PANCE Exam: Cardiovascular Review Questions & Answers

CARDIOMYOPATHIES

Question: Which is the most common type of cardiomyopathy?
Dilated cardiomyopathy (dilation of all four chambers). This condition is often idiopathic but can be induced by progression of ischemia, myocarditis, alcohol consumption, Adriamycin, diabetes, pheochromocytoma, thiamine deficiency, thyroid disease, and valve replacement. The other type of cardiomyopathies are hypertrophic and restrictive.

Question: What is the abnormality seen in the 2-D echocardiogram shown in Figure 2-1?


Figure 2-1 (Reproduced, with permission, from Fuster V et al. Hurst’s The Heart. 12th ed. New York, NY: McGraw-Hill: 2008, Fig. 16-106.)
Hypertrophic cardiomyopathy. Note the very thickened septum.

Question: What drugs have been shown to regress LV hypertrophy and reduce LV mass?
Beta-blockers, alpha-methyldopa (Aldomet), ACE inhibitors, and thiazide diuretics.

What is the most common mechanism responsible for supraventricular tachycardia (SVT)?
AV node reentry.

Question: What are the common causes of SVT?
Myocardial ischemia, myocardial infarction, congestive heart failure, pericarditis, rheumatic heart disease, mitral valve prolapse, preexcitation syndromes, COPD, ethanol intoxication, hypoxia, pneumonia, sepsis, and digoxin toxicity.

Question: What are the physiologic characteristics of dilated cardiomyopathies?
Reduced ventricular ejection fraction, high end-diastolic filling volumes and pressures, reduced cardiac output, and high pulmonary capillary wedge pressures.

Question: What are the common clinical presentations that can occur with a dilated cardiomyopathy?
Fatigue, exertional dyspnea, and orthopnea. They commonly have an S3 and a LV/RV heave. Other presentations that could occur include mitral and/or tricuspid regurgitation, jugular venous distention, rales and edema, low voltage on EKG, and signs of cardiomegaly by CXR.

Question: What are the physiological aspects of restricted cardiomyopathy?
Normal systolic contractility, reduction in diastolic relaxation and filling capacity, high LV end-diastolic filling pressures, and high pulmonary wedge pressures especially with exercise.

Question: What are the common causes of restrictive cardiomyopathy?
Most are idiopathic but other causes include infiltrative diseases, e.g., sarcoid and amyloid, and storage diseases, e.g., hemochromatosis. Other potential causes include radiation exposure and cancer.

Question: What are the common clinical presentations associated with restrictive cardiomyopathy?
Symptoms are very similar to dilated cardiomyopathy with fatigue, exertional dyspnea, and orthopnea but could present with syncope/near syncope and palpitations. Restrictive cardiomyopathy is more likely to have an S4 as opposed to S3. The symptoms often present with a resting tachycardia and typically will not show signs of cardiomegaly on CXR.

Question: What is hypertrophic cardiomyopathy?
It is a genetic disorder resulting in abnormal hypertrophy of the ventricular walls. It often results in asymmetric hypertrophic changes, which can create outlet obstruction. Typically, there is normal LV systolic contractility but increased diastolic stiffness resulting in reduced LV filling volumes. Patients often present with high pulmonary capillary wedge pressures and pulmonary hypertension.

Question: What are the common clinical presentations of hypertrophic cardiomyopathy?
In young patients, clinical signs and symptoms may be difficult to ascertain. Commonly, they may present with complaints of palpitations, chest pain, dyspnea, syncope, or dizziness. Sudden death is not an uncommon presentation for this disorder. Resting tachycardia is common.

Question: What are the key management options for patients with hypertrophic cardiomyopathy?
Patients may be advised to avoid vigorous physical activity. Avoid preload and afterload reducing agents and positive inotropes such as digoxin. Beta-blockers and calcium channel blockers may be used to slow the heart rate. Myomectomy and septal ablation by catheter or chemical means may be needed to decrease outflow tract obstruction. ICDs are often considered because of the increased risk for ventricular dysrhythmias in these patients. Also, the immediate family should be screened for undiagnosed individuals at risk.


CONDUCTION DISORDERS

Question: What are the common causes of multifocal atrial tachycardia?
COPD, CHF, sepsis, valvular heart disease, and methylxanthine toxicity. Treat the arrhythmia with magnesium, verapamil, or beta-blocking agents.

Question: How is atrial flutter treated?
Initiate AV nodal blockade with beta-blockers, calcium channel blockers, or digoxin. If necessary, treat a stable patient with chemical cardioversion by using a class IA agent, such as procainamide or quinidine, after digitalization. If this treatment fails or if the patient is unstable, electrocardiovert at 25 to 50 J.

Question: What are some causes of atrial fibrillation?
Hypertension, rheumatic heart disease, pneumonia, thyrotoxicosis, ischemic heart, pericarditis, ethanol intoxication, PE, CHF, valvular heart disease, and COPD.

Question: How is atrial fibrillation treated?
Control rate with beta-blocker or calcium channel blocker (such as verapamil or diltiazem), and then convert with procainamide, quinidine, or verapamil. Digoxin may be considered, although its effect will be delayed. Synchronized cardioversion at 100 to 200 J should be performed on an unstable patient. In a stable patient with a-fib of unclear duration, anticoagulation should be considered for 3 weeks prior to chemical or electrical cardioversion. A transesophageal echocardiogram is commonly used to determine the timing of cardioversions. Watch for hypotension with the administration of negative inotropes.

Question: What is the treatment of SVT caused by digitalis toxicity?
Stop the digitalis, treat hypokalemia, and administer magnesium or phenytoin. Provide digoxin-specific antibodies to the unstable patient. Avoid cardioversion.

Question: What is the treatment for stable SVT not caused by digitalis toxicity or WPW syndrome?
Vagal maneuvers, adenosine, verapamil, or beta-blockers.

Question: Describe the key feature of Mobitz I (Wenckebach) second-degree AV block:
A progressive prolongation of the PR interval until the atrial impulse is no longer conducted. If symptomatic, atropine and transcutaneous/transvenous pacing may be required.

Question: Describe the key feature of Mobitz II second-degree AV block:
A constant PR interval in which one or more beats fail to conduct.

What is the treatment for Mobitz II second-degree AV block?
Atropine and transcutaneous/transvenous pacing, if symptomatic.

Question: Carotid massage or Valsalva maneuver is useful for slowing supraventricular rhythms. When is carotid massage contraindicated?
With ventricular dysrhythmias, digitalis toxicity, stroke, syncope, seizures, known carotid artery disease, or in those with a carotid bruit.

Question: What are some common vagal maneuvers?
Breath holding, Valsalva (bearing down as if having a bowel movement), stimulating of the gag reflex, squatting, pressure on the eyeballs, and immersing the face in cold water.

Question: What is more common: premature atrial beats or ventricular beats?
Premature atrial beats. Palpitations that occur because of premature atrial beats are generally benign and asymptomatic. Reassurance is the only treatment. Less frequent but more serious causes of atrial premature beats include pheochromocytoma and thyrotoxicosis. Random unifocal PVCs are also benign but common in the general population. Runs of PVCs and/or associated symptoms of dyspnea, angina, or syncope require investigation and are most likely related to an underlying heart disease.

Question: How do the fixed-rate demand modes of pacemakers differ?
Fixed-rate mode produces an impulse at a continuous specific rate, regardless of the patient’s own cardiac activity. Demand mode detects the patient’s electrical activity and triggers only if the heart is not depolarizing.

Question: What is the treatment for ventricular fibrillation in a patient with a pacemaker?
Defibrillation, but be sure to keep the paddles away from the pacemaker.

Question: What is the average lifespan of a pacemaker battery?
7 to 15 years.

Question: What are the most common causes of MAT (multifocal atrial tachycardia)?
COPD with exacerbation is the most common cause, followed by CHF, sepsis, and methylxanthine toxicity. Treatment consists of treating the underlying disorder as well as the use of verapamil, magnesium, or digoxin for slowing the arrhythmia.

Question: What are the most common causes of atrial fibrillation?
Coronary artery disease with myocardial ischemia and hypertensive heart disease are the most common causes. Other common causes are mitral or aortic valvular heart disease, cor pulmonale, dilated cardiomyopathy, hypertrophic cardiomyopathy (particularly the obstructive type), alcohol intoxication or “holiday heart syndrome,” hypo- or hyperthyroidism, pulmonary embolism, sepsis, hypoxia, preexcitation syndrome, and pericarditis.

How is atrial fibrillation treated?
The treatment of atrial fibrillation consists of three major considerations:

1. Control of ventricular rate
2. Conversion, if possible or feasible, to sinus rhythm
3. Prevention of thromboembolic events, particularly CVA
Rate control is best managed with beta-adrenergic blocker or calcium channel blockers (diltiazem or verapamil), or less desirable, digoxin. Digoxin should be used in patients with poor LV systolic function and those with a contraindication to beta-blockers and calcium channel blockers. Digoxin provides good rate control at rest, but often suboptimal rate control during exertion. For conversion to sinus rhythm, in the stable patient with a duration of symptoms <48 hours, it is best managed, initially, with antiarrhythmic agents (amiodarone, ibutilide, propafenone, or procainamide). In the unstable patient or the patient with acute ischemia, hypotension or pulmonary edema, immediate synchronized electrical cardioversion, starting at 200 J should be performed without interruption of antiarrhythmic therapy. Patients with atrial fibrillation of 1 year duration or longer, or those with left atrial size of >5.0 cm on echocardiography cardioversion, are not recommended this therapy because of its low success rate. Patients with recent atrial fibrillation >2 days duration should be started on warfarin and anticoagulated to an INR between 2 and 3 for at least 3 weeks, before any attempt to cardiovert to sinus rhythm because of the significant risk for embolic CVA. Earlier cardioversion attempts could be considered if the patient is at adequate anticoagulation levels and no evidence of intrachamber thrombus by transesophageal echocardiography. Those patients with chronic atrial fibrillation should be on lifelong warfarin unless an absolute contraindication to warfarin exists or the patient cannot reliably take warfarin.

Question: What percentage of patients with atrial fibrillation converted to sinus rhythm will revert into atrial fibrillation?
50% will revert to atrial fibrillation within 1 year of cardioversion, regardless of medical therapy.

Question: What is the risk of CVA in patients with atrial fibrillation, with or without anticoagulation?
Patients with atrial fibrillation, not anticoagulated with warfarin, have a 25% incidence of CVA within 5 years (5% per year). Those patients anticoagulated to therapeutic levels have a 4% incidence of CVA within 5 years (0.8%). Aspirin is a clearly inferior substitute to warfarin, but is much more preferable to no anticoagulant or antithrombotic therapy.

Question: What is the key feature of Mobitz I second-degree AV block (Wenckebach)?
A progressive prolongation of the PR interval until the atrial impulse is no longer conducted through to the ventricle, resulting in a dropped QRS. Almost always transient, atropine and transcutaneous/transvenous pacing is required for the rare instances of symptoms or cardiac stability.

Question: What is the feature of Mobitz II second-degree AV block?
A constant PR interval until one sinus beat fails to conduct through the ventricle, resulting in a dropped QRS. Since this rhythm is indicative of His bundle damage, and 85% of patients with this rhythm eventually develop complete heart block, temporary pacing followed by permanent pacing is usually required.

A 57-year-old man is scheduled for a total colectomy for ulcerative colitis. He has stable angina for several years and has hypertension. His pre-op EKG reveals NSR, LVH, and first-degree AV block. What is the likelihood of high-degree AV block occurring in the perioperative period?
Patients with first-degree AV block have an extremely low incidence of developing high-degree AV block in the perioperative period. Thus, no temporary pacing in the perioperative period is required.

Question: A 26-year-old man presents to your clinic for an insurance physical. An EKG reveals Wolff-Parkinson-White syndrome. He is asymptomatic and has no history of palpitations or arrhythmia. What is the most appropriate management of this patient?
No therapy or work-up is required at this time since there is no evidence that the risk of sudden death can be safely mitigated or that individuals with asymptomatic WPW can be reliably risk stratified with regard to sudden death.

Question: What is the most commonly occurring form of ventricular tachycardia?
Ventricular tachycardia (VT) occurring in patients with healed myocardial infarction. Other causes include bundle branch reentry VT, VT of right ventricular outflow tract origin, idiopathic left ventricular tachycardia, drug-induced VT (proarrhythmia), and VT due to right ventricular dysplasia. Rare causes include long QT syndrome and lymphocytic myocarditis.

Question: A 48-year-old male patient with no history of angina, MI, or other cardiac symptoms is referred to you for evaluation of palpitations. A 24-hour Holter monitor reveals 4 three-beat runs of ventricular tachycardia without any symptoms. The patient has no risk factors for coronary artery disease, is not a smoker, and has a normal resting EKG. His echocardiogram is normal. What is the best management strategy for this patient?
No therapy or further work-up is required. The patient should be reassured that the risk of sudden death is very low and that medical therapy will either worsen his arrhythmia or be of no significant benefit.

Question: A 28-year-old male patient with two previous episodes of palpitations and shortness of breath in the last year is brought in the emergency department by EMS presenting with severe palpitations, hypotension, and shortness of breath. His BP is 90/55 and HR is 195 bpm. A rhythm strip reveals narrow complex QRS tachycardia. A 12-lead EKG reveals what appears to be atrial fibrillation. Synchronized cardioversion is successful in terminating the arrhythmia, and the postcardioversion EKG reveals Wolff-Parkinson-White syndrome. What is the most appropriate management strategy in this patient?
Electrophysiology testing with intracardiac mapping, followed by catheter ablation of the accessory conduction pathway.

Question: A 67-year-old woman with severe three-vessel coronary artery disease with very small distal vessels, deemed inoperable, is brought into the emergency department following a syncopal episode. The paramedics caught the final beats of what looked like a wide-complex QRS tachycardia on a rhythm strip and you confirm this on inspection of the tracing. She is now awake, alert, and breathing comfortably. An echocardiogram performed 1 month ago revealed a dilated left ventricle with poor systolic function (estimated ejection fraction is 20%–25%). What is the most appropriate management strategy for this patient?
Empiric therapy with amiodarone.

What medications, used to maintain sinus rhythm in a patient recently cardioverted from atrial fibrillation, should be avoided in patients with stress test proven myocardial ischemia?
Class IC antiarrhythmics, such as flecainide and propafenone, and class IA agents, such as quinidine and procainamide. They can lead to lethal proarrhythmia in patients with active myocardial ischemia. Amiodarone, an agent that has anti-ischemic properties, is the preferred agent.

Question: What drugs can increase serum digoxin levels?
Quinidine, procainamide, verapamil, and amiodarone.

Question: What are the end points in procainamide loading infusion for patient with unstable VT?
Hypotension, QRS widened more than 50% of pretreatment width, arrhythmia suppression, or a total of 17 mg/kg.

Question: If a defibrillator is available, what is the immediate treatment of a patient with ventricular fibrillation?
Unsynchronized countershock at 200 J (biphasic) or 360 J (monophasic).

Question: What is the differential diagnosis for pulseless electrical activity (PEA)?
- Hypoxia/hypovolemia/hyper- or hypokalemia/hyperthermia
- Acute MI/acidosis
- Tension pneumothorax/tamponade/thrombosis (pulmonary)/tablets (drug overdose)

Question: What is the differential diagnosis of asystole?
Drug overdose, acidosis, hyperkalemia, hypothermia, hypokalemia, and hypoxia.

Question: What is the treatment for unstable supraventricular tachycardia?
Synchronized cardioversion.

Question: A patient in the emergency department suddenly demonstrates ventricular fibrillation on the monitor. The patient is alert and has a pulse. What should you do?
Check the monitor leads.

Question: Inferior wall MIs commonly lead to what two types of heart block?
First-degree AV block and Mobitz I second-degree AV block (Wenckebach). Sinus bradycardia can also occur. Progression to complete AV block is not common. The mechanism for this is damage to autonomic fibers in the atrial septum giving increased vagal tone impairing AV node conduction.

Question: Anterior wall MIs may directly damage intracardiac conduction. This may lead to which type of arrhythmias?
A Mobitz II second-degree AV block that can suddenly progress to complete AV block.

Question: Which type of drug is contraindicated for the treatment of Torsades de pointes?
Any drug that prolongs repolarization (QT interval). For example, class IA antiarrhythmics, such as quinidine and procainamide, are contraindicated for treating torsades de pointes. Other drugs that share this effect include TCAs, disopyramide, and phenothiazine.

What is this cardiac arrhythmia shown in Figure 2-2?


Figure 2-2
Atrial fibrillation.

Question: What is the cardiac arrhythmia seen in Figure 2-3?


Figure 2-3
Accelerated junctional rhythm with retrograde P waves.

Question: What is the cardiac arrhythmia seen in Figure 2-4?


Figure 2-4
Ventricular pacemaker rhythm.

What is the cardiac arrhythmia seen in Figure 2-5?


Figure 2-5 (Reproduced, with permission, from Stone CK, Humphries RL. Current Diagnosis & Treatment Emergency Medicine. 6th ed. New York, NY: McGraw-Hill, 2008, Fig. 33-28.)
Mobitz type II second-degree AV block.

Question: What is the EKG rhythm abnormality seen in Figure 2-6?


Figure 2-6
Ventricular tachycardia degrading into ventricular fibrillation.

Question: What is the cardiac arrhythmia seen in Figure 2-7?


Figure 2-7
Atrial tachycardia with 2:1 conduction.

What is the abnormality seen in the EKG in Figure 2-8?


Figure 2-8
Multifocal atrial tachycardia.

Question: What is the abnormality seen in the EKG in Figure 2-9?


Figure 2-9
Junctional rhythm.

Question: What is the abnormality seen in the rhythm strip in Figure 2-10?


Figure 2-10
Junctional rhythm with escape ventricular beat.

What is the abnormality seen in the rhythm strip in Figure 2-11?


Figure 2-11
Idioventricular rhythm.

Question: What is the abnormality seen in the rhythm strip in Figure 2-12?


Figure 2-12 
2:1 AV block.

What is the abnormality seen in the rhythm strip in Figure 2-13?


Figure 2-13
Atrial flutter.

Question: What is the abnormality seen in the rhythm strip in Figure 2-14?


Figure 2-14
Rhythm strip erroneously mounted upside down. When viewed with right side up, it shows normal sinus rhythm.

Question: What is the abnormality seen in the rhythm strip in Figure 2-15?


Figure 2-15
Ventricular fibrillation.

What is the interpretation of the EKG shown in Figure 2-16?


Figure 2-16
Ventricular tachycardia.

Question: What is the interpretation of the EKG shown in Figure 2-17?


Figure 2-17
Ventricular tachycardia with hyperkalemia. Note the very wide QRS complex with the early stages of a “sine wave.”

What is the interpretation of the EKG shown in Figure 2-18?


Figure 2-18
Acute inferior myocardial infarction with posterior wall involvement, and atrial fibrillation with slow ventricular rate.

Question: What is the interpretation of the EKG shown in Figure 2-19?


Figure 2-19
Atrial fibrillation with rapid ventricular rate of 155 bpm, LVH, and ischemic-type ST depression in the inferior and lateral leads.

What is the interpretation of the EKG shown in Figure 2-20?


Figure 2-20
Acute inferior myocardial infarction and atrial fibrillation with slow ventricular rate.

Question: In the EKG shown in Figure 2-20, does the patient absolutely have myocardial ischemia?
Not necessarily. Patients with supraventricular tachycardia of any type with ST depression can have “ischemic” appearing ST depression without having myocardial ischemia. The ST depression can be as a result of abnormal repolarization that occurs in any tachydysrhythmia. Nonetheless, it would be incorrect to automatically assume that this patient’s ST depression is not due to myocardial ischemia.

What is the interpretation of the EKG shown in Figure 2-21?


Figure 2-21
Ventricular tachycardia with a ventricular rate of 103 bpm. Note the VA conduction evidenced by the retrograde P waves, which occur in the early part of the ST segment.

Question: What is the interpretation of the EKG shown in Figure 2-22?


Figure 2-22
Ectopic atrial rhythm with an old inferior infarction and nonspecific ST-T abnormality.

What is the interpretation of the EKG shown in Figure 2-23?


Figure 2-23
Idioventricular rhythm (rate of 40 bpm).

Question: What is the interpretation of the EKG shown in Figure 2-24?


Figure 2-24
Supraventricular tachycardia.

How do you treat ventricular fibrillation and pulseless ventricular tachycardia?
Defibrillate at 360 J monophasic for the first and subsequent shocks. Continue CPR with an emphasis on chest compressions to respirations at a 30:2 ratio for 2 minutes between shocks. Epinephrine should be given at 1 mg IV/IO every 3 to 5 minutes or vasopressin 40 IU IV/IO × once and in place of the first two doses of epinephrine. Consider antidysrhythmic medications such as amiodarone 300 mg IV/IO or lidocaine (if amiodarone is not available) at 1 to 1.5 mg/kg.

Question: How do you treat pulseless electrical activity?
Treat the underlying causes first (hypovolemia, hypoxia, hyper/hypokalemia, hypothermia, acidosis, acute MI, tamponade (cardiac), tension pneumothorax, thrombus (pulmonary), and drug overdose). If unknown cause or unsuccessful attempts to treat underlying cause, then give 1 mg of epinephrine IV/IO every 3 to 5 minutes or vasopressin 40 U IV/IO once and in place of the first two epinephrine doses. Atropine can be attempted for slow rates at 1 mg IV/IO every 3 to 5 minutes up to 3 mg maximum.

Question: How do you treat stable, narrow complex, paroxysmal supraventricular tachycardia?
First attempt vagal maneuvers; but if there is no success, then use adenosine 6 mg rapid IV push (this can be repeated two more times up to 12 mg if needed). If adenosine fails and the ventricular function is preserved (EF >40), then use diltiazem. Other drugs could include beta-blockers, digoxin, DC cardioversion, procainamide, amiodarone, and sotalol. If the ventricular function is compromised (EF <40), then do not attempt cardioversion but attempt chemical conversion with diltiazem, amiodarone, or digoxin.


CONGESTIVE HEART FAILURE

Question: Which is the most common type of cardiac failure: high or low output?
Low output failure. Reduced stroke volume, lowered pulse pressure, and peripheral vasoconstriction are all signs of low output failure.

Question: What is the most common cause of low output heart failure in the United States?
Coronary artery disease. Other causes include congenital heart disease, cor pulmonale, dilated cardiomyopathy, hypertension, hypertrophic cardiomyopathy, infection, toxins, and valvular heart disease.

Question: Compare the mortality rate from CHF between men and women:
Women fare slightly better. The 5-year mortality rate for women with CHF is 45% as compared to 60% for men. The majority of deaths from CHF result from ventricular dysrhythmias.

Question: Describe the three stages of chest radiographic findings in CHF:
Stage I: Pulmonary arterial wedge pressure (PAWP) of 12 to 18 mm Hg. Blood flow increases in the upper lung fields (cephalization of pulmonary vessels).
Stage II: PAWP of 18 to 25 mm Hg. Interstitial edema is evident with blurred edges of blood vessels and Kerley B lines.
Stage III: PAWP >25 mm Hg. Fluid exudes into alveoli with the generation of the classic butterfly pattern of perihilar infiltrates.

What do nitrates affect: preload or afterload?
Predominantly preload.

Question: What does hydralazine affect: preload or afterload?
Afterload.

Question: Do captopril, nifedipine, and prazosin affect afterload?
Yes.

Question: When is dobutamine used in congestive heart failure?
When heart failure is not accompanied with severe hypotension. Dobutamine is a potent inotrope with some vasodilation activity.

Question: When is dopamine selected in congestive heart failure?
When a patient is in shock. Dopamine is a vasoconstrictor and a positive inotrope.

Question: What is the most common cause of right heart failure?
Left ventricular heart failure.

Question: Match the sign or symptom with the most likely associated type of heart failure—left (L) or right (R):

1. Hypotension
2. Hepatomegaly
3. Orthopnea
4. Cough
5. Dyspnea on exertion
6. Abdominal distention
7. Paroxysmal nocturnal dyspnea
8. Hemoptysis
9. S3 gallop
10. Early satiety
11. Jugular venous distention
12. Ascites
13. Rales
(1) L, (2) R, (3) L, (4) L, (5) L, (6) R, (7) L, (8) L, (9) L, (10) R, (11) R, (12) R, (13) L.


HYPERTENSION

Question: What hypertensive medications should be used with caution in diabetic patients?
Diuretics and beta-blockers should be used with caution because they may increase insulin resistance. If considered for the management of hypertension, they should not be a choice for first-line agent and be chosen only if there is a compelling indication such as heart failure or synergistic blood pressure management. ACE inhibitors and ARBs are the preferred first-line drugs of choice in diabetic patients.

Question: What antihypertensive class is most likely to present with a cough as a side effect?
ACE inhibitors may cause a dry, persistent cough in up to 15% of patients who use them.

What percentage of hypertension is secondary?
Approximately 5%. Secondary hypertension should be suspected in patients younger than 35 years, those with sudden-onset hypertension, and those without a family history for hypertension.

Question: What is the most common cause of secondary hypertension?
Renal parenchymal disease. In women, the most common cause is oral contraceptives. In patients older than 50 years, secondary hypertension can usually be contributed to renal artery stenosis. Other causes include pheochromocytoma, coarctation of the aorta, drugs (such as cocaine), hyperthyroidism, aldosteronism, and Cushing disease.

Question: What percentage of patients with aortic dissection are hypertensive?
70% to 90%.

Question: What percentage of hypertensive patients are afflicted with left ventricular hypertrophy?
50%. This is the primary reason that hypertension is a major risk factor for MI, CHF, and sudden death.

Question: What are the side effects of thiazide diuretics?
Hyperglycemia, hyperlipidemia, hyperuricemia, hypokalemia, hypomagnesemia, and hyponatremia.

Question: Which drugs should be administered to lower the BP in a patient with thoracic aortic dissection?
Sodium nitroprusside. A beta-blocker should also be used to reduce the dp/dt (propagation speed).

Question: A patient has a history of episodic blood pressure elevations. She complains of headache, diarrhea, and skin pallor. Probable diagnosis?
Pheochromocytoma.

Question: What is the most common complication of nitroprusside?
Hypotension. Thiocyanate toxicity accompanied by blurred vision, tinnitus, change in mental status, muscle weakness, and seizures is more prevalent in patients with renal failure or prolonged infusions. Cyanide toxicity is uncommon. However, this type of toxicity may occur with hepatic dysfunction, after prolonged infusions, and in rates greater than 10 mg/kg/min.

Question: Define a hypertensive emergency:
In general, a blood pressure of ≥180/115 with evidence of end organ dysfunction or damage.

Question: How quickly should a patient’s blood pressure be lowered in a hypertensive emergency?
Gradually over 2 to 3 hours to 140–160 systolic and 90–110 diastolic. To prevent cerebral hypoperfusion, the blood pressure should not be decreased by more than 25% of the mean arterial pressure.

What drug is preferred for treatment of a hypertensive emergency?
Sodium nitroprusside. It assists in relaxing smooth muscle tissue through the production of cGMP. As a result, there is decreased preload and afterload, decreased oxygen demand, and a slightly increased heart rate with no change in myocardial blood flow, cardiac output, or renal blood flow. The duration of action is 1 to 2 minutes. Sometimes, beta-blocker is required to treat rebound tachycardia.

Question: Define a hypertensive urgency:
In general, a blood pressure of ≥180/115 without evidence of end organ dysfunction or damage. Blood pressure reduction in these individuals should be done gradually over 24 to 48 hours.

Question: What laboratory findings can assist in confirming end organ compromise in a hypertensive emergency?
- Urinalysis: RBCs, red cell casts, and proteinuria
- BUN and CR: Elevated
- X-ray: Cardiomegaly, aortic dissection, pulmonary edema, or coarctation of aorta
- EKG: LVH and cardiac ischemia

Question: What are the signs of symptoms of hypertensive encephalopathy?
Nausea, vomiting, headache, lethargy, coma, blindness, nerve palsies, hemiparesis, aphasia, retinal hemorrhage, cotton wool spots, exudates, sausage linking, and papilledema. Treat with labetalol or sodium nitroprusside and lower the mean arterial pressure to approximately 120 mm Hg.

Question: What is the first-line pharmacologic therapy for a 40-year-old obese white woman with uncomplicated mild hypertension?
ACE inhibitors or a thiazide diuretic. Beta-blockers, ARBs, or calcium channel blockers could be considered if contraindications to ACEI or diuretics.

Question: What is the preferred choice of antihypertensive therapy for a 58-year-old white man with severe COPD and mild hypertension?
Long-acting calcium channel blockers such as amlodipine, diltiazem, or nifedipine. These agents are particularly useful in patients with a likelihood of pulmonary hypertension. If pulmonary hypertension is suspected, verapamil should be avoided because of its significant negative inotropic effects.

Question: What is the agent of choice in diabetic patients with hypertension?
ACE inhibitors or ARBs.

Question: Which agent is more likely to cause bradycardia: verapamil or diltiazem?
Diltiazem. Diltiazem blocks conduction through both the SA and AV node, whereas verapamil blocks only the AV node.

Question: What antihypertensive agents are preferred agents to use in a 63-year-old obese, African American man?
Calcium channel blockers. Diuretics and/or ACE inhibitors can be considered too.

What is the most common side effect of esmolol, labetalol, and bretylium?
Hypotension.

Question: What side effect can occur with a rapid infusion of procainamide?
Hypotension. Other side effects include QRS/QT prolongation, ventricular fibrillation, and torsades de pointes.

Question: What is one of the most common side effect of antihypertensive medications that patients should be warned about?
Orthostatic hypotension

Question: How long can ST and T wave changes persist after an episode of pain in unstable angina?
Several hours.

Question: What are the diagnostic criteria for a Q wave?
More than 0.04 seconds and at least one-quarter the size of the R wave in the same lead. Beware, EKGs can be normal in up to 10% of all acute MIs.

Question: What is the cause of Prinzmetal angina?
Coronary artery vasospasm with or without fixed stenotic lesions. Prinzmetal angina is more often associated with ST segment elevation than with depression. Calcium channel blockers are the drugs of choice to treat this condition. Beta-blockers are contraindicated in patients with vasospasm without fixed stenotic lesions.

Question: Eighty to ninety percent of patients who experience sudden nontraumatic cardiac death are in what rhythm?
Ventricular fibrillation. Early defibrillation is the key. In an acute MI, the infarction zone becomes electrically unstable. Ventricular fibrillation is most common during original coronary occlusion or when the coronaries begin to reperfuse.

Question: What is the rate of restenosis after percutaneous transluminal coronary angioplasty (PTCA)?
20% to 30% within the first 6 months, but bare metal and drug-eluding stents have greatly reduced restenosis rates. PTCA is now rarely used by itself but commonly used prior to stent placement.

Question: What two drugs are commonly used to reduce thrombosis formation in a patient who has received an intracoronary stent?
Aspirin and clopidogrel.

Question: What is the restenosis rate of coronary vessels following a coronary artery bypass graft (CABG)?
When using venous grafts, there is a 50% restenosis rate within 5 to 10 years. When an artery is used, such as the internal mammary artery, the restenosis rate drops to 5% at 10 years. Occlusion of the grafts is caused by anastomy, trauma to the vessel, postoperative adhesions, or atherosclerosis.

How are acute MI, angina pectoralis, and Prinzmetal angina differentiated?
The pain is similar but typically differs in radiation, duration, provocation, and palliation. Obtaining an accurate history is the most important tool for diagnosing chest pain.
- Angina pectoralis is aggravated by exercise, cold, and excitement but is relieved with rest and nitroglycerin.
- Prinzmetal angina occurs at rest during normal activity, and generally at night or in the early morning. It lasts longer than angina pectoralis.
- Acute MIs produce pain with a greater radius of radiation that may last for hours.

Question: Which type of myocardial infarction is more often associated with thrombosis: transmural or subendocardial?
Transmural. Thrombolytic therapy increases left ventricular ejection fraction post-MI, reduces the development of postinfarction CHF, and can reduce early MI mortality by 25%.

Question: How much aspirin should a post-MI patient take daily to reduce the incidence of reinfarction?
75 to 150 mg daily.

Question: What is the most common cause of death during the first few hours of a MI?
Cardiac dysrhythmias, generally ventricular fibrillation.

Question: When treating early MIs, beta-blockers decrease the risk of reinfarction. Which patients should not receive beta-blockers?
Patients presenting with hypotension, congestive heart failure, severe left ventricular dysfunction, AV block, bradycardia, asthma, or other bronchospastic disease.

Question: How common are PVCs in post-MI patients?
90% will have PVCs within the first few weeks. Concern arises if the PVCs are complex, which is the case in 20% to 40% of MI patients. Risk of sudden death in post-MI patients with complex PVCs increases two to five times.

Question: What percentage of the LV myocardium must be damaged to induce cardiogenic shock?
40%. Twenty-five percent or greater damage to the heart typically results in heart failure.

Question: What percentage of MIs are clinically unrecognized?
5% to 10%.

Question: A non–Q-wave infarction is usually associated with what?
Subsequent angina or recurrent infarction. Non–Q-wave infarctions also have lower in-hospital mortality rate compared to Q-wave MIs.

Question: Why do T waves invert in an acute myocardial infarction?
Infarction or ischemia causes a reversal of the sequence of repolarization, i.e., endocardial-to-epicardial as opposed to normally epicardial-to-endocardial.

What EKG changes arise in a true posterior infarction?
Large R wave and ST depression in V1 and V2.

Question: What conduction defects commonly occur in an anterior wall MI?
The dangerous kind. Damage to the conducting system results in a Mobitz type II second- or third-degree AV block.

Question: How should PSVT be treated during an acute myocardial infarction?
Adenosine, cardioversion, or vagal maneuvers could be attempted. Stable patients may be able to tolerate negative inotropes such as calcium channel blockers (verapamil) or even beta-blockers.

Question: A patient presents 1 day after discharge for an acute myocardial infarction with a new harsh systolic ejection murmur along the left sternal border and pulmonary edema. What is the diagnosis?
Ventricular septal rupture. Diagnosis is made by either a Swan-Ganz catheterization or echocardiogram. These patients often present with cardiogenic shock.

Question: When does cardiac rupture usually occur in patients who have suffered acute MIs?
50% arise within the first 5 days and 90% occur within the first 14 days post-MI.

Question: Which type of infarct commonly leads to papillary muscle dysfunction?
Inferior wall MI. Signs and symptoms include a mild transient systolic murmur and pulmonary edema.

Question: A patient presents 2 weeks post–acute MI with chest pain, fever, and pleuropericarditis. A pleural effusion is detected on chest radiography. What is the diagnosis?
Dressler (post–myocardial infarction) syndrome. This syndrome is caused by an immunologic reaction to myocardial antigens.

Question: What percentage of patients older than 80 years experience chest pain with an acute myocardial infarction?
Only 50%. Twenty percent experience diaphoresis, stroke, syncope, and/or acute confusion.

Question: What three secondary processes resulting in myocardial deterioration occur following acute myocardial infarction?
Ventricular remodeling, typically following Q-wave infarctions; infarct expansion, occurring most frequently from anteroapical infarctions and results in thinning of the left ventricular wall; and ventricular dilatation, an early and progressive response to acute myocardial infarction that is an important predictor of increased mortality following myocardial infarction.

Question: What is the most common cause of death related to acute myocardial infarction?
Ventricular fibrillation, usually occurring within the first hour following symptoms.

What percentage of patients with acute myocardial infarction develop cardiogenic shock?
10%.

Question: What percentage of arteries successfully opened with thrombolytic therapy for acute myocardial infarction, reocclude?
15% of arteries successfully opened reocclude during the first few days following thrombolytic therapy.

Question: What is the mortality benefit from aspirin alone in acute myocardial infarction with thrombolytic therapy and in subsequent reinfarction?
Aspirin reduced mortality from acute myocardial infarction by 23% and reduced nonfatal reinfarction by 49%. When used with thrombolytic therapy, there was a 40% to 50% reduction in mortality from acute myocardial infarction.

Question: A 63-year-old man presents to the emergency department with moderate substernal chest pressure and lightheadedness for 90 minutes. His BP on admission is 80/40 and his HR is 110 bpm and regular. Physical examination reveals JVD to the angle of the jaw, a right parasternal S3 gallop, an apical S4 gallop, and clear lungs on auscultation. EKG reveals 2 mm ST elevation in leads II, III, and aVF with reciprocal ST depression in V1 through V3. What is the most likely diagnosis and what is the most appropriate initial therapy?
Inferior wall myocardial infarction with right ventricular infarction. Initial therapy includes 160 to 325 mg of aspirin administration, thrombolytic therapy, and a large bolus of intravenous saline followed by a moderately high infusion rate of saline. If the patient remains hypotensive despite adequate infusion of saline (typically measured by development of lung congestion on auscultation), then intravenous dobutamine is indicated.

Question: A 70-year-old man is admitted to the hospital with chest pain of 3 hours duration. EKG demonstrates anterior ST elevation for which he is given aspirin, r-TPA, heparin, and intravenous nitroglycerin. His symptoms resolve. Serum chemistries reveal a peak CPK of 1800 and CK-MB fraction of 15%. The patient is eventually transferred out of the CCU and his hospitalization is uneventful until day 5, when he develops sudden, severe shortness of breath. BP is 110/75 and his pulse is 125 bpm and regular. Examination reveals a new systolic murmur. What would the most appropriate therapeutic intervention be?
Intravenous sodium nitroprusside. This patient is most likely suffering from rupture of the left ventricular septum and subsequent defect—a not uncommon complication of MI. Afterload reduction is key to stabilization until surgical repair of the VSD can be performed, usually in about 8 to 12 weeks, after the infarct has healed. If nitroprusside fails to stabilize the patient, intra-aortic balloon counterpulsation and intravenous nitroglycerin should be employed.

Question: A 60-year-old patient suffers an acute inferior myocardial infarction. Three hours after he arrives in the hospital, he develops ventricular fibrillation and is successfully defibrillated back to normal sinus rhythm within 30 seconds. He makes a full recovery and has no further post-MI complications. What does his ventricular fibrillation episode indicate with regard to subsequent risk for sudden death?
This episode has no bearing on his subsequent risk of sudden death. Ventricular fibrillation in the immediate setting of an acute myocardial infarction has no prognostic significance.

A 65-year-old female patient presents to the hospital with sudden crushing chest discomfort and moderate shortness of breath. Her initial EKG reveals 2 mm ST depression in leads V1 through V4 and inverted T waves. She has bibasilar rales in the lower half of both lungs on auscultation. CXR reveals moderate pulmonary edema. Serial EKGs, CPKs, and troponins confirm a non–Q-wave myocardial infarction. With diuretics, her pulmonary edema resolves within 24 hours. What is the most appropriate management strategy at this point?
Cardiac catheterization with coronary angiography. A non–Q-wave MI that results in pulmonary edema signifies a larger amount of myocardium at risk for reinfarction within the next year.

Question: What arrhythmias that occur in patients with acute myocardial infarction require temporary pacing?
Complete heart block; new left bundle branch block; new bifascicular block; marked sinus bradycardia with ischemic pain, hypotension, CHF, frequent PVCs or syncope despite atropine; and Mobitz II second-degree AV block.

Question: A 54-year-old man, admitted 2 days ago with an acute anterolateral myocardial infarction, suddenly develops atrial fibrillation with a ventricular rate of 135 bpm. He subsequently complains of substernal chest discomfort. His BP is 135/70. What is the most appropriate immediate action to be taken?
Synchronized DC cardioversion.

Question: What percentage of patients with acute myocardial infarction develop paroxysmal atrial fibrillation?
10% to 15%.

Question: A 58-year-old man is admitted with an acute anteroseptal myocardial infarction. He is in pulmonary edema clinically, confirmed by chest radiography. His blood pressure is 122/76, his HR is 122. Despite two doses of 80 mg of intravenous furosemide, he remains in pulmonary edema. A Swan-Ganz pulmonary artery catheter is inserted and his initial hemodynamics reveal a cardiac output of 3.1 L/min and a pulmonary capillary wedge pressure of 27 mm Hg. What is the most appropriate pharmacologic agent in this setting?
Intravenous dobutamine, at a dose of 5 to 20 μg/kg/min.

Question: What are the major complications of left ventricular aneurysms?
LV thrombus formation (with subsequent risk of thromboembolic events), CHF, and ventricular arrhythmias.

Question: What is the current recommended therapy for patients with large anterior myocardial infarctions?
Reperfusion therapy with thrombolytics, beta-blockers, intravenous nitroglycerin, and ACE inhibitors to limit and retard ventricular remodeling. Intravenous heparin in a sufficient dose to prolong the APTT to 1.5 to 2.0 times control should be started on admission and continued to discharge. In patients with large akinetic apical segments or mural thrombi, oral anticoagulation with warfarin is indicated for at least 6 months.

Question: What is the significance of pericarditis following acute myocardial infarction?
Pericarditis occurs in about 20% of patients with acute myocardial infarction, more likely in Q-wave infarcts than non–Q-wave infarcts. Patients with pericarditis usually have significantly larger infarcts, lower ejection fractions, and a higher incidence of congestive heart failure. The presence of pericarditis and/or pericardial effusion following acute myocardial infarction is associated with higher mortality.

A previously healthy 65-year-old man is admitted with an acute inferior myocardial infarction. Within several hours, he is hypotensive (BP 90/60) and oliguric. Insertion of a pulmonary artery catheter reveals the following pressure: pulmonary artery wedge pressure, 3 mm Hg; pulmonary artery, 21/3 mm Hg; and mean right atrial pressure, 11 mm Hg. What is the best treatment for this man?
Fluids until his wedge pressure is between 16 and 20 mm Hg.

Question: A 60-year-old man with a recent syncopal episode is hospitalized with congestive heart failure and chest pain. His BP is 165/85 mm Hg, his pulse is 85 bpm, and there is a grade III/VI harsh systolic murmur at the apex and aortic area. An echocardiogram reveals a disproportionately thickened septum and anterior systolic motion of the mitral valve. What is this patient’s diagnosis and what physical findings would most likely be present?
Idiopathic obstructive hypertrophic cardiomyopathy (IHSS). The murmur typically decreases with handgrip and squatting and increases with Valsalva, vasodilators, standing, nitroglycerin, diuretics, and digoxin. Mitral regurgitation is frequent as a result of anterior systolic motion of the mitral valve. Congestive heart failure is present because of diastolic dysfunction, thus a S4 gallop is common.

Question: In patients with coronary artery disease, which patients have been shown to benefit from revascularization with bypass grafting?
Patients with left main coronary artery disease (>50% stenosis) and those with three vessel coronary artery disease (>70% stenosis) with depressed LV function (<40% EF).

Question: What are the classic EKG results associated with posterior MI?
A large R wave in leads V1 and V2, ST depression in leads V1 and V2, Q waves in the inferior leads and, occasionally, ST elevation in the inferior leads.

Question: What is the most common complication of extracorporeal circulation?
Stroke occurs in 1% to 2% of patients after open heart operations. Other postoperative complications are arrhythmias, bleeding, renal failure, and respiratory complications.

Question: What drug is used to reverse heparin after open heart surgery?
Protamine.

Question: In 90% of the population, the right coronary artery terminates as the:
Posterior descending artery.

Question: The left main coronary artery gives rise to which two coronary arteries?
The left anterior descending artery and the left circumflex coronary artery.

Question: What is the vessel of preference in coronary bypass grafting?
The internal mammary artery. Other artery grafts such as the radial artery are preferred too. Arterial grafts tend to have higher rates of patency at 10 years compared to venous grafts. Venous grafts are also more susceptible to atherosclerotic disease.


VASCULAR DISEASE

Are aortic aneurysms more common in men or women?
Men (10:1 male-to-female ratio). Other risk factors include hypertension, atherosclerosis, diabetes, hyperlipidemia, smoking, syphilis, Marfan disease, and Ehlers-Danlos disease.

Question: A patient presents with sudden-onset chest and back pain. Further work-up reveals an ischemic right leg. What is your diagnosis?
Suspect an acute aortic dissection when chest or back pain is associated with ischemic and/or neurologic deficits.

Question: What physical findings suggest an acute aortic dissection?
Blood pressure and pulse differences between arms and/or legs, cardiac tamponade, and aortic insufficiency murmur.

Question: What CXR findings occur with a thoracic aortic aneurysm?
Change in aortic appearance, mediastinal widening, hump in the aortic arch, pleural effusion (most commonly on the left), and extension of the aortic shadow.

Question: A 74-year-old male patient presents with acute-onset testicular pain. Ecchymosis is present in the groin and scrotal sac. What is the diagnosis?
A ruptured aortic or iliac artery aneurysm.

Question: What X-ray study should be ordered for a patient with an abdominal mass and a suspected ruptured abdominal aortic aneurysm?
None! The patient should go to the operating room immediately. About 60% of AAAs occur with calcification and appear on a lateral abdominal X-ray.

Question: What may an X-ray of a patient with an aortic dissection reveal?
Widening of the superior mediastinum, a hazy or enlarged aortic knob, an irregular aortic contour, separation of the intimal calcification from the outer aortic contour that is greater than 5 mm, a displaced trachea to the right, and cardiomegaly.

Question: What is the most common symptom of aortic dissection?
Interscapular back pain.

Question: Where do aortic dissections most often occur?
Proximal ascending aorta (60%). Twenty percent of aortic dissections are found between the origin of the left subclavian and the ligamentum arteriosum in the descending aorta, and 10% are found in the aortic arch or the abdominal aorta. Dissection involves intimal tears propagated by hematoma formation.

Question: What aortic aneurysm diameter is generally considered to be an indication for surgery for an aneurysm in the (a) in the thorax and (b) in the abdomen?
Those with a nondissecting thoracic aneurysm larger than 7 cm in diameter are candidates for surgery. However, surgery should be considered with smaller aneurysms for those with Marfan syndrome because of higher incidence of rupture. Nondissecting abdominal aortic aneurysms larger than 4 cm in diameter should be considered for surgical repair.

Describe the Stanford classification of aortic dissections:
Stanford type A: Always involves the ascending aorta but could include the descending aorta. Stanford type B: Involves the descending aorta only.

Question: What dissections can be treated medically?
Patients with Stanford type B and (type III) are eligible for medical, rather than, surgical treatment. Surgical treatment may be required for those with uncontrollable pain, aortic bleeding, hemodynamic instability, increasing hematoma size, or an impending rupture.

Question: What is the prognosis of an untreated aortic dissection?
20% of afflicted individuals die within 24 hours, 60% within 2 weeks, and 90% within 3 months. With surgical treatment, the 10-year survival rate is 40%. Redissection occurs in 25% of these patients within 10 years of the original episode.

Question: Where is the most common site of peripheral aneurysms that develop from arteriosclerosis?
The popliteal artery. Other sites include the femoral, carotid, and subclavian arteries.

Question: What artery is usually affected by arterial occlusive disease in diabetic patients?
The popliteal artery. Because of diabetic neuropathy and the potential for the development of a necrotizing infection in a leg with compromised circulation, it is very important that patients with diabetes are knowledgeable about pedal hygiene.

Question: What is the Budd-Chiari syndrome?
Thrombosis in the hepatic vein resulting in abdominal pain, jaundice, and ascites.

Question: Which arteries are most commonly involved in giant cell arteritis (chronic inflammation of the large blood vessels)?
The carotid arteries and its branches. Treatment includes high doses of corticosteroids.

Question: What is the most common source of acute mesenteric ischemia?
Arterial embolism (40%–50%). The source is usually the heart, generally from mural thrombus. The most common point of obstruction is the superior mesenteric artery.

Question: What laboratory results strongly suggest that a patient has mesenteric ischemia?
Leukocytosis >15,000, metabolic acidosis (sometimes with anion gap), hemoconcentration, and elevated phosphate and amylase.

Question: Describe the Trendelenburg test for varicose veins:
Raise the leg above the heart and then quickly lower it. If the leg veins become distended immediately after this test is performed, valvular incompetency is evident.

A 68-year-old male patient with diabetes and a 60 pack-year history of smoking presents with sudden, severe substernal chest discomfort, radiating through the interscapular area. His BP is 158/80 mm Hg in the right arm and 135/65 mm Hg in the left arm. He complains of right arm numbness and weakness and you hear a grade II/VI diastolic murmur along the left sternal border. EKG reveals 1.5 mm ST elevation in the inferior leads. What is the diagnosis?
Acute proximal thoracic aortic dissection, with involvement of the right coronary artery and brachiocephalic artery, as well as acute aortic regurgitation.

Question: In the patient described in the last question, what other life-threatening complication must one look for, both on auscultation and on chest radiograph?
Pericardial effusion with cardiac tamponade. Listen for a pericardial rub on auscultation and look for marked cardiomegaly on CXR. Pulsus paradoxus of >10 mm Hg is virtually diagnostic of cardiac tamponade in this setting.

Question: What CXR findings occur with a dissecting thoracic aortic aneurysm?
Tortuosity of the proximal aorta with an enlarged aortic knob, mediastinal widening, pleural effusion (most common on the left), extension of the aortic shadow, displaced trachea to the right, cardiomegaly, and separation of the intimal calcification from the outer contour that is greater than 5 mm.

Question: What is the prognosis for an untreated dissecting aortic aneurysm?
25% die within 24 hours, 50% die within one week, 75% die within 1 month, and 90% die within 3 months. With surgical treatment, the 10-year survival is 50%, the 5-year survival is 75% to 80%. Redissection occurs in 25% of patients within 10 years of the original dissection.

Question: What is an ABI and why is it significant?
An ankle/brachial index is the ankle systolic pressure (numerator) compared to the brachial systolic pressure (denominator). It is used as a screening tool for determining the presence of obstructive arterial disease of the lower extremities. A positive ABI is also considered an independent risk factor for coronary artery disease.

Question: What technical factors can affect the accuracy of the ABI?
Probe pressure, rapid deflation of the BP cuff, arterial wall calcifications, and probe placement, which should be longitudinal to the vessel and at a 30- to 60-degree angle to the skin surface.

Question: Matching:

(1) c, (2) d, (3) b, (4) a, (5) f, and (6) e. These are all signs pertaining to aortic insufficiency.


CONGENITAL HEART DISEASE

What are the more common symptoms of a child with an atrial septal defect (ASD)?
In most cases, the patient is asymptomatic. In later teen to adult years, the patient may complain of mild fatigue or dyspnea. In rare cases, heart failure is present.

Question: What is the typical murmur that is heard in a patient with an ASD?
A midsystolic crescendo–decrescendo over the left upper sternal border.

Question: A 5-month-old male infant is brought to the pediatrician’s office because the mother is concerned about his feeding. She notes that the child appears to be short of breath, has poor weight gain, and his feeding is about half of what it should be. On physical examination, you note that his weight is in the 35th percentile, and a gallop is present on auscultation. There is also a slight murmur detected on the intrascapular region of the back on the left side. What is the most likely diagnosis?
Coarctation of the aorta.

Question: What is the difference between the pressures of the upper half of the body compared to the lower in a patient with a coarctation of the aorta?
The pulse pressures in the upper arms will be strong, while the lower extremities will be diminished or in some cases not detected by Doppler.

Question: What is the most common extracardiac congenital anomaly found in children?
Patent ductus arteriosus (PDA).

Question: What is the most characteristic physical examination finding in an infant with a PDA?
The infant will have a systolic thrill that is felt over the pulmonary artery and suprasternal notch. The child will also have a machine-like continuous murmur over the left upper sternal border.

Question: Name the four defects that are characteristic of tetralogy of Fallot:

1. Ventricular septal defect (VSD)
2. Right ventricular hypertrophy
3. RV outflow obstruction from infundibular stenosis (pulmonary valve)
4. Overriding aorta (<50%); a right-sided aortic arch is seen in 25%

Question: What is the preferred test to determine if a child has tetralogy of Fallot?
Echocardiogram.

Question: What is the most common congenital cardiac anomaly?
Ventricular Septal Defect (VSD).

Question: Describe symptoms that can present in a child with a VSD:
The size of the defect will determine the degree of symptoms. Small defects in children may not produce any symptoms, but clinical deterioration may occur at any time. In patients with a large defect, parents may describe grunting, sweating, failure to gain weight, tachypnea, and fatigue.

What are some of the physical examination characteristics found in a patient with a VSD?
The patient may have some respiratory distress, a thrill at the left lower sternal border (common), S2 splits, S3 is common, and a holosystolic murmur at the apex is common. Hepatic enlargement may also be present.

Question: What percentage of VSDs will resolve with conservative medical management?
About 70% of small defects. Larger defects will either be monitored with symptoms and close examinations, or by surgical correction early in the child’s life.

Question: What murmur is expected in patients with substantial aortic stenosis?
A prolonged, harsh, loud (IV, V, or VI) systolic murmur.

Question: What is the most common cause of aortic regurgitation in adults?
Mild aortic regurgitation frequently develops as a result of a bicuspid aortic valve. A severe aortic valve regurgitation is induced by rheumatic heart disease, syphilis, endocarditis, trauma, an idiopathic degeneration of the aortic valve, a spontaneous rupture of the valve leaflets, or aortic dissection.

Question: What are the signs and symptoms of acute aortic regurgitation?
Dyspnea, tachycardia, tachypnea, and chest pain.

Question: What is the most common cause of aortic stenosis in patients younger than 50 years and older than 50 years?
- Younger than 50: Calcification of congenital bicuspid aortic valves (1% of the population has congenital bicuspid valves).
- Older than 50: Calcification of degenerating leaflets.

Question: What triad of symptoms characterizes aortic stenosis?
Syncope, angina, and left heart failure. As the disease progresses, systolic BP decreases and pulse pressure narrows.

Question: What are the findings in a patient with aortic stenosis?
Angina, dyspnea on exertion, syncope, sustained apical impulse, narrow pulse pressure, parvus et tardus, systolic ejection crescendo–decrescendo murmur that radiates to the neck, systolic ejection click (not heard in severe cases when the valve is so stenosed that it is immobile), paradoxically split S1 and soft S2, and audible S4.

Question: How does the heart murmur reflect the severity of aortic stenosis?
A longer duration associated with an increase in intensity indicates severe aortic stenosis. The “loudness” of the murmur is not as important in assessing its severity.

Question: A patient presents to the hospital 1 month after placement of a mechanical prosthetic valve with fever, chills, and a leukocytosis. Endocarditis is suspected. Which bacterium is most commonly encountered in this situation?
Staphylococcus aureus or Staphylococcus epidermidis.

What percentage of non-anticoagulated patients with mitral stenosis experience system emboli?
About 25%. Patients with chronic atrial fibrillation or mitral stenosis should be chronically anticoagulated to prevent atrial mural thrombi.

Question: What is the most common cause of mitral stenosis?
Rheumatic heart disease. The most common initial symptom is dyspnea.

Question: What physical findings may be associated with mitral stenosis?
Prominent a-wave, early systolic left parasternal lift, loud and snapping first heart sound, and early diastolic opening snap with a low-pitched middiastolic rumble that crescendos into S1.

Question: A midsystolic click with a late systolic crescendo murmur is indicative of what cardiac disease?
Mitral valve prolapse (MVP). This is the hallmark sign of MVP.

Question: Is mitral valve prolapse more common among men or women?
Women have a stronger genetic link to the disease. However, only 2% to 5% of the entire population has symptomatic MVP.

Question: What age group typically develops MVP syndrome?
Patients in their twenties and thirties. Most patients with MVP are asymptomatic. MVP syndrome is symptomatic with chest pain, fatigue, palpitations, postural syncope, and dizziness.

Question: Rheumatic heart disease is the most common cause of stenosis of what three heart valves?
Mitral, aortic (along with congenital bicuspid valve), and tricuspid.

Question: What is the most frequent cause of mitral stenosis?
Rheumatic fever. Far less common causes include congenital, malignant carcinoid, SLE, rheumatoid arthritis, infective endocarditis with large vegetation, and the mucopolysaccharidoses of the Hunter-Hurley phenotype.

Question: What percentage of patients with rheumatic heart disease have pure mitral stenosis?
25%. An additional 40% have combined MS and MR.

Question: What are the principal symptoms in mitral stenosis?
Dyspnea is the most common. Patients with severe mitral stenosis can experience orthopnea, hemoptysis, chest pain, and frank pulmonary edema, often precipitated by exertion, fever, URI, sexual intercourse, pregnancy, or the onset of rapid atrial fibrillation.

Question: What are two most serious complications of mitral stenosis?
Thromboembolism, most often occurring in the setting of atrial fibrillation, and pulmonary edema.

What maneuvers can one do to differentiate the opening snap of mitral stenosis from a split S2 sound?
Sudden standing widens the A2-opening snap interval whereas a split S2 narrows on standing. Progressive narrowing of the A2-opening snap interval on serial examinations suggests an increase in the severity of mitral stenosis.

Question: What is the most accurate noninvasive technique for quantifying the severity of mitral stenosis?
Doppler echocardiography.

Question: What is the medical management strategy of rheumatic mitral stenosis?
- Penicillin prophylaxis for beta-hemolytic streptococcal infections and prophylaxis for infective endocarditis
- Aggressive and prompt treatment of anemia and infections
- Avoidance of strenuous exertion
- Oral diuretics and sodium restriction in symptomatic patients
- Beta-blockers to reduce heart rate
- Cardioversion of atrial fibrillation
- Aggressive slowing of refractory atrial fibrillation
- Anticoagulant therapy in patients who have experienced one or more thromboembolic episodes, or who have mechanical prosthetic valves

Question: What is the symptomatic period after an attack of rheumatic fever in patients with mitral stenosis?
In temperate zones, such as the United States and Europe, about 15 to 20 years. In tropical and subtropical areas and in underdeveloped areas, about 6 to 12 years.

Question: What is the indication for mitral valve surgery or balloon valvuloplasty in patients with mitral stenosis?
Moderate symptoms (class II) or greater in a patient with moderate to severe mitral stenosis (mitral valve orifice size of less than 1.0 cm2 per square meter BSA or less than 1.5 to 1.7 cm2 mitral valve area in normal adults).

Question: A 28-year-old Hispanic woman is referred to you for evaluation of dyspnea and palpitations. She has a diastolic murmur consistent with mitral stenosis. Echocardiography confirms severe, noncalcific mitral stenosis with trivial mitral regurgitation, with a mitral valve area of 0.8 cm2. EKG reveals atrial fibrillation. What is the most appropriate course of therapy for this patient?
Open mitral valvotomy (commissurotomy) followed by cardioversion to normal sinus rhythm. This is palliative, obviates the need for anticoagulation for the immediate future, and results in at least 5 to 10 years of symptom-free life for over half of the patients.

Question: What is the most common cause of mitral regurgitation?
Rheumatic fever. It is more frequent in men than women. Other causes include infective endocarditis, mitral valve prolapse, ischemic heart disease, trauma, SLE, scleroderma, hypertrophic cardiomyopathy, dilated cardiomyopathy involving the left ventricle, and idiopathic degenerative calcification of the mitral annulus.

Question: What are the physical findings of patients with chronic mitral regurgitation?
Harsh, pansystolic murmur heard best at the apex, radiating to the axilla or the base. The murmur is diminished by maneuvers that decrease preload or afterload, such as amyl nitrate inhalation, Valsalva, or standing, and increases with maneuvers that increase preload or afterload, such as squatting, handgrip, or phenylephrine administration.

What are the most common causes of acute mitral regurgitation?
Acute myocardial infarction with papillary muscle dysfunction (15% of acute MI results in acute mitral regurgitation) or papillary muscle rupture (3% of acute MI), infective endocarditis, chordate tendinea rupture secondary to chest trauma, rheumatic fever, mitral valve prolapsed, and hypertrophic cardiomyopathy with rupture of chordate tendinea.

Question: Which is the best test to assess the detailed anatomy of rheumatic mitral valve disease and determine whether mitral valve replacement is necessary or whether reconstruction is feasible?
Transesophageal echocardiography.

Question: What is the appropriate medical management of mitral regurgitation?
Vasodilator therapy with ACE inhibitors is the hallmark of therapy, even in patients who are asymptomatic. Diuretics are used in patients with severe MR. Cardiac glycosides, such as digoxin, are indicated in patients with severe MR and clinical evidence of heart failure. Endocarditis prophylaxis is indicated in all patients with MR. Anticoagulation should be given to all patients in atrial fibrillation.

Question: A 33-year-old female patient comes to you for a physical examination and you notice a harsh systolic murmur at the apex that is also heard at the base. The murmur increases on standing and Valsalva and decreases with handgrip. What is the most likely finding on echocardiography?
Mitral valve prolapse. The murmur of pure mitral regurgitation decreases with Valsalva and standing and increases with handgrip or squatting.

Question: A 46-year-old male patient with a history of rheumatic fever at age 12 is admitted with an acute myocardial infarction. The patient’s post-MI course is complicated by congestive heart failure. Echocardiogram reveals severe mitral regurgitation with rupture of one of the papillary muscles and prolapsed posterior mitral valve leaflet without apparent calcification. Systolic function by echocardiogram is mildly reduced. What is the appropriate course of action in this patient?
Mitral valve reconstruction and repair of the papillary muscle.

Question: What is the classic triad of symptoms of aortic stenosis?
Syncope (often exertional), angina, and heart failure.

Question: What is the most common cause of aortic stenosis in patients younger than 65 years?
Calcification of congenitally bicuspid aortic valves (50%) followed by rheumatic heart disease (25%).

Question: What is the most common cause of aortic stenosis in patients older than 65 years?
Calcific degeneration of the aortic leaflets.

Question: Once patients with aortic stenosis become symptomatic, what is their average survival without valve replacement?
From the onset of syncope and/or angina, the mean survival is 2 to 3 years. From the onset of congestive heart failure, the mean survival is 1.5 years.

How does the heart murmur reflect the severity of aortic stenosis?
The longer the duration of the murmur and the greater the increase in intensity of the murmur, the more severe the aortic stenosis. The degree of loudness of the murmur is not as important in assessing severity.

Question: What is the best pharmacologic agent for patients with asymptomatic aortic stenosis?
Without contraindications, beta-blockers are the best agents as they are the most useful in treating left ventricular hypertrophy and its sequelae that develop as a result of aortic stenosis.

Question: A 68-year-old female patient with severe asymptomatic aortic stenosis suddenly complains of dyspnea and palpitations. On EKG, she is found to be in atrial fibrillation with a ventricular rate of 130 bpm. What is the most appropriate action to be taken?
Immediate DC cardioversion followed by a search for previously unrecognized mitral valve disease. Once stabilized, the patient should be referred for cardiac catheterization and aortic valve replacement.

Question: What is a mitral valve prolapsed syndrome?
A symptom complex consisting of palpitations, chest pain, easy fatigability, exercise intolerance, dyspnea, orthostatic phenomena, and syncope or presyncope in patients with mitral valve prolapsed, predominately related to autonomic dysfunction.

Question: What disorders are seen with increased frequency in patients with MVP syndrome?
Graves disease, asthma, migraine headaches, sleep disorders, fibromyositis, and functional gastrointestinal syndromes.

Question: What is the most common cause of isolated severe aortic regurgitation?
Aortic root dilatation resulting from medial disease. Other common causes include congenital (bicuspid) aortic valve, previous infective endocarditis, and rheumatic heart disease.

Question: What is the survival rate of chronic aortic regurgitation after diagnosis?
The 5-year survival, after diagnosis, is 75%. The 10-year survival is 50%. Once symptoms begin, without surgical treatment, death occurs within 4 years after the development of angina, 2 years after the development of CHG.

Question: What is the preferred pharmacologic agent in patients with asymptomatic chronic aortic regurgitation?
Nifedipine or ACE inhibitors. Both have major improvements in LVEF and major reduction in LV end-diastolic volume and mass with significantly lower incidence of the need for aortic valve replacement at 5 years.

Question: What is the most common cause of acute tricuspid regurgitation and what is the preferred management of this situation?
Tricuspid valve endocarditis, often as a result of intravenous drug abuse. The preferred management is complete removal of the valve with immediate or eventual replacement of the valve. Antibiotic therapy usually is futile in preventing valve surgery.

A 38-year-old female patient with known mitral valve prolapse is scheduled for dental cleaning. Her dentist calls for you asking recommendations for endocarditis prophylaxis. She is not allergic to penicillin. What are your recommendations?
No antibiotic prophylaxis is necessary for patients with only the diagnosis of mitral valve prolapse. Antibiotic prophylaxis is recommended for those with prosthetic heart valves, history of infective endocarditis, and other specific congenital heart defects or congenital heart defect repairs utilizing prosthetic material.

Question: A 55-year-old man who underwent a 4-vessel CABG 3 years ago and has mild mitral and tricuspid regurgitation is scheduled for a colonoscopy for rectal bleeding. What recommendations regarding endocarditis prophylaxis would you give this surgeon?
No antibiotic prophylaxis is needed in this setting.

Question: Which valve is most commonly injured during blunt trauma?
The aortic valve.


OTHER HEART DISEASE AND CONDITIONS

Question: What are some adverse drug effects of lidocaine?
Drowsiness, nausea, vertigo, confusion, ataxia, tinnitus, muscle twitching, respiratory depression, and psychosis.

In CPR, what is the ventilation to compression ratio for one or two rescuers?
One and two rescuers should perform 2 breaths to 30 compressions at a rate of 100 compressions per minute. (New guidelines emphasize compressions over ventilations during the first several minutes of a cardiac arrest.)

Question: What are the most common causes of myocarditis in the United States?
Viruses. Other causes include post–viral myocarditis, an autoimmune response to recent viral infection, bacteria (diphtheria and tuberculosis), fungi, protozoa (Chagas disease), and spirochetes (Lyme disease).

Question: A 25-year-old patient presents with splinted breathing and sharp, precordial chest pain that radiates to the back. The pain increases with inspiration and is mildly relieved by placing the patient in a forward sitting position. What might the EKG show?
The patient probably has pericarditis. The EKG may reveal intermittent supraventricular tachycardias, ST-segment depression in leads aVR and VI with ST segment elevation in all of the remaining leads. PR depression and T-wave inversion may also arise.

Question: What is the most common cause of pericarditis?
Idiopathic. Viral pericarditis is a common cause and the most common infectious etiology. Other causes are myocardial infarction, post–viral syndrome, aortic dissection that has ruptured into the pericardium, malignancy, radiation, chest trauma, connective tissue disease, uremia, and drugs, i.e., procainamide or hydralazine.

Question: What physical findings indicates acute pericarditis?
Pericardial friction rub. The rub is heard best at the left sternal border or apex with the patient in a forward sitting position. Other findings include fever, tachycardia, and pleuritic chest pain.

Question: What will be the appearance of a pericardial effusion on an X-ray?
A water bottle silhouette.

Question: What is the treatment for pericarditis without effusion?
A 2-week treatment of 650 mg aspirin every 4 hours, if no contraindications exist. Ibuprofen, indomethacin, or colchicines are other alternatives. The use of corticosteroids is controversial because recurrent pericarditis is common as the dose is tapered.

Question: What is the 1-year recurrence rate for patients who have been resuscitated from sudden cardiac death?
30%.

Question: Splinter hemorrhages, Osler nodes, Janeway lesions, petechiae, and Roth spots can be indications of what process?
They are physical signs associated with infective endocarditis.

Question: True/False: Osler nodes are usually nodular and painful:
True. In contrast, the macular Janeway lesions are painless.

What percentage of patients with infective endocarditis display peripheral manifestations of the disease?
50%.

Question: What is bacterial endocarditis?
An infectious process where bloodborne bacteria that attach onto damaged or abnormal heart valves or on the endocardium near anatomical defects.

Question: How is bacterial endocarditis diagnosed?
By evidence of valvular vegetations on echocardiogram combined with a positive blood culture. The Duke criteria is often utilized as a diagnostic tool for infectious endocarditis.

Question: Who is at high risk for developing endocarditis?
People with prosthetic heart valves, persons with previous incidents of endocarditis, persons with complex congenital heart disease, intravenous drug user, and persons with surgically devised systemic pulmonary shunts.

Question: What are the risk factors for endocarditis?
Risk factors include intravenous drug use, prosthetic valves, acquired valvular heart disease, hypertrophic cardiomyopathy, hemodialysis, peritoneal dialysis, indwelling venous catheters, post–cardiac surgery, rheumatic heart disease, and uncorrected congenital conditions. It is controversial as to whether mitral valve prolapsed with significant regurgitation is a moderate risk factor.

Question: What are the most common organisms associated with endocarditis?
Streptococcus viridians, Staphylococcus aureus, Enterococcus, and fungal organisms. Staph. aureus is responsible for 75% of disease in IVDAs.

Question: What is more common in the general population: left-sided or right-sided endocarditis?
Left-sided (aortic and mitral involvement).

Question: What is more common in intravenous drug abusers: left-sided or right-sided structural disease?
Right-sided (60%) is most common.

Question: How is infective endocarditis treated?
Intravenous antibiotics for 4 to 6 weeks. Close follow-up is necessary and the patient should have a series of two separate negative blood cultures to demonstrate resolution of the condition. If resolution of the infections does not occur promptly, embolization occurs, or fulminant CHF ensues and surgical valve replacement is indicated.

Question: What are the EKG changes associated with pericarditis?
Concave upward ST elevation in at least seven leads except V1 and aVR. PR segment depression may also be present.

Question: What is the most frequently reported bacterial isolate in patients with myocardial abscesses?
Staphylococcus aureus.

What is the clinical picture of myocardial abscesses?
Low grade fevers, chills, leukocytosis, conduction system abnormalities, nonspecific EKG changes, and signs and symptoms of acute MI.

Question: What is mural endocarditis?
Inflammation and disruption of the nonvalvular endocardial surface of the cardiac chambers.

Question: What are the risk factors for mural endocarditis?
Usually, mural endocarditis is from seeding of an abnormal area of endocardium during bacteremia or fungemia. Infectious thrombi from pulmonary veins, ventricular aneurysms, mural thrombi, chordal friction lesions, pacemaker lead insertion sites, idiopathic hypertrophic subaortic stenosis, jet lesions from ventriculoseptal defects, and other congenital defects are other factors. Immunocompromised patients are also at increased risk.

Question: What is the clinical presentation of prosthetic vascular graft infection?
Erythema, skin breakdown, or purulent drainage. Other symptoms may be thrombosis of the graft, fluid around the graft, or pseudoaneurysm formation.

Question: What are the complications from arterial catheterization?
Thrombosis (19%–38%), infection (4%–23%), pseudoaneurysm, and rupture.

Question: How many deaths per year in the United States are due to cardiovascular disease?
864,480 in 2005 or 35.3% of all deaths. CVD death rates have declined with a 26.4% drop between 1995 and 2005.

Question: A radial pulse on examination indicates a BP of at least what level?
80 mm Hg.

Question: A femoral pulse on examination indicates a BP of at least what level?
70 mm Hg.

Question: A carotid pulse on examination indicates a BP of at least what level?
60 mm Hg.


REFERENCES
Crawford MH Current Medical Diagnosis and Treatment: Cardiology. 3rd ed. New York, NY: McGraw-Hill; 2009.
Fauci AS, Braunwald E, Kasper DL, et al., eds. Harrison’s Principles of Internal Medicine, 17th ed. New York: McGraw-Hill; 2008. http://www.accessmedicine.com Fuster Valentin OR-W. Hurst’s The Heart. 12th ed. New York, NY: McGraw-Hill; 2008.
McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment 2009. New York, NY: McGraw-Hill; 2009.
McPhee SJ, Ganong WF. Pathophysiology of Disease: An Introduction to Clinical Medicine. 5th ed. New York, NY: McGraw-Hill; 2006.