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E. 46 year old patient with history of 5 cm abdominal aortic aneurysm

A patient with only an abdominal aortic aneurysm would not be contraindicated to having a TEE (transesophageal echocardiogram) placed or performed. Contraindications to TEE include those with history of mediastinal radiation, dysphagia/odynophagia, cirrhosis, diverticula of the esophagus, thoracic aortic aneurysm, tumor of the esophagus, esophagitis, and recent chest trauma.
The contraindications to TEE are relatively few, but are quite important. The life threatening complications of TEE (esophageal tear, rupture, and upper GI bleed) can be avoided with gentle maneuvering of the probe and avoidance of high risk patients. High risk patients include those with history of mediastinal radiation due to the highly friable esophageal mucosa which can develop as a result of radiation esophagitis. Any patient with a history of mediastinal radiation or history of dysphagia/odynophagia must be screened with EGD prior to any consideration of TEE use. Odynophagia in a patient with a history of GERD may indicate stricture formation and high risk of esophageal perforation with manipulation. Any patient with cirrhosis must be carefully screened as the elevated portal hypertension found in these patients may cause collateral circulation to increase and allow the formation of esophageal varices. These varices can be fragile and irritation with TEE may result in life threatening GI bleeding. A history of recent upper gastrointestinal surgery is also a contraindication as TEE can disrupt or rupture post surgical healing.
C. Initiate intravenous nitroglycerin, furosemide, 100% FiO2, and PEEP

Nitroglycerin is preferred to nitroprusside in situations where cardiac ischemia is a concern due to a possible "coronary steal syndrome" that has been noted with nitroprusside use. Nitroglycerin increases coronary blood flow where nitroprusside may decrease coronary flow via this syndrome.
Hypertensive emergencies are defined as excessive hypertension with evidence of end organ damage. End organ damage can manifest as renal failure, angina/ cardiac ischemia, encephalopathy, congestive heart failure, and intracerebral hemorrhage. These symptoms necessitate rapid blood pressure control with a target of lowering the blood pressure by 20% in the first hour, then more gradually. Normotension is not desired in these patients as chronic autoregulatory mechanisms may cause cerebral or cardiac ischemia in a patient who is not used to normotension. Treatment depends on end organ damage: Nitroprusside is useful for most indications, nitroglycerin for cardiac ischemia or heart failure, beta blockade (esmolol) for aortic dissection, and fenoldopam for renal insufficiency. This patient is suffering from acute left ventricular failure brought about by a hypertensive crisis. Left ventricular failure causes increased pulmonary venous pressures which will eventually cause a transudation of a protein poor fluid across capillary membranes in the lung. This excess fluid is then carried out of the lungs via the lymphatic system. Once the rate of capillary transudation exceeds lymphatic filtration symptoms and pulmonary edema will develop. In patients with no previous history of heart failure this can happen at pulmonary artery pressures as low as 18 mmHg; whereas in patients with chronic heart failure, pulmonary pressures can exceed 25 mmHg before edema develops due to chronic autoregulatory mechanisms. Treatment is focused on reducing intracardiac filling pressures through volume control and venodilation to decrease preload when it can be tolerated. In this patient a decreased preload would likely be well tolerated given his elevated blood pressure, however, in hypotensive patients with cardiogenic pulmonary edema pressure, support with positive inotropes, such as dobutamine, would need to be considered to maintain cardiac output. Increasing Fi02 will improve cardiac perfusion and may help if cardiac ischemia is an underlying cause or if the patient is hypoxic from pulmonary edema which can worsen ventricular function. Positive pressure ventilation will help by increasing the pressure gradient across pulmonary capillary membranes inhibiting diffusion of fluid from the vascular to the alveolar spaces. Lasix will provide rapid relief of symptoms if given in adequate doses but can have deleterious side effects. Generally, in a patient in severe heart failure, the benefits outweigh the risks when appropriate doses are used. While beta blockade is a mainstay of therapy in chronic heart failure, their negatively inotropic properties will exacerbate acute decompensated heart failure and should be avoided in that setting. Similarly true of calcium channel blockers. BP should instead be controlled with a combination of direct vasodilators which avoid myocardial depression. IV albumin can help if an underlying contributing mechanism is a low oncotic pressure but that is not indicated in this question and would not be first line therapy.
B. The patient cannot exercise or walk very far due to arthritis. They have a history of insulin dependent diabetes and stage 4 chronic kidney disease

This patient has an inability to ambulate and comorbidities that increase his or her risk of CAD. Since the patient's METs cannot be determined we do not know his cardiac reserve. For these reasons the patient would need a cardiac consultation before proceeding to an elective procedure.
Preoperative evaluation should focus on determining myocardial reserve as well as signs of ischemic ventricular dysfunction in order to predict response to the stresses of surgery. Questioning to ascertain information on myocardial reserve should focus on exercise tolerance as an estimation of myocardial supply and demand mismatches. This can be estimated using metabolic equivalents (METs) which is the amount of oxygen uptake in a sitting position (about 3.5 mL/Kg/min). A patient with good exercise capacity in the absence of ischemic symptoms ought to do well on the operating table. Generally a patient who can ambulate 4 blocks or up 1-2 flights of stairs without shortness of breath or angina symptoms has adequate capacity for surgery (about 4 MET's). Less than 4 MET tolerance is associated with poor post operative cardiac outcomes. A patient with CABG in the preceding 5 years without changes in symptoms does not need further testing despite exercise tolerance according to current AHA guidelines. A patient with MI in the prior 2 weeks who is already known to be inappropriate for revascularization needs no further testing and an elective procedure should not be attempted for at least 6 weeks post MI and possibly not at all.
B. Senses and paces the ventricles, senses but doesn't pace the atrium, and will trigger or inhibit in response to sensing

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Question 26
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Which of the following pacemaker modes is most likely to cause asynchrounous atrioventricular beats?
Select one:
a. VVIR
b. AAIR
c. DDDR
d. DDIR
e. VDDR
Feedback
VVIR is most likely to cause asynchronus atrioventricular beats. The remaining modes all have some degree of atrial sensing capability which would prevent asynchronous beats.
VVIR pacing (Ventricle sensed, Ventricle paced, ventricle Inhibited by a sensed beat) is one of the most commonly used pacing modes used. Since only the ventricle is sensed it is possible to enter into a situation in which the ventricular beat is asynchronous with the atrial beat resulting in the atria beating against a closed AV valve. AAIR (Atrium sensed, Atrium paced, pacemaker Inhibited by atrial beat), DDDR (Dual sensing, Dual Pacing, Dual mode of action), DDIR (Dual Sensing, Dual pacing, Inhibition by atrial conduction), and VDD (Venticle paced, Dual sensing, Dual mode of action) all are less likely to cause this issue.
The correct answer is: VVIR
Question 27
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A 71 year old female has just underwent induction for right leg arteriogram and left great toe amputation. At this point she developes ventricular tachycardia and a code is called. You decide to use vasopressin insetad of epinepherine for your first dose of pressor agent as you follow your ACLS protocol. What is the proper dose of vasopressin in cardiac arrest?
Select one:
a. 40 units times one dose
b. 40 units every 3-5 mins times 3 doses
c. 80 units initial IV dose followed by 40 units IV in 5 minutes
d. 40 units initial dose IV followed by 20 units IV in 5 minutes
e. Current guidelines have eliminated vasopressin from ACLS protocols
Feedback
Vasopressin has been removed as a medication indicated for patients in ventricular tachycardia or ventricular fibrillation.
Previously ACLS protocol called for 40 Units IVP Vasopressin with one time readministration as a substitute for epinepherine.
If ventricular fibrillation or pulseless ventricular tachycardia persists after at least one attempt at defibrillation and two minutes of CPR, give epinephrine 1 mg every 3 to 5 minutes without interrupting CPR.
The correct answer is: Current guidelines have eliminated vasopressin from ACLS protocols
Question 28
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While under general anesthesia for a below the knee amputation, your 80 kg patient enters into a monomorphic ventricular tachycardia. His vital signs are as follows: blood pressure 45/20, heart rate 210 beats per minute, mechanically ventilated at 10 respirations per minute. Your next step in management should be Which of the following?
Select one:
a. Defibrillate using a biphasic defibrillator
b. Cardiovert using a biphasic defibrillator
c. Start CPR
d. Administer lidocaine 160 mg IV
e. 1 mg epinephrine IV along with CPR
Feedback
Synchronized cardioversion is the initial recommended treatment for a patient with unstable wide complex ventricular tachycardia.
A biphasic defibrillator should be used at 50-100 joules. Synchronized cardioversion is preferred to defibrillation if distinct QRS complexes are present. If distinct QRS complexes are not present, defibrillation at 200 Joules biphasic should be administered. Adenosine may be used if supraventricular tachycardia with aberrancy (wide complex but originates from the atrium) is suspected but only in situations where the patient remains stable and a diagnosis of SVT is highly likely or certain. Other options include amiodarone or lidocaine administration, but the only correct immediate treatment is synchronized cardioversion. If the patient retains a blood pressure and pulse, CPR may be held until cardioversion fails or if the blood pressure is not felt to be adequate for cerebral perfusion. If at any time the patient loses a pulse, immediately defibrillation and use of ACLS guidelines for cardiac arrest should be undertaken.
The correct answer is: Cardiovert using a biphasic defibrillator
Question 29
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A pacemaker is classified VDD. This means the pacemaker:
Select one:
a. Senses and paces the atria, and inhibits pacemaker firing in response to an event, without rate modulation
b. Senses and paces the ventricles, senses but doesn't pace the atrium, and will triggers or inhibits in response to sensing
c. Senses both chambers, paces onliy the atria, inhibits pacemaker firing in response to an event, is capable of rate modulation
d. Senses the ventricles, paces both atria and ventricle, will inhibit or trigger pacemaker firing in response to an event with rate modulation
e. Senses both the the atria and ventricle, Paces only the ventricle, will inhibit or trigger pacemaker firing in response to an event without rate modulation
Feedback
A VDD pacemaker senses the atria and ventricles, paces only the ventricles, and will trigger or inhibit in response to sensing.
Pacemakers are classified via a five letter code. written "ABCDE"
Slot "A" describes chambers paced and will be labeled A for atria, V for ventricle, or D for dual
Slot "B" described which chambers are sensed Atria, Ventricle, Dual
Slot "C" is for mode of modulation. "I" indicates that the pacemaker is inhibited by an event (i.e. pacer is programmed to always fire but is inhibited by a native beat). A "T" indicates the pacer triggers a beat in response to an event (i.e. the pacer fires the ventricle in response to an atrial beat). A "D" indicates dual mode of action (i.e. can perform either function).
Slot "D" describes if the pacer will adjust to patient exertion. (i.e. a faster heart rate during exercise)
Slot "E" Describes locations where there is multi-site pacing Atria, Ventricle, Dual. An O in any of the above positions indicates an absence of the slotted activity. Lack of a described slot, such as in the example VDD, implies that O is in the remaining locations (VDDOO).
As such VDD means Ventricle paced, Dual sensing, Dual mode of action, O rate modulation, and O multi-site pacing.
D. Intra-aortic balloon pumps can be life saving when used appropriately

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Question 31
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Which of the following is a medication NOT used in the treatment of chronic, stable non-ischemic congestive heart failure?
Select one:
a. Lisinopril
b. Carvedilol
c. Clopidogrel
d. Furosemide
e. Spironolactone
Feedback
Clopidogrel and other "blood thinners" are used for patients that have a history of ischemia, certain irregular rhythms, or clotting abnormalities but not heart failure.
The treatment for congestive heart failure is based on multiple trials which have demonstrated a reduction in symptoms and mortality in patients with heart failure using certain medications. Treatment is initially aimed at any underlying contributing factors followed by improvement in myocardial function and maintenance of euvolemia. Ace inhibitors, beta blockers and aldosterone antagonists have all shown to reduce mortality and hospitalization in patients with heart failure. Diuretics reduce the frequency of symptoms and hospitalizations. Clopidogrel (Plavix) is used in the treatment of ischemic heart disease as an antiplatelet agent and has no use in this patient.
The correct answer is: Clopidogrel
Question 32
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A 65 year old female who is to receive a femoral-popliteal bypass is noted to have a diagnosis of aortic regurgitation. When managing a patient with aortic regurgitation which of the following is INCORRECT?
Select one:
a. Acute aortic regurgitation can be life threatening
b. Pulmonary capillary wedge pressure will underestimate left ventricular end diastolic pressure (LVEDP) in severe acute aortic regurgitation
c. Increasing preload is usually beneficial
d. Intra-aortic ballon pumps can be life saving when used appropriately
e. Maintenance of a tachycardic heart rate is of benefit
Feedback
An intra-aortic ballon pump would be detrimental as it increases diastolic pressures and will increase regurgitant flow and left ventricular (LV) wall stress.
Valve regurgitation management = Full, Fast and Forward
Increased HR, Increased Preload and Decreased Afterload to promote forward flow is indicated.
Aortic regurgitation is a disease in which the heart has trouble maintaining forward ventricular output. When this occurs acutely the sudden increase in left ventricular volumes results in significantly increased systemic sympathetic response to produce tachycardia and increased contractile activity. The increased heart rate lessens ventricular diastole and results in a decreased myocardial wall tension which can help reduce ischemia, and the increased contractility will help with forward flow of blood. Many times in acute regurgitation these compensatory mechanisms are inadequate and will result in increased left ventricular end diastolic pressure (LVEDP), heart failure and pulmonary hypertension with cardiovascular collapse. If this process is a chronic one, the left ventricle responds to the abnormally increased volume load through hypertrophy to assist with forward stroke volume. Though left ventricular volume is increased, left ventricular end diastolic volume and pulmonary pressures remain relatively constant until late in the disease where similar processes will occur as stated in acute conditions. Increasing preload during surgery, maintaining a tachycardic rate, and decreasing afterload will help prevent perioperative decompensation. It is important to remember that when assessing LVEDP in acute aortic regurgitation the rapid increases in LV diastolic pressure may exert enough force to close the mitral valve prior to the end of diastole making readings innacurate on the low side even in the setting of severe ventricular failure.
A. Anesthesia management involves maintaining high central venous pressures

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Question 31
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Which of the following is a medication NOT used in the treatment of chronic, stable non-ischemic congestive heart failure?
Select one:
a. Lisinopril
b. Carvedilol
c. Clopidogrel
d. Furosemide
e. Spironolactone
Feedback
Clopidogrel and other "blood thinners" are used for patients that have a history of ischemia, certain irregular rhythms, or clotting abnormalities but not heart failure.
The treatment for congestive heart failure is based on multiple trials which have demonstrated a reduction in symptoms and mortality in patients with heart failure using certain medications. Treatment is initially aimed at any underlying contributing factors followed by improvement in myocardial function and maintenance of euvolemia. Ace inhibitors, beta blockers and aldosterone antagonists have all shown to reduce mortality and hospitalization in patients with heart failure. Diuretics reduce the frequency of symptoms and hospitalizations. Clopidogrel (Plavix) is used in the treatment of ischemic heart disease as an antiplatelet agent and has no use in this patient.
The correct answer is: Clopidogrel
Question 32
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A 65 year old female who is to receive a femoral-popliteal bypass is noted to have a diagnosis of aortic regurgitation. When managing a patient with aortic regurgitation which of the following is INCORRECT?
Select one:
a. Acute aortic regurgitation can be life threatening
b. Pulmonary capillary wedge pressure will underestimate left ventricular end diastolic pressure (LVEDP) in severe acute aortic regurgitation
c. Increasing preload is usually beneficial
d. Intra-aortic ballon pumps can be life saving when used appropriately
e. Maintenance of a tachycardic heart rate is of benefit
Feedback
An intra-aortic ballon pump would be detrimental as it increases diastolic pressures and will increase regurgitant flow and left ventricular (LV) wall stress.
Valve regurgitation management = Full, Fast and Forward
Increased HR, Increased Preload and Decreased Afterload to promote forward flow is indicated.
Aortic regurgitation is a disease in which the heart has trouble maintaining forward ventricular output. When this occurs acutely the sudden increase in left ventricular volumes results in significantly increased systemic sympathetic response to produce tachycardia and increased contractile activity. The increased heart rate lessens ventricular diastole and results in a decreased myocardial wall tension which can help reduce ischemia, and the increased contractility will help with forward flow of blood. Many times in acute regurgitation these compensatory mechanisms are inadequate and will result in increased left ventricular end diastolic pressure (LVEDP), heart failure and pulmonary hypertension with cardiovascular collapse. If this process is a chronic one, the left ventricle responds to the abnormally increased volume load through hypertrophy to assist with forward stroke volume. Though left ventricular volume is increased, left ventricular end diastolic volume and pulmonary pressures remain relatively constant until late in the disease where similar processes will occur as stated in acute conditions. Increasing preload during surgery, maintaining a tachycardic rate, and decreasing afterload will help prevent perioperative decompensation. It is important to remember that when assessing LVEDP in acute aortic regurgitation the rapid increases in LV diastolic pressure may exert enough force to close the mitral valve prior to the end of diastole making readings innacurate on the low side even in the setting of severe ventricular failure.
The correct answer is: Intra-aortic ballon pumps can be life saving when used appropriately
Question 33
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While on the operating room table your patient receiving an implanted venous access device develops ventricular tachycardia with a pulse. The code cart is brought to the room and defibrillator pads are placed on the patient. After unsuccessfully attempting to convert this rhythm with amiodarone the rhythm has now changed to a ventricular fibrillation without a pulse. What is the next step in management?
Select one:
a. 150mg Amiodarone repeat dose
b. 1mg/kg dose of IV lidocaine
c. Defibrillate using a biphasic defibrillator
d. 2 minute cycle of CPR followed by defibrillation
e. IV magnesium sulfate drip while defibrillating
Feedback
As soon as Ventricular Fibrillation is noticed, it is imperative to defibrillate the patient as soon as possible.
According to 2010 guidelines, immediate defibrillation is key when this rhythm (ventricular fibrillation) is first noted on monitors in a witnessed arrest with a defibrillator immediately available. After defibrillation CPR should begin at once for 5 cycles and then attempted again after checking for a pulse. Pause in CPR should only be taken to confirm the loss of a pulse prior to administering defibrillation treatment, and should occur no more often than every 2 minutes. This should be done along with the ACLS pharmacological therapies as indicated (after defibrillation and two minutes of CPR, 1 mg of epinepherine or 40 units of vasopressin should be administered if there is still no pulse). If the rhythm still is not responding additional use of amiodarone or lidocaine may be considered, typically after a second failed defibrillation. In the event a defibrillator is not immediately available, CPR should be started and defibrillation should occur as soon as a defibrillator has arrived and is attached to the patient. The key in treatment of cardiac arrest is continuous, uninterrupted CPR except during defibrillation.
The correct answer is: Defibrillate using a biphasic defibrillator
Question 34
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A patient with an implantable defibrillator presents for emergency intra-abdominal surgery where monopolar cautery will be used. The patient had his defibrillator implanted by an unknown company at a hospital in another state, and it is currently 2 o'clock in the morning. He has no documenation about the device with him at this time. What is the route to take in managing this patient if no information on this device is available?
Select one:
a. Place a doughnut magnet over the device to avoid accidental defibrillation during surgery
b. Advise the surgeon to use electrocautery to reduce blood loss
c. Take an xray of the device to obtain manufacturer information prior to surgery
d. Do not worry about the device as this is an intraabdominal surgery
e. If cardiac arrythmia occurs during surgery and you happen to have a donut magnet in place, leave the magnet in place and defibrillate with external paddles
Feedback
Focused X-rays will reveal manufacturer information for the device.
The specifications of a device which can affect the hemodynamic status of their patient should never be left unknown. The electromagnetic pulses of the Bovie device may be mistaken for V-fib by defibrillators and bipolar settings and a grounding pad ought to be used whenever possible. A donut magnet can be placed after contacting the manufacturers. Some defibrillators resume function after removal of the magnet, others are deactivated and must be reset, so the manufacturer or the placing cardiologist should be contacted for further info prior to deactivating the device whenever possible. When a patient develops an arrhythmia intraoperatively, removing the donut device is much quicker and effective than prepping external paddles if the device reactivates after removal. This should always be done first prior to attempting external defibrillation.
The correct answer is: Take an xray of the device to obtain manufacturer information prior to surgery
Question 35
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Which of the following is true of tricuspid regurgitation?
Select one:
a. Anesthesia management involves maintaining high central venous pressures
b. Beta blockade should be administered prior to induction
c. Phenylepherine is best avoided to prevent increase in SVR
d. Antibiotic prophylaxis is indicated for any invasive procedures
e. Hydralazine should be avoided due to its afterload decreasing properties
Feedback
Anesthesia management involves maintaining high central venous pressures.
Tricuspid regurgitation management includes an increased HR, normal to increased Preload and decreased Afterload to promote forward flow.
Mild tricuspid regurgitation is a common valvular lesion that can be a normal finding in adults and is frequently found in athletes. When more pronounced it is usually due to tricuspid annular dilation as a sequela of right ventricular enlargement. Long standing pulmonary hypertension, infectious endocarditis, congenital prolapse, and rheumatic heart disease are the more common causes of tricuspid insufficiency but it has been associated with carcinoid syndromes (a carcinoid tumor which releases high levels of serotonin into the blood stream - serotonin will cause fibrosis of the myocardium and valves in the right side of the heart with tricuspid regurgitation). Tricuspid regurgitation is rarely considered for surgical replacement as it is almost always well tolerated by the patient. The regurgitation causes elevated right atrial pressures and then jugular venous distention and hepatic congestion, but usually without severe symptomatology. Management of anesthesia includes diminishing pulmonary hypertension, and increasing preload to maintain forward flow. Venodilation and positive pressure ventilation should be avoided to prevent decreased venous return. Avoid situations that increase pulmonary hypertension as well to assist right ventricular forward flow. Care should be taken in these patients to avoid air emboli as elevated right atrial pressures may exceed left atrial pressures and allow transfer of blood and emboli across previously unnoticed patent foramen ovale (PFO).
B. Premedication with beta adrengeric blockade

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Question 36
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The term "chronotropy" refers to:
Select one:
a. Cardiac contractile rate
b. Cardiac contractile strength
c. Cardiac output
d. Cardiac contractile dimensions
e. Cardiac nerve imulse rate
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The term "Chronotropy" refers to cardiac contractile rate.
The correct answer is: Cardiac contractile rate
Question 37
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Your patient is under general anesthesia for cholecsytectomy and develops an increase in blood pressure and heart rate. After administration of 2 mg of hydromorphone, 200 mcg of fentanyl, and an end tidal sevoflurane of 3.2%, you now have a blood pressure of 196/110 and a heart rate of 134. Which of the following is best used for control of the patient's vital signs in the absence of any confounding factors?
Select one:
a. Nicardipine
b. Hydralazine
c. Adenosine
d. Esmolol
e. Nitroglycerin
Feedback
Esmolol would be the best of the choices listed due to its antihypertensive effects, IV route and ability to decrease heart rate.
Adenosine is an AV nodal conduction inhibitor, but is not approved for the treatment of hypertension, which is this patients most pressing concern. Adenosine is further not indicated in this example without any information regarding the type of tachycardia (wide vs narrow complex on ECG). Thus adenosine is not first line therapy here. Nitroglycerin and hydralazine would both cause an undesirable reflex tachycardia in this patient.
The correct answer is: Esmolol
Question 38
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You are reviewing a malpractice case wherein a 75 kg, 16 year old patient with a past medical history of hypertrophic cardiomyopathy and occasional syncope presented for elective laparoscopic surgery. During the course of the procedure pancuronium was used to affect skeletal muscle relaxation and the patient was premedicated with metoprolol. A central catheter was placed for CVP monitoring and, according to documentation, the surgeon was warned to keep abdominal insufflation pressures around 25 mmHg during the procedure. The patients ventilator settings were as follows: tidal volume 675 mL and ventilator rate 15 with 0 of PEEP. As the patient was being monitored the anesthesia practitioner under review documented a sudden decrease in the patient's CVP, followed by a decrease in systolic blood pressure along and a mild hypoxemia (PO2 was 60 with an O2 saturation of 90%). He immediately gave a bolus of crystalloid fluids and started a dobutamine drip as well as initiating 10 mm Hg of PEEP. The patient never recovered and expired within 25 minutes of this initial event despite aggressive CPR efforts. Which of the following interventions listed in the case was the most beneficial in the anesthetic management of this patient?
Select one:
a. Neuromuscular paralysis induced with pancuronium
b. Premedication with beta adrenergic blockade
c. Appropriate ventilator management
d. Initiation of dobutamine drip
e. Asking the surgeon to increase insufflation pressure
Feedback
Hypertrophic Obstructive Cardiomyopathy (HOCM), also commonly known as Idiopathic Hypertrophic Subaortic Stenosis (IHSS), patients should be maintained with increased preload, increased afterload and slow to normal heart rate.
The scenario listed was incorrectly handled from beginning to end except for 2 points. The premedication with beta adrenergic blockers and intravenous fluid administration as a bolus were both correct actions. In the presence of any hypertrophic cardiomyopathy with left ventricular outflow obstruction (LVOT), as evidenced here by a history of syncope, special care must be taken during anesthetic management to prevent any increase in LVOT obstruction. This is achieved by decreasing the pressure gradient across the obstruction, avoiding tachycardia which will increase LVOT obstruction, and by maintaining preload and increasing afterload when necessary. In order to have maintained preload in the case described the following should have been done: 1) During a laparoscopic case, abdominal insufflation pressures should be maintained as low as possible, generally around 15 mmHg. 2) Tidal volumes should be kept on the lower end of the patients tidal volume range to decrease intrathoracic pressure - a tidal volume of around 450-500 ml would have been more appropriate for this patient (6-8ml/kg instead of a more typical 8-10ml/kg tidal volume setting). 3) PEEP should be avoided as it will decrease preload by increasing thoracic pressures. To decrease tachycardia 1) neuromuscular blockers which block muscarinic receptors (pancuronium) or release histamine should be avoided, 2) Only vasopressors which do not act on cardiac beta 1 receptors should be used (phenylephrine), and 3) Care must be taken to avoid hypovolemia or unnecessary sympathetic stimulation (pain). Of note, while CVP (or pulmonary arterial catheter) monitoring may be helpful, it is not a useful indicator of LVOT obstruction. Monitoring is better achieved with transesophageal echocardiography to asses LVOT obstruction in real time.
E. Electric cardioversion

An unstable patient with a wide complex tachyarrhythmia should always be considered for electrical cardioversion immediately.
Adenosine is safe to use when treating regular, narrow complex tachyarrhythmia in most cases. In STABLE patients with regular wide complex tachycardia where SVT with aberrancy is suspected (as when an old EKG shows a bundle branch block) IV adenosine may also be considered prior to cardioversion. However, in patients with an irregular wide complex tachycardia, it is impossible to rule out atrial fibrillation with a pre-excitation syndrome (Wolff-Parkinson-White) and all such arrhythmias must be assumed to be WPW with atrial fibrillation. The reason for this is that AV nodal blocking agents are contraindicated in WPW with A-fib due to the fact that treatment with AV nodal blocking agents promotes transmission of cardiac activity down the accessory pathway worsening the patients condition. In addition AV nodal blocking agents are given to a patient in ventricular tachycardia can precipitate conversion to ventricular fibrillation and death. As such calcium channel blockers, beta blockers, and adenosine are absolutely contraindicated in these situations where the rhythm is not know to be a supra-ventricular rhythm. Class 1 or class III antiarrhythmic medications may be given when WPW with atrial fibrillation is suspected as the conduction slowing mechanism is not as dependent of the AV node. Procainimide is the drug of choice when WPW is suspected. As stated previously however, in an unstable patient, electrical cardioversion is the lifesaving standard of care.
B. Hypotension should be managed through a combination of increasing preload and afterload. Phenylephrine is best used for this

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Question 41
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A patient with previous history of coronary artery disease, congestive heart failure, and palpitations suddenly develops a wide complex, irregular tachycardia. Vital signs are as follows: HR 205, BP 50/22, respirations 18 on mechanical ventilation, and a temperature of temperature 38.9 Celsius. What is the most appropriate management at this time?
Select one:
a. Adenosine
b. IV amiodarone
c. IV magnesium
d. CPR
e. Electric cardioversion
Feedback
An unstable patient with a wide complex tachyarrhythmia should always be considered for electrical cardioversion immediately.
Adenosine is safe to use when treating regular, narrow complex tachyarrhythmia in most cases. In STABLE patients with regular wide complex tachycardia where SVT with aberrancy is suspected (as when an old EKG shows a bundle branch block) IV adenosine may also be considered prior to cardioversion. However, in patients with an irregular wide complex tachycardia, it is impossible to rule out atrial fibrillation with a pre-excitation syndrome (Wolff-Parkinson-White) and all such arrhythmias must be assumed to be WPW with atrial fibrillation. The reason for this is that AV nodal blocking agents are contraindicated in WPW with A-fib due to the fact that treatment with AV nodal blocking agents promotes transmission of cardiac activity down the accessory pathway worsening the patients condition. In addition AV nodal blocking agents are given to a patient in ventricular tachycardia can precipitate conversion to ventricular fibrillation and death. As such calcium channel blockers, beta blockers, and adenosine are absolutely contraindicated in these situations where the rhythm is not know to be a supra-ventricular rhythm. Class 1 or class III antiarrhythmic medications may be given when WPW with atrial fibrillation is suspected as the conduction slowing mechanism is not as dependent of the AV node. Procainimide is the drug of choice when WPW is suspected. As stated previously however, in an unstable patient, electrical cardioversion is the lifesaving standard of care.
The correct answer is: Electric cardioversion
Question 42
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Which of the following would be the most correct management option in an operative case involving hypertrophic cardiomyopathy with outflow tract obstruction?
Select one:
a. An arterial line is the best method of invasive monitoring to asses LVOT obstruction and should always be placed
b. Hypotenstion should be managed through a combination of increasing preload and afterload. Phenylephrine is best used for this
c. Hypertension is best managed through vasodilation, nitroglycerin is excellent for this
d. Hypoxemia and hypercapnia is of deadly concern in these patients and ventilation should be maintained with average to high tidal volumes and PEEP
e. Bradycardia is poorly tolerated and a low threshold for administering atropine is appropriate as premedication
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Hypertrophic Obstructive Cardiomyopathy (HOCM) also commonly known as Idiopathic Hypertrophic Subaortic Stenosis (IHSS) should be maintained with increased preload, increased afterload and slow to normal heart rate.
The goal of management in hypertrophic cardiomyopathy with left ventricular outflow obstruction (LVOT) is to maintain a steady gradient across the obstructing point. Maintaining preload and afterload are essential to decrease as much of a pressure difference as possible before and after the abnormal LVOT obstruction as possible. Tachycardia ought be avoided and cardiac beta receptor blockade is always indicated when can be tolerated by the patient. Tachycardia will increase any obstruction present and is why many of these patients relate a history of syncope during exercise. Vasodilation should be avoided always as the decrease in preload can cause collapse of the LVOT with deadly consequences. An arterial line may be helpful in these cases however pulmonary and arterial pressure monitoring will not be as useful as transesophageal echocardiography for assessment of the myocardial LVOT. High tidal volumes and PEEP should be avoided as they will decrease preload. Lower tidal volumes and the absence of PEEP are preferred in ventilator management.
B. Epoprostenol should be stopped

Epoprostenol is a prostacyclin medication administered via constant infusion by portable pump and should not be stopped for surgery. Any medications taken by these patients for the purpose of treating their pulmonary hypertension should be continued through the surgical period, especially any constantly infused medications as their discontinuation will cause a dramatic increase in their pulmonary artery pressures.
Pulmonary arterial hypertension is a disorder of abnormal pulmonary vascular vasoconstriction, vascular wall remodeling, and, in some cases, pulmonary vascular thrombosis. These conditions lead to an increase in pulmonary vascular resistance. This in turn causes an increase in RV wall tension leading to RV failure (Cor Pulmonale). Care must be taken to avoid exacerbating the underlying causes of the pulmonary hypertension, or the symptoms and sequela of the right ventricular failure. Anything that causes pulmonary vasoconstriction should be desperately avoided. This includes hypoxemic states, acidosis and the use of nitrous oxide. A pulmonary artery catheter can be very useful when monitoring pulmonary physiologic responses to anesthesia or to the surgery. Acute increases in pulmonary hypertension can lead to a worsening of the right ventricular failure via over-distension and increasing of intra-ventricular pressures. This can cause a decrease in coronary perfusion of the ventricle further worsening function. In turn this results in decreasing left ventricular preload and decreased cardiac output possibly resulting in systemic hypotension. Diuresis for elevated venous volume should be performed carefully with close monitoring of pulmonary pressures if available to prevent overdiuresis and decreasing left ventricular preload in this fashion. Nitric oxide and inhaled prostacyclins can quickly decrease pulmonary artery pressures in the event of an acute increase. Nitrous oxide should never be used in these patients due to its sympathomimetic effect on pulmonary artery pressures.
A. Induction with halothane is best as the myocardial relaxation it produces will assist ventricular filling

Halothane's cardiac depressing effects will further exacerbate the problem. Always remember that MAP=SVRxCO.
Pericardial tamponade results in hypotension via impairment of right ventricular diastolic filling. Any myocardial depression in this setting could prove fatal to a patient with already impaired hemodynamic stability. Ketamine would be the induction agent of choice due to its propensity to increase myocardial contractility, systemic vascular resistance, and heart rate, all of which will contribute to continued cardiac output. Isoflurane may be an option as it is less likely to depress cardiac output than other volatile anesthetics, however many have used nitrous oxide without additional inhaled anesthetic due to its sympathomimetic effects and positive effects on cardiac output. This works especially well when used with pancuronium for neuromuscular blockade. Pancuronium has the lowest autonomic margin of safety of all nondepolarizing blockers. This is a reference to the margin between the dose needed to relax skeletal muscle to the dose required to produce circulatory change. Therefore, the dose of pancuronium required to produce skeletal muscle relaxation will also cause a tachycardia beneficial to maintaining cardiac output in this patient. Infusion of fluids (colloids or crystalloids) to increase cardiac preload and pressor support to increase cardiac output and BP is desirable as well.