Section 11: MKSAP Flashcards
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.
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.
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]
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]
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]
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]
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]
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]
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]
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]
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]
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]
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]
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]
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]
