema marginatum, and subcutaneous nodules. Damage to cardiac valves may be chronic and progressive, resulting in cardiac decompensation.
• Acute rheumatic fever occurs most frequently in children from 5 to 15 years of age; it is rare among children in the first three years of life and among adults.
Treatment of Rheumatic Fever
• Course of Penicillin for streptococcal infection
• Aspirin for arthralgia
• Treat HF with standard medications (ACE-I, diuretics, etc.)
• Recurrent attacks are common - Prophylaxis with Monthly Benzathine Penicillin IM should be continued for the first 5-10 years after infection
Murmur of Mitral Stenosis
Low- pitched early diastolic "rumbling" murmur with an opening snap (from the thickened mitral valve opening; high pitched) heard best in the Left Lateral position at the Apex.
Murmur of Mitral Regurgitation
• Loud high pitched pansystolic murmur with maximum intensity at apex
• Louder murmurs radiate to axilla
Mitral Valve Prolapse Causes
▫ Myxomatous degeneration is most commonly idiopathic, but may be familial. May also be caused by connective tissue disorders and muscular dystrophies.
MVP is more common among patients with Graves' disease, Marfan's Syndrome (connective tissue disorder also susceptible to AR and Aortic dissection), von Willebrand's syndrome, sickle cell disease, and rheumatic heart disease.
Murmur of Mitral Valve prolapse
o Auscultation reveals a mid-systolic click and a late systolic crescendo murmur
o Heard best at apex & LLSB with patient in LLDP
MCC of Murmur of Pulmonic Regurgitation
Pulmonary HTN
Murmur of PR
• High pitched basal blowing diastolic decrescendo murmur (Graham Steel)
• Indistinguishable in quality &timing from murmur of AI
• Usually less loud & is transmitted less widely than AI
• Point of maximum intensity usually in 2nd or 3rd LICS

Distinguishing PI from AI?
• Absence of peripheral signs of AI
MCC of Pulmonic stenosis
Congenital
Part of the tetralogy of ballot
Murmur of Pulmonic Stenosis
• Basal systolic murmur heard maximally over 2nd LICS which may radiate to carotids, left > right
• SEM diamond shaped, medium pitch, coarse; often with thril
Holosystolic Murmurs
VSD, MR, and TR
Murmur of Tricuspid Regurgitation
• Holosystolic plateau blowing murmur over RV
• PMI is nearly always near LSB at its inferior end
• May be sharply localized or transmitted to apex
• Usually of high pitch, harsh quality & best heard with diaphragm firmly held
• Inspiration makes murmur audible or accentuates it
• Decreases with expiration & valsalva maneuver
• If Pulmonary HTN present: loud P2 & palpable RV thrust
Tricuspid valve replacement
• TVR performed exclusively with porcine valves because of high incidence of mechanical valve thrombosis even with adequate anticoagulation
Murmur of Tricuspid Stenosis
• Murmur low-pitched, rumbling, diastolic of low intensity (Gr. 2/6) with presystolic crescendo when AF absent
• Best heard with bell
• Point of maximum intensity sharply localized at LLSB in 4thor 5th interspace.
• S1 is accentuated in this region
• OS may be present
• May be obscured by associated MS murmur or difficult to differentiate from MS
In patients with dilated cardiomyopathy who have multiple runs of symptomatic non-sustained ventricular tachycardia, what is the best intervention to treat this condition?

A Ablation therapy
B Heart transplantation
C Medical therapy alone
D Diet modification
E Implantable defibrillator
Implantable defibrillator
It is recommended for patients with a history of dilated cardiomyopathy who have documented non-sustained ventricular tachycardia to have implantable defibrillators inserted for primary prevention of sudden cardiac death. Medical therapy alone does not protect the patient from arrhythmias, and ablation therapy is not indicated for this type of arrhythmia.
A 67-year-old woman with a history of gastric ulcers is admitted with complaints of recent onset of dyspnea with exertion, 3 pillow orthopnea, lower extremity edema, and palpitations, in which she describes her heart as racing. Which of the following is likely to be the cause of her high-output congestive heart failure?

A Mitral regurgitation
B Aortic stenosis
C Uncontrolled hypertension
D Ruptured chordae tendinae
E Severe anemia
Severe anemia
Choice E, severe anemia, may result with progression of gastric ulcers, and is the only high-output cause of congestive heart failure among the choices offered. Other causes include severe anemia, thyrotoxicosis, and arteriovenouis shunting (for example, in hemodialysis patients). Choice A, mitral regurgitation, is a cause of excessive preload leading to heart failure. Choice D, ruptured chordate tendinae, associated with mitral regurgitation, would also be a cause of excessive preload leading to heart failure. Choices B and C, aortic stenosis and uncontrolled hypertension, are causes in which too much afterload leads to heart failure.
Causes of High Output CHF
high-output causes of congestive heart failure include severe anemia, thyrotoxicosis, and arteriovenouis shunting (for example, in hemodialysis patients).
A 47-year-old man presents with dyspnea on exertion, palpitations, and a persistent cough. He had been generally healthy up until about a week ago, when he began complaining of shortness of breath and weakness.

Physical examination of the chest reveals crackles at the bilateral bases and tachycardia. An echocardiogram shows a small mass within the right atrium. Vital signs are as follows: blood pressure 166/110 mm Hg, pulse 91 BPM, respirations 22/min, temperature 98.7°F. Biopsy reveals a malignant tumor.



Question
What is the most likely diagnosis?

Answer Choices
1 Carcinoma
2 Leukemia
3 Myxoma
4 Sarcoma
5 Lymphoma
Sarcoma
The majority of malignant heart tumors are sarcomas. A large portion of sarcomas are angiosarcomas and have a prelidection for the right atrium. They occur mostly in the age group 20 - 40 years; however, no age is spared. These types of tumors may include angiosarcomas, fibrosarcomas, rhabdomyosarcomas, and liposarcomas. Rhabdomyosarcomas and angiosarcomas are more common in men than in women.

Diagnosis of cardiac tumors is usually by echocardiography and biopsy. Left heart disease may present as obstruction of the mitral valve or often subacute bacterial endocarditis. Right heart disease may present as tricuspid valve disease, hypertension, or pulmonary embolism.

Malignant cardiac tumors are very rare, and the majority of them are due to metastatic involvement of the heart. Primary cardiac tumors are even rarer and may arise from mesothelial or epithelial tissue. They may be benign or malignant.
A 56-year-old man presents with primary hypertension. His additional medical history includes only nephrolithiasis. Past analysis of his kidney stones has revealed a calcium oxalate composition. What class of antihypertensives might best be avoided due to his history of nephrolithiasis?

Answer Choices
1 Angiotensin-converting enzyme (ACE) inhibitors
2 Beta blockers
3 Calcium channel blockers
4 Loop diuretics
5 Thiazide diuretics
Loop diuretics
Loop diuretics reduce blood pressure by decreasing fluid retention and normalizing plasma volume. Loop diuretics act on the ascending limp of the loop of Henle and block the Na+/K+/2Cl- cotransporter. They are highly potent because this transporter is responsible for the greatest proportion of renal salt and water absorption. Loop diuretics also increase urinary calcium excretion, which may enhance the formation of calcium oxalate kidney stones.
The thiazide diuretics act in the kidney at the luminal side of the distal convoluted tubule to inhibit the Na+/Cl- cotransporter and therefore increase urinary salt and water excretion. This leads to decreases in extracellular fluid and plasma volumes. Thiazide diuretics also directly reduce peripheral arteriolar resistance, thereby improving both systolic and diastolic blood pressures. In addition to their antihypertensive effect, thiazide diuretics reduce urinary calcium excretion by indirectly increasing the activity of the 2Na+/Ca2+, also in the distal tubule. This occurs because relatively more sodium is delivered to this transporter due to the blockade of the Na+/Cl- cotransporter. Therefore, they can be helpful in controlling kidney stones that occur as a result of hypercalciuria.

Angiotensin-converting enzyme (ACE) inhibitors block the conversion of angiotensin I to angiotensin II. Angiotensin II promotes the production of aldosterone, which causes sodium and water retention. Angiotensin II also stimulates the sympathetic nervous system. ACE is also responsible for the breakdown of the vasodilator bradykinin. Blockade of this enzyme therefore leads to decreased peripheral arterial resistance by a combination of these mechanisms. Because they reduce the secretion of aldosterone, ACE inhibitors can produce hyperkalemia. However, they have no impact on urinary calcium excretion.

Beta-blockers are one of the most commonly prescribed medications to treat hypertension. In the heart, beta-1 receptor blockade has negative inotropic and chronotropic effects, leading to decreased cardiac output. Nonselective beta-blockers such as propranolol also block beta-2-mediated vasodilation. This action, combined with reduced cardiac output, promotes peripheral vasoconstriction. While nonselective beta-blockers still usually lead to net reductions in systolic and diastolic blood pressures, they must be used with caution in patients with peripheral vascular disease because they reduce peripheral circulation. Similarly, since beta-2 activation produces bronchodilation, nonselective beta-blockers may exacerbate respiratory symptoms in patients with reactive airway disease. So-called selective beta-blockers act only upon beta-1 receptors, thereby improving the side effect profile of this class of antihypertensives. Reductions in cardiac output caused by beta-blockers may lead to decreased renal perfusion, promoting aldosterone production and sodium retention. However, beta-blockers do not impact calcium or other electrolyte transport in the kidneys.

Calcium channel blockers reduce intracellular transit of calcium in both cardiac and vascular smooth muscle cells. This causes a reduction in peripheral arterial resistance and coronary artery dilation. Some calcium channel blocks are also used as antiarrhythmics because they block atrial-ventricular conduction. Calcium channel blockers have no impact of renal calcium handling.
A 70-year-old man is in the ICU post-coronary artery bypass grafts. He is post-op day 9 and becomes both hypotensive and tachycardic. His blood pressure improves with 1 bolus of IV fluid. 30 minutes later, however, he becomes hypotensive again. His heart sounds are muffled and the chest tubes draining the pericardium have had decreased output over the past 3 hours. The patient is afebrile.



Question
What is the most likely etiology for this patient's hypotension?

Answer Choices
1 Hypovolemia
2 Cardiomyopathy
3 Pericardial tamponade
4 Sepsis
5 Myocardial infarction
pericardial tamponade

The scenario in this case describes Beck's triad of distended neck veins, muffled heart sounds, and hypotension seen in pericardial tamponade. Pericardial effusions are common after CABG and have been reported to occur in 22%-85% of patients. Cardiac tamponade after cardiac surgery has been reported in 0.8%-6% of patients. When this develops within the first 24 hours, it is termed early cardiac tamponade and requires surgical intervention to control the bleeding. If it occurs at least 5-7 days postoperatively, it is called late cardiac tamponade and is related to excessive mediastinal drainage. Pericardial tamponade can be seen in penetrating and (sometimes) blunt chest trauma. In this case, the patient has developed a pericardial tamponade secondary to obstruction of the chest tubes draining the pericardial sac postoperatively from a cardiac bypass graft operation. Characteristically, a fluid bolus will temporarily elevate the blood pressure in these patients.

Although a patient who is hypovolemic will demonstrate hypotension with tachycardia; they would not experience distended neck veins or rapid fluctuations in blood pressure in response to IV fluids.

The patient's presentation, along with the fact that the chest tube drainage has decreased, is indicative of cardiac tamponade and not myocardial infarction, sepsis, or cardiomyopathy.
A 43-year-old patient presents with an acute onset of palpitations and dyspnea for the past 3 hours. There is no other significant medical history. Chest X-ray and echocardiography are normal. EKG performed in the ED reveals absence of P wave with variable R-R interval with atrial rate of 300/min and ventricular rate of 120/min. Vitals: patient is afebrile, radial pulse- 90/min, BP- 110/70 mm Hg and RR- 18/min. A diagnosis of newly detected atrial fibrillation is made. What is the next course of action?

Answer Choices
1 Start diltiazem therapy
2 Start propafenone
3 Observation only
4 AV (atrioventricular) nodal ablation
5 Start amiodarone therapy
Diltiazem
In atrial fibrillation (AF), ventricular response to atrial fibrillation is usually irregular. AV node is refractory because atrial fibrillation produces a large number of impulses where not all impulses reach the ventricles. The non-conducted atrial impulses due to AV nodal refractory period are known as concealed conduction; therefore, ventricular response is relatively slow compared to atrial rate.

The initial management in a hemodynamically stable (no hypotension or angina) patient with atrial fibrillation involves control of ventricular rate (goal < 100 beats/min) by administering diltiazem or other rate controlling drugs such as verapamil, metoprolol, esmolol, or propranolol. If there is spontaneous conversion to sinus rhythm then the patient can be discharged after assessment for the cause of AF. Otherwise, the patient requires anticoagulation and electrical/chemical cardioversion at a later date. Amiodarone and propafenone are the pharmacological agents used in chemical cardioversion. AV nodal ablation and permanent pacemaker implantation are highly effective in improving symptoms in patients with AF experiencing symptoms related to a rapid ventricular rate during AF, which cannot be adequately controlled with anti-arrhythmic or negative chronotropic medications.
A 4-year-old boy presents with clubbing of his fingers, cyanosis, and a heart murmur; he is easily fatigued. A chest X-ray reveals right ventricular hypertrophy. Cytogenetic analysis of a skin biopsy reveals a 46,XY karyotype.



Question
What is the most likely diagnosis?

Answer Choices
1 Down syndrome
2 Patau syndrome
3 Edwards syndrome
4 Tetralogy of Fallot
5 Atrial septal defect
tetralogy of fallot
This child is most likely suffering from tetralogy of Fallot. This is the most common cyanotic congenital heart defect; it occurs in approximately 1/1000 live births. There are 4 major components to this condition:

Ventricular septal defect
Stenosis of the pulmonary artery
Overriding aorta (right displacement)
Hypertrophy of the right ventricle

Most cases of male patients with Down syndrome will have a 47,XY,+21 karyotype (trisomy 21). Most cases of male patients with Edwards syndrome will have a 47,XY,+18 karyotype (trisomy 18).

Isolated ventricular septal defects and atrial septal defects also occur, but they would not usually be associated with right ventricular hypertrophy.
4 major components of Tetralogy of Fallot
Ventricular septal defect
Stenosis of the pulmonary artery
Overriding aorta (right displacement)
Hypertrophy of the right ventricle
A 4-year-old boy presents with poor weight gain, small size for his age, and dyspnea upon feeding. His mother notes that the child suffers from frequent upper respiratory tract infections.

On physical exam, the child is underweight for his age. You note a precordial bulge, a prominent right ventricular cardiac impulse, and palpable pulmonary artery pulsations. You also find a widely split and fixed second heart sound as well as a mid-diastolic rumble at the left sternal border.



Question
What pharmacologic agent would be most appropriate in the medical management of this patient at this time?

Answer Choices
1 Lasix (Furosemide)
2 Coumadin (Warfarin)
3 Procardia (Nifedipine)
4 Inderal (Propranolol)
5 Indocin (Indomethacin)
The correct response is Lasix (Furosemide).

This patient's manifestations suggest a diagnosis of an atrial septal defect (ASD). ASD with moderate-to-large left-to-right shunts result in increased right ventricular stroke volume across the pulmonary outflow tract, creating a crescendo-decrescendo systolic ejection murmur. This murmur is heard in the second intercostal space at the upper left sternal border. Patients with large left-to-right shunts often have a rumbling middiastolic murmur at the lower left sternal border because of increased flow across the tricuspid valve.

Definitive therapy for ASD includes closure of the defect, which is achieved surgically or through interventional catheterization. No specific or definitive medical therapy is available; however, patients with significant volume overload or atrial arrhythmias may require specific drug therapy. For patients with large shunts and heart failure, diuretics, digoxin, and ACE inhibitors should be used before surgery.

Although patients are at risk for paradoxical emboli formation, this patient does not present with manifestations consistent with vascular occlusion. For prophylaxis following use of transcatheter occlusion devices, a common practice is aspirin for 6 months.

Propranolol may be used along with morphine sulfate, phenylephrine, oxygen, volume expansion, and knee-chest or squatting positioning to manage Tet spells associated with Tetralogy of Fallot.

Indomethacin is indicated in the closure of patent ductus arteriosus.
A 42-year-old woman was diagnosed with deep vein thrombosis of the left leg 3 weeks ago, and therapy was initiated with heparin. History includes smoking and birth control pills for endometriosis several years ago. On exam lungs show a decrease in air entry bilaterally. Which of the following is most likely?
Answer Choices
1 Lupus anticoagulant
2 Oral contraceptive induced thrombosis
3 Trousseau's syndrome
4 Heparin induced thrombosis
5 Paroxysmal nocturnal hemoglobinuria (PNH)
Explanation Trousseau's syndrome, or migratory thrombophlebitis, is a malignancy associated hypercoagulable state that is characterized by a recurrent thrombosis in a migratory pattern and involvement of superficial veins in unusual sites. It is generally associated with an occult neoplasm (50%), usually an adenocarcinoma. This patient has an extensive smoking history and possibly has an adenocarcinoma of the lung. Several mechanisms for enhanced thrombosis by tumor cells have been proposed: (1) release of a thromboplastic tissue factor, which activates the extrinsic clotting pathway (2) activated protein C resistance (3) tumor cell membranes causing direct activation of the platelets (4) tumor cells releasing a procoagulant, which activates factor X directly (5) the indirect effects on tissue factor, thrombomodulin, and other factors by cytokines derived or induced by tumor cells. Treatment is with heparin, since warfarin is ineffective, and is continued till the malignancy has been adequately eradicated.
Lupus anticoagulant is associated with increased thrombosis especially in SLE patients. Arterial and venous thromboses occur, causing placental dysfunction and frequent fetal loss. Lab findings include prolonged PTT that does not reverse when mixed with normal plasma. Presence of lupus anticoagulant and anticardiolipin antibodies confirms diagnosis. Remote single miscarriage is not enough to suspect this condition in this patient.

Oral contraceptives predispose to a hypercoagulable state, but in this patient the history of use is in the past and not current.

Heparin induced thrombosis, or the white clot syndrome, is a well-recognized complication of heparin therapy, usually occurring within 4 to 10 days after heparin treatment has started. Heparin is an anticoagulant used in various conditions like deep vein thrombosis, pulmonary embolism, hemodialysis, during and after percutaneous coronary intervention procedures like angioplasty and stent placement, and in DIC patients with thrombotic tendencies. It is the anticoagulant of choice in pregnancy since warfarin is well known for its teratogenic effects. It can be used intravenously or subcutaneously. Its principle side effect is bleeding. In cases of overwhelming hemorrhage, protamine sulphate can be used as an antidote. Heparin induced thrombosis is associated with a thrombocytopenia and thrombus formation. The more serious form (heparin-induced thrombocytopenia, type II; HIT-II) is an immune-mediated disorder characterized by the formation of antibodies against the heparin-platelet factor 4 complex. White clot syndrome refers to platelet-rich arterial thrombosis (rather than fibrin-rich venous thrombosis), which occurs with high frequency in patients who develop this disorder. Type I heparin induced thrombocytopenia is benign, occurs within two days of starting therapy, and resolves with continued administration of heparin. For other cases, discontinuation of heparin, administration of dextran, and arterial thrombectomy are tried. Urokinase may also help. Platelet count every 3 days for patients on heparin is necessary, and once thrombocytopenia is detected, it should be stopped. This patient had heparin administered to her several weeks ago and is unlikely to have thrombosis due to that.
A 66-year-old man with a past medical history of diabetes mellitus type II, reflux esophagitis, hypothyroidism, and hyperlipidemia presents with constant, severe "squeezing, crushing chest pressure and tightness" that is experienced in left chest, left shoulder pain and epigastrum. He states that he had just eaten breakfast when the pain began and that his pain has persisted over the last 45 minutes. He denies any additional provoking or relieving factors, including an over-the-counter antacid. He admits to associated weakness, lightheadedness, nausea, and 2 episodes of vomiting. He denies fever, chills, cough, shortness of breath, hemoptysis, or pleurisy.

Upon physical exam, he is found to be anxious and restless while his skin was cool and diaphoretic. His blood pressure is 140/91, and he has an obese BMI. His chest is free of deformity or tenderness. His heart rate was normal with a regular rhythm and free of murmurs, gallops, or rubs. His cardiac, musculoskeletal, and pulmonary exams were normal. A bedside EKG revealed ST-segment elevations of 2 mm in 3 anatomically contiguous leads.



Question
What is the most likely diagnosis?

Answer Choices
1 Peptic ulcer disease
2 Bacterial pneumonia
3 Myocardial infarction
4 Acute pericarditis
5 Pulmonary embolism
MI
This patient's most likely diagnosis is acute myocardial infarction. The pain associated with this diagnosis is deep and visceral; it is typically described as heavy, squeezing, and crushing, and less commonly as stabbing or burning. It is similar in character to the discomfort of angina pectoris but commonly occurs at rest, is usually more severe, and lasts longer. Unlike angina, it is not relieved with rest if precipitated by exertion. Typically, the pain involves the central portion of the chest and/or the epigastrium, and, on occasion, it radiates to the arms. Less common sites of radiation include the abdomen, back, lower jaw, and neck. It is often accompanied by weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom. Additional physical exam findings include anxiousness, restlessness, pallor, diaphoresis, cool extremities, an S3 or S4 gallop, paradoxical splitting of the second heart sound, a transient midsystolic or late systolic apical systolic murmur due to dysfunction of the mitral valve, pericardial friction rub with transmural STEMI. Notable ECG findings include ST-T segment (>1-mm elevation or depression) and T-wave (inversion) changes suggest ischemia; Q-wave suggests accomplished infarction; ST-elevation is absent in unstable angina and NSTEMI; new bundle branch block or sustained ventricular tachycardia indicates a higher risk of progression to infarction.

Burning epigastric pain is the most classic symptom of peptic ulcer disease. The pain also may be described as sharp, dull, an ache, or an "empty" or "hungry" feeling. Pain may be relieved by ingestion of milk, food, or antacids, presumably due to buffering and/or dilution of acid.

Pneumonia is characterized by acute or subacute onset of fever, cough with or without sputum production, and dyspnea. Other common symptoms include sweats, chills, rigors, chest discomfort, pleurisy, hemoptysis, fatigue, myalgias, anorexia, headache, and abdominal pain. Common physical findings include fever or hypothermia, tachypnea, tachycardia, and arterial oxygen desaturation. Many patients appear acutely ill. Chest examination often reveals inspiratory crackles and bronchial breath sounds. Dullness to percussion may be observed if lobar consolidation or a parapneumonic pleural effusion is present.

Pericarditis is usually preceded by viral infections, especially infections with coxsackieviruses and echoviruses. It is characterized by chest pain, which is usually pleuritic and postural (relieved by sitting). The pain is substernal but may radiate to the neck, shoulders, back, or epigastrium. Dyspnea may also be present and the patient is often febrile. A pericardial friction rub is characteristic. The ECG usually shows generalized ST and T wave changes and may manifest a characteristic progression beginning with diffuse ST elevation, followed by a return to baseline and then to T wave inversion.

Nearly all pulmonary emboli arise from deep venous thrombosis (DVT) in the lower extremity or pelvic veins. Risk factors for DVT and PE are similar in children and adults and include conditions that impair venous return, conditions that cause endothelial injury or dysfunction, and underlying hypercoagulability disorders. Larger emboli cause acute dyspnea, pleuritic chest pain, or both. Dyspnea may be intermittent or occur only with exercise. Less common symptoms include cough and hemoptysis. The most common signs of PE are tachycardia and tachypnea. Less commonly, patients have hypotension, a loud 2nd heart sound (S2) due to a loud pulmonic component (P2), and crackles or wheezing. ECG most often shows tachycardia and various ST-T wave abnormalities, which are not specific for PE. An S1Q3T3 or a new right bundle branch block may indicate the effect of abrupt rise in right ventricular pressure on right ventricular conduction; these findings are moderately specific but insensitive for PE.
An 86-year-old woman presents with recent onset of intractable headaches, jaw claudication, and visual field changes, including diplopia. Her past medical history is significant for Polymyalgia Rheumatica.

Question
Based on the most likely diagnosis, what is the primary reason for prompt diagnosis and treatment of this condition?

Answer Choices
1 Prevent blindness
2 Prevent stroke
3 Prevent facial palsy
4 Prevent myocardial infarction
5 Prevent hemorrhage
Prevent Blindness
Based on the classic presentation of jaw claudication, intractable headache, and visual field changes, your index of suspicion should be high for Giant Cell Arteritis. Prompt treatment is necessary to prevent permanent blindness; it can be caused by an occlusive arteritis of the ophthalmic artery. Treatment consists of prednisone, 60mg given daily, immediately and a temporal artery biopsy performed after treatment initiated.

The other choices are not the primary reason for prompt diagnosis and treatment of giant cell arteritis; however, the others may also be prevented with prompt treatment.
After successful cardioversion for atrial fibrillation (AF), a 65-year-old woman with rheumatic mitral valve disease patient feels better, with the exception of slight weakness in her left arm as a consequence of previous ischemic stroke. Her blood pressure is 120/80; her EKG is normal and shows sinus rhythm with rate 75.



Question
What chronic medical therapy is recommended?

Answer Choices
1 Warfarin
2 Aspirin
3 Ticlopidine
4 Clopidogrel
5 Propafenone
warfarin
Chronic antithrombotic therapy should be considered for all patients with AF and risk factors for stroke regardless of whether or not they remain in sinus rhythm. Having rheumatic mitral valve disease and previous ischemic stroke, your patient is at high risk for a cerebrovascular event. Other conditions that put patients at high risk are: transient ischemic attack, or other systemic embolic event; age >75 years; moderate or severe systolic dysfunction of the left ventricle and/or congestive heart failure; and hypertension or prosthetic heart valve. Therefore, you will advise chronic warfarin treatment with target INR in the range of 2 to 3 in this patient.

Only patients at low risk (age<65 years with none of the high-risk factors) should receive only aspirin.
Oliguria in CHF
Oliguria is associated with a markedly reduced cardiac output and is usually a sign of terminal heart failure, indicating a poor prognosis.
Symptoms of essential HTN
Mild-to-moderate primary (essential) hypertension is largely asymptomatic for many years. The most frequent symptom, which is a headache, is also very nonspecific. Accelerated hypertension is associated with somnolence, confusion, visual disturbances, and nausea and vomiting; they are common to hypertensive encephalopathy. Hypertensive retinopathy may cause papilledema, intraretinal hemorrhages, nerve fiber layer infarcts (cotton-wool spots), arteriovenous (AV) nicking, banking or beading, or copper or silver wiring of the retinal vessels.
A 73-year-old man with no significant past medical history presents with a 1-month history of light-headedness, dizziness, and near syncope; it has been occurring in response to sitting up and standing from a supine position. He denies chest pain, palpitations, shortness of breath, cough, loss of consciousness, vision or speech changes, nausea or vomiting, numbness, tingling, paresthesias, and focal weakness. His physical exam is noteworthy for a drop of systolic blood pressure of 24 mm Hg from a supine to standing position.



Question
What clinical intervention should be recommended to this patient?

Answer Choices
1 Begin clonidine or a diuretic
2 Fludrocortisone and compression stockings
3 Large, carbohydrate meal consumption
4 Sodium and water restrictions
5 Rise rapidly from seated and supine positions
Fludrocortisone and compression stockings

This patient is presenting with signs and symptoms consistent with orthostatic hypotension. It is defined as a reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mm Hg within 3 minutes of standing or head-up tilt on a tilt table. It is a manifestation of sympathetic vasoconstrictor (autonomic) failure. The use of compression stockings and medications such as fludrocortisone are of benefit in reducing orthostatic hypotension.

Further interventions that should be made include the discontinuance of any provocative medications, if possible. These medications include clonidine, methyldopa, anticholinergics, opioids, muscle relaxants, tricyclic antidepressants, alpha adrenergic or beta blocking medications, vasodilators, diuretics or quinidine, barbiturates, Parkinsonism agents, and phosphodiesterase type 5 inhibitors.

Recommended dietary interventions include increasing salt and water consumption. This is indicated for 24 hour urinary sodium <170 mmol sodium in 24 hours. 1 to 2 grams extra should be supplemented per day; this should be avoided in CHF or edematous states. Water intake should be in excess of 64 ounces daily, with avoidance of alcohol and large carbohydrate-rich meals; instead, smaller and more frequent meals are recommended.

Activities that are helpful in the management include avoiding heat exposure or strenuous exercise, sleeping with the head of bed slightly elevated, and rising slowly from the bed, allowing for equilibration. Other activity modifications such as avoidance of standing for long periods, isometric exercises, frequent movement or crossed legs while standing, avoidance of work with the arms above shoulder height and performance of dorsiflexion of the feet prior to standing are all considered supportive.
WPW
Individuals with Wolff-Parkinson-White syndrome have an additional aberrant muscular or nodal tissue connection (bundle of Kent) between the atria and ventricles. This conducts more rapidly than the slowly conducting AV node, and one ventricle is excited early. The manifestations of its activation merge with the normal QRS pattern, producing a short PR interval and a prolonged QRS deflection slurred on the upstroke, with a normal interval between the start of the P wave and the end of the QRS complex ("PJ interval"). The QRS complexes show an abnormal morphology with a width greater than the baseline QRS complex (often >0.11 second), with the characteristic initial slurring referred to as a delta wave.

The paroxysmal atrial tachycardias seen in this syndrome often follow an atrial premature beat. This beat conducts normally down the AV node but spreads to the ventricular end of the aberrant bundle, and the impulse is transmitted retrograde to the atrium. A circus movement is thus established. Less commonly, an atrial premature beat finds the AV node refractory but reaches the ventricles via the bundle of Kent, setting up a circus movement in which the impulse passes from the ventricles to the atria via the AV node.
An 84-year-old man with poorly controlled hypertension is evaluated for severe chest pain that came on suddenly; the pain is accompanied by an episode of syncope. The chest pain is described as "ripping", and it radiates to the abdomen and back. There is no known history of trauma, injuries or accidents; he denies any fever, chills, cough, dyspnea, palpitations, nausea, vomiting or diarrhea.

The physical exam is notable for tachycardia, a blood pressure of 188/120, and a high-pitched blowing decrescendo murmur at the right 2nd interspace.



Question
What agent is the preferred initial treatment in the management of this patient?

Answer Choices
1 Nitroprusside
2 Diltiazem
3 Morphine sulfate
4 Enalapril
5 Labetalol
Labetalol
This patient is most likely experiencing an aortic dissection. Unless they are leaking or ruptured, medical management remains the treatment of choice for descending aortic dissections. Medical management consists of decreasing the blood pressure and the shearing forces of myocardial contractility in order to decrease the intimal tear and propagation of the dissection. Medical management with antihypertensive therapy, including beta-blockers, is the treatment of choice for all stable chronic aortic dissections. The agent of choice for this patient consists of a negative inotropic medication, such as labetalol, as it has a dual effect of decreasing blood pressure and cardiac contractility. The target heart rate for patients with aortic dissection is 60-80 bpm.

Nitroprusside causes peripheral vasodilation by direct action on venous and arteriolar smooth muscle, thereby reducing peripheral resistance. Before initiating nitroprusside, a beta-blocker should be used to offset the reflex tachycardia that occurs when nitroprusside is used alone. This physiologic response increases shear forces against the aortic wall.

When beta-blockers are contraindicated, (second- or third-degree atrioventricular block), a calcium channel blocker such as diltiazem should be considered.

Pain control may be achieved by morphine sulfate and is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and prevents exacerbations of tachycardia and hypertension, reducing the force of cardiac contraction and the rate of rise of the aortic pressure. It then retards the propagation of the dissection and delays rupture.

ACE inhibitors may be added in conjunction to β-antagonists in the chronic drug therapy of aortic dissections.
A 57-year-old woman presents with progressive dyspnea and lower extremity edema. She has noticed the symptoms occurring over the last 3 months and also notes increasing fatigue over the last year. Past medical history is significant for diabetes and hypertension. Past social history is significant for previous alcohol abuse; patient has been sober for approximately 5 years. On physical examination, an S3 gallop is heard. Electrocardiogram reveals ST-T changes. Echocardiogram reveals left ventricular dilatation with an ejection fraction of 35%.



Question
What is the most likely diagnosis in this patient?

Answer Choices
1 Hypertrophic cardiomyopathy
2 Restrictive cardiomyopathy
3 Dilated cardiomyopathy
4 Inflammatory pericarditis
5 Constrictive pericarditis
Dilated cardiomyopathy is correct. Dilated cardiomyopathy occurs when the left ventricle becomes dilated and weakened. As a result, the heart is unable to efficiently pump blood, leading to symptoms of fluid overload. The majority of cases are idiopathic, but alcohol abuse is a cause. An S3 gallop may be heard on cardiac auscultation. Echocardiogram will reveal a dilated left ventricle with decreased ejection fraction.

Hypertrophic cardiomyopathy is incorrect. Hypertrophic cardiomyopathy occurs when the myocardium is abnormally thickened, causing impaired contractile function. It is associated with a hereditary syndrome. It typically presents with dyspnea, chest pain, and syncope. Echocardiogram will reveal left ventricular hypertrophy.

Restrictive cardiomyopathy is incorrect. Restrictive cardiomyopathy is characterized by impaired diastolic filling with maintenance of the heart's ability to contract. Echocardiogram will reveal a small or normal sized left ventricle with decreased function.



Inflammatory pericarditis is incorrect. Inflammatory pericarditis is caused by inflammation of the pericardium. It may be caused by infection or systemic disease. Patients typically present with pleuritic chest pain. Electrocardiogram commonly reveals diffuse ST elevation. Echocardiogram may be normal but often reveals a pericardial effusion.

Constrictive pericarditis is incorrect. Constrictive pericarditis occurs when the pericardium becomes thickened and dilated. Echocardiogram may occasionally show a thickened pericardium. It is difficult to distinguish from restrictive cardiomyopathy and may require cardiac catheterization for diagnosis.
A 68-year-old man with a past medical history of hypertension, hyperlipidemia, cluster headaches, polymyalgia rheumatica, and diabetes mellitus type II presents due to a 2-day history of left-sided, throbbing, and constant headache of moderate severity. He admits to associated symptoms such as pain across his mandible when he eats, fever, fatigue, and muscle aches. Most alarming to the patient was a single episode of complete left eye blindness that lasted for 30 minutes, but has since resolved. He denies extremity numbness, tingling, muscle weakness, incontinence, and changes in mental status. He further denies rhinorrhea, ocular discharge, nausea, and vomiting. The physical exam was remarkable only for a tender left scalp with a noticeable pulsation underlying the tender area.


Question
What is the most likely diagnosis?
Answer Choices
1 Bell's palsy
2 Herpes Zoster ophthalmicus
3 Cerebrovascular accident
4 Cluster headache
5 Temporal arteritis
Explanation This patient most likely has temporal arteritis. This patient has a past medical history of polymyalgia rheumatica, which portends a risk of clinical temporal arteritis of 10-15%. Symptoms include headache localized to the arteries of the scalp; polymyalgic symptoms (constitutional) may occur in over 50% of patients. Cranial artery tenderness, masseter claudication, and amaurosis fugax are all common manifestations.

The presence of persistent, moderately severe headache, and absence of facial drooping, muscle paresis, drooling, and eyelid weakness reliably exclude the diagnosis of Bell's palsy.

The lack of dermatomal findings on physical exam consistent with Herpes zoster (grouped vesicles on an erythematous base in a dermatomal distribution) and prodromal pruritis, numbness, burning, and tingling make herpes zoster unlikely.

Although this patient has strong risk factors that may contribute to ischemic stroke development, additional stroke manifestations beyond hemianopia, such as hemisensory loss, hemiparesis or paralysis, dysarthia, aphasia, ataxia, vertigo, or changes in consciousness, are not experienced here.

The typical descriptive features of cluster headaches are an intense, nonthrobbing, unilateral retroocular headache that is stabbing or burning and accompanied by ipsilateral lacrimation, nasal stuffiness, and facial flushing. Ipsilateral ptosis and miosis may also be present.
Troponin
Troponin is a complex of regulatory proteins that are integral to the contraction of skeletal and cardiac muscles. It is a marker for several heart disorders, but it is not a cause of myocardial infarction.
roponin tests are sometimes ordered along with other cardiac biomarkers, such as CK-MB or myoglobin.

However, troponin is the preferred test for a suspected heart attack because it is more specific for heart injury than other tests (which may be elevated in the blood with skeletal muscle injury) and remain elevated for a longer period of time.

Levels of troponin can become elevated in the blood within 3 or 4 hours after heart injury and may remain elevated for 10 to 14 days.

Interpretation of Troponins:
The upper limit for normal individuals is <0.01 ng/mL (undetectable by this method).

For patients who present with acute coronary syndromes, troponin T values > or =0.01 ng/mL that are rising make the diagnosis of cardiac injury. Decreasing values are indicative of recent cardiac injury.

Troponin T values > or =0.01 ng/mL are a prognostic sign in patients with ischemic heart disease and most other situations. Clinical judgment is necessary to distinguish patients who have ischemic heart disease from those who do not. However, all patients with > or =0.01 ng/mL troponin T are at increased risk for cardiac events relative to patients with undetectable troponin T.

Patients with low level (<0.20 ng/mL) elevations of troponin T and diagnostic uncertainty for acute coronary syndrome should be evaluated by repeat measurements at 3 and 6 hours including a delta between these time points to determine whether this is an acute or more chronic elevation. However, all patients with > or =0.01 ng/mL troponin T are at increased risk for cardiac events relative to patients with undetectable troponin T.
How do you best describe dilated cardiomyopathy?

Answer Choices
1 Left ventricular volume is either normal or reduced, and diastolic dysfunction is almost always present.
2 Non-dilated ventricles with impaired ventricular filling.
3 Dilatation and impaired contraction of one or both ventricles.
4 Transient systolic dysfunction of the apical and/or mid segments of the left ventricle that is often provoked by stress.
5 Diffuse thickening of the left ventricular endocardium secondary to proliferation of fibrous and elastic tissue.
The description "dilatation and impaired contraction of one or both ventricles" explains dilated cardiomyopathy.

"Left ventricular volume is either normal or reduced and diastolic dysfunction is almost always present" explains hypertrophic cardiomyopathy.

"Nondilated ventricles with impaired ventricular filling" explains restrictive cardiomyopathy.

"Transient systolic dysfunction of the apical and/or mid segments of the left ventricle that is often provoked by stress" explains Takotsubo syndrome.

"Diffuse thickening of the left ventricular endocardium secondary to proliferation of fibrous and elastic tissue" explains endocardial fibroelastosis.
A 35-year-old Caucasian woman presents with consistent Stage I hypertension on 3 separate visits and has already attempted lifestyle changes to decrease blood pressure with little success. You decide to start her on hydrochlorothiazide 25 mg daily and have her return in 1 week for a blood pressure check.
Which of the following statements is true about thiazide diuretics?

Answer Choices
1 They inhibit sodium reabsorption in the distal tubule
2 They inhibit sodium reabsorption in the proximal convoluted tubule
3 They act as aldosterone receptor antagonists in the distal tubule
4 They inhibit sodium-potassium-chloride transport in the ascending Loop of Henle.
5 They inhibit the transport of bicarbonate out of the proximal convoluted tubule
They inhibit sodium reabsorption in the distal tubule
Explanation The correct answer is they inhibit sodium reabsorption in the distal tubule by inhibiting the sodium-chloride transporter. Decreased sodium in the interstitium leads to less water reabsorbed.
Carbonic anhydrase inhibitors act on the proximal convoluted tubule by inhibiting carbonate from being reabsorbed in the interstitium leading to increased sodium, bicarbonate, and water in the urine. Potassium-sparing diuretics act as aldosterone receptor antagonists in the distal tubule causing more water and sodium to pass through the tubule. Loop diuretics inhibit the reabsorption of sodium in the thick ascending loop increasing sodium and water loss and eventually potassium loss in the distal tubule.
An African-American neonate suffers from respiratory distress and cyanosis shortly after birth. On physical examination, you note the presence of IV/VI ejection-type systolic murmur that is heard at the mid and upper left sternal borders. Also present on auscultation is a right ventricular tap along the left sternal border with a systolic thrill at the upper and mid-left sternal borders. The S2 heart sound is single with an absent pulmonic component. Electrocardiogram reveals right axis deviation with mild right ventricular hypertrophy.

Chest X-ray examination reveals: (1) enlarged right atrium (2) decreased pulmonary vascular markings (3) a "boot-shaped" heart.



Question
What defect is part of this patient's condition?

Answer Choices
1 Aortic stenosis
2 Atrial septal defect
3 Transposition of the great vessels
4 Ventricular septal defect
5 Anomalous coronary artery
VSD
A ventricular septal defect is a component of the classic and often tested congenital heart anomaly known as Tetralogy of Fallot. Tetralogy of Fallot consists of 4 structural defects: (1) ventricular outflow tract obstruction (usually sub-pulmonic stenosis), (2) ventricular septal defect (VSD), (3) right ventricular hypertrophy, and (4) an overriding aorta. Physical findings include an ejection click that originates in the aorta and a single S2 because only the aortic component can be heard. A long, loud (grade 3 - 5/6) ejection-type systolic murmur is heard at the mid and upper left sternal borders. This murmur originates from the pulmonary stenosis but may be easily confused with the holosystolic regurgitant murmur of the associated VSD.

The classic radiographic finding of Tetralogy of Fallot is the 'boot-shaped' heart associated with right atrial enlargement and decreased pulmonary vasculature. Electrocardiography findings include right ventricular hypertrophy and right axis deviation. Some patients with Tetralogy of Fallot exhibit frank cyanosis shortly after birth, which usually indicates a more severe right ventricular outflow obstruction; whereas, other patients progressively develop cyanosis in childhood, leading to infamous 'tet spells'. These 'tet spells' are characterized by a paroxysm of hyperpnea (rapid and deep respiration), irritability and prolonged crying, increasing cyanosis, and decreasing intensity of the heart murmur. These hypoxic spells occur in infants, with a peak incidence between 2 and 4 months of age; they usually occur in the morning after crying, feeding, or defecation. A severe spell may lead to limpness, convulsion, cerebrovascular accident, or even death. These 'tet spells' are usually treated by placing the infant in a knee-chest position, giving morphine sulfate to abolish hyperpnea, and adding oxygen. If the hypoxic spell is refractory to these medications, phenylephrine, ketamine, and propanolol may be tried. Tetralogy of Fallot can be repaired by pediatric cardiovascular surgeons using the classic Blalock-Taussig shunt procedure, by which an anastomosis is formed between the subclavian artery and the ipsilateral pulmonary artery.
A 64-year-old woman with a past medical history of hyperthyroidism presents with new-onset palpitations. The patient states that she has intermittent palpitations, and she is worried about heart disease. She is currently asymptomatic and reports no chest pain or shortness of breath. An EKG is obtained. Vital signs reveal a T 98.6° F, BP 134/88 mm Hg, P 119 beats/min R 12/min. The pulse is noted to be irregular. The EKG is shown below.



Question
What arrhythmia does this patient most likely have?

Answer Choices
1 Atrial flutter
2 Atrial fibrillation
3 Supraventricular tachycardia
4 Ventricular tachycardia
5 Torsades de pointes
The correct answer choice is atrial fibrillation. This patient has a history of hyperthyroidism, an irregularly irregular pulse, and an EKG finding of varying R-R interval and fibrillatory F waves in place of P waves, which is consistent with atrial fibrillation. Irregular rhythm as well as lack of P waves is particularly noted in leads II, III, and aVF. AF is typically treated with rate control in stable patients (not pharmaceutically) or cardioversion in an unstable patient.

Atrial flutter would typically present with the classic "saw-tooth" appearance, most noted on leads II, III, and aVF. In addition, the pulse would typically be much faster.

Supraventricular tachycardia is a rhythm that typically has a narrow QRS complex. However, aberrant conduction can lead to wide complex tachycardia that occasionally mimics ventricular tachycardia. This patient is not in ventricular tachycardia. The QRS complexes would be wide.

Torsades de pointes, which literally means 'twisting of the points' in reference to the characteristic appearance, is an uncommon variant of ventricular tachycardia. It typically occurs as a complication of certain drugs, which cause a blockade of potassium channels, leading to a prolonged QT interval.
A 37-year-old Caucasian man has presented with shortness of breath (SOB). Further history reveals that the patient has been extremely fatigued in the last few weeks, experiencing excessive night sweats, possesses a worsening cough, chest pain, as well as general aches and pains. The patient currently is not taking any prescribed medications and is allergic only to penicillin. He has a history of on-and-off intravenous drug use and admits to last using around 1 month ago. Along with an urgent inpatient admission, you are planning to initiate orders to have the patient undergo an echocardiogram and obtain blood cultures, among other actions.



Question
Based on the most likely diagnosis for this patient, which of the following pharmaceutical interventions is most appropriate?

Answer Choices
1 Intravenous corticosteroids
2 Intravenous diuretics
3 Intravenous nafcillin
4 Intravenous cefazolin
5 Intravenous oxacillin
IV cefazolin
the patient in the above scenario is experiencing infective endocarditis, most likely secondary to his injection drug use. In injection drug users, Staphylococcus aureus accounts for at least 60% of bacterial endocarditis cases; up to 90% of patients in these similar scenarios will have the tricuspid valve infected.

Typically all patients with infective endocarditis will have a fever during the course of the disease; this is evident through the patient admitting to have significant night sweats. Duration is usually a few days and progressively worsens over a matter a weeks, which is consistent with the above. Symptoms can include dyspnea, cough, athralgias, arthritis, and diarrhea, as well as abdominal, back, or flank pain.

Blood cultures will confirm the diagnosis of infective endocarditis. An echocardiogram will show the overall mechanical function of the heart as well as possible evidence of the involved valves, such as vegetation.

In regards to pharmaceutical treatment, all penicillins are ruled out due to the patient's history of a penicillin allergy; therefore, intravenous nafcillin and oxacillin are incorrect choices. Intravenous corticosteroids as well as intravenous diuretics would not begin to resolved infective endocarditis. Intravenous cefazolin, a first-generation cephalosporin, or gentamycin would be the most appropriate choices for the patient scenario above.
A 19-year-old man is brought into the ER following a motor vehicle crash in which he, the driver, sustained blunt trauma to the anterior trunk from striking the steering wheel and dashboard. The patient is alert, short of breath, hypotensive, and complains of acute chest pain. On auscultation, muffled heart sounds are heard. What is your initial diagnosis?
Answer Choices
1 Pericarditis
2 Acute Myocardial Infarction
3 Pulmonary Edema
4 Tension pneumothorax
5 Pericardial Tamponade
pericardial tamponade
Explanation The clinical picture is suggestive of pericardial tamponade. Patients with pericardial tamponade often complain of shortness of breath. The most common symptom is dyspnea. The patient can also present with elevated jugular venous pressure, hypotension, and muffled heart sounds.

Pericarditis presents with severe chest pain, sharp retrosternal onset with radiation to the back and worsening with a deep breath or cough. Also, the pain is position dependant, worse when lying flat and better when leaning forward. On physical examination, a pericardial friction rub is pathognomonic of pericarditis. It is a high-pitched squeaking sound. These signs and symptoms are not present in this patient.

Signs and symptoms of an acute myocardial infarction may include sudden development of prolonged anterior chest discomfort that may produce arrhythmias, hypotension, shock, or cardiac failure. Sometimes they may be painless. ECG changes can be noted, specifically ST-segment elevations or depressions, presence of Q-waves or symmetric inversions of T-waves. Elevations of cardiac markers (troponins, CK-MB) may be seen. These are not present in this patient.

Muffled heart sounds are not heard in pulmonary edema or a tension pneumothorax.
Pericarditits
Pericarditis presents with severe chest pain, sharp retrosternal onset with radiation to the back and worsening with a deep breath or cough. Also, the pain is position dependant, worse when lying flat and better when leaning forward. On physical examination, a pericardial friction rub is pathognomonic of pericarditis. It is a high-pitched squeaking sound.

Acute pericarditis. Inflammation of the pericardium can occur as the result of an infectious source (including viruses, bacteria, TB, fungal, and parasitic sources), medications, systemic diseases (such as SLE), post MI (also known as Dressler's syndrome), uremia, or malignancy; there may also be no known cause.1 Pericarditis typically presents with substernal cheat pain that is aggravated by deep breathing and alleviated by leaning forward.1 The hallmark of pericarditis the finding of pericardial friction rub on exam.1 In addition to exam findings, patients with suspected pericarditis should undergo a CXR (may reveal cardiomegaly if a pericardial effusion is present), a CBC (often demonstrates leukocytosis), a BMP (to evaluate for uremia), a BHCG (necessary prior to imaging in a woman of childbearing age), EKG (may demonstrate diffuse ST segment elevation), and an ECHO (needed to evaluate for pericardial effusion and/or tamponade).1
Pericardial Tamponade
Patients with pericardial tamponade often complain of shortness of breath. The most common symptom is dyspnea. The patient can also present with elevated jugular venous pressure, hypotension, and muffled heart sounds.
A 72-year-old man presents with double vision, weakness, fatigue, nausea, and abdominal discomfort. He describes seeing everything greenish. He suffers from congestive heart failure and is treated for that with digoxin, furosemide, and potassium. He has been taking acetylsalicylic acid since a TIA 2 years ago. He also takes amoxicillin for a urinary tract infection. What medication can cause his symptoms?
Answer Choices
1 Digoxin
2 Furosemide
3 Potassium
4 Acetylsalicylic acid
5 Amoxicillin
Digoxin
These symptoms are typical for digitalis toxicity, therefore it is digoxin causing them. Digoxin is a cardiac glycoside. It is used to treat congestive heart failure, mostly supraventricular tachycardia and cardiogenic shock. It increases the force of cardiac contraction and decreases the conduction rate of the AV node. It can be administered orally, intramuscularly, and intravenously.
Furosemide is a loop diuretic used in congestive heart failure, hepatic, or renal disease as well as hypertension. It can be administered orally, intramuscularly, and intravenously. Major side effects can be: blood disorders, bruising, dark urine, dry mouth, gout, impotence, increase in blood sugar, irregular heartbeat, loss of appetite, muscle cramps, rash, tinnitus, paresthesias, vomiting, and jaundice.

Potassium is a metallic element of the alkali group; its salts are used in medicine. It is the chief cation of the muscle cell and most other cells. Low potassium levels are side effects of therapy with loop diuretics and can lead from weakness to paralysis and electrocardiographic abnormalities (depression of T-wave and elevation of U-wave).

Hyperkalemia is usually caused by defective renal excretion. It is characterized by electrocardiographic abnormalities (elevation of T-wave and depression of U-wave) and can also lead to flaccid paralysis.

Acetylsalicylic acid, commonly known as aspirin, is an anti-inflammatory, analgesic, and antipyretic drug. It inhibits the prostaglandin synthesis and is used for relief of fever and pain, the treatment of osteoarthritis and rheumatoid arthritis, and the prevention of cerebrovascular incidents. Common side effects are dizziness, tinnitus, headache, asthma, and intestinal ulceration.

Amoxicillin is a semi-synthetic derivative of ampicillin. It is an antibiotic, and it is especially efficient against gram positive and gram negative bacteria. Common side effects are: diarrhea, loss of appetite, nausea, vomiting, breathing difficulties, joint pain, fever, sore throat, and candidiasis.
A 25-year-old woman had an episode of angina. On physical exam you notice a systolic heart murmur that is best heard at the 2nd right intercostal space. Valsalva, standing, and handgrip maneuvers decrease the intensity of the murmur. A transesophageal echocardiogram reveals a bicuspid aortic valve among other findings.



Question
What adaptive response is most likely to be present in the left ventricular wall muscle of this patient's heart?

Answer Choices
1 Hypertrophy
2 Hyperplasia
3 Fibrosis
4 Metaplasia
5 Atrophy
Hypertrophy
The clinical and echocardiographic findings are consistent with aortic stenosis. Left ventricular hypertrophy is most likely present. Hypertrophy is the increase in cell size and function capacity commonly observed in cardiac muscle cells. In this case, the congenital anomaly in the aortic valve creates an obstacle (aortic stenosis) to the blood flux out of the left ventricle. This leads to the systolic murmur and an increase in pressure inside the ventricle. The increased chamber pressure acts chronically on the cardiac muscle cells, leading to the adaptive response of hypertrophy. Macroscopically, the result is an increase in the thickness of the left ventricular myocardial walls.

Cardiac and skeletal muscle cells are unable to replicate after the embryogenesis period; therefore, they are classified as permanent cells. When they face a stimulus that signals to proliferation, hypertrophy is the only adaptive response that can occur.
A 54-year-old man presents with a 30-minute history of oppressive retrosternal chest pain that radiates to the left arm. The physical examination reveals a BP= 170/100mmHg, P= 90/min, R= 24/min with normal cardiac and lung auscultation. The initial EKG shows an elevation of ST segment in leads V3 and V4. What artery is most likely compromised in this patient?

Answer Choices
1 Septal branch of left anterior descending artery
2 Diagonal branch of left anterior descending artery
3 Circumflex branch of left coronary artery
4 Posterior descending branch of right coronary artery
5 Proximal branches of right coronary artery
Correct Answer: Diagonal branch of left anterior descending artery

The patient's history is compatible with an acute myocardial infarction. The EKG shows an elevation of ST segment in leads V3 and V4, which reflect the anterior wall of the left ventricle. The diagonal branch of the left anterior descending artery-LAD (a branch of left coronary artery) supplies this anatomic area. The LAD-septal branch supplies the septum, represented by leads V1 and V2. LCA-circumflex branch supplies the high lateral wall of left ventricle, represented by V5, V6, DI, and aVL. RCA (Right Coronary Artery) posterior descending branch supplies the inferior and posterior wall of left ventricle, represented by leads DII, DIII, and aVF. RCA-proximal branch supplies right ventricle, inferior, and posterior wall of left ventricle, represented by leads V4R, DII, DIII, and aVF.
Which of the following complications is commonly associated with subarterial VSD?

Answer Choices
1 Infective endocarditis
2 Pulmonary hypertension
3 Congestive cardiac failure
4 Cor pulmonale
5 Aortic insufficiency (AI)
AI
In subarterial VSD, the defect occurs in the outlet septum and is also known as the supracristal, conoseptal, or outlet VSD. It is referred to as subarterial VSD, as the aortic and pulmonary valves are in fibrous continuity with the outlet septum. Subarterial VSDs are commonly associated with aortic insufficiency. The VSDs that are complicated by AI are restrictive with high velocity shunting through the VSD. This creates a low-pressure zone, which impacts the adjacent aortic valve cusp, resulting in aortic valve prolapse (AVP), and subsequent AI.

AI complicates about half of subarterial VSD patients, hence, patients with a subarterial VSD and AVP should undergo surgery to prevent the development of AI, as spontaneous closure is rare.

To prevent development of aortic cusp prolapse, and subsequent AI, subarterial VSD of 5 mm or more should be closed as early as possible.

VSDs create abnormal blood flows that predispose to infective endocarditis. Patients with VSD should be given antibiotic prophylaxis before procedures that produce bacteremia. The patient's risk of developing infective endocarditis is higher for VSD with aortic insufficiency than it is for an isolated VSD.

The left to right shunt of VSD eventually leads to pulmonary hypertension, with a reversal of flow (Eisenmenger's complex). The heart will have an increased load due to VSD, that leads to hypertrophy and dilation, and eventually failure.

The pulmonary hypertension as a late consequence of the VSD will produce right heart failure (cor pulmonale).
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