Section 1. Cardiovascular Medicine (Questions 25-49)
Item 25 [Basic]
An 85-year-old woman is admitted to the coronary care unit following successful thrombolytic therapy for an acute anteroseptal ST -elevation myocardial infarction. Blood pressure is 120/70 mm Hg and heart rate is 90/min. There is no jugular venous distention and no cardiac murmurs. The lung fields are clear. Medications started in the hospital are aspirin, low-molecular-weight heparin, intravenous nitroglycerin, and metoprolol.
On hospital day 3, the patient experiences acute onset of respiratory distress and her systolic blood pressure falls to 80 mm Hg. Her oxygen saturation remains at 80% despite the administration of 100% oxygen by face mask. On physical examination, blood pressure is 96/40 mm Hg, pulse rate is 100/min, and respiration rate is 28/min. Findings include jugular venous distention, crackles throughout both lung fields, and a grade 4/6 systolic murmur associated with a thrill.
Which of the following is the most likely diagnosis?
(A) Aortic dissection
(B) Pericardial tamponade
(C) Pulmonary embolism
(D) Ventricular septal defect
Item 25 Answer: D
Educational Objective: Diagnose ventricular septal defect following ST-elevation myocardial infarction.
The most likely diagnosis is a ventricular septal defect. Mechanical complications occur in roughly 0.1% of patients with ST -elevation myocardial infarction (ST EMI) and usually occur 2 to 7 days after infarction. Late complications following ST EMI include cardiogenic shock, ventricular septal defect, mitral regurgitation, free wall rupture, and left ventricular thrombus. This patient’s progressive hypotension, respiratory distress, and new systolic murmur and thrill suggest either ischemic mitral regurgitation or a ventricular septal defect. Following echocardiography to confirm the diagnosis, this patient should undergo emergent surgery to repair the defect or valve.
Patients with aortic dissection typically present with severe, sharp, tearing chest pain. The pain may radiate widely and be associated with syncope, systemic ischemia (related to impaired blood flow to an organ or limb), or heart failure (aortic valve disruption, tamponade). Ascending aortic dissection is often associated with acute aortic regurgitation (diastolic murmur at the base of the heart), myocardial ischemia, cardiac tamponade or hemopericardium, and hemothorax or exsanguination. A new systolic murmur and thrill are not compatible with aortic dissection.
Pericardial tamponade may occur following an ST EMI from hemorrhagic pericarditis or free wall rupture. Pericardial tamponade from rupture of the left ventricular free wall usually leads to sudden hypotension and death. Ventricular free wall rupture typically occurs 1 to 4 days after acute myocardial infarction. Patients usually present with cardiovascular collapse, tamponade, or pulseless electrical activity. It is not associated with a new, loud systolic murmur or palpable thrill.
A massive pulmonary embolism may produce cardiovascular collapse and hypoxemia but cannot explain the new systolic murmur or left-sided heart failure.
Key Point
A ventricular septal defect following an ST -elevation myocardial infarction results in respiratory distress, hypotension, a new systolic murmur, and a palpable thrill.
Bibliography
Poulsen SH, Praestholm M, Munk K, Wierup P, Egeblad H, Nielsen-Kudsk JE. Ventricular septal rupture complicating acute myocardial infarction: clinical characteristics and contemporary outcome. Ann T horac Surg. 2008;85(5):1591-1596. [PMID: 18442545]
Item 26 [Advanced]
A 77-year-old woman is admitted to the hospital for intermittent dizziness over the past few days. She has hypertension, hyperlipidemia, and paroxysmal atrial fibrillation with a history of rapid ventricular response. Medications are metoprolol, hydrochlorothiazide, pravastatin, lisinopril, aspirin, and warfarin.
On physical examination, blood pressure is 137/88 mm Hg and pulse is 52/min. Estimated central venous pressure is 7 cm H2O. Cardiac auscultation reveals bradycardia with regular S1 and S2, as well as an S4. The lungs are clear to auscultation.
On telemetry, she has sinus bradycardia with rates between 40/min and 50/min, with two symptomatic sinus pauses of 3 to 5 seconds each.
Which of the following is the most likely diagnosis?
(A) Mobitz I atrioventricular block
(B) Mobitz II atrioventricular block
(C) Third-degree atrioventricular block
(D) Sinoatrial node dysfunction
Item 26 Answer: D
Educational Objective: Diagnose sinoatrial node dysfunction.
This patient has symptomatic sinoatrial node dysfunction (also called sick sinus syndrome). Sinoatrial node dysfunction comprises a collection of pathologic findings that result in bradycardia. These include sinus arrest, sinus exit block, and sinus bradycardia. This patient has sinus bradycardia and sinus arrest. Approximately 50% of patients with sinoatrial node dysfunction also have associated supraventricular tachycardia, most often atrial fibrillation or atrial flutter. The tachycardia-bradycardia syndrome is characterized by rapid ventricular conduction during episodes of atrial fibrillation, but resting bradycardia between episodes. Symptomatic sinus node dysfunction is an indication for pacemaker placement, even if the bradycardia occurs as a consequence of drug therapy, if there is no acceptable alternative.
Atrioventricular nodal block is classified as first, second, or third degree. First-degree block is defined by prolongation of the PR interval to greater than 0.2 sec and usually is not associated with alterations in heart rate. There are two types of second-degree block, both recognized electrocardiographically by the presence of a P wave that is not followed by a ventricular complex. Mobitz type I block (Wenckebach block) manifests as progressive prolongation of the PR interval until there is a dropped beat, whereas Mobitz type II block manifests as a dropped beat without progressive PR-interval prolongation. Mobitz type I block usually does not progress to complete heart block, but Mobitz type II block, which is usually associated with a bundle branch block, typically progresses to third-degree block. Second-degree block may be associated with bradycardia, depending upon the frequency of blocked atrial impulses. Third-degree block is the complete absence of conduction of atrial impulses to the ventricle and is the most common cause of marked bradycardia; ventricular rates are usually 30-50/min. This patient has no evidence of atrioventricular block.
Key Point
Sinoatrial node dysfunction comprises a collection of pathologic findings (sinus arrest, sinus exit block, and sinus bradycardia) that result in bradycardia.
Bibliography
Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricular conduction blocks. Emerg Med Clin North Am. 2006;24(1):1-9, v. [PMID: 16308110]
Item 27 [Advanced]
A 70-year-old man is evaluated in the emergency department for bradycardia that was detected in the nursing home and is found to have second-degree atrioventricular block.
The patient has Alzheimer dementia. His medications are donepezil (dosage recently increased); memantine (recently started); vitamin E; and trazodone for agitation.
Which of the patient’s medications is likely to explain the bradycardia?
(A) Donepezil
(B) Memantine
(C) Trazodone
(D) Vitamin E
Item 27 Answer: A
Educational Objective: Diagnose heart block due to donepezil.
The medication most likely responsible for the patient’s heart block is donepezil. Donepezil inhibits acetylcholinesterase. Its activity occurs preferentially in the central nervous system, but mild peripheral cholinergic side effects are common. These effects include increased vagal tone, bradycardia, and, occasionally, atrioventricular block. In this patient, this side effect became manifest when the dosage of donepezil was increased. In patients with preexisting heart block, cholinesterase inhibitors should be used with caution.
Memantine inhibits the glutamatergic N-methyl-D-aspartate receptor on central neurons. The side effects of memantine include hallucinations, confusion, restlessness, anxiety, dizziness, headache, fatigue, and constipation.
Trazodone does not commonly cause slowing of cardiac conduction, although it may be associated with palpitations and ventricular ectopy. Vitamin E at a high dose can cause loose stools and may inhibit vitamin K carboxylase, but it is not associated with cardiac side effects.
Key Point
Donepezil, an acetylcholinesterase inhibitor, may cause mild peripheral cholinergic side effects, including increased vagal tone, bradycardia, and atrioventricular block.
Bibliography
Feldman H, Gauthier S, Hecker J, et al. A 24-week, randomized, double-blind study of donepezil in moderate to severe Alzheimer’s disease. Neurology. 2001;57:613-620.
[PMID: 11524468]
Item 28 [Basic]
A 67-year-old man is brought to the emergency department after he lost consciousness. His wife reports he had been experiencing palpitations and lightheadedness earlier in the day. He has hypertension, dyslipidemia, and chronic obstructive pulmonary disease. His medications are lisinopril, hydrochlorothiazide, pravastatin, and a fluticasone salmeterol inhaler.
On physical examination, the patient is awake but confused and in respiratory distress. He is afebrile, blood pressure is 80/45 mm Hg, pulse rate is 167/min, and respiration rate is 24/min and labored. Oxygen saturation is 86% on ambient air. The cardiac rhythm is irregular, and bibasilar crackles are present on pulmonary examination.
An electrocardiogram shows atrial fibrillation.
Which of the following is the most appropriate immediate management for this patient?
(A) Bedside echocardiography
(B) CT pulmonary angiography
(C) Coronary angiography
(D) Electrical cardioversion
Item 28 Answer: D
Educational Objective: Treat an unstable patient with a cardiac arrhythmia with electrical cardioversion.
Electrical cardioversion is indicated for an unstable patient with any arrhythmia, other than sinus tachycardia, including atrial fibrillation with a rapid ventricular rate. This patient has persistent tachycardia, worsening mental status, hypoxia, and hypotension consistent with significant hemodynamic instability. Immediate cardioversion is often the safest choice even in hemodynamically stable patients, particularly in those with wide complex tachycardia. After termination of the arrhythmia, the electrocardiogram can provide clues regarding the presence of previous myocardial infarction, left ventricular hypertrophy, or long QT syndrome, and an echocardiogram provides evaluation for structural heart disease and assessment of left ventricular function. Exercise testing can screen for significant coronary artery disease and provoke exercise-associated tachycardias. In newly diagnosed cardiomyopathy, cardiac catheterization is often necessary to evaluate for coronary artery disease as the cause of myocardial dysfunction.
CT pulmonary angiography can evaluate the patient for pulmonary emboli; however, none of these studies are indicated until the patient’s cardiac rhythm is stabilized with immediate cardioversion.
Key Point
Electrical cardioversion is indicated in hemodynamically unstable patients with an arrhythmia.
Bibliography
Zimetbaum P. Atrial fibrillation. Ann Intern Med. 2010;153(11):IT C61. [PMID: 21135291]
Item 29 [Basic]
A 62-year-old-woman is evaluated for a 6-month history of difficulty falling asleep and an unexplained 4.5-kg (10 lb) weight loss. She is active and rides her bicycle 5 miles a day. She does not drink alcohol, smoke cigarettes, or use recreational drugs. She has no other medical problems and takes no medications.
On physical examination, she is afebrile, blood pressure is 125/75 mm Hg, pulse rate is 108/min, and respiration rate is 14/min. On cardiac examination, a regular rhythm without murmurs or extra cardiac sounds is heard. The remainder of the physical examination is normal.
A metabolic profile and complete blood count are normal.
An electrocardiogram shows only sinus tachycardia.
Which of the following is the most appropriate management for this patient?
(A) Administer adenosine intravenously
(B) Measure serum thyroid-stimulating hormone level (T SH)
(C) Obtain an exercise stress test
(D) Radiofrequency ablation of the sinoatrial node
Item 29 Answer: B
Educational Objective: Identify hyperthyroidism as the cause of sinus tachycardia.
Measuring the T SH level is an appropriate first step to determine the underlying cause of the sinus tachycardia. Sinus tachycardia originates from the sinoatrial node and is defined as a rate of greater than 100/min. Common causes of sinus tachycardia include normal response to exercise and situations associated with increased catecholamine release (fear, pain, anxiety, alcohol withdrawal) as well as fever, hypovolemia, sepsis, heart failure, pulmonary embolism, and hypoxia. Hyperthyroidism is a relatively common cause of sinus tachycardia. Other clues suggesting hyperthyroidism in this patient include difficulty sleeping and unexplained weight loss. In patients with hyperthyroidism, treatment with a ß-blocker may provide some symptomatic relief until the underlying thyroid disease is treated.
Adenosine bolus injection is highly effective at terminating atrioventricular (AV) nodal reentrant tachycardia and providing diagnostic information in unclear cases such as revealing flutter waves during adenosine-induced AV block or revealing an underlying atrial tachycardia. Adenosine has no role in managing patients with sinus tachycardia.
An exercise stress test is used to diagnose coronary artery disease. This patient is asymptomatic, has good exercise tolerance, and has no other signs or symptoms of coronary artery disease. Therefore, an exercise stress test is not warranted.
Sinoatrial ablation is indicated for patients with atrial tachycardia that uses part of the sinoatrial node as a reentry circuit. Sinoatrial node ablation is rarely used to treat inappropriate sinus tachycardia. This is a condition characterized by an elevated resting sinus rate in the absence of a recognized cause and an exaggerated rate response to exercise. Most patients with inappropriate sinus tachycardia respond to ß-blockers or nondihydropyridine calcium channel blockers, but some refractory cases are treated with sinoatrial node ablation.
Key Point
Determining the underlying cause of sinus tachycardia is necessary to guide appropriate treatment.
Bibliography
DeVoe JE, Judkins DZ, Woods L. Clinical inquiries. What is the best approach to the evaluation of resting tachycardia in an adult? J Fam Pract. 2007;56(1):59-61. [PMID:1721790]
Item 30 [Advanced]
A 79-year-old man is evaluated in the emergency department for a 1-week history of dyspnea and weakness. He has had several such episodes over the past 5 years but has never sought medical attention. He reports that 1 year ago, he had a 10-minute episode of left arm weakness that resolved spontaneously. He was never evaluated for this problem. He has hypertension treated with lisinopril and hydrochlorothiazide.
On physical examination, blood pressure is 135/80 mm Hg and heart rate is 143/min. Other than a rapid heart rate, the cardiopulmonary examination is normal, as is the remainder of the physical examination.
Electrocardiogram shows atrial fibrillation with a rapid ventricular rate without evidence of ischemic changes. Cardiac enzyme values are normal. Following the administration of metoprolol, he converts to sinus rhythm, with a heart rate of 74/min.
Which of the following is the most appropriate long-term treatment for this patient?
(A) Amiodarone
(B) Low-molecular-weight heparin followed by warfarin
(C) Metoprolol
(D) Metoprolol and warfarin
Item 31 [Basic]
A 28-year-old man is evaluated for a pre-employment physical examination and electrocardiogram before entering the police academy. He has no medical problems, describes no worrisome symptoms, and does not take any medications. He does not smoke cigarettes, has one alcoholic drink or less each week, and rarely consumes caffeine. He runs 4 miles a day 3 days a week and bikes 25 to 50 miles on the weekends. His parents are both alive and in good health as are his two older brothers.
On physical examination, vital signs are normal. The cardiopulmonary examination is normal as is the remainder of the examination.
The resting 12-lead electrocardiogram shows 3 unifocal premature ventricular contractions.
Which of the following is the best management plan for this patient?
(A) Begin amiodarone
(B) Begin metoprolol
(C) Exercise stress test
(D) No further investigation or therapy
(E) Order 24-hour ambulatory electrocardiography
Item 32 [Advanced]
A 55-year-old man is evaluated for fatigue, dyspnea with modest exertion, occasional lightheadedness, and palpitations. He has a history of ischemic cardiomyopathy following a large anterolateral myocardial infarction 6 weeks ago. He does not have chest pain, and a postdischarge adenosine stress test with nuclear imaging demonstrated no inducible ischemia. His medications are lisinopril, carvedilol, furosemide, spironolactone, digoxin, and aspirin.
On physical examination, he is afebrile, blood pressure is 130/83 mm Hg, pulse rate is 50/min, and respiration rate is 12/min. He has no jugular venous distension. S1 and S2 are soft, and S3 and S4 are present. A grade 2/6 holosystolic murmur at the cardiac apex is present. The lungs are clear. No peripheral edema is noted.
An electrocardiogram shows an episode of nonsustained ventricular tachycardia. Echocardiography shows diminished anterior wall motion with an ejection fraction of 25%.
Which of the following is the most appropriate treatment for this patient?
(A) Amiodarone
(B) Flecainide
(C) Procainamide
(D) Implantable cardioverter-defibrillator (ICD)
Item 33 [Advanced]
A 67-year-old man presented to the emergency department 2 days ago with an acute ST -elevation myocardial infarction. During the initial evaluation, he became unresponsive due to ventricular fibrillation. He was successfully resuscitated and taken to the cardiac catheterization lab, where a 100% occlusion of his proximal left anterior descending artery was stented. His postinfarction course was notable for mild heart failure, which has now resolved. He is now stable on aspirin, metoprolol, atorvastatin, clopidogrel, and lisinopril.
On physical examination, blood pressure is 115/72 mm Hg, pulse is 65/min, and respiration rate is 12/min. There is no jugular venous distention, crackles, murmur, or S3. The electrocardiogram shows ST -segment changes consistent with a resolving anterior myocardial infarction but is otherwise unremarkable. Transthoracic echocardiogram reveals mild hypokinesis of the anterior wall and a left ventricular ejection fraction of 42%.
Which of the following is the best management option at this time?
(A) Add amiodarone
(B) Continue medical management
(C) Implantable cardioverter-defibrillator placement
(D) Pacemaker placement
Item 34 [Advanced]
An 18-year-old woman is evaluated for recurrent syncope. She has experienced four syncopal episodes in her lifetime, all of which occurred during activity. Episodes have no prodrome, and she has had no dizziness. She is healthy and active, without cardiopulmonary complaints, and takes no medications. Her maternal cousin drowned at age 10 years, and her mother has been evaluated for recurrent episodes of loss of consciousness.
On physical examination, blood pressure is 112/65 mm Hg, and pulse is 67/min and regular. The cardiopulmonary and general physical examinations are normal. An echocardiogram examination is normal. An electrocardiogram is ordered.
Which of the following electrocardiographic findings is most likely to provide a diagnosis?
(A) Left bundle branch block
(B) Long PR interval
(C) Long QT interval
(D) Right bundle branch block
Item 35 [Basic]
A 50-year-man with a 6-month history of New York Heart Association class IV heart failure secondary to idiopathic dilated cardiomyopathy is evaluated following a recent hospitalization for worsening heart failure symptoms. The patient is adherent to his medications and his fluid and sodium restrictions. His medications are lisinopril, carvedilol, spironolactone, and furosemide.
On physical examination, vital signs are normal. He has no jugular venous distention. The cardiac rhythm is regular. Cardiac auscultation reveals an S3 and holosystolic murmur at the cardiac apex. The chest is clear, and no peripheral edema is noted.
In the hospital, no evidence of ischemia, infection, arrhythmia, or thyroid disease was present. An echocardiogram demonstrated global hypokinesis of the left ventricle, moderate mitral regurgitation, and an ejection fraction of 25%
Which of the following medications should be initiated for this patient?
(A) Digoxin
(B) Metolazone
(C) Valsartan
(D) Warfarin
Item 36 [Basic]
A 35-year-old woman is evaluated for progressive dyspnea 3 weeks after delivery of her first child. The pregnancy and delivery were uncomplicated. She has no history of cardiovascular disease.
On physical examination, blood pressure is 110/70 mm Hg in both arms, heart rate is 105/min and regular, and respiratory rate is 28/min. The estimated central venous pressure is 10 cm H2O and there are no carotid bruits. The apical impulse is displaced and diffuse. There is a grade 2/6 holosystolic murmur at the apex. Third and fourth heart sounds are present. There is dullness to percussion at the posterior lung bases bilaterally, and there are crackles extending up half of the lung fields. Lower extremity pulses are normal and without delay. Pedal edema is present.
The electrocardiogram demonstrates sinus tachycardia. There are no ST -segment or T -wave changes. The chest radiograph demonstrates bilateral pleural effusions and interstitial infiltrates. The aortic contour is unremarkable.
Which of the following is the most likely cause of the patient’s current symptoms?
(A) Acute myocardial infarction
(B) Aortic dissection
(C) Coarctation of the aorta
(D) Heart failure
Item 37 [Advanced]
A 65-year-old man is evaluated for 2 months of central chest pain with exertion and relief with rest, exertional dyspnea, orthopnea, and lower-extremity edema. The chest discomfort is increasing in frequency and severity. He has a 25-year history of hypertension and a 44-year history of smoking. His only medication is hydrochlorothiazide.
On physical examination, blood pressure is 118/80 mm Hg, pulse is 95/min, and respiration rate is 16/min. There is jugular venous distention. Cardiac examination reveals a regular rhythm. S1 and S2 are normal, and an S3 and S4 are present. Crackles are heard at both lung bases. There is edema at the ankles. Laboratory studies show a normal serum troponin T level. Electrocardiogram is normal. Echocardiogram shows an ejection fraction of 40%, global hypokinesis, and left ventricular hypertrophy.
Which of the following is the most appropriate diagnostic test?
(A) Cardiac angiography
(B) Nuclear medicine stress test
(C) Radionuclide ventriculography
(D) Standard exercise stress test
Item 38 [Basic]
A 40-year-old woman is evaluated for 2 months of progressive dyspnea on exertion, orthopnea, and lower extremity edema. She denies chest discomfort and has no other medical problems and takes no medications. She does not smoke cigarettes and rarely drinks alcohol. There is no family history of heart disease.
On physical examination, she is afebrile. Blood pressure is 120/80 mm Hg and pulse is 80/min. Estimated central venous pressure is 10 cm H2O. The lungs are clear. Cardiac examination reveals a regular rhythm, an S3, and no murmurs. There is ankle edema. Chest radiograph shows vascular congestion. Electrocardiogram is normal. Initial laboratory evaluation reveals a normal hemoglobin level and metabolic profile, including thyroid studies.
Which of the following is the most appropriate initial diagnostic test?
(A) B-type natriuretic peptide level
(B) Echocardiography
(C) Radionuclide ventriculography
(D) Stress test
Item 39 [Basic]
A 70-year-old woman is evaluated for a 1-month history of dyspnea on exertion and fatigue. She can still perform activities of daily living, including vacuuming, grocery shopping, and ascending two flights of stairs carrying laundry. She has a history of hypertension. Her medications are lisinopril and hydrochlorothiazide.
On physical examination, blood pressure is 110/80 mm Hg and pulse is 70/min. Jugular veins are not distended. S1 and S2 are normal, and there is no S3 or murmur. The pulmonary examination is normal and there is no edema. Laboratory studies show normal hemoglobin and thyroid-stimulating hormone levels. Electrocardiogram shows low voltage and left axis deviation. Echocardiogram shows a left ventricular ejection fraction of 45% and global hypokinesis. Chest radiograph is normal.
Which of the following is the most appropriate additional treatment?
(A) Amlodipine
(B) Carvedilol
(C) Digoxin
(D) Losartan
(E) Spironolactone
Item 40 [Basic]
A 60-year-old woman is diagnosed with heart failure due to nonischemic cardiomyopathy. Her ejection fraction is 40%. She currently has mild shortness of breath with moderate exertion but no orthopnea or lightheadedness. She has a history of hypertension treated with hydrochlorothiazide and metoprolol.
On physical examination, she is afebrile. Blood pressure is 120/80 mm Hg and pulse is 65/min. The jugular veins are not distended, and the lungs are clear. Cardiac examination discloses a regular rate and rhythm with no S3 or murmurs. There is no edema.
Which of the following agents should be added to her regimen?
(A) Digoxin
(B) Eplerenone
(C) Hydralazine and a nitrate
(D) Lisinopril
Item 41 [Basic]
A 60-year-old woman is evaluated for dyspnea with mild activity (ascending less than one flight of stairs, walking less than one block on level ground) that has been stable for the past year. She has a history of nonischemic cardiomyopathy (most recent left ventricular ejection fraction, 20%). Her current medications are lisinopril, carvedilol, digoxin, and furosemide. She had an implantable cardioverter-defibrillator placed 1 year ago.
On physical examination, blood pressure is 115/75 mm Hg and pulse rate is 70/min. Jugular veins are not distended, and the lungs are clear. Cardiac examination discloses a regular rhythm, no murmurs, normal S1 and S2, and no S3. There is no edema. Laboratory studies show normal serum creatinine and potassium levels.
Which of the following is the most appropriate addition to this patient’s treatment?
(A) Losartan
(B) Metolazone
(C) Nifedipine
(D) Spironolactone
Item 42 [Basic]
An 81-year-old woman with aortic stenosis is evaluated for increased shortness of breath and exercise intolerance. She was asymptomatic until 2 weeks ago when she noted increased shortness of breath with exertion. She reports no chest pain, orthopnea, paroxysmal nocturnal dyspnea, or palpitations. She has had no fever, chills, or recent procedures that might increase the risk for infective endocarditis. She has no other medical problems and takes no medications.
On physical examination, she is afebrile, blood pressure is 116/72 mm Hg, pulse rate is irregularly irregular at 112/min, and respiration rate is 12/min. No jugular venous distention is present. Cardiac auscultation reveals an irregular rhythm with a grade 3/6 crescendo-decrescendo systolic murmur loudest at the second left intercostal space with radiation to the carotid arteries. Bibasilar pulmonary crackles are present, as is 1+ bilateral lower extremity edema.
Which of the following is most likely responsible for the new symptoms?
(A) Atrial fibrillation
(B) Infective endocarditis
(C) Development of mitral stenosis
(D) Development of mitral regurgitation
Item 43 [Basic]
A 54-year-old man is evaluated for increased shortness of breath of 3 weeks’ duration. He has dyspnea on exertion, orthopnea, and occasional paroxysmal nocturnal dyspnea.
He reports no chest pain, fever, or chills. He had an aortic bioprosthetic valve replacement for bicuspid valve aortic stenosis 15 years ago. He takes no medications.
On physical examination, he is afebrile, blood pressure is 140/50 mm Hg, pulse rate is 100/min, and respiration rate is 14/min. The carotid pulse is hyperdynamic. The S2 is diminished. Cardiac auscultation reveals a grade 2/6 diastolic murmur, heard loudest at the third left intercostal space. A few scattered crackles can be heard at the lung bases.
No peripheral edema is present.
Which of the following is the most likely diagnosis?
(A) Aortic regurgitation
(B) Atrial septal defect
(C) Coarctation of the aorta
(D) Mitral stenosis
(E) Ventricular septal defect
Item 44 [Basic]
A 65-year-old woman is evaluated as a new patient during a routine office visit. She is healthy and active and swims laps three or four times per week. She does not smoke and she takes no medications.
On physical examination, blood pressure is 118/60 mm Hg. There are no carotid bruits. There is a normal S1 and a physiologically split S2. There is a grade 2/6 midsystolic murmur that does not radiate and is heard best at the second right intercostal space. The rest of the physical examination is unrevealing.
Which of the following is the most appropriate management?
(A) Antibiotic endocarditis prophylaxis
(B) Transthoracic echocardiography
(C) Treadmill stress echocardiography
(D) No further intervention
Item 45 [Advanced]
A 30-year-old woman is evaluated in the emergency department for shortness of breath, palpitations, and pedal edema. She is gravida 1, para 0, and she is 30 weeks pregnant.
She has not received prenatal care until this point.
On physical examination, the patient is sitting upright to breathe. Blood pressure is 112/80 mm Hg, and pulse is 96/min. There is jugular venous distention to her jaw line while sitting upright. Cardiac auscultation demonstrates an irregularly irregular rhythm, a loud P2, and an opening snap followed by a low-pitched diastolic murmur heard best at the cardiac apex. Bibasilar crackles are present.
Which of the following is the most likely diagnosis?
(A) Acute aortic regurgitation
(B) Atrial septal defect
(C) Mitral stenosis
(D) Tricuspid regurgitation
Item 46 [Advanced]
An 18-year-old woman is evaluated during a routine examination prior to entering college. She has had no major medical problems and there is no family history of cardiovascular disease.
On physical examination, blood pressure is 110/60 mm Hg and pulse is 70/min. S1 and S2 are normal and there is an S4 present. There is a harsh grade 2/6 midsystolic murmur heard best at the lower left sternal border. The murmur does not radiate to the carotid arteries. A Valsalva maneuver increases the intensity of the murmur; moving from a standing position to a squatting position decreases the intensity. Rapid upstrokes of the carotid pulses are present. Blood pressures in the upper and lower extremities are equal.
Which of the following is the most likely diagnosis?
(A) Aortic coarctation
(B) Bicuspid aortic valve
(C) Hypertrophic cardiomyopathy
(D) Ventricular septal defect
Item 47 [Basic]
A 25-year-old asymptomatic man is evaluated during a routine examination. His blood pressure is 150/40 mm Hg and his heart rate is 90/min. Estimated central venous pressure is normal. The carotid upstroke is brisk and collapses quickly. The apical impulse is displaced. A grade 3/6 high-pitched decrescendo diastolic murmur is heard at the second right intercostal space with radiation down the left sternal border. The murmur is heard best with the patient leaning forward and in end-expiration. There is evidence of nailbed pulsation. Femoral pulsations are full and collapse quickly. There is no change in the murmur with inspiration.
Which of the following is the most likely diagnosis?
(A) Aortic valve regurgitation
(B) Mitral valve stenosis
(C) Patent ductus arteriosus
(D) Tricuspid regurgitation
Item 48 [Basic]
A 35-year-old woman is evaluated during a routine examination. She has no cardiovascular risk factors and no family history of cardiovascular disease. She is not currently on any medications.
On physical examination, vital signs are normal. There is a midsystolic click and a grade 2/6 late systolic murmur at the cardiac apex that radiates toward the left axilla.
Following squat-to-stand maneuvers, the midsystolic click moves closer to the S1, and murmur duration and intensity are increased. Carotid upstrokes are normal. The rest of the examination is unremarkable.
Which of the following is the most likely diagnosis?
(A) Aortic stenosis
(B) Coarctation of the aorta
(C) Hypertrophic cardiomyopathy
(D) Mitral valve prolapse
Item 49 [Advanced]
A 43-year-old man is evaluated during a routine examination. He has a history of a cardiac murmur diagnosed during childhood. He exercises regularly without restriction to activity and has no history of syncope, palpitations, or edema. He takes no medications.
On physical examination, blood pressure is 120/64 mm Hg, pulse is 80/min and regular, and respiration rate is 16/min. Cardiac examination reveals a normal S1 and a physiologically split S2. There is a grade 2/6 decrescendo diastolic murmur at the upper left sternal border. Distal pulses are brisk. There is no pedal edema.
A transthoracic echocardiogram demonstrates normal ventricular size and function, with ejection fraction of 60% to 65%. There is a bicuspid aortic valve with moderate regurgitation. Pulmonary pressure estimates are in the normal range.
Which of the following is the most appropriate management option for this patient?
(A) Antibiotic endocarditis prophylaxis
(B) Aortic valve replacement
(C) Begin metoprolol
(D) Clinical follow-up in 1 year
Item 30 Answer: D
Educational Objective: Treat atrial fibrillation with metoprolol and warfarin.
This patient is best treated with metoprolol and warfarin. There are two strategies in the treatment of persistent or paroxysmal atrial fibrillation: controlling the ventricular response rate to atrial fibrillation (rate control) and using antiarrhythmic drugs to maintain sinus rhythm (rhythm control). There is no survival advantage associated with either of these strategies, but for older patients (age >70 years), rate control is associated with improved quality-of-life scores. More hospitalizations and adverse drug reactions occur in patients receiving rhythm control compared with rate control. This elderly patient would be at significant risk of drug side effects from antiarrhythmic therapy. Therefore, this patient should receive medication to control the ventricular rate, such as metoprolol, and not an antiarrhythmic agent, such as amiodarone. The use of anticoagulation for stroke prevention is not affected by choice of approach.
In patients with nonvalvular atrial fibrillation, warfarin with a target INR of 2.0 to 3.0 has been shown to decrease stroke risk by an average of 62%, compared with a 19% decrease with aspirin therapy. To determine whether the risk of stroke is high enough to warrant chronic anticoagulation, risk stratification scores have been developed. The CHADS2 risk score for assessing the risk of stroke associated with atrial fibrillation has been validated in a large population. Points are scored for the presence of the following specific risk factors for stroke: Congestive heart failure, Hypertension, Age >75 years, Diabetes, and Stroke or transient ischemic attack (T IA). Patients are given 2 points for a history of stroke or T IA (the strongest risk factor) and 1 point for all other risk factors. The risk of stroke is lowest in patients with a CHADS2 score of 0 (1.2%). The risk is 18% for a CHADS2 score of 6 (maximum score). Patients with a CHADS2 score of 3 or greater and patients with a history of T IA or stroke are at high risk and should be considered for chronic anticoagulation with warfarin. This patient’s 10-minute episode of arm weakness is very suggestive of T IA, placing him in the highest risk category for stroke. Patients with a CHADS2 score of 1 or 2 should be assessed on an individual basis for aspirin versus warfarin therapy.
Not all patients with newly diagnosed atrial fibrillation require acute anticoagulation with heparin. Asymptomatic patients with good rate control who require long-term anticoagulation with aspirin or warfarin can have this therapy initiated as an outpatient.
Key Point
Most patients with atrial fibrillation are treated with a combination of rate control and long-term anticoagulation.
Bibliography
Zimetbaum P. Atrial fibrillation. Ann Intern Med. 2010;153(11):IT C61. [PMID: 21135291]
Item 31 Answer: D
Educational Objective: Manage benign premature ventricular contractions.
The most appropriate management for this patient is no additional investigation or therapy. He is very active and has no symptoms associated with the premature ventricular contractions (PVCs). Physical examination is normal and no findings suggest structural heart disease. Finally, the family history includes no worrisome features to suggest premature or sudden cardiac death syndromes. PVCs often are not associated with symptoms, although they can cause palpitations or a sensation that the heart has stopped, owing to the post-PVC compensatory pause. PVCs at rest in the setting of a structurally normal heart appear to be associated with little to no increased risk of cardiovascular events, particularly in patients younger than 30 years. Repetitive or complex ectopy in the setting of heart disease is associated with increased mortality risk, although the risk is due to the underlying pathophysiologic substrate, and suppression of ambient ventricular arrhythmias does not reduce mortality. Some patients have bothersome symptoms associated with PVCs. If symptoms can be clearly correlated with PVCs, treatment may be appropriate, although many patients respond well to simple reassurance. First-line therapy is almost always a ß-blocker such as metoprolol or a calcium channel blocker such as verapamil. However, antiarrhythmic drug therapy is associated with side-effects, so treatment cannot be undertaken without a discussion of its risks and benefits. Additional investigation in this asymptomatic young and healthy patient is unlikely to change his management. Therefore, echocardiography, arrhythmia monitoring, and exercise stress testing is not indicated.
Key Point
Premature ventricular contractions at rest in the setting of a structurally normal heart appear to be associated with little to no increased risk of cardiovascular events, particularly in patients younger than 30 years.
Bibliography
Ng GA. Treating patients with ventricular ectopic beats. Heart. 2006;92 (11):1707-12. [PMID: 17041126]
Item 32 Answer: D
Educational Objective: Treat patients at risk for sudden death with an implantable cardioverter-defibrillator.
The most appropriate treatment for this patient is an ICD. Sustained ventricular tachycardia (VT ) occurs most commonly in patients with previous myocardial infarction, and it is the scar formed by the infarction that provides the anatomic substrate for reentry. Areas of fibrosis interspersed with viable myocardial tissue are present in the border zone of dense scar tissue and impart the required conduction delay critical to the establishment of reentry circuits. Symptoms depend on the underlying state of the patient, and some patients can be asymptomatic, particularly if the VT rate is slow. In general, medical therapy (amiodarone, procainamide, flecainide) does not improve survival in patients with VT and structural heart disease; thus, most patients are candidates for ICD placement. Large clinical trials have demonstrated ICD therapy improves survival rates in patients with hemodynamically unstable VT after cardiac arrest who have ischemic or nonischemic cardiomyopathy and ejection fractions less than 35%. In patients with left ventricular dysfunction in the absence of VT , ICD implantation has also been shown to improve survival. The primary eligibility criterion for ICD implantation for primary prevention of sudden cardiac death in the setting of heart failure is left ventricular ejection fraction less than 35%, regardless of the presence or absence of coronary disease or the occurrence of arrhythmia.
Key Point
The primary eligibility criterion for implantable cardioverter-defibrillator implantation for primary prevention of sudden cardiac death in the setting of heart failure is left ventricular ejection fraction less than 35%.
Bibliography
Cevik C, Nugent K, Perez-Verdia A, Fish RD. Prophylactic implantation of cardioverter defibrillators in idiopathic nonischemic cardiomyopathy for the primary prevention of death: a narrative review. Clin Cardiol. 2010;33(5):254-60. [PMID: 20513063]
Item 33 Answer: B
Educational Objective: Manage a patient with ventricular fibrillation arrest in the setting of acute myocardial infarction.
The best option for the patient at this time is to continue medical management. Ventricular tachyarrhythmias are common in the setting of acute myocardial infarction, occurring in up to 20% of patients. Despite a sixfold increase in in-hospital mortality, the overall mortality at 1 year is not increased in patients with ventricular fibrillation that occurs early in this setting. Therefore, unlike sudden cardiac death occurring in other settings, cardiac arrest occurring within the first 48 hours of transmural acute myocardial infarction does not require defibrillator placement.
Primary ventricular fibrillation should be distinguished from ventricular fibrillation that occurs later in the course, usually as a result of heart failure. Before the advent of the implantable cardioverter-defibrillator, ventricular fibrillation occurring late in the hospital course was associated with an 85% 1-year mortality rate. All patients, even those who have not suffered arrhythmia during myocardial infarction, should be reevaluated after myocardial infarction by transthoracic echocardiogram to further stratify risk. If the ejection fraction is found to be reduced (<35%), the patient may be a candidate for defibrillator placement.
Amiodarone has not been shown to improve overall mortality following myocardial infarction. In the general population of cardiac arrest survivors, amiodarone does not improve mortality.
Implantable cardioverter-defibrillator placement is not indicated for patients who experience ventricular arrhythmias less than 48 hours after an acute ST -elevation myocardial infarction. Implantable cardioverter-defibrillators have demonstrated a mortality benefit for essentially all other groups of cardiac arrest survivors.
The typical indications for a pacemaker include symptomatic sinoatrial node dysfunction (sinus bradycardia, intra-atrial block, exit block) and symptomatic bradycardia due to advanced second- or third-degree heart block. This asymptomatic man with no evidence of bradycardia or advanced heart block on his electrocardiogram has no indication for a pacemaker. Pacemaker placement does not prevent sudden death due to ventricular tachyarrhythmias.
Key Point
Cardiac arrest occurring within the first 48 hours of an acute, transmural myocardial infarction does not require secondary prevention therapy other than standard postmyocardial infarction care.
Bibliography
Kusumoto F. A comprehensive approach to management of ventricular arrhythmias. Cardiol Clin. 2008;26(3):481-496, vii. [PMID: 18538192]
Item 34 Answer: C
Educational Objective: Diagnose familial long QT syndrome.
This patient most likely has long QT syndrome (LQT S). Cardiac events in patients with LQT S include syncope and cardiac arrest due to torsade de pointes ventricular tachycardia. LQT S may be either congenital or acquired. This patient probably has congenital LQT S, suggested by recurrent syncope triggered by activity and a family history of early sudden death (cousin drowning). Her mother is probably affected as well. Risk factors for acquired LQT S include female sex, hypokalemia, hypomagnesemia, structural heart disease, previous QT -interval prolongation, and a history of drug-induced arrhythmia. (An extensive list of offending agents can be found at www.azcert.org/medical-pros/drug-lists/drug-lists.cfm.) Other cardiac causes of syncope and sudden death in young patients include hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia.
Left bundle branch block (LBBB) and right bundle branch block (RBBB) are electrocardiographic patterns that increase in frequency with age. LBBB most often occurs in patients with underlying heart disease. In older patients, LBBB is associated with increased mortality. In younger patients, however, LBBB is not associated with syncope or sudden death and the prognosis is generally excellent. RBBB is similarly associated with increased mortality in older patients with underlying heart disease. When RBBB is not associated with underlying cardiac disease, patient outcomes are generally excellent, and RBBB is an unlikely cause of this patient’s symptoms.
First-degree atrioventricular block is characterized by prolongation of the PR interval to longer than 0.2 sec; it usually is not associated with alterations in heart rate and has no association with syncope or sudden death.
Key Point
Cardiac events in patients with long QT syndrome include syncope and cardiac arrest due to torsade de pointes ventricular tachycardia.
Bibliography
Goldenberg I, Zareba W, Moss AJ. Long QT syndrome. Curr Probl Cardiol. 2008;33(11):629-694. [PMID: 18835466]
Item 35 Answer: A
Educational Objective: Treat New York Heart Association class IV heart failure with digoxin.
Digoxin is the most appropriate therapy to initiate in this patient. The role of digoxin in treating heart failure patients in sinus rhythm is primarily for symptom control rather than improving survival. Treatment with digoxin has not been shown to affect mortality but has been shown to reduce hospitalizations. Digoxin can be added to other therapy in patients with New York Heart Association class III or IV heart failure for symptom control. Maintaining lower serum concentrations of digoxin is as effective as maintaining higher concentrations, and potential toxicities are avoided. Higher digoxin levels (=1.2 ng/mL [1.5 nmol/L] versus 0.5-0.8 ng/mL [0.6-1.0 nmol/L]) appear to be associated with higher mortality in patients with systolic heart failure. The primary reason to use an angiotensin receptor blocer (ARB) instead of an angiotensin-converting enzyme (ACE) inhibitor, such as lisinopril, is to avoid the side effect of cough. Combined treatment with an ACE inhibitor and an ARB is generally not recommended, because concurrent therapy is significantly associated with increased risk of medication nonadherence and adverse effects, including worsening renal function and symptomatic hypotension, whereas the additional benefit of using these two medications together is not well established. ACE inhibitors are currently preferred over ARBs for most patients, because there is more clinical experience with these agents.
There is no role for the routine anticoagulation of heart failure patients with warfarin (or aspirin) because there is no apparent benefit and an increased risk of bleeding. Major guidelines generally agree that warfarin should be considered in a patient with a heart failure and a previous thrombotic event (for example, stroke or pulmonary embolism) and in patients with an underlying atrial fibrillation heart rhythm.
Key Point
Digoxin alleviates symptoms and decreases hospitalizations, but it provides no survival benefit in patients with heart failure.
Bibliography
Goldberg LR. Heart failure. Ann Intern Med. 2010;152(11):IT C61-15; quiz IT C616. [PMID: 20513825]
Item 36 Answer: D
Educational Objective: Diagnose heart failure due to peripartum cardiomyopathy.
This patient most likely has heart failure due to peripartum cardiomyopathy. Peripartum cardiomyopathy is defined as heart failure with a left ventricular ejection fractionless than 45% that is diagnosed between 3 months before and 6 months after delivery in the absence of an identifiable cause. It is usually diagnosed during the first month postpartum. This patient has clinical features consistent with heart failure (progressive dyspnea), evidence of left ventricular dysfunction (tachycardia, elevated central venous pressure, S3 and S4, displaced and diffuse apical impulse, mitral regurgitant murmur, pulmonary crackles), and confirmatory chest radiography (pleural effusions and interstitial infiltrates).
Acute myocardial infarction may occur during pregnancy and in the postpartum period. It may be related to atherosclerotic coronary artery disease or coronary artery dissection and vasculitis and carries a high risk of maternal mortality and morbidity. This patient’s presentation, however, does not suggest an acute coronary syndrome, given the absence of chest pain or electrocardiographic changes.
Aortic dissection may occur in the peripartum or postpartum period and is a particular concern in patients with aortopathy related to Marfan syndrome, familial thoracic aortic aneurysmal disease, or bicuspid aortic valve-related aortopathy. However, the current presentation does not suggest aortic dissection given the absence of chest pain, the presence of equal and normal blood pressures in the upper extremities, and the presence of normal lower extremity pulses. Additionally, aortic dissection is usually associated with an abnormal chest radiograph (widened mediastinum, abnormal aortic contour), and the absence of these findings argues strongly against the diagnosis. Aortic dissection cannot explain the patient’s findings of a dilated left ventricle and signs of heart failure.
Coarctation of the aorta may rarely present initially as hypertension during pregnancy. However, the patient’s current physical examination findings of easily palpable lower extremity pulses without delay and the absence of hypertension argue against coarctation. In addition, rib notching is not reported on the chest radiograph.
Key Point
The presence of elevated central venous pressure, pulmonary crackles, ventricular gallops (S3 or S4), any cardiac murmur, and lower extremity edema all increase the likelihood of heart failure.
Bibliography
Goldberg LR. Heart failure. Ann Intern Med. 2010;152(11):IT C61-15; quiz IT C616. [PMID: 20513825]
Item 37 Answer: A
Educational Objective: Evaluate a patient with new-onset heart failure with cardiac angiography.
The most appropriate diagnostic test for this patient is a cardiac angiography. This patient has typical angina (substernal chest pain precipitated by exertion and relieved by rest) and new-onset heart failure, as evidenced by symptoms (exertional dyspnea and orthopnea), examination findings (elevated jugular venous pressure, pulmonary crackles, and an S3 and S4), and echocardiogram with a subnormal ejection fraction. Definitive testing for coronary artery disease (CAD) by cardiac catheterization is warranted. The primary aim of an evaluation for CAD is to identify possible targets for revascularization (percutaneous or surgical) with the goals of reducing angina, improving systolic function, reducing the risk of heart failure progression, and improving survival.
For patients with an intermediate likelihood of CAD who have no features of unstable angina, stress testing is the preferred approach when assessing for CAD. An exercise stress test is recommended in a patient with an intermediate probability of disease and a normal resting electrocardiogram (ECG). A nuclear medicine stress test is helpful if the resting ECG is abnormal. In this patient, however, the pretest probability for CAD is high based on his age, sex, and the presence of typical anginal symptoms. Because a negative result on stress testing in a patient with a high pretest probability of CAD would have a high likelihood of being a false negative, catheterization would still be needed for a definitive diagnosis, as well as for planning therapy.
A radionuclide ventriculogram can be useful in confirming the ejection fraction if clarification is needed. In this patient, however, the ejection fraction value is provided by the echocardiogram. Furthermore, a radionuclide ventriculogram would not assist in determining the cause of the new-onset heart failure.
Key Point
Patients with new-onset heart failure and angina should be evaluated with cardiac catheterization and angiography if they are possible candidates for revascularization.
Bibliography
Goldberg LR. Heart failure. Ann Intern Med. 2010;152(11):IT C61-15; quiz IT C616. [PMID: 20513825]
Item 38 Answer: B
Educational Objective: Evaluate new-onset heart failure with echocardiography.
An echocardiogram should be obtained in all patients with newly diagnosed or suspected heart failure to determine whether the heart failure is systolic or diastolic and whether there are any structural or functional abnormalities that may be causing the heart failure (such as regional wall abnormalities, pericardial disease, or valvular abnormality). All of these issues may have a significant impact on management and prognosis.
B-type natriuretic peptide (BNP) is a hormone synthesized by the cardiac ventricles in response to increased wall stress due to pressure or volume overload. BNP assays have become a useful tool in the diagnosis of acute heart failure and differentiating it from noncardiac causes of dyspnea. A patient with a BNP concentration below 100 pg/mL is unlikely to have acute heart failure, whereas a patient with a concentration higher than 500 pg/mL has a high likelihood of having heart failure. BNP level will likely be elevated in this patient, confirming the presence of volume overload. The physical examination, history, and chest radiograph concordantly suggest volume overload and heart failure, and a BNP level confirming this would not be helpful.
A radionuclide ventriculogram would accurately assess ventricular ejection fraction but would not provide other cardiac structural or functional information that may impact management. A radionuclide ventriculogram, therefore, is not the most appropriate next test.
Ischemia is a major cause of left ventricular dysfunction. Given the potential significant benefits of revascularization in appropriate candidates, including improved ventricular function and reduced morbidity and mortality, diligent evaluation for coronary artery disease should be undertaken for most patients with heart failure. A stress test would be appropriate in this patient if there were a higher clinical suspicion for coronary disease or ischemia causing new-onset heart failure. However, given the lack of anginal symptoms, the patient’s relatively young age, and lack of risk factors, clinical suspicion at this point is low. Finally, and importantly, an exercise stress test is contraindicated in a patient with decompensated heart failure, such as this patient.
Key Point
An echocardiogram should be obtained in all patients with newly diagnosed or suspected heart failure.
Bibliography
Abraham J, Abraham T P. The role of echocardiography in hemodynamic assessment in heart failure. Heart Fail Clin. 2009;5(2):191-208. [PMID: 19249688]
Item 39 Answer: B
Educational Objective: Treat New York Heart Association class I or II systolic heart failure with a ß-blocker.
Treatment with an angiotensin-converting enzyme (ACE) inhibitor (such as lisinopril) and a ß-blocker (such as carvedilol) is indicated for all patients with systolic heart failure regardless of symptoms or functional status, including asymptomatic or very functional patients. The combination of these two classes of medications has additivebenefits with regard to morbidity and mortality in systolic heart failure. This patient is already taking an ACE inhibitor, so a ß-blocker such as carvedilol should be added. ß-Blockers should not be initiated or increased during decompensated states, such as volume overload or hypotension, because the transient decline in cardiac output may worsen a decompensated state.
Amlodipine is the only calcium channel blocker demonstrated to have a neutral (rather than detrimental) effect on morbidity and mortality in heart failure. Thus, it is an acceptable agent to use for angina or hypertension that is not adequately controlled with ACE inhibitors or ß-blockers. However, this patient has neither angina nor uncontrolled hypertension, and amlodipine is not indicated.
Digoxin is indicated for patients with moderately to severely symptomatic heart failure (New York Heart Association [NYHA] class III-IV) or for rate control in patients with atrial fibrillation. Digoxin improves symptoms and reduces hospitalizations, but it does not affect survival. Spironolactone is indicated only for treatment of NYHA class III or IV heart failure; in this setting, its use is associated with a 30% reduction in mortality. This patient, however, is only minimally symptomatic (NYHA class II);treatment with either digoxin or spironolactone is not indicated.
There are currently no robust data to support addition of an angiotensin receptor blocker (ARB), such as losartan, to ACE inhibitor therapy for treatment of systolic heart failure. No definitive improvement in survival has been demonstrated using the combination of these two agents. ARBs are currently recommended only for patients who are intolerant of ACE inhibitors, primarily owing to ACE inhibitor-induced cough.
Key Point
Treatment with an angiotensin-converting enzyme inhibitor and a ß-blocker is indicated for all patients with systolic heart failure regardless of symptoms or functional status, including asymptomatic or very functional patients.
Bibliography
Goldberg LR. Heart failure. Ann Intern Med. 2010;152(11):IT C61-15; quiz IT C616. [PMID: 20513825]
Item 40 Answer: D
Educational Objective: Treat a patient with heart failure with a ß-blocker and an angiotensin-converting enzyme inhibitor.
This patient should be started on lisinopril in addition to metoprolol. Angiotensin-converting enzyme (ACE) inhibitors, such as lisinopril, are indicated for treatment of all New York Heart Association (NYHA) functional classes of systolic heart failure, including asymptomatic (NYHA class I) patients. ACE inhibitors reduce mortality and morbidity in asymptomatic and symptomatic patients and delay the onset of clinical heart failure in patients with asymptomatic left ventricular dysfunction. Overall, ACE inhibitor therapy reduces mortality by about 20%, risk for myocardial infarction by about 20%, and hospitalization for heart failure by 30% to 40%.
For patients intolerant of ACE inhibitors owing to hyperkalemia or renal insufficiency, the combination of hydralazine and a nitrate is a suitable alternative, with hemodynamic effects of vasodilation and afterload reduction. Treatment with this combination is also associated with a reduction in mortality, although to a lesser degree than is seen with ACE inhibitors, and this combination does not have the same positive impact on quality of life as an ACE inhibitor.
The role of digoxin in treating heart failure patients in sinus rhythm is primarily for symptom control rather than improving survival. Treatment with digoxin has not been shown to affect mortality but has been shown to reduce hospitalizations. Digoxin can be added to other therapy in patients with NYHA class III or IV heart failure for symptom control. Maintaining lower serum concentrations of digoxin is as effective as maintaining higher concentrations, and potential toxicities are avoided.
Eplerenone is a selective aldosterone blocker that is currently approved for treatment of hypertension and for left ventricular dysfunction after myocardial infarction.
Eplerenone is a suitable alternative to spironolactone in treatment of severe heart failure (NYHA class III or IV) if gynecomastia develops as a side effect of spironolactone treatment.
This patient has NYHA class II heart failure (symptoms with moderate exertion) and does not meet the criteria for treatment with digoxin or an aldosterone agonist.
Key Point
Angiotensin-converting enzyme inhibitors are indicated for treatment of all New York Heart Association (NYHA) functional classes of systolic heart failure, including asymptomatic (NYHA class I) patients.
Bibliography
Goldberg LR. Heart failure. Ann Intern Med. 2010;152(11):IT C61-15; quiz, IT C616. [PMID: 20513825]
Item 41 Answer: D
Educational Objective: Treat a patient with New York Heart Association functional class III or IV heart failure with spironolactone.
The most appropriate addition to this patient’s treatment is spironolactone. She has symptoms consistent with New York Heart Association (NYHA) class III functional status (symptoms develop with mild activity), and she does not appear volume-overloaded on examination (normal central venous pressure and no S3, pulmonary crackles, or edema). Spironolactone is indicated for treatment of severe (NYHA functional class III or IV) systolic heart failure in addition to standard therapy with an angiotensinconverting enzyme (ACE) inhibitor, ß-blocker, and diuretic as needed. Spironolactone further blocks the actions of aldosterone, which is not completely suppressed by chronic ACE inhibitor therapy; aldosterone has adverse effects of sodium retention, potassium wasting, and myocardial fibrosis. The addition of spironolactone is associated with a 30% relative reduction in mortality.
Serum creatinine and potassium levels should be serially monitored in patients taking spironolactone. Contraindications to spironolactone therapy include a serum creatinine level greater than 2.5 mg/dL (221 µmol/L) in men or 2.0 mg/dL (176.8 µmol/L) in women or a potassium level greater than 5 meq/L (5 mmol/L).
It is generally not recommended to add angiotensin receptor blocker therapy, such as losartan, to ACE inhibitor therapy because the risk of adverse side effects, such as hyperkalemia and hypotension, is increased.
The addition of metolazone to loop diuretic therapy can be useful to increase diuretic effectiveness. However, this patient appears euvolemic on her current diuretic regimen, so enhanced diuresis is not needed.
First-generation calcium channel blockers (such as nifedipine) have been shown to increase the risk of heart failure decompensation and hospitalization. Amlodipine and felodipine are the only calcium channel blockers with demonstrated neutral effects on mortality in patients with heart failure. These agents can be used in patients with heart failure for the management of hypertension or angina not adequately controlled with other agents such as ACE inhibitors or ß-blockers.
Key Point
Angiotensin-converting enzyme inhibitors, ß-blockers, and spironolactone reduce mortality in patients with New York Heart Association class III or IV heart failure.
Bibliography
Goldberg LR. Heart failure. Ann Intern Med. 2010;152(11):IT C61-15; quiz IT C616. [PMID: 20513825]
Item 42 Answer: A
Educational Objective: Diagnose atrial fibrillation as the cause of clinical deterioration in a patient with aortic stenosis.
New-onset atrial fibrillation is the most likely cause of the patient’s new symptoms. Aortic valve sclerosis, or valve thickening without outflow obstruction, is present in more than 25% of persons older than 65 years. Patients are often diagnosed when an asymptomatic murmur is auscultated or following an incidental echocardiographic finding. The progression from aortic sclerosis to stenosis is slow, and fewer than 20% of patients develop valve obstruction over the next 10 years. When mild stenosis is present, however, progressive valve stenosis proceeds more rapidly. Classic manifestations of aortic stenosis are angina, syncope, and heart failure. In early stages, aortic stenosis may present subtly with dyspnea or a decrease in exercise tolerance. Atrial fibrillation can be associated with rapid and severe clinical deterioration due to the more rapid rate and loss of atrial contribution to left ventricular filling. Angina occurs in more than 50% of patients with severe stenosis, due in part to maldistribution of coronary flow in the hypertrophied myocardium. Patients with aortic stenosis have increased sensitivity to ischemic injury, and subsequently have higher mortality. Frank syncope associated with aortic stenosis is rare, with prospective studies documenting sudden cardiac death rates less than 1% annually.
Endocarditis should be suspected if an abnormal murmur is heard on examination, particularly in patients with a compelling history or concurrent fever. Incidence is higher in patients with underlying valve abnormalities and prosthetic valves. Because of the absence of fever and the presence of atrial fibrillation as a more likely cause of clinical deterioration, infective endocarditis is unlikely.
Patients with a history of rheumatic fever may have involvement of multiple heart valves, but this is not the case in patients with degenerative aortic sclerosis. Furthermore, the physical examination findings of chronic mitral regurgitation include a holosystolic murmur, heard best at the apex, with radiation laterally or posteriorly. The auscultatory findings for mitral stenosis include an opening snap with a low-pitched middiastolic murmur that accentuates presystole. These findings are not present, making mitral stenosis or regurgitation unlikely.
Key Point
In patients with aortic stenosis, atrial fibrillation can be associated with rapid and severe clinical deterioration due to the more rapid rate and loss of atrial contribution to left ventricular filling.
Bibliography
Kappetein AP, van Geldorp M, T akkenberg JJ, Bogers AJ. Optimum management of elderly patients with calcified aortic stenosis. Expert Rev Cardiovasc T her.
2008;6(4):491-501. [PMID: 18402539]
Item 43 Answer: A
Educational Objective: Diagnose failure of a prosthetic aortic heart valve.
Failure of a prosthetic aortic valve often leads to aortic insufficiency. Bioprosthetic valves are less durable than mechanical valves because of the progressive degenerative calcification of the biologic material. In the first generation of bioprosthetic valves, only about 50% of aortic and 30% of mitral prostheses were still working after 15 years.
Although newer valves are more durable and have larger valve areas and improved hemodynamics, they are still prone to progressive calcific degeneration. Physical examination in patients with chronic aortic regurgitation shows a widened pulse pressure with bounding peripheral and carotid pulses. Auscultatory findings include an early to holodiastolic murmur along the left upper sternal border, which is high pitched and may be better heard when the patient is at end-expiration, leaning forward.
The characteristic physical examination findings in atrial septal defect are fixed splitting of the S2 and a right ventricular heave. A pulmonary midsystolic flow murmur and a tricuspid diastolic flow rumble caused by increased flow through the right-sided valves from a large left-to-right shunt may be heard.
Aortic coarctation is usually diagnosed in childhood by the association of a systolic murmur with systemic hypertension and reduced femoral pulse amplitude. More than 50% of patients with aortic coarctation also have a bicuspid aortic valve. When coarctation is severe, the murmur may be continuous and a murmur from collateral intercostal vessels may also be audible and palpable. An ejection click and aortic systolic murmur suggest the presence of a bicuspid aortic valve. An S4 is common.
The auscultatory findings for rheumatic mitral stenosis include an opening snap with a low-pitched middiastolic murmur that accentuates presystole and is best heard over the mitral valve area. The S1 may be intensified owing to higher left atrial pressures.
New-onset ventricular septal defect in adults usually occurs 5 to 7 days following a myocardial infarction. It is characterized by the development of cardiogenic shock and a new systolic murmur. A thrill along the left sternal border may also be present. This patient does not have a history consistent with myocardial infarction and does not have the typical findings.
Key Point
Failure of a prosthetic aortic valve often leads to aortic insufficiency.
Bibliography
Choudhry NK, Etchells EE. The rational clinical examination. Does this patient have aortic regurgitation? JAMA. 1999;281(23):2231-8. [PMID: 10376577]
Item 44 Answer: D
Educational Objective: Manage an asymptomatic benign murmur.
This patient has a benign midsystolic murmur that is grade 2/6 in intensity and requires no further evaluation or intervention. Midsystolic murmurs grade 2/6 or less are considered innocent murmurs, especially when they are short in duration, associated with a physiologically split (normal) S2, and are not accompanied by any other abnormal cardiac sounds or murmurs. The most common etiology of this type of murmur in persons older than 65 years is minor valvular abnormalities due to aortic sclerosis. Aortic sclerosis is characterized by focal areas of valve thickening leading to mild valvular turbulence, producing the auscultated murmur. A hyperdynamic circulation (for example, from severe anemia, thyrotoxicosis, or pregnancy) also may produce an innocent midsystolic pulmonary or aortic flow murmur. A physiologically split S2 (apparent during inspiration, absent during exhalation) excludes severe aortic stenosis.
Endocarditis prophylaxis is not indicated. The only patients who should receive endocarditis prophylaxis are those with prosthetic cardiac valves, those with a known history of prior infective endocarditis, those with unrepaired cyanotic congenital heart disease, those with complex congenital heart disease with residual abnormalities, and cardiac transplant recipients with valve abnormalities.
Transthoracic echocardiography is indicated when a grade 3/6 or greater systolic murmur is heard on examination, in the presence of any diastolic or continuous murmur, or if a new murmur is diagnosed in the interval since a normal prior physical examination; none of these criteria are met by this patient.
A screening cardiac stress test is not warranted because she has no symptoms indicative of angina or risk factors for coronary artery disease. In a patient with a low pretest probability of coronary artery disease, an exercise stress test would carry a high false-positive rate.
Key Point
Short, soft, midsystolic murmurs in the elderly are usually benign and caused by minor, age-related changes of the aortic valve (aortic sclerosis).
Bibliography
Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA. 1997;277(7):564-571. [PMID: 9032164]
Item 45 Answer: C
Educational Objective: Diagnose mitral stenosis.
This patient’s clinical history and physical examination findings are consistent with rheumatic mitral valve stenosis. Cardiac auscultation reveals the typical findings of mitral stenosis, including an accentuation of P2 (evidence of elevated pulmonary arterial pressure), an opening snap (a high-pitched apical sound best heard with the diaphragm of the stethoscope), and a low-pitched, rumbling diastolic murmur.
Mitral stenosis is usually caused by rheumatic valve disease. In the United States, clinical presentation tends to be 20 to 30 years after the initial episode of rheumatic fever, and most cases occur in women. Patients with mitral stenosis may be asymptomatic for some time, but become symptomatic with additional hemodynamic stress, such as the increased volume load of pregnancy. This hemodynamic stress may precipitate an arrhythmia, such as atrial fibrillation, that can further exacerbate heart failure symptoms.
The diagnosis of acute aortic regurgitation is suggested in patients with rapid onset of dyspnea, exercise intolerance, or chest pain (aortic dissection). Physical findings include tachycardia, hypotension, a soft S1 (due to premature closure of the mitral valve), an S3 and/or S4 gallop, an accentuated pulmonic closure sound, and pulmonary crackles. The typical murmur of aortic regurgitation may not be prominent in acute disease as aortic and left ventricular diastolic pressures equilibrate quickly, resulting in a short and soft (sometimes inaudible) diastolic murmur at the base of the heart.
The characteristic physical examination finding in atrial septal defect is fixed splitting of the S2. A pulmonic midsystolic murmur at the base of the heart and a tricuspid diastolic flow rumble may be heard at the lower left sternal border owing to increased flow through the valves from the left-to-right shunt.
The murmur of tricuspid regurgitation is a systolic murmur that is best heard at the lower left sternal border and characteristically increases in intensity with inspiration.
Tricuspid regurgitation usually occurs as a secondary consequence of pulmonary hypertension, right ventricular chamber enlargement with annular dilatation, or endocarditis.
Key Point
T ypical findings of mitral stenosis include an opening snap and a low-pitched, rumbling diastolic murmur.
Bibliography
Chizner MA. The diagnosis of heart disease by clinical assessment alone. Dis Mon. 2002;48(1):7-98. [PMID: 11807426]
Item 46 Answer: C
Educational Objective: Diagnose hypertrophic cardiomyopathy.
In this patient, the physical examination is most consistent with hypertrophic cardiomyopathy. The systolic murmur of hypertrophic cardiomyopathy is caused by obstruction in the left ventricular outflow tract from the thickened interventricular septum. In severe cases, systolic anterior motion of the mitral valve apparatus into the left ventricular outflow tract contributes to the systolic murmur. If mitral valve leaflet coaptation is affected, there may be concurrent mitral regurgitation. The stand-tosquat maneuver and passive leg lift transiently increase venous return (preload), which increases left ventricular chamber size and volume. As a consequence, there is less relative obstruction and turbulence in the left ventricular outflow tract, decreasing murmur intensity. Handgrip exercise also diminishes murmur intensity, by increasing afterload and decreasing the relative pressure gradient across the left ventricular outflow tract. The Valsalva maneuver and the squat-to-stand maneuver transiently decrease venous return, with the septum and anterior mitral leaflet brought closer together. Turbulent flow—and the murmur—are increased. Transthoracic echocardiography can confirm a diagnosis of hypertrophic cardiomyopathy.
Aortic coarctation in an adult is characterized by hypertension and a continuous or late systolic murmur that may be heard over the back. Because pulses distal to the aortic obstruction are decreased, aortic coarctation is also associated with abnormal differences in upper and lower extremity blood pressures. The carotid upstroke is normal in coarctation.
A congenital bicuspid aortic valve is a common cause of calcific aortic stenosis. The murmur of aortic stenosis is an early systolic murmur that often radiates toward the carotid arteries. Hypertrophic cardiomyopathy is associated with rapid upstrokes of the carotid arteries, helping to distinguish it from aortic stenosis, which is associated with a carotid artery pulsation that has a slow up-rise and is diminished in volume. In addition, the murmur of aortic stenosis decreases with the Valsalva maneuver. Finally, although the presence of a bicuspid aortic valve accelerates the process of aortic calcification, patients typically develop stenosis in their thirties or forties, not in the late teens or early twenties.
The murmur associated with a ventricular septal defect is a harsh systolic murmur located parasternally that radiates to the right sternal edge and may be associated with a palpable thrill but no change in the carotid artery pulsation. Maneuvers that increase afterload, such as isometric handgrip exercise, increase the left-sided murmurs of mitral regurgitation and ventricular septal defect.
Key Point
The Valsalva maneuver and the squat-to-stand maneuver increase the murmur of hypertrophic cardiomyopathy.
Bibliography
Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA. 1997;277(7):564-571. [PMID:9032164]
Item 47 Answer: A
Educational Objective: Diagnose aortic valve regurgitation.
This patient most likely has aortic regurgitation. Physical findings of chronic aortic regurgitation may include cardiomegaly, tachycardia, a widened pulse pressure, a thrill at the base of the heart, a soft S1 and a sometimes absent aortic closure sound, and an S3 gallop. The characteristic high-pitched diastolic murmur begins immediately after S2 and is heard best at the second right or third left intercostal space with the patient leaning forward, and in end-expiration. Manifestations of the widened pulse pressure may include the T raube sign (pistol-shot sounds over the peripheral arteries), the de Musset sign (head bobs with each heartbeat), the Duroziez sign (systolic and diastolic murmur heard over the femoral artery), and the Quincke sign (systolic plethora and diastolic blanching in the nail bed with nail compression).
Mitral stenosis is associated with accentuation of P2 (evidence of elevated pulmonary arterial pressure), an opening snap (a high-pitched apical diastolic sound best heard with the diaphragm of the stethoscope) followed by a low-pitched, rumbling diastolic murmur best heard with the bell of the stethoscope at the apex with the patient in the left lateral decubitus position. Presystolic accentuation of the murmur may be present. As the severity of the stenosis worsens, the opening snap moves closer to S2 as a result of increased left atrial pressure, and the murmur increases in duration.
A small patent ductus arteriosus in an adult produces a continuous murmur that envelopes the S2 and is characteristically heard beneath the left clavicle. Patients with a moderate-sized patent ductus arteriosus may present with symptoms of heart failure, a continuous “machinery-type” murmur best heard at the left infraclavicular area, and bounding pulses with a wide pulse pressure.
Tricuspid valve regurgitation usually occurs as a secondary consequence of pulmonary hypertension, right ventricular chamber enlargement with annular dilatation, or endocarditis. The murmur of tricuspid regurgitation occurs during systole and is loudest at the lower left sternal border and becomes louder with inspiration.
Key Point
The characteristic high-pitched diastolic murmur of chronic aortic regurgitation begins immediately after S2 and is heard best with the patient leaning forward, and in endexpiration at the second right or third left intercostal space.
Bibliography
Choudhry NK, Etchells EE. The rational clinical examination. Does this patient have aortic regurgitation? JAMA. 1999;281(23):2231-2238. [PMID: 10376577]
Item 48 Answer: D
Educational Objective: Diagnose mitral valve prolapse.
Mitral valve prolapse is the most common cause of mitral regurgitation. The prevalence in the United States is 2% to 3% with equal sex distribution. The classic auscultatory findings are a midsystolic click followed by a late apical systolic murmur. A squat-to-stand maneuver transiently decreases preload on the heart. This decreases left ventricular chamber size and increases systolic buckling of the redundant mitral valve into the left atrium, moving the midsystolic click earlier in systole and increasing mitral regurgitation.
Most patients with mitral valve prolapse have either minimal or no mitral regurgitation, and the prognosis is benign, with annual mortality below 1%. Serious complications, which are rare, include significant mitral regurgitation, infective endocarditis, and arrhythmia.
The murmur of aortic stenosis is an early systolic murmur that is heard best at the right second intercostal space but can be heard anywhere from the cardiac base to the apex.
The murmur often radiates toward the carotid arteries. The murmur of aortic stenosis decreases with the Valsalva maneuver.
Aortic coarctation in an adult is characterized by hypertension and a continuous or late systolic murmur that may be heard over the back. Because pulses distal to the aortic obstruction are decreased, aortic coarctation is also associated with abnormal differences in upper and lower extremity blood pressures.
The murmur of hypertrophic cardiomyopathy is a harsh systolic murmur heard best near the lower left sternal border between the sternum and apex. The Valsalva maneuver and the squat-to-stand maneuver transiently increase the intensity of the murmur. Handgrip exercise increases afterload and decreases the relative pressure gradient across the left ventricular outflow tract, so murmur intensity for hypertrophic cardiomyopathy is decreased. Carotid upstrokes are brisk. There is no midsystolic click.
Key Point
The classic auscultatory findings of mitral valve prolapse are a midsystolic click followed by a late apical systolic murmur.
Bibliography
Foster E. Clinical practice. Mitral regurgitation due to degenerative mitral-valve disease. N Engl J Med. 2010;363(2):156-65. [PMID: 20647211]
Item 49 Answer: D
Educational Objective: Follow a patient with an asymptomatic bicuspid aortic valve and preserved left ventricular function.
The most appropriate management for this patient is clinical follow-up in 1 year. This patient has a bicuspid aortic valve with moderate aortic regurgitation.
Echocardiography demonstrates normal left ventricular size and systolic function. Pulmonary pressures are in the normal range, and there is no evidence of adverse hemodynamic effects of valve regurgitation on the ventricle (ventricular size and function are normal). No specific treatment is needed at this time. However, because worsening of aortic regurgitation can be insidious, routine clinical follow-up is indicated in at least yearly intervals, typically with repeat transthoracic echocardiography to monitor for disease progression. The presence of a bicuspid aortic valve is associated with ascending aorta dilatation, and transthoracic echocardiography can also monitor for aortic enlargement. Most patients with bicuspid valves will eventually develop aortic stenosis, regurgitation, or aortic root dilatation or dissection that will require surgery.
Antibiotic endocarditis prophylaxis is now recommended only in patients with prosthetic cardiac valves, those with a known history of prior infective endocarditis, cardiac transplant recipients with valve abnormalities, those with unrepaired cyanotic congenital heart disease, and those with complex congenital heart disease with residual abnormalities. This patient, therefore, should not receive antibiotic endocarditis prophylaxis.
Aortic valve replacement surgery is recommended in patients with severe aortic regurgitation and cardiopulmonary symptoms. In asymptomatic patients with severe regurgitation, surgery is recommended once there are signs of left ventricular enlargement or adverse hemodynamic effects on the left ventricle, or if the ejection fraction falls below 50% to 55%. This patient is asymptomatic, and his left ventricular size and function are normal.
A ß-blocker (such as metoprolol) is indicated for all stages of systolic heart failure, even asymptomatic patients with left ventricular ejection fractions less than 50%. This patient has no evidence of systolic heart failure either by symptoms or echocardiographic evidence. There is no evidence that treatment with a ß-blocker delays the time to aortic valve replacement; therefore, metoprolol is not indicated.
Key Point
Asymptomatic patients with chronic aortic regurgitation and normal left ventricular size and function have an excellent prognosis and do not require prophylactic surgery.
Bibliography
Maurer G. Aortic regurgitation. Heart. 2006;92(7):994-1000. [PMID: 16775114]