Section 1. Cardiovascular Medicine (Questions 1-24)
Item 1 [Basic]
A 66-year-old man is evaluated in the emergency department for left-sided chest pain that began at rest, lasted for 15 minutes, and has since resolved. A similar episode occurred at rest yesterday. Pertinent medical history includes hypertension and type 2 diabetes mellitus. Current medications are amlodipine, glyburide, and aspirin.
On physical examination, blood pressure is 125/65 mm Hg, heart rate is 70/min, and respiratory rate is 12/min. Estimated central venous pressure is 6 cm H2O, carotid upstroke is normal, there are no cardiac murmurs, and the lung fields are clear.
Laboratory findings include an elevated serum troponin I level. Electrocardiogram is shown. Chest radiograph is normal.
Which of the following is the most likely diagnosis?
(A) Chronic stable angina
(B) Non-ST -elevation myocardial infarction
(C) ST -elevation myocardial infarction
(D) Unstable angina
Item 2 [Basic]
A 63-year-old woman is admitted to the hospital with pleuritic chest pain, diaphoresis, and dyspnea of 1 hour’s duration. The pain is not affected by food, antacids, or exertion. It may be worse when supine and with deep breathing. She has a 10-year history of hypertension and hyperlipidemia. Her medications are chlorthalidone and lovastatin.
On physical examination, temperature is 37.8°C (100.0°F), blood pressure is 145/90 mm Hg (both arms), heart rate is 108/min, and respiration rate is 22/min. Cardiovascular examination reveals a regular rhythm and a biphasic, scratchy sound best heard at the lower left sternal border. No murmur, S3, or S4 is heard. The lungs are clear to auscultation. The jugular venous pressure is normal and no peripheral edema is noted.
The electrocardiogram shows sinus tachycardia with diffuse ST elevation. Troponin level and chest radiograph findings are normal.
Which of the following is the most likely diagnosis?
(A) Acute myocardial infarction
(B) Acute pericarditis
(C) Aortic dissection
(D) Pulmonary embolism
Item 3 [Basic]
A 78-year-old man is evaluated in the emergency department for new-onset chest pain. He describes a crushing pain that is located in the left substernal area and has been present for 10 hours. He has had no prior episodes of chest pain. His medical history is notable for hypertension and hyperlipidemia. Current medications are aspirin, hydrochlorothiazide, and atorvastatin.
On physical examination, blood pressure is 100/70 mm Hg in both arms, pulse is 100/min, and respiration rate is 16/min. There is no jugular venous distention and no cardiac murmurs or rubs. The lungs are clear.
Laboratory results are notable for elevated levels of serum creatine kinase and troponin I. The initial electrocardiogram is shown. Chest radiograph is normal.
Which of the following is the best management for this patient?
(A) Chest CT with contrast
(B) Echocardiogram
(C) Percutaneous coronary intervention
(D) Thrombolytic therapy
Item 4 [Basic]
A 50-year-old man is evaluated for a 2-hour episode of epigastric discomfort and dyspnea during exercise that is relieved by rest. He is now pain free. The patient states a similar episode occurred on three previous occasions, but he did not seek medical advice. He has been using antacids for the past 6 weeks with partial relief. He reports no fever, chills, nausea, vomiting, diaphoresis, or postprandial abdominal pain. He has a 15-year history of hypertension and hyperlipidemia; his only medication is chlorthalidone.
On physical examination, he is afebrile, blood pressure is 150/85 mm Hg, pulse rate is 88/min, and respiration rate is 14/min. BMI is 28. Estimated central venous pressure is normal. Cardiac examination reveals a regular rhythm. The S2 is normal, and an S4 is heard at the apex; no murmurs or other extracardiac sounds are heard. The lungs are clear to auscultation. The abdomen is not tender to palpation.
Complete blood count and troponin level are normal as are the electrocardiogram and chest radiograph.
Which of the following is the most likely diagnosis?
(A) Acute pericarditis
(B) Aortic dissection
(C) Ischemic heart disease
(D) Peptic ulcer disease
Item 5 [Advanced]
A 52-year-old woman is evaluated in the emergency department for ongoing substernal chest pressure associated with nausea, diaphoresis, and lightheadedness. Her symptoms began 3 hours ago. She has hypertension and hypercholesterolemia. Her medications are hydrochlorothiazide, pravastatin, and aspirin.
On physical examination, her blood pressure is 84/62 mm Hg, pulse is 68/min, and respiration rate is 20/min. Cardiac auscultation reveals distant heart sounds with an S4. The lungs are clear bilaterally; estimated central venous pressure is elevated at 11 cm H2O.
Electrocardiogram with right-sided precordial leads is shown. (Leads V1 through V6 are recorded from the right side of the chest.)
Which of the following should be given next in the treatment of this patient?
(A) Dobutamine intravenously
(B) Metoprolol intravenously
(C) Nitroglycerin sublingually
(D) 0.9% saline intravenous bolus
Item 6 [Basic]
A 58-year-old woman is evaluated in the emergency department for substernal chest pain of 18 hours’ duration. She describes the pain as a tightening that is not associated with eating or exertion and that radiates to the neck. The pain is not accompanied by dyspnea, nausea, or diaphoresis and is not associated with exertion. She also reports symptoms of occasional heartburn and acid regurgitation. She had a similar episode of substernal chest pain 1 month ago, and an exercise stress test that achieved 90% her predicted maximal heart rate showed no ischemia. The patient’s medical history is otherwise unremarkable.
On physical examination, temperature is 37.2°C (99.0°F), blood pressure is 130/74 mm Hg, pulse rate is 88/min, and respiration rate is 16/min; BMI is 32. The cardiopulmonary examination is normal. Electrocardiography shows nonspecific ST -segment and T -wave abnormalities, which are unchanged from several previous examinations.
Which of the following is the most appropriate management for this patient?
(A) Ambulatory esophageal pH monitoring
(B) Coronary angiography
(C) Esophagogastroduodenoscopy
(D) Oral proton pump inhibitor therapy
(E) Repeat exercise stress test
Item 7 [Advanced]
A 22-year-old man is evaluated during the month of June in the emergency department for intermittent palpitations and dizziness for the past week. He has not experienced chest pain, dyspnea, or orthopnea. He has no prior medical history and is healthy and active. He reports being ill 6 to 8 weeks ago with fever, fatigue, myalgia, and a gradually expanding, flat, erythematous rash on his abdomen measuring a minimum of 5 cm at widest point. He works as a forester in Massachusetts and has not traveled out of the area recently.
On physical examination, his temperature is normal, blood pressure is 120/70 mm Hg, and pulse is 45/min. There are cannon waves in the jugular pulsation. There is no rash, and results of cardiac and pulmonary auscultation are normal.
The electrocardiogram is shown.
Which of the following is the most likely diagnosis?
(A) First-degree atrioventricular block
(B) Mobitz type I atrioventricular block
(C) Mobitz type II atrioventricular block
(D) Third-degree atrioventricular heart block
Item 8 [Basic]
A 46-year-old man is evaluated for an 8-year history of episodic chest pain associated with dyspnea, tachycardia, diaphoresis, and dizziness that occurs several times each week. The symptoms develop suddenly, are often so severe that he feels that he is going to die, and improve significantly within 20 to 30 minutes. The patient does not know what precipitates these episodes or whether anything makes the symptoms better or worse.
Previous medical evaluations have been unremarkable. Studies have included electrocardiographic exercise stress testing, 24-hour electrocardiographic monitoring, echocardiography, cardiac catheterization, and upper endoscopy. The patient takes no medications. Findings on physical examination are unremarkable. Medical records reveal that during these episodes, hypertension or tachycardia have never been documented.
Which of the following is the most likely diagnosis?
(A) Acute coronary syndrome
(B) Panic disorder
(C) Pheochromocytoma
(D) Pneumothorax
(E) Pulmonary embolism
Item 9 [Basic]
A 65-year-old woman is hospitalized for chest pain secondary to an acute coronary syndrome. Her immediate treatment consists of metoprolol, heparin, nitroglycerin, and aspirin, which results in immediate relief of her chest discomfort. A rhythm strip is shown.
Which of the following is the most likely electrocardiographic diagnosis?
(A) First-degree atrioventricular block
(B) Mobitz type I second-degree atrioventricular block
(C) Mobitz type II second-degree atrioventricular block
(D) Third-degree atrioventricular block (complete heart block)
Item 10 [Advanced]
A 65-year-old man is evaluated during a routine follow-up examination for coronary artery disease. He was diagnosed with a myocardial infarction 5 years ago, and was started on aspirin, metoprolol, atorvastatin, lisinopril, and sublingual nitroglycerin. He was asymptomatic until 3 months ago, when he noted exertional angina after walking two blocks. He now uses sublingual nitroglycerin on a daily basis. He has not had any episodes of pain at rest or prolonged chest pain that were not relieved by sublingual nitroglycerin.
On physical examination, blood pressure is 146/94 mm Hg and heart rate is 87/min. Carotid upstrokes are normal with no bruits. Cardiac examination is normal. The lungs are clear.
His electrocardiogram is unchanged since the last visit, with no evidence of acute changes.
In addition to adding a long-acting nitrate, which of the following is the most appropriate management for this patient?
(A) Add ranolazine
(B) Coronary angiography
(C) Exercise treadmill stress testing
(D) Increase metoprolol
Item 11 [Advanced]
A 48-year-old woman is evaluated in the emergency department 3 hours after the sudden onset of central anterior chest pain and dyspnea. There is constant chest pressure, tightness, and dyspnea. She is not on any medications.
On physical examination, the patient is afebrile. Blood pressure is 144/76 mm Hg bilaterally, pulse is 118/min, and respiration rate is 18/min. Estimated central venous pressure is 15 cm H2O. There are no murmurs, rubs, or gallops on cardiac auscultation. Her lungs are clear. There is mild pedal and lower leg edema that is more pronounced on the right side.
The electrocardiogram shows ST -segment depression in the lateral leads. The chest radiograph is normal. Handheld echocardiography shows a small, hyperdynamic left ventricle with normal regional wall motion.
Which of the following tests should be performed next?
(A) CT pulmonary angiography
(B) Coronary angiography
(C) Radionuclide perfusion imaging
(D) Transesophageal echocardiography
Item 12 [Basic]
A 68-year-old woman is evaluated for chest pain of 3 months’ duration. She describes the pain as a left-sided burning that occurs both at rest and when she exercises. It lasts for about 10 minutes, and is relieved by eating and by rest. She has hypertension, for which she takes hydrochlorothiazide. She has asthma, for which she takes inhaled corticosteroids and inhaled albuterol as needed. If she pretreats herself with the inhaled bronchodilator, she can walk long distances at a brisk pace without dyspnea. She continues to smoke cigarettes and has smoked 1 pack per day for 40 years.
On physical examination, she is afebrile. Blood pressure is 138/84 mm Hg, pulse is 64/min, and respiration rate is 18/min. Cardiopulmonary examination is normal. The results of an electrocardiogram are normal.
Which of the following is the most appropriate diagnostic test for this patient?
(A) Adenosine nuclear perfusion stress test
(B) Coronary angiography
(C) Dobutamine stress echocardiography
(D) Exercise stress test
Item 13 [Basic]
A 54-year-old man is evaluated for 2 days of fatigue and dyspnea on exertion. He denies chest pain and lightheadedness. He has no other medical problems, and his only medication is aspirin.
On physical examination, his blood pressure is 123/65 mm Hg and his pulse is 100/min. Cardiac examination reveals a normal S1 and S2 and no murmurs or gallops. Lungs are clear to auscultation.
The electrocardiogram is shown.
Which of the following is the most likely diagnosis?
(A) Atrial fibrillation
(B) Atrial flutter
(C) Sinoatrial node dysfunction
(D) Ventricular tachycardia
Item 14 [Basic]
A 75-year-old man with chronic stable angina is evaluated during a routine appointment. He had a myocardial infarction 5 years ago treated medically and has had no complications. He only gets chest pain with significant exertion, typically occurring less than once a week. The pain is relieved by one sublingual nitroglycerin tablet or resting. He reports no shortness of breath or edema. Medications are lisinopril, carvedilol, simvastatin, aspirin, and nitroglycerin, as needed.
On examination, temperature is 37.0°C (98.6°F), blood pressure is 118/70 mm Hg, pulse rate is 60/min, and respiration rate is 14/min. BMI is 22. Cardiovascular examination reveals normal heart sounds without murmurs, gallops, or rubs. Lungs are clear to auscultation. The remainder of the examination is normal.
Total cholesterol 140 mg/dL (3.6 mmol/L)
Triglycerides 100 mg/dL (1.1 mmol/L)
HDL cholesterol 44 mg/dL (1.1 mmol/L)
LDL cholesterol 76 mg/dL (2.0 mmol/L)
Which of the following is the best management for this patient?
(A) Add clopidogrel
(B) Add ranolazine
(C) Coronary angiography
(D) No changes
Item 15 [Basic]
A 43-year-old man is evaluated in the emergency department for dyspnea. He has no prior personal or family history of cardiovascular disease, diabetes mellitus, or hypertension. On physical examination, the lungs are clear. Cardiovascular examination is unremarkable with the exception of a rapid heart rate.
The chest radiograph is normal. The electrocardiogram is shown.
Which of the following is the most likely diagnosis?
(A) Atrial fibrillation
(B) Atrial flutter
(C) Sinus tachycardia
(D) Ventricular tachycardia
Item 16 [Basic]
A 48-year-old man is evaluated after a coworker had a myocardial infarction; he is worried about having a heart attack. He reports no episodes of chest pain or shortness of breath. He jogs on a treadmill 30 minutes a day four times a week. He does not smoke. He has hypertension for which he takes hydrochlorothiazide. Family history is negative for coronary artery disease.
On physical examination his vital signs are normal. The cardiopulmonary examination is normal, as is the remainder of the physical examination.
The most recent lipid panel shows: total cholesterol 208 mg/dL (5.4 mmol/L), HDL cholesterol 70 mg/dL (1.8 mmol/L), and LDL cholesterol 114 mg/dL (3.0 mmol/L).
The patient’s Framingham Risk Score for a major cardiac event is calculated as 4% over the next 10 years.
Which of the following is the best diagnostic test for this patient?
(A) Coronary angiography
(B) Coronary calcium scoring
(C) CT angiography
(D) Exercise stress test
(E) No additional testing
Item 17 [Advanced]
A 26-year-old nurse is evaluated in the emergency department after an episode of syncope. While working in the intensive care unit, she developed tachycardia and then lost consciousness. She has had brief episodes of rapid palpitations in the past but no prior syncope.
Physical examination is unremarkable and the patient is in sinus rhythm. The chest radiograph is unremarkable. The electrocardiogram is shown.
Which of the following is the most likely diagnosis?
(A) Accelerated idioventricular tachycardia
(B) Atrial flutter
(C) Atrioventricular reentrant tachycardia
(D) Multifocal atrial tachycardia
Item 18 [Basic]
A 62-year-old man with coronary artery disease is evaluated for angina. He was diagnosed with coronary artery disease 4 years ago. Medical therapy was started with aspirin, metoprolol, isosorbide mononitrate, pravastatin, and sublingual nitroglycerin. He was asymptomatic until 8 months ago, when he noted exertional angina; his dosages of metoprolol and isosorbide mononitrate were increased and long-acting diltiazem was added, resulting in control of his symptoms. Over the past 2 months, however, he has had gradually increasing symptoms, and currently he requires daily nitroglycerin for angina relief during exercise. He has not had any episodes of angina at rest.
On physical examination, blood pressure is 100/60 mm Hg and heart rate is 48/min. Carotid upstroke is normal with no bruits. Cardiac examination reveals no murmurs, and the lungs are clear.
An electrocardiogram shows no acute ischemic changes.
Which of the following should be the next step in this patient’s management?
(A) Coronary angiography
(B) Exercise treadmill stress testing
(C) Increase metoprolol
(D) Intravenous heparin and nitroglycerin
Item 19 [Basic]
A 62-year old man with a history of a myocardial infarction 1 year ago is evaluated in the emergency department for sudden episodes of dyspnea and weakness. He is diaphoretic, cool, clammy, and pale; cannon waves are noted in the jugular pulsations. An electrocardiogram taken at the beginning of a typical episode is shown.
Which of the following is the most likely diagnosis?
(A) Atrial fibrillation with left bundle branch block
(B) Atrial fibrillation with preexcitation (Wolf-Parkinson-White syndrome)
(C) Supraventricular tachycardia with right bundle branch block
(D) Ventricular tachycardia
Item 20 [Basic]
A 54-year-old woman is evaluated in the emergency department for jaw and shoulder pain that has occurred intermittently for the past week. The symptoms occur with activity and are relieved by rest. Medical and family history is unremarkable. She is not taking any medications.
Physical examination shows a blood pressure of 150/68 mm Hg and a pulse of 90/min. There is no jugular venous distention and carotid upstrokes are normal. There are no cardiac murmurs and the lung fields are clear. Extremities show no edema and peripheral pulses are normal bilaterally. The troponin I level is elevated.
Electrocardiogram shows 1.0-mm ST -segment depression in leads V1 through V4 with T -wave inversions.
The patient is given aspirin, intravenous nitroglycerin, low-molecular-weight heparin, clopidogrel, and atorvastatin.
Which of the following is the most appropriate additional immediate treatment for this patient?
(A) Intra-aortic balloon pump
(B) Metoprolol
(C) Verapamil
(D) Warfarin
Item 21 [Advanced]
A 72-year-old man is evaluated in the emergency department for dyspnea. One week ago, an episode of severe chest pain and dyspnea awoke him from sleep. Over the next several days his dyspnea stabilized. On the morning of admission, the patient noted a sudden increase in dyspnea. His medical history is significant for hypertension and hyperlipidemia. He has no history of heart murmur. He currently takes simvastatin, aspirin, and lisinopril.
On physical examination, the patient is sitting up with labored breathing. Blood pressure is 86/52 mm Hg, pulse is regular at 110/min, and respiration rate is 24/min. Oxygen saturation is 92% on 6 L of oxygen. Jugular veins are distended to the angle of the jaw while sitting upright. Cardiac examination reveals a grade 3/6 holosystolic murmur at the cardiac apex radiating toward the left axilla. Bibasilar crackles are present.
An electrocardiogram is shown. A chest radiograph shows pulmonary vascular congestion.
Which of the following is the most likely diagnosis?
(A) Acute mitral regurgitation
(B) Left ventricular aneurysm
(C) Pulmonary embolism
(D) Ventricular free wall rupture
Item 22 [Advanced]
A 62-year-old woman is brought to the emergency department for chest pain that has been present for 5 hours. Medical history is notable for type 2 diabetes mellitus, hyperlipidemia, and hypertension. Medications are glyburide, lisinopril, atorvastatin, and aspirin.
On physical examination, blood pressure is 160/80 mm Hg, pulse rate is 88/min, and respiration rate is 16/min. Cardiac examination shows no murmurs, extra sounds, or rubs.
The lungs are clear. Neurologic examination is normal.
The electrocardiogram shows 2-mm ST -segment elevation in leads II, III, and aVF.
A coronary catheterization laboratory is not available, and the nearest hospital with percutaneous intervention capability is 3 hours away.
Which of the following is the best management option for this patient?
(A) Aggressive medical therapy without reperfusion attempt
(B) Immediate thrombolytic therapy
(C) Transfer for coronary artery bypass graft surgery
(D) Transfer for percutaneous coronary intervention
Item 23 [Basic]
A 65-year-old man is evaluated before beginning an exercise program. He is asymptomatic and his only medical problem is chronic hypertension that is well controlled on hydrochlorothiazide. He takes no other medications.
On physical examination, blood pressure is 138/76 mm Hg, and pulse is 80/min and regular. Physical examination is normal, except for a soft S1. His electrocardiogram is shown.
Which of the following best describes the electrocardiographic findings?
(A) First-degree atrioventricular block
(B) Second-degree atrioventricular block
(C) Third-degree (complete) atrioventricular block
(D) Ventricular preexcitation (Wolff-Parkinson-White) syndrome
Item 24 [Advanced]
A 56-year-old man is evaluated in the emergency department for chest discomfort that began 3 hours ago. He describes the pain, which is well localized to the left chest, as pressure. He denies prior episodes. Medical history is notable for type 2 diabetes mellitus and hyperlipidemia. Medications are aspirin, metformin, and atorvastatin.
On physical examination, he is diaphoretic. Blood pressure is 95/60 mm Hg and heart rate is 110/min. There is jugular venous distention, with an estimated central venous pressure of 14 cm H2O. An S3 is heard on cardiac auscultation, but no murmurs are present. The lung fields are clear and there is no peripheral edema.
The electrocardiogram shows sinus tachycardia, 2-mm ST -segment elevation in leads II, III, and aVF, and 0.5-mm ST -segment elevation in lead V1. The chest radiograph is normal.
Which of the following is the most likely cause of hypotension in this patient?
(A) Increased vagal tone
(B) Pericardial tamponade
(C) Right ventricular infarction
(D) Ventricular septal defect
Answers and Critiques
Item 1 Answer: B
Educational Objective: Diagnose non-ST-elevation myocardial infarction.
The most likely diagnosis is a non-ST -elevation myocardial infarction (NST EMI). This patient has had chest pain at rest, an elevated serum troponin I level, and an electrocardiogram that shows ST -segment depression that is particularly prominent in leads V2 through V6. These features indicate a NST EMI.
In an acute coronary syndrome, obstruction to coronary blood flow results in either transient or prolonged episodes of severe myocardial ischemia. ST -elevation myocardial infarction (ST EMI) is diagnosed in patients with a clinical presentation consistent with acute myocardial infarction together with electrocardiographic evidence of ST – segment elevation. Although most patients with ST EMI ultimately develop Q waves on electrocardiogram, some exhibit diagnostic ST -segment elevation and cardiac enzyme elevations without Q waves.
Patients who present with ischemic chest pain but without diagnostic ST -segment elevation are categorized as having unstable angina or NST EMI. These two conditions are closely related and have similar pathophysiology and clinical presentations, but they differ in the severity of the myocardial ischemia. Patients with either condition typically present with angina at rest; however, some patients describe a pattern of new-onset or increasing angina. In NST EMI, ischemia is severe and results in a detectable release of biomarkers of myocardial injury hours after the onset of ischemic chest pain, most commonly cardiac troponin I, troponin T , and the MB isoenzyme of creatine kinase. In
unstable angina, there is no detectable increase in these enzymes.
Chronic stable angina refers to a coronary artery syndrome that is characterized by chest discomfort that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin. Ischemic pain that occurs with rest is not compatible with the diagnosis of chronic stable angina, and the presence of positive serum biomarkers for myocardial necrosis also excludes this diagnosis.
Key Point
Non-ST -elevation myocardial infarction is characterized by chest pain at rest, absence of ST -elevation on the electrocardiogram, and elevated biomarkers of myocardial injury.
Bibliography
Hillis LD, Lange RA. Optimal management of acute coronary syndromes. N Engl J Med. 2009;360(21):2237-2240. [PMID: 19458369]
Item 2 Answer: B
Educational Objective: Diagnose acute pericarditis
The most likely diagnosis is acute pericarditis. Chest pain from acute pericarditis is sharp and pleuritic and worsened by assuming a supine position. Acute pericarditis is diagnosed by the presence of at least two of the three classic features: (1) pleuritic chest pain; (2) friction rub; and (3) diffuse concordant ST -segment elevation on electrocardiography, often with depression of the PR segment. The classic pericardial friction rub has three components (not all components may be heard) related to cardiac motion and occurs during atrial systole, ventricular contraction, and rapid ventricular filling. The sound of the rub can be squeaky, scratchy, and high-pitched.
Patients with an acute aortic dissection present with the abrupt onset of severe pain in the thorax. Blood pressure is variable. Pain described as “ripping” or “tearing” occurs in only about 50% of patients. The physical finding of a pulse deficit is uncommon. At least one third of patients have no electrocardiographic abnormality, and at least 40% of patients lack widening of the mediastinum on plain chest radiograph. However, pleuritic chest pain, pericardial friction rub, and diffuse ST elevations are not compatible with aortic dissection.
The pain of an acute myocardial infarction is usually retrosternal in location, may radiate to the shoulders or arms, and may be associated with nausea and vomiting, diaphoresis, or shortness of breath. Although the initial electrocardiogram is nondiagnostic in up to 50% of patients, compatible changes would include focal ST elevations with reciprocal ST depression associated with elevation of cardiac biomarkers such as troponin.
Patients with pulmonary embolism may present with the classic symptoms of dyspnea, chest pain, hemoptysis, or syncope, but the presentation is often more subtle. At times, only nonspecific respiratory or hemodynamic manifestations may occur. Pulmonary embolism is not associated with a pericardial friction rub or diffuse ST -segment changes.
Key Point
Diagnosis of acute pericarditis is made by the presence of at least two of the three classic features: (1) pleuritic chest pain; (2) friction rub; and (3) diffuse concordant ST – segment elevation on electrocardiography.
Bibliography
Lee T H, Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med. 2000;20;342(16):1187-95. [PMID: 10770985]
Item 3 Answer: C
Educational Objective: Treat a patient with ST-elevation myocardial infarction with percutaneous coronary intervention.
The best management for this patient is percutaneous coronary intervention (PCI). This patient is presenting with an ST -elevation inferior wall myocardial infarction (ST EMI). The diagnosis is based upon the presence of chest pain, elevated cardiac biomarkers, and ST -segment elevations in the inferior leads (II, III, and aVF). Reperfusion strategies for ST EMI patients include either thrombolytic therapy or PCI. Percutaneous angioplasty and stent placement is the preferred therapy for most patients with ST EMI because it is associated with a lower 30-day mortality rate compared to thrombolytic therapy. PCI is also indicated in patients with a contraindication to thrombolytic therapy and in patients with cardiogenic shock. Contraindications to thrombolytic therapy include prior intracerebral hemorrhage, ischemic stroke within 3 months, suspected aortic dissection, or active bleeding. PCI is most effective if completed within 12 hours of the onset of chest pain; the earlier the intervention, the better the outcome.
A chest CT can be a useful diagnostic tool in patients being evaluated for chest pain if there is a high clinical suspicion for an aortic dissection. This patient does not have any characteristics of ascending aortic dissection—back pain, unequal blood pressures or pulses, or a widened mediastinum on chest radiograph. Given these factors, the possibility of an acute aortic dissection is extremely low, and further imaging with a chest CT would likely further delay treatment for the ST EMI.
An echocardiogram is occasionally useful in the management of patients presenting with chest pain and a nondiagnostic electrocardiogram (ECG). A focal wall motion abnormality suggests a cardiac basis to the symptoms. In this patient presenting with a markedly abnormal ECG with ST -segment elevation and elevated cardiac biomarkers, echocardiography would not add to the management.
Key Point
Percutaneous angioplasty and stent placement is the preferred therapy for most patients with ST -elevation myocardial infarction.
Bibliography
Hillis LD, Lange RA. Optimal management of acute coronary syndromes. N Engl J Med. 2009;360(21):2237-2240. [PMID: 19458369]
Item 4 Answer: C
Educational Objective: Diagnose angina pectoris.
Symptoms of ischemic heart disease are fairly predictable for an individual patient, but great heterogeneity exists between patients. Patients may have a difficult time describing the pain and may use words such as discomfort, pressure, or heaviness. Although the location of the pain is classically substernal, it may be difficult for patients to localize the pain; they may indicate the entire chest or upper abdomen is involved. Sharp pain, well-localized pain, and back pain are infrequently associated with ischemic heart disease. Ischemic cardiac pain has a predictable relation to exercise and relief with rest or nitroglycerin. In some patients, exertional dyspnea may be the only manifestation of cardiac ischemia (angina equivalent). A normal electrocardiogram at rest does not exclude ischemic heart disease nor does a normal troponin level.
The pain of acute pericarditis is often pleuritic, may radiate to the top of the shoulder, and is often worse when the patient is supine. Fever and a pericardial friction rub are usually evident. Characteristic electrocardiographic changes include diffuse ST elevations and PR depression.
The classic presentation of aortic dissection consists of sudden-onset severe chest pain radiating to the back. Other findings may include a blood pressure differential between the right and left arms, murmur of aortic regurgitation, and a widened mediastinum on chest x-ray. Aortic dissection should always be considered in the differential diagnosis of acute chest pain, but this patient’s pain is not consistent with this diagnosis.
Most patients with peptic ulcer disease do not have pain at diagnosis; ulcers are usually detected during an evaluation for potential ulcer-related complications such as overt or obscure bleeding. When symptoms are present, they include dyspepsia or a nonspecific, gnawing epigastric pain. Other presentations include bleeding, perforation (sometimes with penetration into adjacent organs), and gastric outlet obstruction. Finally, discomfort caused by a duodenal ulcer is not typically relieved by rest, worsened by exertion, or accompanied by shortness of breath.
Key Point
Ischemic cardiac pain has a predicable relation to exercise and relief with rest or nitroglycerin.
Bibliography
Lee T H, Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med. 2000;342(16):1187-95. [PMID: 10770985]
Item 5 Answer: D
Educational Objective: Treat right ventricular myocardial infarction with normal saline infusion.
Volume expansion with normal saline is the primary supportive treatment for the hemodynamic abnormalities of a right ventricular myocardial infarction. The physical examination findings of hypotension, clear lung fields, and elevated estimated central venous pressure represent the classic triad of right ventricular myocardial infarction.
However, the most predictive finding is ST -segment elevation on right-sided electrocardiographic lead V4R. Therefore, all patients with an inferior ST -elevation myocardial infarction (ST EMI) should have a right-sided electrocardiogram performed at the time of presentation. This patient’s electrocardiogram shows ST -segment elevation in frontal inferior leads II, III, and aVF, and 1-mm ST -segment elevation in right-sided precordial lead V4R. These findings indicate inferior and right ventricular injury in the setting of an inferior ST EMI, likely related to a right coronary artery occlusion.
In the setting of right ventricular myocardial infarction, right ventricular contractility is reduced, resulting in higher right ventricular diastolic pressure, lower right ventricular systolic pressure, and reduced preload or filling of the left ventricle. Volume expansion improves the hemodynamic abnormalities of right ventricular myocardial infarction because the gradient of pressure from the right atrium to the left atrium maintains filling of the left ventricle. In addition to reperfusion therapy for ST EMI, the acute treatment of right ventricular myocardial infarction is supportive.
Inotropic support, specifically using intravenous dobutamine, is appropriate treatment in patients with right ventricular myocardial infarction whose hypotension is not corrected after 1 L of saline infusion. However, volume expansion should be tried before giving inotropic agents. By increasing cardiac contractility, inotropic agents increase myocardial oxygen demand and potentially extend the infarction.
Bradycardia, potentially caused by increased vagal activity or sinoatrial node ischemia, exacerbates the hemodynamic abnormalities of right ventricular myocardial infarction, so ß-blocker therapy with metoprolol is contraindicated in this patient.
Nitroglycerin is contraindicated in patients with hypotension and patients with the potential for hypotension, particularly right ventricular myocardial infarction. In right ventricular infarction, nitrate-induced venodilation impairs right ventricular filling and thereby cardiac output.
Key Point
Volume expansion is the primary supportive treatment for the hemodynamic abnormalities of a right ventricular myocardial infarction.
Bibliography
Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008;117(5):686-697. [PMID: 18250279]
Item 6 Answer: D
Educational Objective: Manage noncardiac chest pain caused by gastroesophageal reflux disease with an oral proton pump inhibitor.
The most appropriate management for this patient is empiric treatment with a proton pump inhibitor. Esophageal disease is the most common cause of noncardiac chest pain. Gastroesophageal reflux disease (GERD) is caused by reflux of gastric contents into the esophagus. Symptoms of GERD can mimic cardiac ischemia, with substernal squeezing or burning that may radiate widely, including to the back, neck, jaw, or arms. Chest pain due to GERD may last minutes to hours and can resolve spontaneously or with antacids. Most patients with GERD-induced chest pain also have typical reflux symptoms, including regurgitation and heartburn. The recommended approach in patients with suspected esophageal chest pain is to rule out cardiac ischemia and then treat the patient empirically with a proton pump inhibitor.
Ambulatory esophageal pH monitoring can be used if the patient’s condition does not respond to empiric therapy or if the patient has atypical symptoms.
Esophagogastroduodenoscopy is indicated in patients with long-standing reflux disease to screen for Barrett esophagus and in patients with such alarm symptoms as anemia, weight loss, or dysphagia, but not as the initial screening test for GERD.
This patient’s previous normal stress test makes cardiac disease very unlikely and a repeat exercise stress test or coronary angiography is unlikely to provide additional diagnostic information. Because ischemic heart disease has been ruled out, it is reasonable in this patient to attempt empiric acid suppression therapy with a proton pump inhibitor. A complete response to empiric therapy is considered diagnostic of GERD.
Key Point
Empiric proton pump inhibitor therapy is the first step in the management of esophageal noncardiac chest pain.
Bibliography
Fass R. Evaluation and diagnosis of noncardiac chest pain. Dis Mon. 2008;54(9):627-641. [PMID: 18725005]
Item 7 Answer: D
Educational Objective: Diagnose third-degree atrioventricular heart block.
This patient most likely has third-degree (complete) atrioventricular heart block due to Lyme carditis. The presence of the characteristic skin rash (erythema migrans) with or without a history of tick bite in an endemic region, has a probability greater than 80% of being caused by Borrelia burgdorferi infection. Lyme carditis is manifested by acute-onset, high-grade atrioventricular conduction defects that may occasionally be associated with myocarditis.
Atrioventricular block is classified as first, second, or third degree. First-degree block is characterized 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. Patients with atrioventricular block may be asymptomatic or have severe bradycardiarelated symptoms (weakness, presyncope, syncope) and ventricular arrhythmias.
Key Point
Third-degree block is the complete absence of conduction of atrial impulses to the ventricle and is the most common cause of marked bradycardia.
Bibliography
Barold SS. Atrioventricular block revisited. Compr T her. 2002;28(1):74-78. [PMID: 11894446]
Item 8 Answer: B
Educational Objective: Diagnose panic disorder.
This patient’s presentation is characteristic of panic disorder. Panic disorder is characterized by recurrent, unexpected panic attacks that feature the abrupt onset of numerous somatic symptoms, such as palpitations, sweating, tremulousness, dyspnea, chest pain, nausea, dizziness, and numbness. Symptoms typically peak within 10 minutes of onset, and attacks usually last from 15 to 60 minutes. The most appropriate treatment for panic disorder is cognitive-behavioral therapy and a selective serotonin reuptake inhibitor, such as paroxetine.
Because the symptoms of panic disorder are primarily physical, most patients with this disorder present to their primary care physicians or to emergency departments for evaluation. Patients with panic disorder are evaluated, on average, by 10 clinicians before the diagnosis is established. The alarming nature of their symptoms prompts patients with panic disorder to seek medical attention; consequently, they have very high health care utilization rates.
The clinical manifestations of pheochromocytomas are variable, with hypertension (episodic or sustained) observed in more than 90% of patients. Other major symptoms include diaphoresis, pallor, palpitations, and headaches; the classic triad of sudden severe headache, diaphoresis, and palpitations is highly suggestive of pheochromocytoma.
Other manifestations include hyperglycemia, weight loss, arrhythmias (atrial and ventricular fibrillation), and catecholamine-induced cardiomyopathy. The absence of hypertension and the long duration of symptoms make this diagnosis unlikely.
The diagnosis of acute coronary syndrome is unlikely in a patient with recurrent, self-limited attacks and previous normal results of coronary angiography. The current nature of the symptoms and normal physical examination findings are not compatible with the diagnosis of pneumothorax. Symptoms that resolve after 20 minutes or recur frequently over many years are not compatible with the diagnosis of pulmonary embolism.
Key Point
Panic disorder is characterized by recurrent, unexpected panic attacks that feature the abrupt onset of numerous somatic symptoms such as palpitations, sweating, tremulousness, dyspnea, chest pain, nausea, dizziness, and numbness.
Bibliography
Culpepper L. Identifying and treating panic disorder in primary care. J Clin Psychiatry. 2004;65(suppl 5):19-23. [PMID: 15078114]
Item 9 Answer: B
Educational Objective: Diagnose Mobitz type I second-degree atrioventricular block.
This patient has evidence for Mobitz type I second-degree atrioventricular (AV) block. Second-degree heart block is characterized by intermittent nonconduction of P waves and subsequent “dropped” ventricular beats. Second-degree heart block is divided into types, Mobitz I and Mobitz II. Mobitz type I second-degree heart block is characterized by progressive prolongation of the PR interval until a dropped beat occurs. Mobitz type I block can occur in the absence of heart disease, including in athletes and older adults; in patients with underlying heart disease, including acute ischemia; and in patients who are taking drugs that block the AV node, such as ß-blockers (metoprolol), calcium channel blockers, and digoxin. This type of heart block is characteristically transient and usually requires no specific treatment; however, some patients may develop excessively slow heart rates and experience symptoms related to decreased cerebral or coronary perfusion. If treatment is necessary, it begins by identifying and correcting reversible causes of slowed conduction, such as myocardial ischemia, increased vagal tone (for example, from pain or vomiting), and discontinuation of drugs that depress AV conduction.
Mobitz type II second-degree AV block is characterized by a regularly dropped beat (for example, a nonconducted P wave every second or third beat) without progressive prolongation of the PR interval. It is often associated with evidence of additional disease in the conduction system, such as bundle branch block or bifascicular or trifascicular block. Mobitz type II second-degree block suddenly and unpredictably progresses to complete heart block and is usually treated with a pacemaker.
First-degree AV block is recognized, electrocardiographically, as a prolongation of the PR interval to greater than 0.2 sec. All P waves are conducted. First-degree block requires no specific treatment.
Third-degree AV block, or complete heart block, refers to a lack of AV conduction, characterized by lack of conduction of all atrial impulses to the ventricles.
Key Point
Mobitz type I second-degree atrioventricular block is characterized by progressive prolongation of the PR interval until a dropped beat occurs.
Bibliography
Da Costa D, Brady WJ, Edhouse J. Bradycardias and atrioventricular conduction block. BMJ. 2002;324:535-538. [PMID: 11872557]
Item 10 Answer: D
Educational Objective: Treat chronic stable angina with worsening symptoms with increased dosage of a ß-blocker.
The most appropriate management at this point is to increase the patient’s dose of metoprolol. Medical therapy for chronic stable coronary artery disease (CAD) includes both antianginal and vascular-protective agents. Antianginal therapy includes ß-blockers, calcium channel blockers, and nitrates. Vascular-protective therapy includes aspirin, angiotensin-converting enzyme (ACE) inhibitors, and statins. This patient is already on a ß-blocker, aspirin, a statin, and an ACE inhibitor. Switching to a long-acting nitrate will help relieve his angina symptoms. However, his resting heart rate of 87/min and high blood pressure suggest a suboptimal dose of ß-blocker, and the patient’s dosage of metoprolol should be increased. The ß-blocker dose should be titrated to achieve a resting heart rate of approximately 55 to 60/min and approximately 75% of the heart rate that produces angina with exertion. The patient should be reevaluated in a few weeks to assess the response to therapy.
Ranolazine is a novel antianginal agent that is approved for the treatment of chronic stable angina. It should only be used, however, in addition to baseline therapy with a ß-blocker, a calcium channel blocker, and a long-acting nitrate. Given that this patient was on suboptimal doses of metoprolol and is just being started on a long-acting nitrate, the addition of ranolazine would be premature.
Coronary angiography would not be indicated at this time because the patient is not receiving maximal medical therapy. In the setting of continued angina despite maximal medical therapy, coronary angiography could be considered.
Exercise treadmill stress testing would not provide useful information in this setting. It would only confirm the high pretest probability that this patient has underlying CAD as a cause for the current symptoms.
Key Point
In the treatment of chronic stable angina, the ß-blocker dose should be titrated to achieve a resting heart rate of approximately 55 to 60/min and approximately 75% of the heart rate that produces angina with exertion.
Bibliography
Jawad E, Arora R. Chronic stable angina pectoris. Dis Mon. 2008;54(9):671-689. [PMID: 18725007]
Item 11 Answer: A
Educational Objective: Diagnose pulmonary embolism with CT pulmonary angiography.
This patient’s symptoms of chest pain and dyspnea in combination with the physical findings of asymmetric leg edema, elevated central venous pressure, tachypnea, and tachycardia suggest the possibility of pulmonary embolism. The most appropriate diagnostic test to perform next is CT pulmonary angiography to look for pulmonary emboli.
A normal echocardiogram between episodes of chest pain does not rule out unstable angina because wall motion returns to normal between ischemic episodes. However, this patient had no wall motion abnormalities during her ongoing chest pain, making acute myocardial ischemia very unlikely. Because an acute coronary syndrome is highly unlikely, coronary angiography is not indicated as the next diagnostic test.
A resting radionuclide perfusion study can be helpful in the diagnosis of coronary ischemia when the electrocardiogram is nondiagnostic but does not provide additive information to that already obtained by echocardiography.
Transesophageal echocardiography is not sensitive for detection of pulmonary emboli but may be useful in acute chest pain if aortic dissection is suspected. Ascending aortic dissection is often associated with acute aortic regurgitation, myocardial ischemia, cardiac tamponade or hemopericardium, and hemothorax or exsanguination. Considerable (>20 mm Hg) variation in systolic blood pressure in the arms may be present. Descending thoracic aortic aneurysm is more commonly associated with splanchnic ischemia, renal insufficiency, lower extremity ischemia, or focal neurologic deficit due to spinal cord ischemia. This woman has no physical findings to suggest this diagnosis.
Key Point
Normal wall motion on echocardiography during chest pain excludes coronary ischemia or infarction.
Bibliography
Chunilal SD, Eikelboom JW, Attia J, et al. Does this patient have pulmonary embolism? JAMA. 2003;290(21):2849-2858. [PMID: 14657070]
Item 12 Answer: D
Educational Objective: Evaluate suspected coronary artery disease using an exercise stress test.
The most appropriate diagnostic test for this patient is an exercise stress test. This 68-year-old woman has cardiac risk factors of smoking and hypertension, with an intermediate Framingham risk score (18% likelihood of a coronary event in 10 years). (A tool to calculate the Framingham risk score can be accessed at www.acponline.org/acp_press/essentials/calculator.htm.) In addition, she has atypical chest pain, so further evaluation is appropriate. An exercise stress test is recommended in patients with intermediate probability of coronary artery disease with a normal baseline electrocardiogram (ECG) who are able to exercise because it provides information about exercise tolerance and hemodynamic response to exercise.
An adenosine nuclear perfusion stress test is contraindicated in patients with significant bronchospastic disease and hence is not the correct choice for a patient with asthma.
Furthermore, exercise stress testing is preferred over pharmacologic stress testing because of the additional physiologic information on exercise tolerance and the blood pressure and heart rate response to exercise.
Coronary angiography would only be appropriate if the patient were presenting with an acute coronary syndrome or after an abnormal stress test to determine if there is an indication for revascularization.
Dobutamine stress echocardiography is an appropriate choice in patients who are unable to exercise and are not hypertensive at rest. This patient is able to exercise, so treadmill testing is the more appropriate choice.
Key Point
Exercise electrocardiographic stress testing is the primary approach to the diagnosis of coronary artery disease in patients who can exercise and have a normal resting electrocardiogram.
Bibliography
Wilson JM. Diagnosis and treatment of acquired coronary artery disease in adults. Postgrad Med J. 2009;85(1005):364-365. [PMID: 19581247]
Item 13 Answer: B
Educational Objective: Diagnose atrial flutter.
The most likely diagnosis for this patient is atrial flutter. The presence on the electrocardiogram of multiple P waves in a “sawtooth” pattern, typically with 2:1 ventricular conduction, characterizes atrial flutter and eliminates atrial fibrillation as a diagnostic consideration. Electrocardiographically, atrial fibrillation is characterized by an absence of discernible P waves, which are replaced by fibrillatory waves that vary in amplitude, shape, and timing. The ventricular response is grossly irregular and often rapid, except when there is concomitant atrioventricular block.
Sinoatrial node dysfunction (sick sinus syndrome) is a frequent cause of pacemaker implantation. It consists of symptomatic sinus bradycardia and the tachycardia-bradycardia syndrome (alternating atrial tachyarrhythmias and bradycardia). In patients with “tachy-brady” syndrome, bradycardia usually occurs after termination of the tachycardia; atrial fibrillation is the most common tachyarrhythmia observed in this group of patients. The patient does not fulfill the diagnostic criteria for sinus node dysfunction.
Ventricular tachycardia is characterized by wide-complex QRS morphology (QRS >0.12 sec) and a ventricular rate that is greater than 100/min. In ventricular tachycardia, theventricular rate typically ranges from 140/min to 250/min. The patient does not have a wide-complex tachycardia and, therefore, does not have ventricular tachycardia.
Key Point
Atrial flutter is typically a narrow-complex tachycardia characterized by multiple regular atrial contractions (flutter waves) creating a “sawtooth” baseline pattern prior to the QRS complex.
Bibliography
Sawhney NS, Anousheh R, Chen WC, Feld GK. Diagnosis and management of typical atrial flutter. Cardiol Clin. 2009;27(1):55-67, viii. [PMID: 19111764]
Item 14 Answer: D
Educational Objective: Treat chronic stable angina with appropriate medical therapy.
The most appropriate treatment of this patient would be to continue his current medical management. Medical therapy for chronic coronary artery disease (CAD) can be classified as antianginal or vascular protective. Antianginal medications include ß-blockers, calcium channel blockers, nitrates, and ranolazine. ß-Blockers reduce mortality by approximately 20%. Patients with chronic stable angina can be treated with calcium channel blockers if they are unable to tolerate ß-blockers, or calcium channel blockers can be added to ß-blocker therapy for difficult-to-control symptoms. All patients with chronic stable angina should carry either a sublingual or a spray form of nitroglycerin for emergency use. Ranolazine should only be considered in patients who remain symptomatic despite optimal doses of ß-blockers, calcium channel blockers, and nitrates.
Vascular-protective medications include aspirin, clopidogrel, angiotensin-converting enzyme (ACE) inhibitors, and statins. Aspirin reduces the risk of stroke, myocardial infarction, sudden death, and vascular death by 33%. Although clopidogrel is beneficial in patients with acute coronary syndromes, it has small clinical benefit in patients with chronic stable angina and is associated with an increased risk of bleeding. ACE inhibitors reduce cardiovascular mortality by 17% to 23%. Statins reduce future cardiovascular events by approximately 25% to 30%. Current guidelines specify an LDL cholesterol target level of less than 100 mg/dL (2.6 mmol/L) for patients with coronary artery disease. This patient is receiving standard therapy for chronic stable angina with aspirin, ß-blocker (carvedilol), ACE inhibitor (lisinopril), a statin (simvastatin), and nitroglycerin. His blood pressure is well controlled, pulse rate is appropriately reduced, and the lipid profile is at target. His symptoms are infrequent and stable; no change in his medical therapy is needed.
Coronary angiography is reserved for patients with acute coronary symptoms, angina increasing in severity, markedly abnormal stress tests, sudden cardiac death, or diagnostic difficulties and is not indicated in this clinically stable patient. Because this patient’s symptoms are well controlled with the current therapy, it is not necessary to add ranolazine.
Key Point
Most patients with chronic stable angina are treated with aspirin, a ß-blocker, an ACE inhibitor, nitroglycerin, and a statin.
Bibliography
Pfisterer ME, Zellweger MJ, Gersh BJ. Management of stable coronary artery disease. Lancet. 2010;375(9716):763-72. [PMID: 20189028]
Item 15 Answer: A
Educational Objective: Diagnose atrial fibrillation.
The electrocardiogram is characteristic for atrial fibrillation, showing a rapid, irregularly irregular rhythm with no discernible P waves and atrial fibrillatory waves at a rate between 350 and 600 beats/min. The fibrillatory waves vary in amplitude, morphology, and intervals, creating a rough, irregular baseline between the QRS complexes. The patient’s evaluation should minimally include a transthoracic echocardiogram to exclude occult valve or other structural heart disease and also to assess the size of the left atrial appendage; in addition, thyroid studies should be performed to exclude hyperthyroidism.
Atrial flutter is recognized by its saw-tooth pattern of flutter waves, most noticeable in the inferior leads II, III, and aVF; flutter waves are distinctly different from the small, chaotic fibrillation waves that are characteristic of atrial fibrillation.
Sinus tachycardia is a regular rhythm associated with P waves prior to each QRS complex. In each lead, the P-wave morphology and PR interval remain constant in shape and duration. The absence of well-defined P waves in this electrocardiogram rules out sinus tachycardia.
Ventricular tachycardia is characterized by wide-complex QRS morphology (QRS >0.12 sec) and a ventricular rate ranging from 140-250/min. This patient’s QRS complexes are narrow, excluding ventricular tachycardia as a diagnosis.
Key Point
Atrial fibrillation is characterized electrocardiographically by an irregularly irregular rhythm with no discernible P waves and atrial fibrillation waves creating an irregular baseline.
Bibliography
Zimetbaum P. Atrial fibrillation. Ann Intern Med. 2010;153(11):IT C61. [PMID: 21135291]
Item 16 Answer: E
Educational Objective: Avoid screening for asymptomatic coronary artery disease.
No additional testing for coronary artery disease (CAD) is the best management option for this patient. He is at low risk for CAD, and he is asymptomatic. In addition, he only has a 4% probability of a major coronary event over the next 10 years (www.acponline.org/acp_press/essentials/calculator.htm). The American College of Cardiology/American Heart Association, American College of Physicians, and U.S. Preventive Services T ask Force all agree that there is little evidence to support routinetesting for CAD in adults who are low risk and asymptomatic. Screening for CAD in adults who are asymptomatic is not recommended because the probability of a falsepositive test is much greater than the probability of a true positive test. For patients with an intermediate probability of CAD, noninvasive stress testing with an exercise stress test provides the most useful information.
Coronary angiography should be reserved for patients with chronic CAD who have lifestyle-limiting angina despite medical therapy, markedly positive results on noninvasive stress testing, successful resuscitation from sudden cardiac death, or documented ventricular tachycardia. Coronary angiography can also be considered in patients with nonspecific chest pain to completely exclude CAD as a cause for the current symptoms if they have had recurrent hospitalizations. Coronary calcium testing may be considered in asymptomatic persons with a 10% to 20% Framingham 10-year risk category (intermediate risk) and in young persons with a strong family history of premature cardiovascular disease. The diagnostic accuracy of CT angiography to detect obstructive CAD is approximately 90%. Because CT angiography provides no functional information (that is, the extent of ischemia), a markedly abnormal study is followed by referral to coronary angiography or stress testing to determine the ischemic burden. Recent consensus guidelines suggest that the benefits of CT angiography are greatest in symptomatic patients with an intermediate pretest probability of CAD.
Key Point
There is little evidence to support routine testing for coronary artery disease in adults who are low risk and asymptomatic.
Bibliography
Snow V, Barry P, Fihn SD, Gibbons RJ, Owens DK, Williams SV, Weiss KB, Mottur-Pilson C; ACP; ACC Chronic Stable Angina Panel. Evaluation of primary care patients with chronic stable angina: guidelines from the American College of Physicians. Ann Intern Med. 2004;141 (1):57-64. [PMID: 15238371]
Item 17 Answer: C
Educational Objective: Diagnose atrioventricular reentrant tachycardia (Wolff-Parkinson-White syndrome).
The most likely diagnosis is atrioventricular reentrant tachycardia. The patient presents with a history of tachycardia and recent syncope. The electrocardiogram shows a short PR interval and the presence of a delta wave, which signifies preexcitation. These features, together with tachycardia, make the diagnosis of Wolff-Parkinson-White syndrome, a type of atrioventricular reentrant tachycardia.
There are no clinical features to suggest idioventricular tachycardia or slow ventricular tachycardia, which is demonstrated electrocardiographically as a wide QRS complex and a heart rate between 60/min and 100/min. Atrial flutter is recognized by the characteristic negative sawtooth deflections in ECG leads II, III, and aVF, with a positive deflection in V1, findings that are not present in this patient’s electrocardiogram. Multifocal atrial tachycardia characteristically occurs in the setting of chronic lung disease and is manifested by three or more P-wave configurations on the electrocardiogram with associated tachycardia.
Key Point
The combination of a short PR interval and a delta wave plus tachycardia confirms the diagnosis of Wolff-Parkinson-White syndrome, a type of atrioventricular tachycardia.
Bibliography
Lee KW, Badhwar N, Scheinman MM. Supraventricular tachycardia-part I. Curr Probl Cardiol. 2008;33(9):467-546. [PMID: 18707990]
Item 18 Answer: A
Educational Objective: Evaluate progressive chronic angina pectoris with coronary angiography.
Coronary angiography is the most appropriate option in this patient with continued anginal symptoms despite optimal medical therapy. Compared with optimal medical therapy, a strategy of coronary angiography and revascularization provides no benefit in patients with chronic stable angina. This patient, however, remains highly symptomatic despite optimal medical therapy, and therefore may benefit from coronary angiography and revascularization. Coronary revascularization is beneficial in patients with chronic stable angina and the following conditions: angina pectoris refractory to medical therapy; a large area of ischemic myocardium and high-risk criteria on stress testing; high-risk coronary anatomy, including left main coronary artery stenosis or three-vessel disease; and significant coronary artery disease with reduced left ventricular systolic function. In appropriately selected patients, revascularization, either a percutaneous coronary intervention or coronary artery bypass grafting surgery, has been shown to reduce angina, increase longevity, and improve left ventricular performance.
Exercise treadmill stress testing would not be useful for this patient’s management as it would only confirm the known diagnosis of coronary artery disease. Results of an exercise stress test would not influence therapeutic decisions.
ß-Blockers, such as metoprolol, reduce myocardial oxygen demand by reducing heart rate and contractility, thereby reducing myocardial oxygen consumption. However, this patient’s heart rate is already reduced to 48/min and his blood pressure is under excellent control. Increasing the dose of metoprolol in these circumstances is unlikely to produce further benefit and may not be tolerated because of unacceptably low pulse rate and blood pressure.
For patients with unstable angina, admission to the coronary care unit and intravenous heparin and nitroglycerin would be beneficial. This patient has chronic stable angina,
characterized by progressive exertional angina for 2 months without episodes of pain while at rest or prolonged episodes of pain.
Key Point
Coronary angiography is indicated in patients with chronic stable angina who experience lifestyle-limiting angina despite optimal medical therapy.
Bibliography
Jawad E, Arora R. Chronic stable angina pectoris. Dis Mon. 2008;54(9):671-689. [PMID: 18725007]
Item 19 Answer: D
Educational Objective: Diagnose ventricular tachycardia.
The most likely diagnosis is ventricular tachycardia. The electrocardiogram demonstrates sinus rhythm that is suddenly interrupted by the onset of ventricular tachycardia.
Ventricular tachyarrhythmias consist of ventricular tachycardia, ventricular fibrillation, and torsades de pointes (a special subset of polymorphic ventricular tachycardia).
Ventricular tachyarrhythmias are characterized by wide QRS complex morphology (QRS >0.12 sec) and ventricular rates greater than 100/min. In ventricular tachycardia, theventricular rate typically ranges from 140 to 250/min; in torsades de pointes, the ventricular rate ranges from 200 to 300/min; and in ventricular fibrillation, the rate is typically above 300/min.
Atrial fibrillation is characterized by an irregularly irregular rhythm, an irregular baseline (atrial fibrillatory waves), and the absence of P waves, which is inconsistent with this patient’s electrocardiographic findings.
Supraventricular tachycardia with a wide QRS complex, usually due to coexisting bundle branch block or preexcitation (Wolff-Parkinson-White syndrome), can mimic ventricular tachycardia. Differentiating ventricular tachycardia from supraventricular tachycardia with aberrant conduction is important because the treatment differs markedly. Ventricular tachycardia is more common than supraventricular tachycardia with aberrancy, particularly in patients with structural heart disease. A key point is that any wide QRS tachycardia should be considered to be ventricular tachycardia until proven otherwise. The most important differentiating point is the history of ischemic heart disease. In the presence of known structural heart disease, especially a prior myocardial infarction, the diagnosis of ventricular tachycardia is almost certain. The presence of cannon waves (large a waves) in the jugular venous pulsations and varying intensity of the first heart sound support the diagnosis of atrioventricular dissociation caused by either ventricular tachyarrhythmias or heart block.
Key Point
A wide QRS tachycardia in the presence of known structural heart disease, especially a prior myocardial infarction, is almost certainly ventricular tachycardia.
Bibliography
Srivathsan K, Ng DW, Mookadam F. Ventricular tachycardia and ventricular fibrillation. Expert Rev Cardiovasc T her. 2009;7(7):801-809. [PMID: 19589116]
Item 20 Answer: B
Educational Objective: Treat non-ST-elevation myocardial infarction with a ß-blocker.
The most appropriate additional treatment for this patient is metoprolol. This patient’s elevated troponin I level and ST -segment depression and T -wave inversions on electrocardiogram are indicative of a non-ST -elevation myocardial infarction (NST EMI). Early intravenous ß-blocker therapy reduces infarct size, decreases the frequency of recurrent myocardial ischemia, and improves short- and long-term survival. ß-Blockers diminish myocardial oxygen demand by reducing heart rate, systemic arterial pressure, and myocardial contractility; in addition, prolongation of diastole augments perfusion to the injured myocardium. ß-Blocker therapy can be used in left ventricular dysfunction if heart failure status is stable.
An intra-aortic balloon pump is indicated for an acute coronary syndrome with cardiogenic shock that is unresponsive to medical therapy, acute mitral regurgitation secondary to papillary muscle dysfunction, ventricular septal rupture, or refractory angina. The intra-aortic balloon pump reduces afterload during ventricular systole and increases coronary perfusion during diastole. Patients with refractory cardiogenic shock who are treated with an intra-aortic balloon pump have a lower in-hospital mortality rate than patients who are not treated. This patient has no indication for an intra-aortic balloon pump.
Calcium channel blockers, such as verapamil, are also effective antianginal medications, but data are conflicting as to whether calcium channel blockers reduce mortality in patients with NST EMI. Therefore, ß-blockers are first-line therapy for unstable angina and NST EMI unless contraindications are present. With ongoing ischemia despite ß-blocker therapy, a calcium channel blocker can be added. However, there is no indication for starting verapamil rather than metoprolol at this time.
There is no role for the routine use of warfarin in the treatment of acute coronary syndrome, including NST EMI. Warfarin is not associated with improved patient outcome as compared to treatment without warfarin. Warfarin may be considered in patients at increased risk for thromboembolism, such as those with atrial fibrillation.
Key Point
In patients with myocardial infarction, early intravenous ß-blocker therapy reduces infarct size, decreases the frequency of recurrent myocardial ischemia, and improves short- and long-term survival.
Bibliography
Hillis LD, Lange RA. Optimal management of acute coronary syndromes. N Engl J Med. 2009;360(21):2237-2240. [PMID: 19458369]
Item 21 Answer: A
Educational Objective: Diagnose acute severe mitral regurgitation due to papillary muscle rupture.
The most likely diagnosis is acute mitral valve regurgitation due to papillary muscle rupture. The clinical history of chest pain and dyspnea a week ago and the electrocardiographic findings of Q waves in leads II, III, and aVF strongly suggest an acute inferior wall myocardial infarction. The presence of a new systolic murmur and respiratory distress several days after an acute myocardial infarction indicates the possibility of either a ventricular septal rupture or mitral regurgitation. Papillary muscle rupture generally presents several days after the infarct event. Severe mitral regurgitation complicating an acute myocardial infarct is more common with inferior versus anterior infarcts and should be suspected in patients with pulmonary edema and respiratory distress in that setting. The murmur of mitral regurgitation may not be prominent because of the acutely elevated left atrial pressure and relatively lower transmitral systolic pressure gradient. Echocardiography is diagnostic, and early clinical recognition with aggressive support (intra-aortic balloon pump, afterload reduction if blood pressure allows) is essential, providing a bridge to surgical repair.
A left ventricular aneurysm may result in late-appearing complications of acute myocardial infarction. A ventricular aneurysm may be associated with intractable ventricular tachyarrhythmias, systemic emboli, or heart failure. It is not associated with a new holosystolic murmur.
Pulmonary embolism can complicate acute myocardial infarction and should be considered in any patient with new-onset pleuritic chest pain, dyspnea, and hypotension.
However, pulmonary embolism is not associated with a new holosystolic murmur.
Ventricular free wall rupture typically leads to pericardial tamponade manifesting as 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.
Key Point
The presence of a new systolic murmur and respiratory distress several days after an acute myocardial infarction indicates the possibility of either a ventricular septal rupture or mitral regurgitation.
Bibliography
T opalian S, Ginsberg F, Parrillo JE. Cardiogenic shock. Crit Care Med. 2008;36:S66-S74. [PMID: 18158480]
Item 22 Answer: B
Educational Objective: Treat ST-elevation myocardial infarction with thrombolytic therapy.
The best management option for this patient is immediate thrombolytic therapy. The patient is experiencing an acute inferior wall ST -elevation myocardial infarction (ST EMI). The diagnosis is established by the presence of chest pain and ST -segment elevations in leads II, III, and aVF. The treatment for an acute ST EMI is either revascularization or thrombolytic therapy. The patient has no contraindications for thrombolytic therapy. She is currently hemodynamically stable without cardiogenic shock. The treatment of choice is percutaneous coronary intervention (PCI) provided that it can be done immediately or in less than 60 minutes if transfer to another hospital is necessary. Since the nearest hospital with PCI capability is 3 hours away, immediate thrombolytic therapy is the most appropriate treatment for this patient.
Thrombolytic agents are an alternative to primary PCI in suitable candidates with ST EMI. By lysing the clot that is limiting blood flow to the myocardium, thrombolytics restore perfusion to the ischemic area, reduce infarct size, and improve survival. Thrombolytics should be administered within 12 hours after the onset of chest pain; the earlier the administration, the better the outcome.
Aggressive medical therapy would not be the correct option for this patient given the electrocardiographic findings, her relatively young age, and the ability to treat her with a thrombolytic agent.
Transfer for coronary artery bypass graft surgery would not be the correct option given that the patient’s coronary anatomy has not yet been defined and there would be an unacceptable delay if she were transferred for coronary angiography. Most patients presenting with a ST EMI can be treated effectively with percutaneous coronary intervention or thrombolytic therapy. Bypass surgery in the setting of an acute infarction is therefore rarely performed. Bypass surgery may be preferred in patients who have a large amount of myocardium at ischemic risk owing to proximal left main disease or multivessel disease, especially if the left ventricular ejection fraction is reduced.
However, this is predicated by first performing coronary angiography and knowing the coronary anatomy.
Key Point
Thrombolytic agents are an alternative to primary percutaneous coronary intervention in suitable candidates with ST -elevation myocardial infarction and should be administered within 12 hours after the onset of chest pain.
Bibliography
Hillis LD, Lange RA. Optimal management of acute coronary syndromes. N Engl J Med. 2009;360(21):2237-2240. [PMID: 19458369]
Item 23 Answer: A
Educational Objective: Diagnose first-degree atrioventricular block.
This electrocardiogram shows first-degree atrioventricular block and is otherwise unremarkable. First-degree atrioventricular block is diagnosed when the PR interval is greater than 0.20 sec. It is often associated with a soft S1. The presence of first-degree heart block suggests atrioventricular nodal disease but rarely requires therapy. First-degree atrioventricular block is also associated with acute reversible conditions, including inferior myocardial infarction, rheumatic fever, and digitalis intoxication. Additionally, any medication that slows conduction through the atrioventricular node (for example, diltiazem) can potentially produce a first-degree atrioventricular block.
Second-degree atrioventricular block is established when not all beats are conducted from the atria to the ventricles (“dropped beats”). It is recognized in the tracing by the presence of isolated P waves that are not followed by a QRS complex.
Third-degree (complete) atrioventricular heart block is characterized by complete absence of conduction from the atria to the ventricles; the P waves and the QRS complexes are completely independent of each other. Careful analysis will show that the P wave rate and the QRS rate are different and that the PR interval is different for every QRS complex.
The electrocardiographic diagnosis of ventricular preexcitation is based on a short PR interval (<0.11 sec), prolonged QRS duration, and slurred onset of the QRS (delta wave) complex. None of these findings are present.
Key Point
First-degree atrioventricular block is diagnosed when the PR interval is greater than 0.20 sec.
Bibliography
Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricular conduction blocks. Emerg Med Clin North Am. 2006;24(1):1-9, v. [PMID: 16308110]
Item 24 Answer: C
Educational Objective: Diagnose right ventricular infarction complicating an inferior wall ST-elevation myocardial infarction.
The most likely cause of hypotension in this patient is right ventricular infarction. Right ventricular infarction occurs in approximately 20% of patients with an inferior wall ST -elevation myocardial infarction (ST EMI). This diagnosis should be considered in patients with the clinical triad of hypotension, clear lung fields, and jugular venous distention. The diagnosis can be made using a right-sided electrocardiogram, on which ST -segment elevation in leads V3R and V4R will be seen. Treatment for right ventricular infarction consists of rapid restoration of blood flow to the right ventricle with either thrombolytic therapy or primary percutaneous coronary intervention, aggressive volume loading with intravenous normal saline to increase filling of the right ventricle, and dopamine or dobutamine if hypotension persists.
Increased vagal tone can cause bradycardia and decreased right ventricular preload, resulting in hypotension early in the course of a myocardial infarction. Although increased vagal tone is commonly associated with inferior wall myocardial infarction, the patient’s tachycardia suggests an alternative diagnosis.
Pericardial tamponade from rupture of the left ventricular free wall usually leads to sudden hypotension and death. Free wall rupture is second only to heart failure as the most
common cause of death for patients who die in hospitals after myocardial infarction. Ventricular free wall rupture typically occurs 1 to 4 days after acute myocardial infarction. It would be unlikely for pericardial tamponade to be present upon initial presentation unless the patient had chest pain for several days prior to the hospitalization.
A ventricular septal defect manifests as a new systolic murmur, hypotension, and respiratory distress 1 to 3 days following the onset of a myocardial infarction. It would be exceedingly uncommon for a patient to present initially with a ventricular septal defect unless symptoms of chest pain were present for several days.
Key Point
In the setting of an inferior wall ST -elevation myocardial infarction, the clinical triad of hypotension, clear lung fields, and jugular venous distention suggests a right ventricular infarction.
Bibliography
Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008;117(5):686-697. [PMID: 18250279]