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Flashcards in Section 11: MKSAP Deck (25)
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1

A 56-year-old man is evaluated in the office during a routine physical examination. He has no cardiovascular complaints. His medical history is unremarkable.

On physical examination, heart rate is approximately 90/min and irregularly irregular, and blood pressure is 130/78 mm Hg. Except for the abnormal cardiac rhythm, the remainder of the examination is unremarkable.

The electrocardiogram demonstrates atrial fibrillation with a heart rate of 92/min. The chest radiograph is unremarkable. Laboratory test results, including assessment of thyroid function, are normal. The patient is not aware of the abnormal rhythm or its duration.

In addition to heart rate control, which of the following would be most appropriate for this patient?

  • A. Aspirin
  • B. Clopidogrel
  • C. Direct-current cardioversion
  • D. Warfarin

 

Answer and Critique (Correct Answer = A)
 

This patient with asymptomatic atrial fibrillation has no risk factors for stroke; therefore, aspirin would be sufficient thromboembolic risk protection. The CHADS2 score is used to assess stroke risk in patients with atrial fibrillation. The CHADS2 score assigns 1 point each for the presence of congestive heart failure, hypertension, age 75 years or older, and diabetes mellitus and 2 points for a history of stroke or transient ischemic attack. This patient's CHADS2 score is 0; therefore, risk of stroke is low and anticoagulation other than aspirin is not necessary.

Cardioversion is recommended primarily for patients with symptoms related to atrial fibrillation or patients with hemodynamic deterioration due to the loss of sinus rhythm. There are no data to suggest that conversion to sinus rhythm improves survival; cardioversion is therefore not indicated in this patient. If the patient's symptoms progressed to a point at which cardioversion would be indicated, anticoagulation with warfarin would be required first because of the potential of having an atrial clot that could embolize upon the restoration of sinus rhythm. Clopidogrel has not been demonstrated to be effective thromboprophylaxis for patients with atrial fibrillation. The combination of clopidogrel and aspirin has been shown to worsen outcomes in patients with atrial fibrillation by increasing the risk of bleeding.

Key Point
Aspirin is sufficient thromboembolic risk protection in patients with asymptomatic atrial fibrillation and no risk factors for stroke.

2

A 68-year-old man is evaluated in the emergency department for chest pain that has lasted 90 minutes. He was eating dinner when he had the sudden onset of sharp precordial pain radiating toward both shoulders and his back. The pain is described as 9/10 in severity. Medical history is significant for hypertension and hyperlipidemia.

Physical examination shows a heart rate of 90/min, respiration rate of 19/min, blood pressure of 110/60 mm Hg, and oxygen saturation of 94% with the patient breathing room air. Bibasilar crackles are heard. Heart sounds are distant. There is a normal S1 and S2 and no S4 or S3. An electrocardiogram is shown (Figure 23).

Which of the following is the most likely diagnosis?

  • A. Acute anterior wall myocardial infarction
  • B. Acute inferior wall myocardial infarction
  • C. Acute lateral wall myocardial infarction
  • D. Acute pericarditis
  • E. Acute posterior wall myocardial infarction

Answer and Critique (Correct Answer = B)

This patient's clinical presentation is consistent with an acute inferior wall myocardial infarction; i.e., sudden onset of anterior chest pain radiating to the shoulders and ST elevation in the inferior leads (II, III, aVF). Posterior wall myocardial infarction may be associated with ST depression in leads V1 and V2. Posterior wall infarction is often associated with an inferior wall infarction, but this is not the case for this patient. Anterior (anteroseptal) wall myocardial infarction is associated with ST elevation in the anterior chest leads (V1–V3) and lateral wall and apical infarction with ST elevation in the lateral chest leads (V4–V6). Acute pericarditis is associated with PR-segment depression and widespread ST segments that are upwardly concave. PR-segment depression is virtually pathognomonic for acute pericarditis, but is seen in several other possible but rare entities (e.g., atrial myocardial ischemia). ST segments that are upwardly concave are useful findings to help distinguish acute pericarditis from an acute myocardial infarction, in which a downwardly concave pattern is seen.

Key Points

    Acute myocardial infarction can be localized according to ST elevation in specific electrocardiographic leads: inferior infarction in leads II, III, and aVF; anteroseptal infarction in leads V1–V3; lateral and apical infarctions in leads V4–V6.
    Acute posterior wall myocardial infarction is often associated with inferior wall infarction and may be associated with ST depression in leads V1–V2.

3

A 33-year-old man is evaluated in the office for palpitations. He reports intermittent symptoms that do not correlate with any particular activity. He is only mildly disturbed by the palpitations but wants to have his heart evaluated. His medical history is unremarkable, and he takes no medications. His physical examination and electrocardiogram also are unremarkable. A 24-hour electrocardiogram shows a normal sinus rhythm with 3004 total premature ventricular contractions in 24 hours. An echocardiogram shows a structurally normal heart. Thyroid function studies and electrolyte levels are normal.

Which of the following is the most appropriate treatment for this patient?

  • A. Atenolol
  • B. Flecainide
  • C. Radiocatheter ablation
  • D. Reassurance

Answer and Critique (Correct Answer = D)

In healthy adults, premature ventricular contractions at rest are common and are not a cause for concern. Even very frequent premature ventricular contractions on a 24-hour electrocardiogram are not of concern in the absence of underlying structural heart disease. This otherwise healthy patient needs reassurance. Suppression of premature ventricular contractions is indicated only in patients with severe and disabling symptoms, which may include palpitations, fatigue, and lightheadedness. In these patients, β-blockers are the safest initial choice. Antiarrhythmic agents such as flecainide are associated with more side effects and thus are a second-line option for patients who continue to have debilitating symptoms despite β-blocker therapy. Catheter ablation of premature ventricular contractions is feasible; however, because of the technical demands of the procedure and its variable success rate, it is reserved for the most refractory cases.

Key Point
In healthy adults, premature ventricular contractions are common and are not a cause for concern.

Bibliography

    Ng GA. Treating patients with ventricular ectopic beats. Heart. 2006;92:1707-12. [PMID: 17041126] [PubMed]

 

4

A 42-year-old man is evaluated at a rural emergency department for severe left shoulder and chest pain that radiates to the jaw and is associated with diaphoresis and mild dyspnea. The patient has no prior medical history and takes no medications.

In the emergency department, intravenous heparin and an aspirin are administered. On physical examination, blood pressure is 90/79 mm Hg and heart rate is 54/min. There is no jugular vein distention and no carotid bruits. The lungs are clear. Cardiac examination reveals a normal S1 and S2 and no murmurs. Electrocardiogram is shown (Figure 25).

The receiving hospital does not have a cardiac catheterization laboratory, and the closest hospital with one is 62 miles away. It usually takes at least 2 hours to arrange transfer.

Before transfer, which of the following therapeutic agents should be given?

  • A. Clopidogrel
  • B. Esmolol
  • C. Fibrinolytic therapy
  • D. Glycoprotein receptor blocker
  • E. Nitroglycerin

Answer and Critique (Correct Answer = C)

The electrocardiogram shows Q waves and ST elevation in leads II, III, and aVF diagnosing an inferior ST-elevation myocardial infarction (STEMI). Patients presenting less than 12 hours after the onset of symptoms of STEMI are best treated with a percutaneous coronary intervention. However, if the receiving hospital does not have a catheterization laboratory with interventional capabilities and transfer would take more than 2 hours, the patient should undergo prompt fibrinolysis. Fibrinolytic therapy should be given within 30 minutes of arrival in the emergency department. Percutaneous coronary intervention reperfusion is achieved for 90% to 95% of vessels compared with 60% to 75% of vessels with fibrinolytic therapy. The goal of all reperfusion strategies for patients with STEMI is to achieve a patent vessel within 90 minutes from the onset of symptoms.

The patient with STEMI arriving more than 12 hours after symptom onset who is asymptomatic is not a candidate for fibrinolytic therapy. Studies have also shown that the risk of fibrinolysis outweighs the benefit in patients with ST-segment depression.

In some patient groups, percutaneous coronary intervention is preferred over fibrinolysis even when transfer to a facility with a cardiac catheterization laboratory will take more than 2 hours: 1) patients in whom fibrinolysis is contraindicated (e.g., those with recent surgery, stroke, bleeding diathesis, uncontrolled hypertension, or peptic ulcer disease); 2) STEMI patients presenting more than 12 hours after symptoms who still have residual ST-segment elevation or a complicated presentation (e.g., heart failure, high-grade ventricular arrhythmias, shock); 3) STEMI occurring in patients who have had coronary artery bypass graft surgery (owing to the high likelihood of saphenous vein graft thrombosis); and 4) patients with cardiogenic shock (pulmonary edema and systolic blood pressure <100 mm Hg), especially those <75 years old.

Although both glycoprotein receptor blockers and clopidogrel are given to patients with acute myocardial infarction undergoing percutaneous coronary intervention, these drugs should not precede or delay the administration of fibrinolytic therapy. β-Blockers are beneficial in acute STEMI. However, β-blockers do not replace prompt reperfusion therapy and are relatively contraindicated in this patient with a low heart rate and blood pressure at presentation. Nitroglycerin provides symptom relief but does not affect clinical outcome and is relatively contraindicated in patients who have marginal blood pressure (<100 mm Hg systolic in the setting of acute STEMI).

Key Point
STEMI patients who cannot be reperfused by a direct coronary intervention within 90 to 120 minutes should receive fibrinolytic therapy if there are no contraindications.

Bibliography

    Pinto DS, Southard M, Ciaglo L, Gibson CM. Door-to-balloon delays with percutaneous coronary intervention in ST-elevation myocardial infarction. Am Heart J. 2006;151:S24-9. [PMID: 16777506] [PubMed]

 

5

A 38-year-old man is hospitalized with palpitations and dyspnea. He has no significant medical history and does not take any medications. He has a 20-pack-year smoking history and drinks alcohol daily. He does not use illicit drugs.

On physical examination, temperature is 36.9 °C (98.5 °F), blood pressure is 120/80 mm Hg, and heart rate is 115/min. Jugular venous pressure is normal. The lungs are clear. Cardiac examination shows an irregularly irregular rhythm. There is trace edema at both ankles.

Laboratory Studies


Hemoglobin - 14 g/dL
Mean corpuscular volume - 101 fL
Aspartate aminotransferase - 55 U/L
Alanine aminotransferase - 45 U/L
Thyroid-stimulating hormone - 4.5 μU/mL

Electrocardiogram shows normal voltage, normal axis, and atrial fibrillation. Echocardiogram shows dilated ventricles with normal wall thickness and severely decreased systolic function (left ventricular ejection fraction, 15%). The patient is started on lisinopril, carvedilol, and warfarin. Later in the hospital course, he spontaneously converts to normal sinus rhythm, he feels well, and has a blood pressure of 105/75 mm Hg and a heart rate of 63/min. Electrocardiogram confirms normal sinus rhythm.

Which of the following is the most likely type of cardiomyopathy in this patient?

  • A. Alcoholic
  • B. Amyloid
  • C. Hypertrophic
  • D. Ischemic

 

Answer and Critique (Correct Answer = A)
 

This patient likely has alcoholic cardiomyopathy, which generally occurs after many years of heavy alcohol consumption, although it may also occur after a short period of heavy consumption. Typically, both ventricles are dilated and globally hypokinetic. The patient reports that he drinks alcohol daily, and his laboratory test results suggest chronic alcohol use (macrocytosis) and possibly an acute episode of heavy alcohol use (mild elevation of aminotransferases, new-onset atrial fibrillation). In addition to medical therapy for heart failure, therapy for alcoholic cardiomyopathy must include total abstinence from alcohol. Abstinence may reverse the cardiomyopathy in patients with less advanced disease.

Cardiac amyloidosis results in increased left ventricular wall thickness due to deposition of amyloid, and, as a result, typically presents with restrictive cardiomyopathy, which is characterized by diastolic rather than systolic dysfunction. On echocardiography, ventricular chambers are typically small with thick walls, and the atria are dilated. Because increased left ventricular wall thickness is caused by infiltration of the myocardium rather than hypertrophy, the electrocardiographic voltage is generally low.

Hypertrophic cardiomyopathy is characterized by inappropriate, marked, and asymmetric hypertrophy of the left ventricle. The hypertrophy usually involves the interventricular septum, although there is a wide range of severity and location of hypertrophy, hemodynamic consequences, and symptoms. The left ventricular cavity is small, unlike the cavity in this patient.

Ischemic cardiomyopathy is often, but not invariably, associated with symptomatic coronary artery disease. The electrocardiogram may show evidence of previous infarction and the echocardiogram typically shows focal, not global, hypokinesis.

Key Point
Alcoholic cardiomyopathy is a dilated cardiomyopathy.


Bibliography

    Piano MR. Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology. Chest. 2002;121:1638-50. [PMID: 12006456] [PubMed]

6

A 43-year-old man is evaluated in the emergency department for palpitations. 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 (Figure 27). The patient converts to sinus rhythm spontaneously while in the emergency department, and the subsequent electrocardiogram is normal.

Which of the following is the most likely rhythm disorder responsible for this patient's symptoms?

A Atrial fibrillation
B Atrial flutter
C Atrioventricular nodal re-entrant tachycardia
D Atrioventricular re-entrant tachycardia

Answer and Critique (Correct Answer = A)

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. There is no evidence of structural heart disease in this patient on the basis of the history and physical examination. The follow-up normal electrocardiogram also suggests that cardiac structure and function are likely normal. These findings are most consistent with a diagnosis of lone atrial fibrillation. In this setting, aspirin and additional outpatient evaluation should be recommended. This should include a transthoracic echocardiogram to exclude occult valve or other structural heart disease and also to assess the size of the left atrial appendage. Thyroid studies and a careful family history should also be obtained to exclude familial atrial fibrillation.

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 characteristic of atrial fibrillation. In the typical form of atrioventricular (AV) nodal re-entrant tachycardia, the atria and ventricles are simultaneously activated, and either no P wave is visible, or a small pseudo r′ deflection in lead V1 and a pseudo S-wave deflection inferiorly are seen. AV nodal re-entrant tachycardia is easily distinguished from atrial fibrillation by the regularity of the rhythm and smooth baseline denoting the absence of chaotic atrial fibrillation waves. AV re-entrant tachycardia (bypass-tract-mediated tachycardia) is associated with an accessory AV pathway. Bypass-tract-mediated tachycardias are re-entrant tachycardias in which the anterograde conduction (atria-to-ventricle) is typically via the AV node, and retrograde conduction is via the bypass tract. Because bypass-tract conduction is typically faster than conduction via the AV node, atrial activation occurs rapidly after the QRS complex (within the ST segment), resulting in a “short RP” tachycardia. Only accessory pathways with anterograde conduction will show a pre-excitation (Wolff-Parkinson-White) pattern consisting of a short PR interval and a delta wave initiating the R wave deflection on the sinus rhythm electrocardiogram. Like AV nodal re-entrant tachycardia, the rhythm in AV re-entrant tachycardia is regular and the baseline is smooth, making the distinction from atrial fibrillation straightforward.

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

    Dewar RI, Lip GY; Guidelines Development Group for the NICE clinical guideline for the management of atrial fibrillation. Identification, diagnosis and assessment of atrial fibrillation. Heart. 2007;93:25-8. Epub 2006 Sep 4. [PMID: 16952973] [PubMed]

 

7

A 26-year-old woman is hospitalized because of a 7-day history of increasing shortness of breath. Two weeks ago, she had flu-like symptoms of fever, muscle aches, and chest pain, which have since resolved. She does not take any medications.

On physical examination, temperature is 37 °C (98.6 °F), blood pressure is 120/79 mm Hg, and heart rate is 100/min and regular. The lungs are clear. Cardiac examination shows a normal S1 and S2. Echocardiogram shows normal-sized ventricles, decreased systolic function (left ventricular ejection fraction, 40%) that is global and most severe in the anterior wall, and no significant valvular abnormalities. Coronary angiography discloses no evidence of coronary artery disease.

Which of the following is the most appropriate next step in treating this patient?

A Azithromycin
B Enoxaparin
C Ibuprofen
D Lisinopril
E Prednisone

Answer and Critique (Correct Answer = D)
 

This patient's presentation, including a viral prodrome, chest pain, symptoms and findings of heart failure in the absence of significant coronary artery disease, is consistent with acute myocarditis, which can range in presentation from asymptomatic to acute cardiogenic shock. Wall motion abnormalities on echocardiography can be regional or global during acute myocarditis. There is no specific treatment for acute myocarditis other than supportive care and the usual treatment for heart failure, including an angiotensin-converting enzyme inhibitor such as lisinopril, in the absence of contraindications.

The patient's normal blood pressure is not consistent with a serious infection, such as sepsis, and in the absence of other, more concrete evidence for infection, antibiotics are not indicated. The results of the coronary angiography rule out acute coronary syndrome, and therefore enoxaparin is not indicated. Although myocarditis is characterized by inflammation, there is no proven role for ibuprofen or corticosteroids for treatment.

Key Point
Therapy for acute myocarditis generally consists of standard care for heart failure tailored to the severity of the myocarditis.


Bibliography

    Magnani JW, Dec GW. Myocarditis: current trends in diagnosis and treatment. Circulation. 2006;113:876-90. [PMID: 16476862] [PubMed]

 

8

A 73-year-old man is evaluated in the office for shortness of breath and decreased exercise tolerance for the past 3 days. He has no other medical problems, and his only medication is low-dose aspirin daily.

On physical examination, heart rate is 148/min and blood pressure is 118/68 mm Hg. The lungs are clear. Cardiac examination demonstrates tachycardia with no murmur. The electrocardiogram is shown (Figure 29).

Which of the following is most likely causing this patient's symptoms?

A. Atrial fibrillation
B. Atrial flutter
C. Multifocal atrial tachycardia
D. Sinus tachycardia

Answer and Critique (Correct Answer = B)
 

This patient has an electrocardiogram consistent with atrial flutter. Atrial flutter waves are evident in the inferior leads, and appear as a “saw-tooth” pattern. In this electrocardiogram, atrioventricular conduction occurs once every two flutter waves (2:1 atrioventricular conduction) and is very typical for atrial flutter.

Atrial fibrillation is characteristically associated with an irregularly irregular rhythm, no discernible P waves, and atrial fibrillatory waves at a rate between 350 and 600/min. The fibrillatory waves vary in amplitude, morphology, and intervals, creating a rough, irregular baseline between the QRS complexes. Multifocal atrial tachycardia is defined by the electrocardiographic presence of discrete P waves with at least three different morphologic patterns with varying P-P, P-R and R-R intervals. P wave morphology is generally best seen in leads II, III and V1. In adults, multifocal atrial tachycardia is often associated with other serious illnesses, often hypoxic chronic obstructive pulmonary disease. Sinus tachycardia is a sinus rhythm with a ventricular rate >100/min. The P waves have a normal morphology but can become difficult to see with heart rates >140/min since they begin to merge with the preceding T wave. Slowing the heart rate with carotid sinus massage can often reveal the hidden P waves and establish the diagnosis.

Key Point
Atrial flutter is characterized by saw-tooth pattern flutter waves most noticeable in the inferior electrocardiographic leads.


Bibliography

    Fitzpatrick AP, Earley M, Petkar S, Diab I, Fox D, Williams P. Practical management of common atrial arrhythmias 2: common atrial flutter. Br J Hosp Med (Lond). 2007;68:201-4. [PMID: 17465101] [PubMed]

 

 

9

A 68-year-old woman is hospitalized with palpitations and shortness of breath. She has a history of hypertension and chronic atrial fibrillation, and her medications are furosemide, candesartan, and warfarin. On physical examination, the heart rate is 120/min with an irregularly irregular rhythm, and blood pressure is 130/80 mm Hg with no evidence of pulsus paradoxus. She has an elevated jugular venous pressure with normal x and y descent, crackles in both lungs, and marked lower extremity edema. Echocardiography shows left ventricular hypertrophy, an ejection fraction of 70%, and no significant valvular disease.

After intravenous diuretics are begun, the patient's symptoms improve, and the crackles and peripheral edema resolve. Her heart rate is now 99/min, and her blood pressure is 120/75 mm Hg.

Which of the following is the most likely primary mechanism of her heart failure?

A Constrictive pericarditis
B Diastolic dysfunction
C Systolic dysfunction
D Valvular disease

Answer and Critique (Correct Answer = B)
 

This patient has a history and echocardiographic findings consistent with diastolic dysfunction. She has hypertension, which predisposes to the development of left ventricular hypertrophy and associated impaired ventricular relaxation.

Although she presented with evidence of heart failure, the echocardiogram demonstrated normal systolic function and no significant valvular abnormalities that could account for the heart failure. Therefore, systolic dysfunction and valvular disease are unlikely. Constrictive pericarditis is also unlikely in the absence of pulsus paradoxus, normal x and y descent, and no echocardiographic evidence of constrictive pericarditis, such as pericardial thickening or abrupt posterior motion of the ventricular septum in early diastole with inspiration.

The primary treatment goals in patients with diastolic heart failure are to treat the underlying cause (if possible), manage any potentially exacerbating factors, and optimize diastolic filling by slowing the heart rate with β-blockers. To date, there have been no medications shown to reduce morbidity and mortality in patients with diastolic dysfunction.

Key Point
The diagnosis of diastolic heart failure is generally made when signs and symptoms of systolic heart failure are present but the echocardiogram shows a normal left ventricular ejection fraction and an absence of significant valvular abnormalities.


Bibliography

    Chinnaiyan KM, Alexander D, Maddens M, McCullough PA. Curriculum in cardiology: integrated diagnosis and management of diastolic heart failure. Am Heart J. 2007;153:189-200. [PMID: 17239676] [PubMed]

10

A 68-year-old man is evaluated in the emergency department for shortness of breath and palpitations. He reports a 3-day history of progressive shortness of breath, with productive cough and wheezing. In addition, his heart “has been racing” since last night. He has a 50-pack-year smoking history and bronchospastic lung disease, for which he uses inhaled bronchodilators.

On physical examination, temperature is 37.8 °C (100 °F), and heart rate is 122/min. The patient is in moderate respiratory distress. Examination of the chest shows decreased airflow with expiratory wheezing. The cardiac examination demonstrates distant heart sounds. Electrolytes are normal. The electrocardiogram is shown (Figure 31).

Which of the following is the most likely electrocardiographic diagnosis?

A. Accelerated idioventricular tachycardia
B. Atrioventricular nodal re-entrant tachycardia
C. Atrioventricular re-entrant tachycardia
D. Multifocal atrial tachycardia

Answer and Critique (Correct Answer = D)

Multifocal atrial tachycardia is most commonly seen in acutely ill patients, most often in the setting of pulmonary disease. Multifocal atrial tachycardia is defined by the electrocardiographic presence of discrete P waves with at least three different morphologic patterns with varying P-P, P-R, and R-R intervals. P wave morphology is generally best seen in leads II, III, and V1. Therapy is directed at the underlying disease process because otherwise the arrhythmia will be refractory to therapy or will recur. In this patient, treatment should be directed at the pulmonary disease and correction of any electrolyte imbalances, especially magnesium. Therefore, the treatment of choice in this patient is oxygen, inhaled bronchodilators, and possibly oral antibiotics. Second-line therapy in patients with refractory tachycardia is a calcium-channel blocker such as diltiazem or verapamil. Electrolytes should be corrected, and magnesium should be administered even if serum magnesium levels are normal.

There are no clinical features to suggest idioventricular tachycardia (slow ventricular tachycardia), which is demonstrated electrocardiographically as a wide QRS complex (without preceding conducting P waves) and a heart rate between 60 and 100/min. Atrioventricular (AV) re-entrant tachycardia is a bypass-tract-mediated re-entrant tachycardia, in which the anterograde conduction (atria-to-ventricle) is typically via the AV node, and retrograde conduction is via the bypass tract. Because bypass-tract conduction is typically faster than conduction via the AV node, atrial activation occurs rapidly after the QRS complex, resulting in a “short RP” tachycardia, and the P wave is usually located within the ST segment. In AV nodal re-entrant tachycardia, the atria and ventricles are activated simultaneously from the AV node; the QRS complex is narrow, and there are no P waves.

Key Point
Multifocal atrial tachycardia is characterized on electrocardiograms by three or more P wave morphologic patterns and variable PR intervals.


Bibliography

    McCord J, Borzak S. Multifocal atrial tachycardia. Chest. 1998;113:203-9. [PMID: 9440591] [PubMed]

 

 

11

A 28-year-old man is evaluated in the office for a 5-year history of palpitations. These episodes used to occur once or twice a year, but over the past 6 months he has been experiencing them on a monthly basis. He reports that his heart starts “racing” suddenly for no reason, and the episode usually terminates abruptly after he takes a few deep breaths. Episodes typically last 10 to 15 minutes, although one episode last month lasted 30 minutes. He is otherwise healthy, has no other symptoms, and takes no medications. Physical examination is normal.

A baseline electrocardiogram is shown (Figure 33).

Which of the following is the most likely cause of his arrhythmia?

A Atrial flutter
B Atrial tachycardia with block
C Atrioventricular re-entrant tachycardia (Wolff-Parkinson-White syndrome)
D Atrioventricular nodal re-entrant tachycardia

Answer and Critique (Correct Answer = C)

 

The combination of manifest pre-excitation (short PR segment and delta wave [slurred initial upstroke of the QRS complex]) in this patient's baseline electrocardiogram plus tachycardia establishes the diagnosis of the Wolff-Parkinson-White syndrome, which can cause an atrioventricular (AV) re-entrant tachycardia. AV re-entrant tachycardia is a bypass-tract-mediated re-entrant tachycardia, in which the anterograde conduction (atria-to-ventricle) is typically via the AV node, and retrograde conduction is via the bypass tract. Because bypass-tract conduction is typically faster than conduction via the AV node, during episodes of atrial tachycardia, atrial activation occurs rapidly after the QRS complex, resulting in a “short RP” tachycardia and the P wave is usually located within the ST segment. Because the ventricle is activated normally during tachycardia, the QRS complex is narrow. Patients with Wolff-Parkinson-White syndrome should be offered radiofrequency catheter ablation as first-line therapy. This recommendation is based on the high success rate of catheter ablation and the presence of a small but persistent risk of sudden cardiac death if the arrhythmia is untreated.

Sinus tachycardia, AV nodal re-entrant tachycardia, atrial tachycardia, and atrial flutter can cause paroxysmal episodes of palpitations, but none of these conditions is associated with a short PR segment and delta wave.

Key Point
Atrioventricular re-entrant tachycardia (Wolff-Parkinson-White syndrome) is characterized electrocardiographically by a short PR segment, delta wave, and tachycardia.


Bibliography

    Esberger D, Jones S, Morris F. ABC of clinical electrocardiography. Junctional tachycardias. BMJ. 2002;324:662-5. [PMID: 11895828] [PubMed]

 

12

A 50-year-old man is evaluated during a routine follow-up office visit for heart failure, which was diagnosed 1 year ago. A stress test at the time of diagnosis was negative for ischemia. At his most recent evaluation 4 months ago, an echocardiogram showed left ventricular enlargement and hypertrophy, a left ventricular ejection fraction of 40%, and no significant valvular disease. An electrocardiogram was unchanged, showing left ventricular hypertrophy but no evidence of previous myocardial infarction. The patient is currently asymptomatic, and his medications are hydrochlorothiazide and lisinopril.

On physical examination, heart rate is 85/min and blood pressure is 135/85 mm Hg. There is no jugular venous distention or peripheral edema. The lungs are clear. There is a soft S4 but no murmur.

Which of the following medications should be added to the patient's regimen?

A Carvedilol
B Digoxin
C Diltiazem
D Losartan
E Spironolactone

Answer and Critique (Correct Answer = A)

Treatment with an angiotensin-converting enzyme (ACE) inhibitor and a β-blocker is indicated for all patients with any degree of systolic heart failure, including this asymptomatic patient with a low ejection fraction, because treatment with both agents has been shown to reduce morbidity and mortality.

Losartan, an angiotensin-receptor blocker (ARB), is an acceptable alternative in a patient who cannot tolerate an ACE inhibitor, but there is no benefit to adding an ARB to an ACE inhibitor. Calcium-channel blockers are indicated in patients with heart failure who have hypertension or angina that is not adequately controlled with an ACE inhibitor or β-blocker. First-generation calcium-channel blockers, such as nifedipine, diltiazem, and verapamil, cause a reactive increase in sympathetic activity in response to peripheral vasodilatation and negative inotropic effects, whereas second-generation calcium-channel blockers, such as amlodipine, are more vasoselective, less cardiodepressant, and do not appear to have a deleterious effect on outcome in patients with heart failure. Spironolactone and digoxin are not indicated for patients with asymptomatic systolic heart failure. Spironolactone reduces mortality in patients with severe symptomatic heart failure (New York Heart Association class III or IV) and a left ventricular ejection fraction ≤35%. Digoxin alleviates symptoms and reduces hospitalizations related to heart failure, but has not been shown to reduce mortality.

Key Points

    An angiotensin-converting enzyme inhibitor and a β-blocker are indicated in all patients with systolic heart failure, including asymptomatic patients with low ejection fractions. Spironolactone and digoxin are not indicated in patients with asymptomatic systolic heart failure.


Bibliography

    O’Connor CM. The new heart failure guidelines: strategies for implementation. Am Heart J. 2007;153:2-5. [PMID: 17394896] [PubMed]

 

13

A 63-year-old man is evaluated in the emergency department after calling 911 for chest pain and diaphoresis. He had an anterior wall myocardial infarction 5 years ago, after which he underwent coronary artery bypass grafting. He has a history of New York Heart Association class II congestive heart failure, hypertension, and hypercholesterolemia. His current medications are furosemide, potassium chloride, enalapril, digoxin, atorvastatin, metoprolol, and aspirin.

On physical examination he is diaphoretic. Heart rate is 192/min, and blood pressure is 85/43 mm Hg. He has jugular venous distention, and the cardiac examination reveals tachycardia with no murmurs. Bibasilar crackles are heard.

The electrocardiogram is shown (Figure 37).

Which of the following is the most likely electrocardiographic diagnosis?

A. Atrial fibrillation
B. Left bundle branch block
C. Right bundle branch block
D. Ventricular tachycardia

Answer and Critique (Correct Answer = D)

This patient has ventricular tachycardia. Ventricular tachycardia is defined as three or more consecutive beats originating below the atrioventricular node (wide-complex beats not associated with a conducted P wave), with a heart rate >100–120/min. Patients with sustained ventricular tachycardia in the setting of significant structural heart disease have a high risk of future recurrence, with a mortality rate as high as 25% per year. An implantable cardioverter-defibrillator reduces sudden cardiac death in patients with ventricular fibrillation or sustained ventricular tachycardia associated with hemodynamic compromise and is superior to amiodarone therapy. It is therefore recommended in this population unless there is a contraindication.

The electrocardiogram for a patient with atrial fibrillation shows a rapid, irregularly irregular rhythm with no discernible P waves and atrial fibrillatory waves at a rate between 350 and 600/min. The fibrillatory waves vary in amplitude, morphology, and intervals, creating a rough, irregular baseline between the QRS complexes. Unless there is co-existing bundle branch block, the QRS complex is narrow. Electrocardiographically, left bundle branch block is associated with absent Q waves in leads I, aVL, and V6; a large, wide, and positive R wave in leads I, aVL, and V6 (“tombstone” R waves); and prolongation of the QRS complex to >0.12 sec. Repolarization abnormalities are present consisting of ST segment and T wave vectors directed opposite to the QRS complex. In right bundle branch block, lead I will show a small Q wave and tall R wave; lead V6 will show a small positive R wave and a small negative S wave followed by a large positive deflection (the “rabbit ear”). There is ST depression and T wave inversion in right precordial leads and upright T waves in left precordial and limb leads. The QRS complex is >0.12 sec.

Key Points

  •     Patients with sustained ventricular tachycardia in the setting of significant structural heart disease are at high risk of future recurrence with a high mortality rate.
  •     An implantable cardioverter-defibrillator improves survival in patients with sustained ventricular tachycardia and concomitant structural heart disease.


Bibliography

    Kokolis S, Clark LT, Kokolis R, Kassotis J. Ventricular arrhythmias and sudden cardiac death. Prog Cardiovasc Dis. 2006;48:426-44. Erratum in: Prog Cardiovasc Dis. 2006;49:58. [PMID: 16714162] [PubMed]

 

14

A 29-year-old woman is evaluated in the emergency department at 30 weeks gestation for increasing dyspnea on exertion. On physical examination, blood pressure is 110/70 mm Hg and heart rate is 98/min and regular. Bilateral crackles are heard. Cardiac examination shows a normal S1, a fixed split S2, a grade 2/6 early systolic murmur at the base, a grade 2/6 holosystolic murmur at the apex radiating to the axilla, and an S3 gallop. There is trace peripheral edema. Echocardiography shows global left ventricular hypokinesis, with an ejection fraction of 30% and moderate mitral regurgitation. Peripartum cardiomyopathy and heart failure are diagnosed.

Which of the following medications is contraindicated at this time?

A. Atenolol
B. Furosemide
C. Isosorbide dinitrate
D. Lisinopril

Answer and Critique (Correct Answer = D)

The principles of management of heart failure in the pregnant patient parallel therapy in the nonpregnant patient, with the modification that some medications should be avoided during pregnancy. This patient with a low left ventricular ejection fraction should be started on afterload reduction therapy. Because angiotensin-converting enzyme inhibitors may cause fetal renal agenesis and should be avoided during pregnancy, hydralazine is the most appropriate choice for this patient. Furosemide can be used to control volume overload, but attention must be paid to avoiding hypovolemia and its deleterious effect on the fetus. Nitrates often are added to hydralazine to improve the effectiveness of vasodilator therapy. On a long-term basis, the addition of a β-blocker may be helpful; however, β-blockers should be avoided in patients with decompensated heart failure and considered only after afterload reduction has been established and volume status has been optimized.

Key Points

  • The use of angiotensin-converting enzyme inhibitors should be avoided during pregnancy.
  • Hydralazine and nitrates are the vasodilators of choice to treat heart failure during pregnancy.


Bibliography

    Sliwa K, Fett J, Elkayam U. Peripartum cardiomyopathy. Lancet. 2006;368:687-93. [PMID: 16920474] [PubMed]

15

A 70-year-old man is evaluated in the emergency department for palpitations and substernal chest pain that began 30 minutes ago. He has a history of coronary artery disease and hypertension. His medications are hydrochlorothiazide, pravastatin, metoprolol, sublingual nitroglycerin, and aspirin.

Physical examination reveals a diaphoretic man who is anxious and short of breath. Blood pressure is 100/60 mm Hg, heart rate is 160/min, and respiration rate is 22/min. He has large jugular venous a waves, varying intensity of S1, and an S3. There are crackles at the lung bases. Bilateral lower extremity edema is present.

His electrocardiogram is shown (Figure 39).

Which of the following intravenous drugs should be administered at this time?

A Dopamine
B Lidocaine
C Tissue plasminogen activator
D Verapamil

Answer and Critique (Correct Answer = B)
 

This patient has symptomatic monomorphic ventricular tachycardia and needs emergent treatment. Sustained monomorphic ventricular tachycardia in hemodynamically stable patients is treated initially with intravenous lidocaine, procainamide, or amiodarone. If the patient is hemodynamically unstable, direct-current cardioversion is used.

Ventricular tachyarrhythmias have wide-complex QRS morphology (QRS complex >0.12 sec) and a ventricular rate greater than 100/min. Ventricular tachyarrhythmias are classified as either sustained or nonsustained and either monomorphic or polymorphic. Sustained ventricular tachycardia persists for more than 30 seconds or requires termination because of hemodynamic collapse; nonsustained ventricular tachycardia is characterized by three or more beats lasting up to 30 seconds. Ventricular tachycardia is monomorphic if the QRS complexes in the same leads do not vary in contour or polymorphic if the QRS complexes in the same leads vary in contour. Physical examination findings of cannon a waves and variable intensity S1 are suggestive of atrioventricular dissociation and support the diagnosis of ventricular tachycardia in this patient.

Thrombolytic agents such as recombinant tissue plasminogen activator (rtTPA) are not used unless a diagnosis of acute myocardial infarction is established. Although myocardial infarction is highly probable in this patient, the initial electrocardiogram is not diagnostic. If myocardial infarction is ultimately diagnosed in this patient, given the presence of ventricular tachycardia and heart failure, a primary coronary intervention (e.g., coronary angioplasty and stenting) is preferred to thrombolytic therapy. Intravenous dopamine does not terminate ventricular tachycardia and could trigger ventricular fibrillation. Verapamil does not terminate ventricular tachycardia occurring in the setting of coronary artery disease and could trigger hemodynamic collapse. If this patient had supraventricular tachycardia with aberrant conduction, adenosine or verapamil is an acceptable treatment.

Key Point

 

  • Hemodynamically stable but symptomatic monomorphic ventricular tachycardia is treated emergently with intravenous lidocaine, procainamide, or amiodarone.

Bibliography

    ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005;112:IV1-203. Epub 2005 Nov 28. [PMID: 16314375] [PubMed]

 

16

A 65-year-old woman with heart failure due to nonischemic cardiomyopathy (left ventricular ejection fraction is 25%) is evaluated in the office for a 1-week history of increasing dyspnea on exertion. Her symptoms have progressed to the point that she is no longer able to perform even minimal activities of daily living. She has not had any chest pain or pressure, and her weight has not fluctuated more than a few pounds over the past month. She takes furosemide, lisinopril, and carvedilol and is compliant with a salt-restricted diet.

On physical examination, blood pressure is 105/60 mm Hg, heart rate is 75/min and regular, and respiration rate is 18/min. Findings include jugular venous distention, scattered bibasilar crackles, an S3 gallop, and trace bilateral pretibial edema.

Addition of which of the following medications will most likely improve this patient's symptoms and prolong her survival?

A Amlodipine
B Digitalis
C Metolazone
D Milrinone
E Spironolactone

Answer and Critique (Correct Answer = E)
 

The use of low-dose anti-aldosterone agents such as spironolactone should be carefully considered in selected patients with recently decompensated New York Heart Association class III–IV heart failure. When added to standard therapy of angiotensin-converting enzyme (ACE) inhibitors and β-blockers, spironolactone substantially reduces the risk of morbidity and death in patients with severe heart failure due to systolic dysfunction. ACE inhibition may not completely reduce or inhibit aldosterone production. Aldosterone causes salt and water retention and myocardial fibrosis; the addition of spironolactone may blunt these effects. The original spironolactone heart failure clinical trial included patients with serum creatinine levels <2.6 mg/dL and potassium levels <5.0 meq/L. Because the risk of hyperkalemia may be higher in patients who do not meet these criteria, spironolactone should be used with caution in these patients.

Calcium channel blockers such as amlodipine can lead to worsening heart failure and an increased risk of cardiovascular events in patients with a reduced left ventricular ejection fraction. Digitalis (e.g., digoxin) may improve symptoms and reduce the need for hospitalization in patients with current or prior symptoms of heart failure due to systolic dysfunction, but the drug's narrow risk/benefit ratio and the lack of survival benefit limit its usefulness. The addition of metolazone to a loop diuretic may help overcome diuretic resistance in patients with refractory edema, but diuretic therapy has not been shown to improve survival in patients with heart failure. Long-term studies with other oral positive inotropic agents, such as milrinone, have shown little efficacy and were terminated early because of an increased risk of death in patients with heart failure.

Key Point

  • When added to standard therapy of angiotensin-converting enzyme inhibitors and β-blockers, spironolactone substantially reduces the risk of morbidity and death in patients with severe heart failure due to systolic dysfunction.


Bibliography

    Hunt SA; American College of Cardiology; American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2005;46:e1-82. Erratum in: J Am Coll Cardiol. 2006;47:1503-1505. [PMID: 16168273] [PubMed]

 

17

A 45-year-old woman with a 20-year-history of type 2 diabetes mellitus is evaluated for a 1-month history of progressive shortness of breath. Two months ago, she had a flu-like illness with nausea, vomiting, and sweating.

On physical examination, the patient is obese (BMI 32.9). Heart rate is 75/min, and blood pressure is 185/93 mm Hg. Jugular venous pressure is elevated. Bibasilar crackles are present. Cardiac examination shows regular rhythm, normal S1 and S2, and the presence of an S3. There is peripheral edema. An electrocardiogram is shown (Figure 41). An echocardiogram is notable for left ventricular hypertrophy and severely decreased systolic function (left ventricular ejection fraction, 20%).

Which of the following is the most appropriate next diagnostic test?

A. Cardiac catheterization
B. Exercise stress test
C. Endomyocardial biopsy
D. Measurement of B-type natriuretic peptide
 

Answer and Critique (Correct Answer = A)
 

The patient's electrocardiogram shows a previous anteroseptal myocardial infarction (Q waves in leads V1–V3). She may have had a myocardial infarction 2 months ago, resulting in systolic dysfunction. Her risk factors for coronary artery disease include diabetes mellitus, obesity, and hypertension. The American College of Cardiology/American Heart Association class I (evidence or general agreement that therapy is useful and effective) indications for cardiac catheterization include patients who have angina and who may be candidates for revascularization.

Measuring B-type natriuretic peptide would likely confirm mild volume overload but would not add to the diagnosis; the physical examination already suggests volume overload, and the echocardiogram already confirms severe systolic dysfunction. The priority in diagnosis should be to rule out coronary artery disease as a treatable cause of heart failure. The pretest probability of coronary artery disease is very high in this patient, and a cardiac stress test, which is most useful diagnostically for risk stratification in patients with an intermediate pretest probability of disease, would not be helpful. Few patients with new-onset heart failure require endomyocardial biopsy as part of their diagnostic evaluation. Endomyocardial biopsy is useful in patients with unexplained cardiomyopathy, in whom a definitive diagnosis, such as amyloidosis or sarcoidosis, would affect treatment and prognosis.

Key Point
In patients with new-onset heart failure, ischemia should be ruled out if risk factors are present.


Bibliography

    Onwuanyi A, Taylor M. Acute decompensated heart failure: pathophysiology and treatment. Am J Cardiol. 2007;99:25D-30D. Epub 2007 Jan 25. [PMID: 17378992] [PubMed]

 

 

18

A 34-year-old man is seen in the office for a routine evaluation. He is asymptomatic and has no personal or family history of cardiovascular disease. He jogs 2 to 3 miles three times per week.

On physical examination, temperature is normal, heart rate is 70/min, and blood pressure is 140/58 mm Hg. There is no jugular venous distention. Lungs are clear. Cardiovascular examination reveals a point of maximal impulse that is displaced 1 cm from the midclavicular line and is diffuse. There is an early decrescendo diastolic murmur heard at the left parasternal third intercostal space that does not radiate or change with respiration. There are brisk, prominent distal pulses throughout the extremities, with a “pistol shot” sound heard when auscultating over the peripheral arteries. A transthoracic echocardiogram is scheduled

Which of the following is the most likely diagnosis?

A Aortic dissection
B Aortic valve regurgitation
C Aortic valve stenosis
D Pulmonary valve regurgitation
E Pulmonary valve stenosis

Answer and Critique (Correct Answer = B)
 

This young, asymptomatic patient has a bicuspid aortic valve and significant aortic regurgitation. Transthoracic echocardiography is the diagnostic test of choice. The physical examination findings that support aortic regurgitation include the displaced and diffuse apical impulse (left ventricular dilatation), the diastolic murmur at the left sternal border, and the peripheral artery findings that include brisk pulses with rapid collapse and a “pistol shot” sound that can be auscultated over large peripheral arteries.

Aortic valve stenosis is associated with a systolic, not diastolic, murmur, and the apex beat is hyperkinetic and prolonged, not displaced and diffuse. Aortic valve stenosis is also associated with a small, delayed carotid pulse that is distinctly different from the rapidly rising and collapsing pulse of aortic regurgitation. Aortic dissection can produce acute aortic insufficiency, but patients typically have severe chest pain that radiates through to the back, an absent S1 due to premature closure of the mitral valve, and a soft S2. Pulmonary valve stenosis, like aortic valve stenosis, causes a systolic murmur, and murmurs of both pulmonary valve stenosis and pulmonary valve regurgitation increase with inspiration, a finding that is absent in this patient. Finally, pulmonary valve abnormalities are not associated with peripheral artery findings.

Key Point

  • Chronic aortic valve regurgitation is associated with a basal, left-sided diastolic murmur that does not change with respiration.


Bibliography

    Maurer G. Aortic regurgitation. Heart. 2006;92:994-1000. [PMID: 16775114] [PubMed

19

A 79-year-old woman is seen in the office for an annual examination. She walks regularly to and from the bus stop several times per week. It now takes her 25 minutes to get to the bus stop, whereas it only took her 10 minutes a year ago. She describes dyspnea midway in her walk, causing her to stop and catch her breath. She does not have angina, presyncope, syncope, or pedal edema.

On physical examination, heart rate is 80/min, and blood pressure is 165/86 mm Hg. Carotid artery upstrokes are delayed. The lungs are clear. There is a sustained apical impulse. S1 is normal, and there is a single S2 and an S4. A grade 3/6 late-peaking systolic murmur is heard best at the right second intercostal space with radiation into the right carotid artery. Transthoracic echocardiogram is scheduled.

Which of the following is the most likely diagnosis?

A. Aortic valve stenosis
B. Hypertrophic cardiomyopathy
C. Mitral valve regurgitation
D. Tricuspid valve regurgitation
E. Ventricular septal defect

Answer and Critique (Correct Answer = A)

This patient has severe aortic stenosis based upon her symptoms and quality of the murmur. Severe aortic stenosis is associated with carotid artery pulsations that are low volume and late (in relation to the apical impulse), a late peaking murmur (indicating an increased pressure gradient across the aortic valve), and a sustained apical impulse and absent splitting of S2 (both indicating a prolonged ejection time). The most common cause of aortic stenosis is progressive calcific valve disease of a normal trileaflet valve. The primary indication for aortic valve replacement in patients with aortic stenosis is onset of cardiac symptoms. This patient has symptomatic disease with exertional dyspnea and decreased exercise tolerance. Referral for aortic valve replacement should be the next step in her management.

Physical examination findings in patients with hypertrophic cardiomyopathy and left ventricular outflow obstruction show a variable and dynamic systolic murmur that is increased by a Valsalva maneuver and standing and is diminished by hand gripping, leg elevation, and squatting. Carotid upstrokes are brisk. Mitral regurgitation is associated with a holosystolic murmur that radiates to the cardiac apex and is associated with a displaced, not sustained, apical impulse. Tricuspid regurgitation causes a systolic murmur heard best along the left sternal border; the murmur increases with inspiration and does not radiate to the carotid arteries. Ventricular septal defect would be an unusual cause of a systolic murmur in an elderly person in the absence of a recent myocardial infarction. Ventricular septal defects can be associated with a precordial thrill, and if pulmonary hypertension develops, fixed splitting of the S2 occurs. The murmur of a ventricular septal defect does not radiate to the carotid arteries.

Key Point

  • The physical findings of severe aortic stenosis include small and late carotid pulsations, late peaking systolic murmur, absence of splitting of the S2, and a sustained apical impulse.


Bibliography

    Otto CM. Valvular aortic stenosis: disease severity and timing of intervention. J Am Coll Cardiol. 2006;47:2141-51. [PMID: 16750677] [PubMed]

 

 

20

A 78-year-old woman is evaluated in the office for a 1-year history of progressively decreasing exercise tolerance. She has been in good health other than hypertension and osteoarthritis.

On physical examination, heart rate is 84/min and regular, respiration rate is 12/min, and blood pressure is 170/90 mm Hg. Carotid upstrokes are brisk, and jugular venous pressure is 8 cm H2O. The lungs are clear. S1 is soft, and there is a physiologically split S2. A grade 2/6 mid-systolic murmur is present at the base with radiation to the apex but not to the carotid arteries, and there is a grade 1/6 early diastolic decrescendo murmur at the left sternal border. There is no peripheral edema.

Which of this patient's physical examination findings is the most helpful for excluding severe aortic stenosis?

A Blood pressure
B Carotid upstroke
C Murmur intensity
D Radiation of the murmur
E Second heart sound (S2)

Answer and Critique (Correct Answer = E)

Physical examination is helpful for defining the presence of heart valve disease but is less useful for evaluation of disease severity. In this elderly woman with symptoms that may be due to aortic stenosis, the presence of a systolic murmur on examination is of concern. The most helpful physical examination finding in this patient is a physiologically split S2, which has a specificity of 76% for excluding severe aortic stenosis. With severe stenosis, the stiff aortic valve leaflets do not “snap” shut, thus the aortic component of the S2 is absent. In addition, a physiologically split S2 rules out the delay in left ventricular ejection that is associated with severe aortic valve stenosis.

About one third of adults with severe aortic stenosis have systemic hypertension, so this finding does not exclude the diagnosis. In fact, concurrent hypertension and aortic stenosis “double loads” the left ventricle, resulting in increased wall stress and earlier symptom onset. In patients with hypertension, the increased stiffness of the peripheral vessels may mask the expected delay and decrease in carotid upstroke that is classically associated with severe aortic stenosis. The loudness of the murmur in aortic stenosis is only helpful when a grade 4/6 murmur (murmur and a palpable thrill) is present because this finding is specific for severe valve obstruction. Most patients with severe aortic stenosis have a grade 3/6 murmur and some have a grade 2/6 murmur. In the elderly, the murmur of aortic stenosis may radiate to the apex instead of to the carotid arteries. Severe aortic stenosis is very unlikely with a grade 1 or absent systolic murmur, but severe stenosis may be present with a grade 2 murmur.

In clinical practice, most physicians would obtain an echocardiogram in this patient because aortic valve disease almost certainly is present, even if not yet severe. Echocardiography provides prognostic information in this setting. In patients with mild aortic stenosis (aortic jet velocity <3 m/s, valve area >1.5 cm2), progression to symptoms occurs in only 8% of patients per year. In contrast, in patients with asymptomatic severe stenosis (aortic jet velocity >4 m/s, valve area <1.0 cm2), about 40% develop symptoms that prompt valve surgery within 1 year. Outcomes are intermediate with moderate aortic stenosis (jet velocity 3–4 m/s, valve area 1–1.5 cm2), with an annual rate of symptom onset of about 17%.

Key Points

  • Physical examination is helpful in identifying the presence, but not the severity, of heart valve disease.
  • The most sensitive physical examination finding excluding the diagnosis of severe aortic stenosis is a physiologically split S2.


Bibliography

    Etchells E, Glenns V, Shadowitz S, Bell C, Siu S. A bedside clinical prediction rule for detecting moderate or severe aortic stenosis. J Gen Intern Med. 1998;13:699-704. [PMID: 9798818] [PubMed]
    Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA. 1997;277:564-71. [PMID: 9032164] [PubMed]

 

 

21

A 68-year-old man is evaluated in the office during a routine physical examination. A heart murmur was diagnosed at age 28 years, and echocardiography 20 years ago revealed a bicuspid aortic valve with minimal obstruction to aortic outflow. He works full time, is very active, and has no physical limitations. He does not have chest pain, dyspnea on exertion, or syncope and takes no medications.

On physical examination, heart rate is 68/min and blood pressure is 128/78 mm Hg. The carotid pulses are full and not delayed. A long, late-peaking grade 3/6 systolic crescendo–decrescendo murmur is present at the second right intercostal space with radiation to the carotid arteries; no diastolic murmur is heard. S1 is normal, and S2 is diminished and paradoxically split. An S4 gallop is heard at the cardiac apex. The lungs are clear. There is no lower extremity edema.

Electrocardiography shows a heart rate of 70/min, normal sinus rhythm, left atrial enlargement, and prominent R waves in leads V5 and V6.

Which of the following findings suggests the presence of advanced aortic stenosis in this patient?

A Absent aortic ejection click
B Left atrial enlargement
C Long, late-peaking systolic murmur
D Radiation of the systolic murmur to the carotid arteries
E S4 gallop

Answer and Critique (Correct Answer = C)
 

This patient's long, late-peaking systolic murmur suggests severe aortic stenosis. In adults, aortic stenosis is most commonly caused by rheumatic heart disease, a bicuspid aortic valve, and degenerative disease of a tricuspid aortic valve. Significant obstruction to aortic outflow typically develops gradually over many years. Signs of severe stenosis may include angina, dyspnea, or syncope, as well as a lengthening murmur with a peak later in systole, paradoxical splitting of S2, and the presence of pulsus parvus et tardus (a small and slow-rising peripheral pulse). Evaluation for possible surgical valve replacement may be warranted if any of these findings are present.

Electrocardiographic evidence of left atrial enlargement and an S4 gallop suggestive of left ventricular hypertrophy are often present years before surgical intervention for aortic stenosis is needed and do not correlate well with the severity of the obstruction. A characteristic systolic murmur at the base of the heart with radiation to the carotid arteries often is present regardless of disease severity. The primary importance of an aortic ejection click is its etiological association. In patients with aortic stenosis the presence of an ejection click implies that the stenosis is at the valvular level and there is some mobility to the valve. Elderly patients with calcific aortic stenosis and immobile valves do not have ejection clicks. The absence of an ejection click is not well correlated with severity of stenosis.

Key Point
A long, late-peaking systolic murmur is associated with advanced aortic stenosis.


Bibliography

    Carabello BA. Clinical practice. Aortic stenosis. N Engl J Med. 2002;346:677-82. [PMID: 11870246] [PubMed]

 

22

A 32-year-old man is evaluated in the office during an annual physical examination. He is asymptomatic, and there is no personal or family history of cardiovascular disease. On physical examination, vital signs are normal. S1 and S2 are normal, and an S4 is present. There is a grade 2/6 crescendo-decrescendo systolic murmur heard best at the lower left sternal border. The murmur does not radiate to the carotid arteries. The Valsalva maneuver increases the intensity of the murmur, and moving from a standing to a squatting position, performing a passive leg lift while recumbent, and performing isometric handgrip exercises decrease the intensity. Rapid upstrokes of the peripheral pulses are present.

Which of the following is the most likely diagnosis?

A Aortic valve stenosis
B Atrial septal defect
C Hypertrophic cardiomyopathy
D Mitral valve prolapse
E Ventricular septal defect

Answer and Critique (Correct Answer = C)
 

In this patient, the physical examination is most consistent with hypertrophic cardiomyopathy. Rapid upstrokes of the peripheral pulses help differentiate hypertrophic cardiomyopathy from aortic stenosis, which is characterized by low volume and delayed peripheral pulses (pulsus parvus et tardus). The murmur of hypertrophic cardiomyopathy is caused by obstruction of the left ventricular outflow tract from a thickened interventricular septum. In contrast to aortic stenosis, the murmur of hypertrophic cardiomyopathy rarely radiates to the level of the carotid arteries. The stand-to-squat maneuver and passive leg lift transiently increase venous return (preload) and therefore increase left ventricular chamber size and volume. If preload is transiently increased, the end-systolic dimension of the left ventricle increases, and there is less relative obstruction/turbulence in the left ventricular outflow tract with a resulting decrease in murmur intensity. If venous return is transiently decreased, as with the Valsalva maneuver or the squat-to-stand maneuver, left ventricular chamber size decreases and the septum and mitral leaflet are brought closer together. As a consequence, turbulent flow in the outflow tract is increased, increasing the intensity of the murmur. A murmur that increases with the Valsalva maneuver is a strong indicator that hypertrophic cardiomyopathy is present, with a positive likelihood ratio of 14.0. An absence of change in a murmur with the squat-to-stand, passive leg lift, and handgrip exercise maneuvers provides strong evidence against a diagnosis of hypertrophic cardiomyopathy, with a negative likelihood ratio of 0.1.

In contrast to the murmur of hypertrophic cardiomyopathy, the murmur associated with mitral valve prolapse and regurgitation is a holosystolic to late systolic murmur. This murmur is usually associated with a midsystolic click and is located at the apex. A Valsalva maneuver causes the click and murmur to occur earlier in systole. Having the patient squat from the standing position, perform leg raising, and do maximal isometric exercises moves the click-murmur complex toward S2. The murmur associated with a ventricular septal defect is a harsh systolic murmur located parasternally that radiates to the right sternal edge. Maneuvers that increase afterload, such as isometric handgrip exercise, increase the regurgitant left-sided murmurs of mitral regurgitation and ventricular septal defect.

An atrial septal defect is associated with a wide, fixed split S2 and a soft systolic murmur that may or may not be audible. If present, the murmur is heard best over the pulmonic area.

The murmur of aortic stenosis is a mid-peaking systolic murmur that often radiates superiorly, toward the carotid arteries. There are no accentuating maneuvers for the murmur of an atrial septal defect or aortic stenosis.

Key Point

  • The murmur of hypertrophic cardiomyopathy increases after a Valsalva maneuver and decreases with standing to squatting.


Bibliography

    Lembo NJ, Dell’Italia LJ, Crawford MH, O’Rourke RA. Bedside diagnosis of systolic murmurs. N Engl J Med. 1988;318:1572-8. [PMID: 2897627] [PubMed]

23

A 57-year-old woman with a 6-month history of progressive dyspnea on exertion is evaluated in the office. Physical examination reveals an elevated jugular venous pressure, bibasilar crackles, a grade 2/6 holosystolic murmur at the apex that radiates to the axilla and does not vary with respiration, a loud pulmonic component of S2, an enlarged point of maximal impulse, and moderate edema up to both shins. An electrocardiogram shows left atrial and ventricular enlargement. Chest radiograph shows mild cardiomegaly and pulmonary congestion.

Which of the following is the most likely diagnosis?

A Aortic valve regurgitation
B Aortic valve stenosis
C Mitral valve regurgitation
D Mitral valve stenosis
E Tricuspid valve regurgitation

Answer and Critique (Correct Answer = C)
 

This patient has findings consistent with chronic mitral regurgitation with associated hemodynamic and structural sequelae, ultimately leading to the development of symptomatic heart failure. The location of the murmur is characteristic of mitral valve regurgitation (holosystolic, loudest at the apex, and radiating to the axilla). The prominent pulmonic component of the S2 suggests pulmonary hypertension secondary to chronic mitral valve regurgitation. She has evidence of left-sided heart failure, including left atrial and ventricular enlargement on the electrocardiogram, crackles on lung examination, and pulmonary congestion on the chest radiograph. The signs of right-sided heart failure (peripheral edema, jugular venous distention) are the upstream effects of elevated left-sided filling pressures.

Chronic aortic valve stenosis can also cause left-sided heart failure, but the murmur of aortic stenosis is diamond-shaped, loudest at the right sternal border, and radiates to the carotid arteries. Mitral valve stenosis is characterized by an opening snap after the S2 followed by a low-frequency decrescendo murmur (diastolic “rumble”). Significantmitral valve stenosis results in elevated left atrial pressure, secondary pulmonary hypertension, and, ultimately, right-sided heart failure. Because the left ventricle is protected from pressure or volume overload, mitral stenosis does not lead to left ventricular hypertrophy. The murmur of aortic valve regurgitation is an early blowing diastolic murmur heard loudest at the left sternal border. Chronic aortic regurgitation may lead to left ventricular enlargement and left-sided heart failure. The murmur of tricuspid valve regurgitation is systolic, loudest at the lower left sternal border, and becomes louder with inspiration. Significant tricuspid valve regurgitation will lead to right-sided heart failure but should not cause signs and symptoms of left-sided heart failure.

Key Point

  • Physical examination findings of mitral valve regurgitation include a holosystolic murmur at the apex that radiates to the axilla without respiratory variation.

Bibliography

    Otto CM. Clinical practice. Evaluation and management of chronic mitral regurgitation. N Engl J Med. 2001;345:740-6. [PMID: 11547744] [PubMed]

 

24

A 23-year-old woman who is 23 weeks pregnant is evaluated in the office because of a 2-month history of increasing shortness of breath. On physical examination, blood pressure is 100/60 mm Hg, heart rate is 88/min and regular, and respiration rate is 26/min. Jugular venous pressure is 18 cm H2O, carotid upstrokes are brisk, and bibasilar crackles are present. On cardiac examination, the apical impulse is faint in the mid left 6th intercostal space, and there is a forceful sternal heave. The S1 is loud, and there is fixed splitting of S2, a soft apical systolic murmur, and an opening snap followed by a grade 2/6 mid-diastolic murmur.

Which of the following is the most likely diagnosis?

A Aortic valve stenosis
B Mitral valve stenosis
C Normal findings of pregnancy
D Patent ductus arteriosus
E Peripartum cardiomyopathy

Answer and Critique (Correct Answer = B)

This patient has symptoms of mitral valve stenosis. Her physical examination shows a loud S1 due to the forceful closing of the stenotic mitral valve. The S2 has a fixed split due to accompanying pulmonary hypertension and a prolonged right ventricular ejection time. The classic findings of mitral stenosis, an opening snap and a low-pitched diastolic rumble, are often difficult to hear, particularly in a pregnant patient. The opening snap follows the S2 and has an audible quality similar to a normal S2. The opening snap may be mistaken for a split S2 unless it is recognized that the sound is loudest at the apex, instead of the base. Both the opening snap and the diastolic rumble are heard best with the bell of the stethoscope at the apex and are enhanced when the patient is in a left lateral decubitus position. Often accompanying mitral regurgitation is easier to hear. The diagnosis can be confirmed by echocardiography.

Mitral valve stenosis is more common in women than men, and the age at symptom onset varies worldwide. Patients are often asymptomatic until there is a superimposed hemodynamic stress, such as pregnancy.

Aortic valve stenosis is characterized by a loud systolic murmur at the cardiac base. Peripartum cardiomyopathy typically presents later in pregnancy; although physical examination findings of heart failure might be similar, peripartum cardiomyopathy is not associated with an opening snap or diastolic murmur. A patent ductus arteriosus results in a continuous cardiac murmur. In pregnancy, a basal systolic ejection murmur is normal, but signs of heart failure are definitely abnormal.

Key Points

  •  Classic findings of mitral stenosis include a loud S1 and an opening snap followed by a rumbling diastolic murmur.
  • Previously undiagnosed mitral stenosis often first becomes symptomatic during pregnancy.


Bibliography

    Carabello BA. Modern management of mitral stenosis. Circulation. 2005;112:432-7. [PMID: 16027271] [PubMed]

 

25

A 19-year-old woman is evaluated in the office for palpitations described as isolated “extra beats” that do not occur with any regularity. She has no history of syncope or presyncope, no cardiovascular risk factors, and no family history of cardiovascular disease. She does not have signs or symptoms of congestive heart failure and takes no medications.

On physical examination, vital signs are normal. Her lungs are clear. There is no S4 or S3. A grade 2/6 late systolic murmur is present that is heard best at the cardiac apex and radiates toward the left axilla. A midsystolic click is heard. Following a Valsalva maneuver and a squat-to-stand maneuver, the midsystolic click moves closer to the S1, but the intensity of the murmur does not change. The remainder of her examination is unremarkable.

Which of the following is the most likely diagnosis accounting for the heart murmur?

A. Benign (innocent) flow murmur
B. Hypertrophic cardiomyopathy
C. Mitral valve regurgitation
D. Mitral valve prolapse

Answer and Critique (Correct Answer = D)

The auscultatory feature of mitral valve prolapse is a “click-murmur” complex—a midsystolic click, thought to be from the sudden tensing of the mitral subvalvular apparatus as the leaflets prolapse into the left atrium, is followed by a late systolic murmur. The Valsalva maneuver and standing from a squatting position decrease end-diastolic volume and move the click-murmur complex closer to the S1.

Mitral valve prolapse occurs in approximately 2% of the general population and is the most common cause of mitral regurgitation. In the absence of significant mitral regurgitation, primary mitral valve prolapse is usually asymptomatic but can present with palpitations or atypical chest discomfort. Palpitations are common and are usually associated with benign premature atrial or ventricular contractions. Sustained arrhythmias are exceedingly rare.

Hypertrophic cardiomyopathy is associated with a harsh crescendo-decrescendo systolic murmur that begins slightly after S1 and is heard best at the apex and lower left sternal border. The Valsalva maneuver and standing from a squatting position increase the intensity of the murmur. The murmur of hypertrophic cardiomyopathy is the only murmur that increases in intensity with the Valsalva maneuver. Benign (innocent) flow murmurs are typically midsystolic grade 1–2/6 murmurs associated with normal heart sounds and no other findings. The presence of a click, an S4, abnormal splitting of S2, or increased intensity or duration of the murmur with the Valsalva maneuver or standing are not compatible with a benign (innocent) flow murmur. The murmur of mitral valve regurgitation begins shortly after S1 and ends just prior to S2 (holosystolic murmur). It is not associated with clicks, and the intensity is not increased with standing from a squatting position or with the Valsalva maneuver.

Key Points

  • The auscultatory feature of mitral valve prolapse is a midsystolic click followed by a late systolic murmur.
  • In mitral valve prolapse, the Valsalva maneuver and standing from a squatting position move the click-murmur complex closer to S1.


Bibliography

    Hayek E, Gring CN, Griffin BP. Mitral valve prolapse. Lancet. 2005; 365:507-18. [PMID: 15705461] [PubMed]