PAeasy Cardiovascular

Terms in this set (228)

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).
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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.
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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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