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A 65-year-old African-American man is brought to the emergency department (ED) with a two-hour history of sudden onset of sharp, stabbing chest pain under his sternum. He was doingsome physical activity when the symptoms started. The pain reached its maximum intensitywithin a few minutes, and is now radiating to his upper back and shoulder tips. His pastmedical history is significant for hypertension for the past 10 years. He is a heavy smoker. Hisblood pressure is 196/112 mmHg in the right arm and 120/62 mmHg in the left arm. His pulserate is 120/min and respiratory rate is 18/min. The lung examination is clear to auscultationbilaterally. The cardiovascular examination reveals a regular heart rhythm with an earlydiastolic murmur heard at the right sternal border. A stat transesophageal echocardiogram isdone in the ED, which confirms the diagnosis of acute aortic dissection with extension into theleft subclavian artery. What is the best next step in the management of this patient?

A. Aspirin B. Heparin

C. Propranolol D. Sodium nitroprusside E. Hydralazine

Explanation:

Acute aortic dissection refers to a tear in the aortic intima with separation of the intima fromthe media, thereby creating a false lumen within the aortic wall. The dissection may propagateeither distal or proximal to the intimal tear, causing the associated clinical manifestations. It isusually seen in elderly males with a longstanding history of hypertension and atherosclerosis;however, some conditions associated with or predisposing to aortic dissection in youngerpatients include a history of connective tissue disorder (Marfan's syndrome, Ehler-Danlossyndrome), inflammatory vasculitis (Takayasu's arteritis, giant cell arteritis, syphilis aortitis),bicuspid aortic valve, coarctation of aorta, use of crack cocaine and trauma.

Most of the patients present with a sudden onset of sharp tearing chest or back pain. Patientswith ascending aortic dissection may also develop acute aortic insufficiency, thereby causingacute heart failure (with early diastolic decrescendo murmur), acute myocardial infarction dueto the dissection extending into coronary vessels, cardiac tamponade or hemothorax orneurological deficits due to the direct extension of dissection into the carotid arteries. Physicalexamination may reveal a significant difference in the blood pressure between the two armsdue to the involvement of the subclavian vessels. The diagnosis is usually suspected based onthe history and physical examination, along with mediastinal widening on chest radiograph andthe absence of typical electrocardiographic findings of myocardial ischemia or infarction.Transesophageal echocardiography is the modality of choice for rapid confirmation of thediagnosis.

Acute aortic dissection involving the ascending aorta is a life-threatening emergency, and allsuch patients should have emergent surgical intervention. The goal of early medical treatmentis to rapidly reduce the shearing stress on the aortic wall and prevent the further propagation of

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dissection. This is achieved by rapidly lowering the systolic blood pressure and left ventricularcontractility with the use of intravenous beta-blockers. Intravenous beta-blockers are the initialdrugs of choice in the management of patients with aortic dissection. The goal is to reduce thesystolic blood pressure to 100 to 120 mmHg, and to reduce the heart rate to less than 60/min.An intravenous loading dose of propanolol or labetalol followed by an IV infusion can be usedto achieve the desired heart rate and blood pressure in most patients. If the blood pressurecontinues to remain high (systolic blood pressure greater than 100 mmHg), direct vasodilatorsodium nitroprusside should be added to the beta-blockers to achieve the desired bloodpressure goal.

(Choice A) Aspirin has no role in the management of patients with aortic dissection.

(Choice B) Heparin is absolutely contraindicated in patients with aortic dissection.

(Choice D) Sodium nitroprusside should only be used in conjunction with beta-blockers. Whenused alone, it can cause reflex activation of the sympathetic nervous system, thereby causingan increase in the heart rate and ventricular contractility. This, in turn, leads to an increase inthe shearing stress on the aortic wall and causes worsening of the aortic dissection.

(Choice E) Hydralazine is another direct vasodilator and causes reflex activation ofsympathetic nervous system. It has a less predictable blood pressure response and should beavoided in patients with acute aortic dissection.

Educational Objective:Intravenous beta-blockers (propranolol or labetalol) should be used in the initial managementof patients with acute aortic dissection. Sodium nitroprusside should not be used alone forblood pressure control without prior beta blockade.

41% of people answered this question correctly;

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A 53-year-old Caucasian sales clerk presents to the emergency department after spitting upblood while at work. She is very concerned and says this has never happened before. Shereports a lengthy history of shortness of breath, fatigue, palpitations, and cough while lyingdown, but has never sought medical attention for these symptoms because she has no healthinsurance. Her medical history is significant for atrial fibrillation and iron-deficient anemia, andshe underwent a cholecystectomy ten years ago. Physical examination reveals a thin, fatigued,anxious woman in no acute distress. She is mildly tachypneic. Jugular venous distention ispresent, and there is a questionable apical low-pitched rumbling murmur. Bilateral rales arenoted. An electrocardiogram shows a broad notched P wave in lead II as well as some rightaxis deviation. Chest radiograph shows Kerley B lines, a redistribution of blood flow towardthe apices, prominent pulmonary arteries at the hilum, elevation of the left mainstem bronchus,and left atrial enlargement with a flattening of the left heart border. What is the most likelydiagnosis?

A. Mitral stenosis B. Mitral regurgitation C. Aortic stenosis D. Aortic insufficiency E. Pulmonic stenosis

Explanation:

Mitral stenosis (Choice A) is a narrowing of the outflow tract from the left atrium to the leftventricle, resulting in increased pressure in the left atrium, pulmonary vasculature, and rightside of the heart. It is more common in women, and is most commonly linked to a remoteepisode of rheumatic fever, though congenital mitral stenosis may be found as well. Onphysical examination, mitral stenosis produces a diastolic thrill palpable over the apex and alow-pitched, rumbling diastolic murmur best heard over the apex when the patient is lying in aleft lateral decubitus position.

Mitral regurgitation (Choice B) causes an apical holosystolic murmur, and is most oftensecondary to myocardial infarction, mitral valve prolapse, rheumatic heart disease, or coronaryartery disease.

Aortic stenosis (Choice C) causes a crescendo-decrescendo systolic murmur with a normalS1, a diminished A2, and a paradoxical splitting of S2. It is most often secondary to seniledegenerative calcification, or congenital malformation.

Aortic insufficiency (Choice D) causes a diastolic murmur best heard adjacent to the sternumin the second to fourth intercostal space. It is most often secondary to infective endocarditis,congenital malformation, connective tissue disorders, or rheumatic heart disease.

Pulmonic stenosis (Choice E) causes a systolic crescendo-decrescendo ejection murmur inthe left upper sternal border. It is most often secondary to congenital malformation, rheumatic

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heart disease, or carcinoid.

Educational Objective: Mitral stenosis can result in hemoptysis. It causes a low-pitched, rumbling diastolic murmurand is most commonly linked to a remote episode of rheumatic fever. Prominent pulmonaryarteries at the hilum, elevation of the left mainstem bronchus, and left atrial enlargement with aflattening of the left heart border are the other clues for the diagnosis.


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A 55-year-old male with a history of leukemia comes to the emergency department andcomplains of shortness of breath and weakness. He is tachycardic, hypotensive, and ill-looking. Auscultation reveals distant heart sounds. Which of the following statements regardinghis diagnosis and tests is true?

A. An inspiratory fall in blood pressure of 10 mmHg is diagnostic of cardiactamponade.

B. A diffuse ST segment elevation in the electrocardiogram is diagnostic forconstrictive pericarditis.

C. Echocardiogram will show pericardial effusion with evidence of right atrial and/orventricular wall collapse during diastole, thereby leading to a diagnosis of cardiactamponade.

D. A chest x-ray showing an enlarged heart with evidence of pulmonary edema will leadto a diagnosis of acute pericarditis.

E. Soft heart sounds on auscultation are reflective of a stenotic valve and lead to adiagnosis of mitral stenosis.

Explanation:

A pericardial effusion may occur in response to any cause of pericarditis or frommalignancies. The pericardial effusion may develop slowly or rapidly; however, sudden fillingof the pericardial space with fluid can have catastrophic consequences by limiting ventricularfilling.

Patients with pericardial tamponade often complain of shortness of breath. The typicalphysical signs and symptoms arise from the limited filling of the ventricle. The classic Beck'striad is hypotension, muffled or distant heart sounds, and elevated jugular venous pressure.Cardiac tamponade is a surgical emergency, and an ECHO should be obtained urgently. TheECHO will reveal the large pericardial effusion, with prominent collapse of the right atrium andventricle during diastole. Cardiac catheterization can confirm the diagnosis by showingequalization of diastolic pressures in all chambers. However, if the patient is collapsing, oneshould not wait for an ECHO. Rapid pericardiocentesis is life-saving.

(Choice A) Arterial systolic blood pressure normally drops 10 -12 mmHg with inspiration. Amarked inspiratory drop in systolic blood pressure (> 20 mmHg) is an important physicalfinding in cardiac tamponade; however, this can also be seen in severe obstructive pulmonarydisease and constrictive pericarditis.

(Choice B) Diffuse ST segment elevations present in all leads may indicate acutepericarditis. In pericardial tamponade, low limb voltage with alternating size of QRS complexdue to swinging of the heart is seen.

(Choice D) The chest x-ray in cardiac tamponade will show an enlarged cardiac silhouette.When a chest x-ray shows an enlarged heart with pulmonary edema, congestive heart failure should be

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suspected. In cardiac tamponade, ther is usually no pulmonary edema.

(Choice E) The heart sounds are muffled or distant in cardiac tamponade because of the fluidaround the heart. In mitral stenosis, the first heart sound is loud. There is an opening snap anda diastolic murmur. Mitral stenosis is usually caused by rheumatic fever.

Educational Objective:Cardiac tamponade will cause a limitation of fluid entering the ventricles, and an ECHO willreveal diastolic collapse of both the right atrium and ventricle.


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The following vignette applies to the next 2 items

A 55-year-old Caucasian man comes to the emergency department with a sudden onset ofretrosternal chest pain that began eight hours ago. An electrocardiogram revealed thepresence of ST segment elevation in leads V2 to V5. He is taken emergently for cardiaccatheterization, where he undergoes percutaneous transluminal coronary angioplasty withstent placement to the left anterior descending artery. After the procedure, the ST changesresolve, and the patient has an uneventful hospital course. On the third night, just prior to hisdischarge, he called for the nurse due to a sudden onset of sharp, retrosternal chest pain. Hefirst noticed the pain while he was turning around in the bed. The pain gets worse with deepbreathing. His vital signs are as follows: temperature 37.8C (100F), blood pressure 134/80mmHg, heart rate 108/min, and respiratory rate 22/min. Physical examination reveals jugularvenous distention (3 cm), regular heart sounds without any murmurs, and clear lung fields.There is a scratchy sound heard during ventricular systole over the left sternal border. An EKGdone during the episode reveals the presence of sinus tachycardia with Q waves in leads V2to V5.

Item 1 of 2

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

A. Acute pericarditis B. Left ventricular aneurysm C. Chordae tendineae rupture D. Acute myocardial infarction E. Dressler's syndrome

Explanation:

The patient has a clinical syndrome consistent with a diagnosis of acute pericarditis. Acutepericarditis (infarct associated or infarction pericarditis) can occur within one to four days as adirect complication of a transmural myocardial infarction. The recurrence of chest pain threedays after a myocardial infarction, which gets worse with position changes and deepinspiration, is suggestive of infarction pericarditis. It is usually a clinical diagnosis, and issupported by the presence of pericardial friction rub and EKG changes of pericarditis (sinustachycardia, diffuse ST segment elevations with PR segment depression). A pericardial rub isusually heard over the left sternal border and can be present during any of the phases of thecardiac cycle. It is heard as a superficial scratchy or grating sound, which gets morepronounced when the patient leans forward. The EKG changes of pericarditis are not alwaysseen, but usually resemble that of an acute myocardial infarction.

Infarction pericarditis is seen less frequently in patients with early and complete reperfusion. Itis usually a transient episode and does not affect the management of acute myocardialinfarction, unless it is complicated by a large pericardial effusion or tamponade.

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(Choice B) A left ventricular aneurysm usually occurs as a late complication of a transmuralmyocardial infarction (usually a large anterior wall MI). It may result in heart failure, ventriculararrhythmias, or peripheral arterial embolization due to the formation of a left ventricularthrombus. It develops over a longer period of time, and is usually not associated with chestpain. Persistent ST elevation can be present in these patients.

(Choice C) Chordae tendineae or papillary muscle rupture is a life threatening mechanicalcomplication of an acute myocardial infarction. It usually occurs two to seven days after theinfarction and causes acute hemodynamic instability. Patients also develop acute pulmonaryedema.

(Choice D) Acute myocardial infarction is unlikely in the absence of any specific EKGchanges of ischemia or infarction. The presence of 'Q' waves indicates an old infarction in thispatient.

(Choice E) Dressler's syndrome, or post-cardiac injury syndrome, occurs in patients withmyocardial infarction and after cardiac surgery. It is an autoimmune mediated syndrome,which usually develops weeks to months after an acute MI. It usually presents with fever,leukocytosis, pleuritic chest pain, and a pericardial rub.

Educational Objective:Acute pericarditis (infarction pericarditis) can occur within one to four days as a complicationof transmural myocardial infarction.


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Item 2 of 2

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

A. High-dose aspirin B. Glycoprotein IIb/IIIa inhibitors C. Oral corticosteroids D. Urgent cardiac catheterization for in-stent restenosis E. Immediate cardiothoracic surgical referral

Explanation:

Acute pericarditis occurring after a myocardial infarction is usually transient (lasts for only afew days). It should be managed with close clinical observation and adequate pain control.Aspirin (anti-inflammatory doses) is effective in alleviating the pain associated with acutepericardial inflammation. There are some concerns that other NSAIDs may increase the risk ofmyocardial rupture after a transmural MI.

(Choices B and D) There is no evidence of myocardial ischemia or infarction in this patient.Glycoprotein IIb/IIIa inhibitors and emergent cardiac catheterization are therefore not indicatedin this patient.

(Choice C) Corticosteroids are useful in refractory cases of Dressler's syndrome, whennonsteroidal antiinflammatory drugs fail to control the symptoms. Its use has been reported toincrease the incidence of ventricular aneurysm formation.

(Choice E) The patient in the above vignette does not exhibit any signs of acute mitralregurgitation (MR) or chordae tendinae rupture. Urgent cardiothoracic surgical evaluation andmanagement are required for patients with chordae tendineae rupture since it leads to anacute MR and hemodynamic instability.

Educational Objective:Acute pericarditis following a transmural myocardial infarction is usually transient and shouldbe managed by pain control with aspirin.


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A 44-year-old Caucasian woman presents to the ER after sudden onset of weakness anddizziness. She denies any chest pain but feels her heart pounding in her chest. A portion of herEKG is shown below.

Which of the following is the best initial treatment for this patient's condition?

A. Quinidine B. Digoxin

C. Adenosine D. Isoproterenol E. Lidocaine

Explanation:

This patient has a narrow QRS complex tachycardia consistent with a supraventriculartachycardia (SVT). Given this patient's age, gender, and the regularity of the QRS complexes,she may have paroxysmal SVT (PSVT). However, it is often difficult to distinguish betweenPSVT and the numerous other types of SVT (e.g., sinus tachycardia, AV nodal reentranttachycardia, AV reentrant tachycardia, atrial fibrillation, and atrial flutter). One diagnostic andtherapeutic maneuver to distinguish between these entities is to increase vagal tone to theheart by Valsalva or adenosine administration. This will slow the heart rate until a rhythm canbe recognized. It can also potentially "break" the SVT and return the patient to normal sinusrhythm.

(Choice A) Quinidine is a class IA antiarrhythmic used to treat a spectrum of rhythmdisturbances. Notably, quinidine has anti-vagal actions and often induces a tachycardia. Thisdrug may be associated with increased mortality in atrial fibrillation. It is not a first-linetreatment for SVT.

(Choice B) Digoxin is a cardiac glycoside used to treat symptomatic heart failure. Itdecreases heart failure symptoms and hospitalizations but does not prolong life. Digoxin isalso an AV node blocker and can be useful in treating atrial fibrillation. It is not, however, afirst-line agent for SVT.

(Choice D) Isoproterenol is a -1 and -2 adrenergic agonist. As a result, administration ofisoproterenol will increase heart rate and contractility due to its -1 effects and decreasemean arterial blood pressure due to -2-mediated vasodilation.

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(Choice E) Lidocaine is a class IB antiarrhythmic used predominantly to treat ventriculararrhythmias. Lidocaine is not recommended for SVT.

Educational Objective:Supraventricular tachycardias are characterized by narrow QRS complexes. The initialdiagnostic and therapeutic maneuver is to increase a patient's vagal tone via the Valsalvamaneuver or adenosine administration.


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A 53-year-old Caucasian businessman is brought in to the emergency department bycoworkers. He was in a meeting at work when he suddenly experienced severe pain andtightness in his chest. The pain radiates to his jaw. He reports feeling very anxious andlightheaded, and is extremely sweaty upon arrival. He was given supplemental oxygen andintravenous access was established. His vital signs include temperature of 36.9C (98F), bloodpressure of 132/90 mm Hg, pulse of 82/min, and respirations are 20/min. Noelectrocardiogram results are yet available. What medication should be administered next?

A. Aspirin B. Captopril C. Heparin D. Metoprolol E. Streptokinase

Explanation:

Unless there is clear evidence to the contrary, clinicians managing chest pain should alwaysassume it is ischemic in origin. Supplemental oxygen should be administered, pulse oximetryreadings obtained, and intravenous access established. Ideally, 325 mg of aspirin (Choice A)should be chewed en route to the hospital. Nitroglycerin is typically given next, unlesscontraindications exist (e.g., hypotension or recent usage of sildenafil).

ACE inhibitors such as captopril (Choice B) are not as commonly given in the acute setting.However, they are known to significantly improve cardiac hemodynamics and reduce mortalitywhen given for a several week period following myocardial infarction.

Heparin (Choice C) may be given intravenously after aspirin, nitroglycerin, and morphine havebeen administered and the electrocardiogram performed.

Beta-blockers such as metoprolol (Choice D) are of help in controlling heart rate anddecreasing myocardial oxygen demand, and are typically given after aspirin, nitroglycerin, andmorphine have been administered.

Streptokinase (Choice E) is used for thrombolysis as an alternative to primary coronaryintervention (e.g., stent placement or balloon dilation), but is not one of the first medicationsadministered after myocardial infarction.

Educational Objective: In patients whose chest pain may be ischemic in origin, supplemental oxygen and aspirinshould be administered immediately, followed by nitroglycerin, morphine, and beta-blockers(presuming no contraindications exist).


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A 70-year-old African-American woman is brought to the emergency department because shewoke up this morning with a sudden onset of shortness of breath. She has never had angina orshortness of breath. She denies wheezing, chest pain, leg swelling, palpitations, and loss ofconsciousness. Her other medical problems include hypertension, diabetes mellitus-type 2,and hypercholesterolemia. She had bronchial asthma when she was a child. Her only hospitaladmission occurred two months ago, when she underwent a spinal fusion for lower backproblems. She denies the use of alcohol or tobacco. Her family history is not significant. Hertemperature is 36.1 C (97 F), blood pressure is 210/106 mmHg, pulse is 65/min, andrespirations are 34/min. Her pulse oximetry reading is 81% at room air. Physical examinationshows diffuse crackles all over the lung fields. Her labs reveal the following:

CBC

Hb 11.4 g/dLPlatelet count 180,000/cmmLeukocyte count 8,000/cmm

Her chest x-ray is shown below. Oxygen is administered.

Item 1 of 3

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

A. Give IV nitroglycerine B. Give intravenous metoprolol

C. Administer furosemide D. Start intravenous heparin E. Albuterol nebulization

Explanation:

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The patient's chest x-ray is characteristic of flash pulmonary edema, which is most likely due tohypertensive crisis. The initial steps in management of patients with acute pulmonary edemaincludes the administration of oxygen, morphine, and loop diuretics (IV furosemide).

Educational objective:Patients with acute pulmonary edema are initially managed with oxygen, morphine and loopdiuretics (IV furosemide).


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Item 2 of 3

The patient is given the appropriate treatment. She also undergoes further evaluation. HerEKG reveals left ventricular hypertrophy with repolarization changes. The first set of cardiacenzymes is negative. She is still in moderate distress, and has similar vital signs. What is thenext best step in the management of this patient?

A. Add intravenous steroids B. Start dopamine C. Increase metoprolol

D. Start IV nitroglycerine E. Continue heparin

Explanation:

This patient's flash pulmonary edema is most likely due to hypertensive crisis. The two mostcommonly used antihypertensive agents in the management of hypertensive crisiscomplicated by acute pulmonary edema are IV nitroglycerine and IV nitroprusside.

(Choice B) Dopamine is indicated in patients with cardiogenic shock complicated byhypotension. This patient has hypertensive crisis; therefore, the use of dopamine in this caseis very inappropriate.

(Choice E) Heparin is indicated in either pulmonary embolism (PE) or acute coronary event;however, there is no evidence of ischemia (normal EKG), no chest pain, and no elevatedcardiac enzymes, which could suggest the latter. PE is also unlikely in this case, given thepatient's findings of pulmonary edema in the chest x-ray, as well as hypertension.

(Choice C) Beta-blockers are not usually given in acute pulmonary edema.

(Choice A) Steroids are indicated in acute bronchial asthma or COPD exacerbation, which isnot the case here.

Educational objective: The two most commonly used antihypertensive agents in the management of hypertensivecrisis complicated by acute pulmonary edema are IV nitroglycerine and IV nitroprusside.


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Item 3 of 3

The patient is responding well to the treatment. The second set of cardiac enzymes isnegative. What other test is necessary for this patient?

A. Echocardiogram B. Coronary angiogram C. Pulmonary function tests D. V/Q scan and D-dimer E. Renal duplex scan

Explanation:

Mitral stenosis and acute aortic or mitral regurgiation can sometimes present with flashpulmonary edema; therefore, an echocardiogram should be performed to evaluate the systolicand diastolic function, and to check for any left ventricular hypertrophy or valvular disease.

(Choice E) A renal duplex scan is indicated in patients with severe, uncontrolled hypertensionand recurrent episodes of flash pulmonary edema.

Educational objective:All patients with flash pulmonary edema of unknown etiology should be evaluated with anechocardiogram.


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A 62-year-old man comes to the emergency department because of shortness of breath, chestpain, and palpitations. His other medical problems include hypertension, obesity, chronicobstructive pulmonary disease, myocardial infarction requiring a coronary artery bypass graft,and carotid artery stenosis. His medications include metoprolol, aspirin, tiotropium, andlisinopril. Electrocardiogram shows atrial fibrillation with a rapid ventricular response(140150/min). The patient is connected to a cardiac monitor. While the team is securingintravenous access, the patient becomes unresponsive. He has no palpable pulses over themajor arteries. The cardiac monitor continues to show atrial fibrillation at a rate of 145/min.Which of the following is the most appropriate next step in the management of this patient?

A. Arterial blood gas testB. Chest compressions

C. Defibrillation D. Intravenous bicarbonate and digoxin E. Synchronized cardioversion

Explanation:

This patient's condition would be classified as pulseless electrical activity (PEA), which isdefined as the presence of an organized electrocardiographic rhythm (such as atrial fibrillationwith a rapid ventricular rate, as in this patient) without sufficient cardiac output to produce apalpable pulse or measurable blood pressure. The absence of a palpable pulse also meansthat the brain is not being appropriately perfused; therefore, cardiopulmonary resuscitation(CPR) is necessary despite the presence of an organized rhythm. The most important initialstep in the management of PEA is chest compressions. The airway should also be secured,but the 2010 Advanced Cardiac Life Support (ACLS) guidelines place a greater importanceon circulation than on airway and breathing.

It is important to distinguish this patient's condition from unstable tachycardia. In unstabletachycardia, the patient has hypotension, ischemic chest pain, altered mental status, or heartfailure, but a pulse is present. Cardioversion would be the best choice if this patient hadunstable tachycardia. However, defibrillation and cardioversion are not a component of ACLSguidelines for PEA management. The patient should be evaluated and treated for anunderlying metabolic cause of his atrial fibrillation as resuscitation is taking place. If the patientregains a pulse, then the situation would change, and cardioversion would likely be warrantedgiven that the patient would then be in an unstable tachycardia, assuming his rhythm remainsthe same. It is important to adjust to a different ACLS algorithm as the clinical situationchanges.

(Choice A) Obtaining an arterial blood gas test is a reasonable step while the patient is beingresuscitated. However, the most important first step is to begin chest compressions in anattempt to adequately perfuse the brain.

(Choice C) Defibrillation is only effective if there is a shockable rhythm, such as ventricular

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fibrillation or pulseless ventricular tachycardia.

(Choice D) The most important initial step is to initiate chest compressions. Epinephrine is animportant component of resuscitation in PEA patients, but bicarbonate or digoxin would not beindicated at this time.

(Choice E) Synchronized cardioversion would be indicated for unstable tachycardia, but giventhat this patient has no pulse, the PEA algorithm as opposed to the tachycardia algorithmshould be followed.

Educational objective:Pulseless electrical activity (PEA) is defined as the presence of an organizedelectrocardiographic rhythm without sufficient cardiac output to produce a palpable pulse ormeasurable blood pressure. Immediate cardiopulmonary resuscitation with chestcompressions should be started. Defibrillation or cardioversion are not a component ofresuscitation for PEA, although cardioversion is the best choice in patients who have unstabletachycardia with a pulse.


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A 66-year-old man presents to the emergency department for evaluation of left-sided chestpain. He describes his pain as sharp, non-radiating, and lasting several minutes at a time. Hischest pain is present both at rest and with exertion. He also has intermittent claudication withwalking that manifests as a crampy, right-sided thigh pain. His past medical history otherwiseincludes hypertension, type 2 diabetes mellitus, osteoarthritis of the right knee, and obesity(BMI of 42 kg/m 2 ). His daily medications are aspirin, insulin detemir, lisinopril, metoprolol,and atorvastatin. He also takes omeprazole for occasional heartburn. He has a 50-pack yearsmoking history. He has no known allergies. His physical examination and electrocardiogramare unremarkable. Which of the following is the most appropriate test for further evaluation ofthis patient?

A. Adenosine myocardial perfusion imaging B. Ambulatory 24-hour EKG monitoring C. Exercise echocardiography D. Exercise electrocardiography E. Radionuclide ventriculography

Explanation:

The first concern when evaluating a patient such as this in the emergency department isassessment of risk for coronary artery disease and possible acute coronary syndrome. Thispatient's history of smoking, hypertension, diabetes, and obesity all place him at risk forcoronary artery disease. His symptoms of intermittent extremity claudication are almostcertainly secondary to atherosclerosis in the lower extremity arteries, which makes thepresence of atherosclerosis in the coronary arteries highly likely. However, it is unclear at thispoint if this patient's symptoms are secondary to coronary artery disease or an unrelatedproblem as his presentation is not entirely specific. Further evaluation with measurement ofcardiac markers would be recommended at this time. If his cardiac markers are negative,stress testing before discharge would be ideal to help risk-stratify the patient. Given hisintermittent claudication and osteoarthritis, however, he will likely be unable to effectivelyexercise for the stress test. An adenosine myocardial perfusion test would therefore be thebest choice for this particular patient.

(Choice B) Ambulatory 24-hour EKG monitoring is most useful when there is suspicion for anintermittent arrhythmia, for example, in patients being evaluated for syncope.

(Choice C) This patient is unlikely to be able to exercise effectively and therefore an exerciseechocardiogram would not be a good choice. A dobutamine echocardiogram could beconsidered, but given the patient's obesity, finding an appropriate acoustic window cansometimes be difficult.

(Choice D) Exercise electrocardiography is currently less frequently used as a stress testingmodality (compared to exercise echocardiography). This test's sensitivity is lower than ifimaging with echocardiography or radionuclides are used. Therefore in a patient like this one

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with a reasonably high pretest probability, coronary artery disease could not be reliablyexcluded even in the presence of a negative test.

(Choice E) Radionuclide ventriculography is a highly accurate method for determiningejection fraction, and is often used to follow patients receiving cardiotoxic chemotherapy.

Educational objective:Stress testing is needed to risk-stratify patients suspected of having coronary artery disease.Exercise echocardiography or nuclear perfusion studies are preferred for most patients,although a pharmacologic stress test may be needed in patients unable to exercise. Exerciseelectrocardiography is less sensitive than exercise echocardiography or nuclear perfusionstudies.


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A 65-year-old female presents to the emergency room with a chief complaint of headache.Upon further questioning, she states that the headache is localized to the right side of herhead. The patient has no other complaints. Her only regular medications are acetaminophenfor arthritis in her left shoulder and metformin for recently diagnosed DM type II. On physicalexam you notice that the patients right pupil is smaller than the left and her right eyelid isslightly drooping. Initial labs reveal:

Hemoglobin 12.2g/LPlatelets 206,000/mm3Leukocyte count 4,500/mm3ESR 20 mm/hr

What is the next best step in the management of this patient?

A. CT head without contrastB. MRA of the head and neck

C. Begin oral prednisone D. Order temporal artery biopsy E. Perform lumbar puncture

Explanation:

This patient has a unilateral headache with associated Horners syndrome, which consists ofmiosis (small pupil), ptosis (eyelid drooping), and often anhidrosis (lack of sweating) on theaffected side. This patient should be considered to have a carotid dissection until provenotherwise. The key to the presentation is the presence of Horners syndrome, which occursbecause the sympathetic chain providing innervation to the head travels on the carotid artery.Carotid artery dissections can be due to trauma, connective tissue disease, smoking, neckmanipulation, hypertension, and three point restraint seatbelts in motor vehicle accidents.Once carotid artery dissection is suspected, the preferred method of noninvasive imaging isMRA. If the MRA results are unclear but carotid dissection is still suspected, catheterangiography is the definitive test. These patients are at a high risk for developing cerebralinfarction. Treatment consists primarily of anticoagulation with platelet agents and/or heparin.

(Choice A) CT head would be useful if an intracranial process were suspected, especially asubarachnoid hemorrhage or bleed. However, the presence of Horners syndrome pointsmore towards carotid dissection.

(Choice C) Oral prednisone would be indicated if temporal arteritis were suspected. Hornersyndrome is not seen typically in temporal arteritis. A highly elevated ESR would also behelpful in distinguishing temporal arteritis from carotid dissection.

(Choice D) A temporal artery biopsy would be indicated if temporal arteritis was suspected,but this is unlikely given the presence of Horners syndrome. Of note, treatment with

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prednisone should not be delayed while waiting for a temporal artery biopsy to be done.

(Choice E) A lumbar puncture is useful if one suspects meningitis or a subarachnoidhemorrhage, but neither of these entities would normally present in this fashion.

Educational objective:A unilateral headache with associated Horners syndrome (miosis, ptosis, and anhidrosis) isgenerally a carotid dissection until proven otherwise, and MRA is the initial diagnostic modalityof choice.


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A 28-year-old Mexican-American woman comes to the emergency room because ofpalpitations. She has no other medical problems. She does not use tobacco, alcohol, ordrugs. She takes no medications. Her temperature is 36.7C (98F), blood pressure is100/60 mmHg, pulse is 172/min, and respirations are 20/min. A 12-lead EKG is taken, whichshows a heart rate of 172 beats/min with no P waves, and with regular and narrow- appearingQRS complexes.

Item 1 of 2

Which of the following is the most likely diagnosis?

A. Atrial fibrillation B. Ventricular tachycardia C. Sinus tachycardia

D. Paroxysmal supraventricular tachycardia E. Atrial flutter

Explanation:

The patient's EKG findings (narrow and regular QRS complexes, absent P wave) arecharacteristic of a paroxysmal supraventricular tachycardia (SVT). SVT includes suchcommon entities as AV nodal reentrant tachycardia (AVNRT) and AV reentrant tachycardia.The term 'paroxysmal SVT' excludes atrial fibrillation and atrial flutter, other common forms ofsupraventricular arrhythmias.

(Choice C) P waves, along with narrow QRS complexes, are present in sinus tachycardia.

(Choice A) Atrial fibrillation is an "arrhythmic arrhythmia"; the rhythm is completely irregular,and P waves are absent.

(Choice B) Ventricular tachycardia presents with wide QRS complexes (more than 0.12 sec).

(Choice E) Atrial flutter is characterized by the presence of "flutter waves" in a saw toothpattern. The heart rate for 'typical' atrial flutter with 2:1 conduction is usually around 150 bpm.

Educational Objective:Paroxysmal SVT and sinus tachycardia are frequent types of tachyarrhythmias. Narrow andregular QRS complexes, and absent P waves suggest paroxysmal SVT.


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Item 2 of 2

The patient receives antiarrhythmic therapy, and her heart rate decreases from 172/min to68/min. The palpitations resolve, and the patient begin to feel better. A new 12-lead EKG istaken, which shows a heart rate of 70/min, regular rhythm, presence of P waves, a PR intervalof 0.10 sec, a slurred initial part of activation of the QRS complex, a QRS of 0.12 sec, andnonspecific T wave abnormalities. Which of the following is the most likely diagnosis?

A. Mahaim tachycardiaB. Wolff-Parkinson White (WPW) syndrome

C. Dual AV nodal pathways D. James fibers preexcitation E. Right bundle branch block

Explanation:

The abovementioned features are characteristic of Wolff-Parkinson White (WPW) Syndrome.The slurred upstroke of the QRS complex during the initial part or ventricular activation isknown as the delta wave. QRS duration is generally equal to 0.12 sec, but may have greatervalues. Another feature of WPW syndrome is a PR interval less than 0.12 sec.

(Choices A and D) Mahaim and James fibers tachycardias are preexcitation forms that lackdelta waves.

(Choice E) A right bundle branch block (RBBB) has wide QRS complexes, but does not havedelta waves or short PR intervals. Furthermore, an RBBB will not explain the paroxysmal SVTof the patient.

(Choice C) AV nodal reentrant tachycardias are the most common etiologies of paroxysmalSVT. On resting EKG, there is no delta wave and the QRS complex is narrow.

Educational Objective:WPW Syndrome can be identified in around 0.2% of the population. It is characterized by ashort PR interval (less than 0.12sec), a delta wave at the beginning of the QRS complex, QRSduration of 0.12sec or wider, and non-specific ST segments or T wave abnormalities.


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A 60-year-old man is brought to the emergency department due to acute-onset shortness ofbreath. His past medical history is significant for hypertension, coronary artery disease, andtype 2 diabetes mellitus. His current medications are hydrochlorothiazide, insulin, simvastatin,aspirin, and a daily multivitamin. His blood pressure is 128/72 mmHg, pulse is 116/min,temperature is 36.7C (98F), and respirations are 28/min. Physical examination shows ananxious-appearing, diaphoretic man. There is jugular venous distention, a regular heart rhythm,and an ejection murmur over the cardiac base. Lung examination reveals crackles to the mid-lung level bilaterally. He has pitting edema in both lower extremities. Which of the following isthe best initial approach to improving this patient's symptoms?

A. Blocking sympathetic activityB. Decreasing cardiac preload

C. Decreasing heart rate D. Improving myocardial contractility E. Increasing coronary perfusion pressure

Explanation:

This patient's shortness of breath accompanied by jugular venous distention, crackles onexam, and pitting edema are all consistent with congestive heart failure. The acuity of hissymptom onset would classify this as acute decompensated heart failure, or flash pulmonaryedema. The patient's tachycardia is likely secondary to poor myocardial contractility, althoughthere is no hypotension at this point to suggest cardiogenic shock. This patient will needfurther evaluation to determine the underlying cause of his acute decompensated heart failure;at this point the most emergent concern would be a myocardial infarction. A pulse oximetryreading should be obtained, with administration of oxygen and/or noninvasive ventilationadministered as needed. Given that this patient is clearly volume overloaded, decreasing thecardiac preload with a diuretic such as furosemide would be indicated at this time.

(Choice A) While morphine does not directly block sympathetic activation, it does relievepatient anxiety which in turn may reduce sympathetic outflow. Data as to the safety andefficacy of morphine in this setting is limited. If morphine is administered, it should not take theplace of diuretic therapy.

(Choice C) Decreasing the heart rate with medications such as beta-blockers does improvemortality in the long-term in patients with chronic CHF. However, in this patient's acutedecompensated heart failure, his tachycardia is attempting to counteract the low cardiacoutput. Heart rate-lowering medications would risk detrimental hypotension here.

(Choice D) Improving myocardial contractility with inotropic agents such as dobutamine ormilrinone should only be considered in patients with hypotension causing hypoperfusion.

(Choice E) Coronary artery vasodilators such as nitroglycerine may be indicated here if theresponse to diuretic therapy is inadequate. It should not be given if the patient is hypotensive.

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Educational objective:There are multiple possible causes of acute decompensated heart failure, or flash pulmonaryedema, with myocardial infarction being the most pressing entity on the differential diagnosis.Initial management should involve ensuring adequate oxygenation and ventilation followed bydiuretic therapy.


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A 64-year-old healthy male comes to your office after a local emergency department (ED) visitfor an episode of paroxysmal atrial fibrillation, which ceased spontaneously three weeks ago.The ED doctor gave him a prescription for metoprolol, and advised a follow-up appointmentwith you, the primary care physician. He currently has no complaints. He takes no othermedications. Physical examination revealed no abnormalities. EKG showed normal sinusrhythm. A 2D-Echocardiogram is ordered, which revealed cardiac dilatation and an ejectionfraction of 45%. Which of the following is the most appropriate next step in diagnosis?

A. Refer the patient for ambulatory monitoring of blood pressure (AMBP).B. Refer the patient for cardiac stress test.

C. Refer the patient for renal artery Doppler ultrasound. D. Refer the patient for polysomnography. E. Check BNP (B-Natriuretic peptide) and troponins.

Explanation:

Ischemic heart disease is the most common cause of congestive heart failure (CHF),especially dilated cardiomyopathy, in the United States. Approximately 50 to 75% of thepatients with heart failure (HF) have coronary disease as the etiology. Other known etiologiesare: hypertension (13%), valvular disease (10-to12%), renovascular disease, and very rarecauses, such as obstructive sleep apnea, myocarditis, alcohol or cocaine abuse, etc.

Although this patient is asymptomatic, his echocardiogram results (cardiac dilatation and lowejection fraction) are very suggestive of CHF. The next step in the management of this patientis to identify the etiology of his CHF. Since ischemic heart disease is the most commonetiology, a cardiac stress test should be done first. The objective here is to quickly identify thepresence of ischemia to address the need for coronary angiography (for possiblerevascularization).

(Choices A, C and D) Hypertension, renovascular disease, and sleep apnea are lesscommon causes of CHF.

(Choice E) Troponin and BNP level determination is not useful in this setting. Troponins canbe elevated in any type of heart failure or coronary ischemia. This is also true for BNP (-natriuretic peptide), which is mainly used to distinguish cardiogenic pulmonary edema fromprimary pulmonary conditions.

Educational Objective:The most common cause of heart failure (CHF) is ischemic heart disease. In a new case ofCHF with unknown etiology, efforts must first be made to rule out the presence of coronarylesions which may be corrected by an angioplasty. Other important causes of CHF arehypertension, valvular and renovascular disease.


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A 42-year-old Caucasian woman is brought to the emergency room by paramedics with achange in mental status. She has a past medical history of hypothyroidism, major depression,and chronic back pain. She takes levothyroxine, amitriptyline, and oxycodone regularly. In theemergency room, she is markedly confused, agitated, and keeps talking to herself. Onphysical examination, her temperature is 38.9 C (102 F), respiratory rate is 22/minute, heartrate is 110/minute, and blood pressure is 92/52 mmHg. There is marked flushing, mydriasis,and hyperreflexia. Her EKG reveals the presence of sinus tachycardia, with widening of theQRS interval. You start her on sodium bicarbonate infusion. While waiting for more data, shehas an episode of sustained ventricular tachycardia. Which of the following is the mostappropriate antiarrhythmic in this setting?

A. Lidocaine B. Procainamide C. Propranolol D. Disopyramide E. Quinidine

Explanation:

Tricyclic Antidepressants (TCA) are a frequently prescribed group of medications fordepression, despite having the highest risk for overdose and suicide attempts. TCA overdoseis the leading cause of hospitalization and death. The signs of TCA overdose includehypotension, anticholinergic effects, CNS manifestations, and cardiac arrhythmias.Cardiotoxic effects are responsible for most of the mortality in patients with TCA overdose.

TCAs inhibit fast sodium channels, which result to slowing of the phase 0 depolarization in His-Purkinje tissue and the myocardium. This may lead to QRS prolongation and reentrantarrhythmias, like ventricular tachycardia, ventricular fibrillation, and torsades de pointes.Sodium bicarbonate is the most effective agent for the management of TCA-inducedcardiotoxic effects. Lidocaine is the antiarrhythmic drug of choice for TCA-induced ventriculardysrhythmias.

(Choice C) Propranolol depresses myocardial contractility and conduction and, thus,enhances the tricyclic toxicity.

(Choices B, D, and E) Antiarrhythmic drugs should be used with caution in patients with TCAoverdose. Procainamide, disopyramide, and quinidine have membrane-stabilizing effects andenhance TCA toxicity.

Educational Objective: Lidocaine is the drug of choice for patients with TCA-induced ventricular arrhythmias.


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A 62-year-old Caucasian male is brought to the emergency department (ED) because of painand numbness of his right leg. He says, "I was watching TV two hours ago, when this painstarted, and then my leg turned numb." His past medical history is significant for recent acuteanterior wall myocardial infarction, hypertension, and hyperlipidemia. His current medicationsare metoprolol, ramipril, simvastatin, and aspirin. He admits to not being regularly adherentwith his medications. He does not smoke, and he occasionally consumes alcohol. Histemperature is 36.7C(98F), blood pressure is 150/90 mm Hg, pulse is 80/min, andrespirations are 14/min. Physical examination reveals a cool, right lower extremity withdelayed capillary refill and significant pulse deficits over the popliteal and dorsalis pedisarteries, compared to the left lower extremity. Which of the following is the best next step in themanagement of this patient?

A. Order Doppler Echocardiography. B. Proceed with angiography. C. Refer the patient to the vascular surgeon.

D. Administer IV heparin. E. Hydrate the patient and observe.

Explanation:

This patient's history and presentation suggest a diagnosis of acute arterial occlusion, which ispresumably caused by arterial thromboembolism. Recent myocardial infarction and atrialfibrillation are two most common causes of arterial thromboembolism. The single mostimportant step in the early management of the patients with acute arterial occlusion diagnosedby history and physical examination is immediate IV heparin therapy followed by continuousheparin infusion. Heparin therapy will prevent further propagation of thrombus, and inhibitthrombosis distally in the arterial and venous systems due to low flow and stasis.

(Choices A, B, and C) Immediate anticoagulation therapy should be started in patients withacute arterial occlusion. It cannot wait until after diagnostic procedures are performed, or afterother therapeutic measures (i.e., surgery) are planned.

(Choice E) Delaying anticoagulation therapy may lead to loss of the limb if the ischemia issevere.

Educational Objective:The single most important step in the management of a clinical diagnosis of acute arterialocclusion is immediate IV heparin therapy followed by continuous heparin infusion.


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A 52-year-old male comes to the emergency department because of chest tightness andshortness of breath. The symptoms started two hours ago and woke him up from the sleep. Healso complains of lightheadedness and dry cough. He has type 1 diabetes mellitus and mildintermittent asthma controlled with an albuterol inhaler for symptomatic relief. He was startedon trimethoprim-sulfamethoxazole therapy three days ago for the right big toe infection. Hedoes not use tobacco, alcohol, or drugs. His daughter, who is seven years old, has had anupper respiratory infection recently. His temperature is 37.2C (99.0F), blood pressure is155/92 mmHg, pulse is 100/min and respirations are 22/min. His oxygen saturation is 92% on2L of nasal canula oxygen. His BMI is 27 kg/m2. Scattered wheezes are heard bilaterally.Crackles are heard at lung bases. His initial EKG is shown on the slide below.

Two months ago his EKG was reported to be 'normal.' Which of the following is the mostappropriate next step in management?

A. Anticoagulation, aspirin and close observation B. Cardiac enzymes followed by coronary angiography, if positive

C. Coronary angiography D. CT angiography of the chest E. D-dimer followed by CT angiography, if positive

Explanation:

This patient's EKG shows new onset left bundle branch block (LBBB). Left bundle branch block(LBBB) suggests underlying heart disease and is present in nearly 7 percent of patients withacute myocardial infarction. The LBBB can mask Q waves and change the early and laterventricular depolarization stages, leading to secondary ST segment and T wave changes in the

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same direction as the QRS complex. The left anterior descending artery (LAD) provides themain blood supply to the left bundle branch and a complete blockage of the artery can cause anew LBBB on EKG. There should be a high suspicion of a possible new anterior MI in patientswith a previously normal EKG who present with a new LBBB. The next step should be animmediate coronary angiography in addition to medical therapy.

(Choice A) Aspirin and anticoagulation are indicated in patients with both ST elevation MI(STEMI) and non-ST elevation MI (NSTEMI). However, STEMI patients must get immediatecoronary angiography without delay. New onset LBBB in an appropriate clinical setting issynonymous with STEMI. NSTEMI patients who have evidence of hemodynamic instability,heart failure, ongoing angina, or persistent arrhythmias must also get immediate coronaryintervention. NSTEMI patients who do not have high risk characteristics should undergocoronary intervention as early as possible, preferably within 24 hours.

(Choice B) Cardiac enzymes are a sensitive marker for cardiac injury and also predict bothshort-term and long-term prognosis in acute MI. They may take two to three hours to bepositive and decrease the therapeutic window for coronary angiography in the setting of anacute MI.

(Choice D) CT angiography of the chest is currently most useful for diagnosing pulmonaryembolism. New onset right bundle branch block in an appropriate clinical setting should makeyou think about large pulmonary embolism. CT angiogram is not indicated in acute coronarysyndrome.

(Choice E) D-dimer is elevated in a variety of conditions but is most useful for ruling outpulmonary embolism in patients with low pretest probability.

Educational objective:A new left bundle branch block on an EKG in patients with acute chest pain is suggestive of apossible acute myocardial infarction and should be managed aggressively with coronaryangiography and medical therapy.


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A 36-year-old man comes to the emergency department because of loss of consciousness.He was standing on the crowded subway station when he felt lightheaded, had a poundingsensation in his chest, and then passed out. Upon awakening, he felt short of breath for a littlewhile and then was "completely fine." He denies any chest pain, confusion, tongue biting, orurinary incontinence. He has never had similar episodes. The night before, he was at a partywith his friends and consumed some alcohol. Later he was nauseated and had three episodesof vomiting and one episode of diarrhea. In the emergency department, his blood pressure is124/68 mm Hg and pulse is 80/min. There is a small laceration above his right eyebrow. Heartexamination shows normal heart sounds with regular rhythm. Lungs are clear to auscultation.Neurologic examination shows no abnormalities. Electrocardiogram is shown on the slidebelow.

Item 1 of 2

Which of the following is the most likely cause of this patient's syncope?

A. Acute coronary syndrome B. Bradyarrhythmia C. Orthostatic hypotension

D. Tachyarrhythmia E. Vasovagal syncope

Explanation:

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The electrocardiogram (EKG) presented on the slide above is consistent with Wolff-Parkinson-White (WPW) pattern, a type of preexcitation syndrome caused by an accessorypathway. Normal electric impulses pass from the atria to the ventricles via a specializedconduction pathway, the atrioventricular (AV) node/His-Purkinje system. In patients with WPWsyndrome, there is an extra conduction pathway (also known as bypass tract or accessorypathway) that directly connects the atria to the ventricles, bypassing the AV junction. Theaccessory pathway conducts faster than the AV node and excites the ventricles prematurely,manifesting as a short PR interval with characteristic delta wave on EKG. QRS complex isprolonged (>0.12 sec). All these findings are seen on resting EKG.

Although patients with WPW pattern on EKG can be completely asymptomatic, some developtachyarrhythmias. Paroxysmal supraventricular tachycardia is the most common arrhythmia; itis usually a regular, narrow complex tachycardia. If patients with ventricular preexcitationdevelop atrial fibrillation, they can conduct down the accessory pathway from the atria to theventricles at a very fast rate; therefore, syncope and collapse are common. Progression to life-threatening ventricular arrhythmias may sometimes lead to sudden death. This patient'spresentation, especially drinking the night before (a well-known precipitant of atrial fibrillation),definitely raises that possibility.

(Choice A) Acute coronary syndrome (ACS) can present with symptoms, including nauseaand vomiting, palpitations, and/or syncope, without any chest pain. However, this patient hasno known cardiac risk factors for ACS and does not have the characteristic EKG findings,such as ST segment elevation/depression or T-wave inversions.

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(Choice B) Bradyarrhythmias generally arise from either sinoatrial (SA) node dysfunction orconduction blocks through the AV node and typically present with syncope or presyncope.However, this patient has a WPW pattern on his EKG and felt palpitations before passing out,which make a tachyarrhythmia a more likely possibility.

(Choice C) Orthostatic hypotension is defined as a change in blood pressure and heart ratewith positional change and can be due to an inadequate autonomic response, seen in manyautonomic nervous system disorders, or volume depletion. Although this patient had episodesof vomiting, his presentation is more consistent with WPW syndrome given the palpitationswith the episode and classic EKG.

(Choice E) Vasovagal syncope, also known as neurocardiogenic syncope, can have manytriggering factors, such as stress and pain, and is caused by decreased sympathetic drive(causing vasodilation) combined with increased parasympathetic response (causingbradycardia). The EKG findings in this patient make this a less likely cause of the syncope.

Educational objective:The classic resting electrocardiogram findings in a patient with Wolff-Parkinson-Whitesyndrome are short PR interval, delta wave, and wide QRS complex. Patients becomesymptomatic with tachyarrhythmias. Development of atrial fibrillation can be dangerous as itcan result in ventricular fibrillation and cardiac arrest.


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Item 2 of 2

The patient's serum potassium level is 3.4 mEq/L, blood urea nitrogen level is 12 mg/dL, andcreatinine level is 0.9 mg/dL. Chest x-ray shows no infiltrates or cardiomegaly.Echocardiogram shows normal left ventricular size and function and no significant valvularabnormalities. Which of the following is the most appropriate next step in management?

A. Order 24-hour Holter monitoringB. Refer for catheter ablation

C. Refer for coronary angiography D. Refer for nuclear stress testing E. Refer for tilt-table testing

Explanation:

Catheter-ablation therapy is the recommended therapy in symptomatic patients with Wolff-Parkinson-White (WPW) syndrome. Catheter-ablation therapy has a nearly 90% efficacy rateand a

Educational objective:Catheter-ablation therapy is the preferred treatment of Wolff-Parkinson-White syndrome inpatients with symptomatic arrhythmias.


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A 54-year-old heavyset Caucasian man presents to the emergency department complaining ofchest pain that began approximately thirty minutes ago while he was mowing the lawn. He ispanting and sweating heavily. He describes the chest pain as intense pressure, "like a pickuptruck is right on top of me." The pain radiates to his neck, jaw, and left arm. He has neverexperienced an episode like this before. He has been diagnosed with diabetes mellitus,hypertension, hypercholesterolemia, peptic ulcer disease, and onychomycosis. He smokesone pack of cigarettes per day and consumes 1-3 alcoholic drinks per night. He denies usageof recreational drugs. Vital signs include temperature of 37.7C (99.9F), blood pressure of142/90 mm Hg, pulse of 114/min, and respirations of 21/min. There is diffuse mild chesttenderness to palpation. No edema of the extremities is evident and the remainder of theexamination is unremarkable. He was given oxygen and aspirin while en route to the hospital.Nitroglycerin is now administered, which provides moderate pain relief. Which of the followingfindings on electrocardiogram most strongly indicates the need for thrombolytic therapy?

A. ST depression >1mm in the lateral leadsB. ST elevation >1mm in the lateral leads

C. T wave inversion in the inferior leads D. Poor R wave progression E. QT prolongation

Explanation:

Patients stricken with chest pain suggestive of an acute myocardial infarction are eligible forthrombolytic therapy if they present within 12 (and sometimes 24) hours of symptom onset andif an electrocardiogram demonstrates ST elevations >1mm in two contiguous leads (ChoiceB). It is important to administer nitroglycerin in these patients before performing theelectrocardiogram to rule out coronary vasospasm. Additional candidates for thrombolytictherapy include individuals with persistent symptoms of new left bundle branch block. There isno indication that thrombolytic therapy is of benefit in patients with non-ST elevation acutecoronary syndrome. Contraindications for thrombolytic therapy include evidence of activebleeding, adverse intracerebral history (history of hemorrhage, ischemic stroke, or neoplasm),systolic blood pressure greater than 180 mm Hg, recent trauma, or drug allergy.

ST depression >1mm (Choice A) is commonly caused by ischemia, "strain," digitalis effect,and hypokalemia or hypomagnesemia. ST segment depression is not an indication forthrombolysis unless it is evidence of a posterior or dorsal MI.

T wave inversion (Choice C) commonly occurs in myocardial infarction, angina, andventricular hypertrophy. However, T wave inversion rarely indicates ischemia if the QRS is alsonegative in those leads.

Poor R wave progression (Choice D) occurs when the R wave in leads V1 through V4remains the same size or increases very little. Common pathologic causes of poor R waveprogression include LVH, RVH, COPD, anterior infarction, conduction defects, and

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cardiomyopathy.

The QT interval is considered prolonged (Choice E) if it measures more than half the R-Rinterval, though measurement of the interval is of little clinical significance if the patient istachycardic. Common causes of QT prolongation include drugs (eg, antiarrhythmic agents andtricyclic antidepressants), electrolyte imbalances (eg, hypokalemia), and CNS catastrophes(eg, stroke, seizure).

Educational Objective:Patients with chest pain suggestive of an acute myocardial infarction are eligible forthrombolytic therapy if they present within 12 hours of symptom onset and if anelectrocardiogram demonstrates ST elevations >1mm in two contiguous leads.


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A 45-year-old Caucasian male is brought to the emergency department after losingconsciousness in a shopping mall. He regains consciousness in 5 minutes, and eyewitnessessay that he had no seizure-like activity during the episode. He does not understand whathappened, and describes no preliminary symptoms such as nausea, vomiting andlightheadedness. He has never had such an episode before. He is alert and oriented. His pastmedical history is insignificant. His blood pressure is 130/90 mmHg while supine and 128/87mmHg while sitting. The physical examination findings are within normal limits. What is thebest next step in the management of this patient?

A. Electroencephalogram B. CT scan of the head

C. Electrocardiogram D. Echocardiogram E. Holter monitoring

Explanation:

The cause of syncope can be often established by careful history taking, physical examination,simple lab tests and ECG. Examples of significant diagnostic clues in the history arepreliminary nausea or lightheadedness (neurocardiogenic syncope), convulsions, chest pain,dyspnea, palpitations, etc. Physical examination findings that also provide important clues areorthostatic blood pressure changes, abnormal cardiac examination, response to carotidmassage, etc. ECG helps to reveal brady- or tachyarrhythmias and conduction abnormalitiesthat can explain the symptoms, as well as provide other clues to the presence of organic heartdisease. It has been estimated that this simple evaluation (i.e., history, physical exam andECG) establishes the diagnosis in up to 70% of patients. More complex diagnostic studiesare indicated if specific clues are present; otherwise, these are not cost-effective.

(Choices D and E) When suggested by the history, physical examination or ECG findings, anorganic heart disease can be further evaluated by echocardiography, Holter monitoring,exercise testing and electrophysiological tests. Routine use of these tests in all patients withsyncope is not reasonable.

(Choices A and B) Neurologic tests, including electroencephalogram, brain CT scan, brainmagnetic resonance imaging, and carotid Doppler ultrasound, are frequently obtained inpatients with syncope; however, these are usually of limited value unless specificallysuggested by the history or physical examination.

Educational Objective: The cause of syncope can be established by careful history taking, physical examination,simple lab tests and ECG in 70% of cases.


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A 65-year-old male comes to the emergency department with a two week history ofprogressive shortness of breath. He has been sleeping in a chair for the last three daysbecause he cannot lie flat in bed. His past medical history is significant for hypertension,hyperlipidemia, coronary artery disease, and type 2 diabetes mellitus. He experienced amyocardial infarction two years ago but refused cardiac catheterization. His currentmedications are metoprolol, metformin, losartan, pioglitazone, atorvastatin, glyburide, and low-dose aspirin. He is a lifelong non-smoker. His blood pressure is 151/82 mmHg and his heartrate is 72/min, regular in rhythm. His oxygen saturation is 92% on room air. An S3 heart soundis present on cardiac auscultation. Bilateral crackles are heard on chest examination. There is2+ symmetric bilateral pitting edema. EKG shows normal sinus rhythm with no acute STsegment or T wave changes. Cardiac enzymes are negative. Chest X-ray reveals increasedinterstitial markings with Kerley B lines and small bilateral pleural effusions. Which of thefollowing medications most likely contributed to this patient's current condition?

A. Atorvastatin B. Glyburide C. Losartan D. Metformin

E. Pioglitazone

Explanation:

This patient's orthopnea, hypoxia, bilateral crackles on exam, and chest radiograph findingsare all consistent with pulmonary edema. Of the medications listed, the most likely to result inpulmonary edema is the PPAR- agonist pioglitazone, a member of the thiazolidinedioneclass. PPAR- receptors are present in the collecting tubule of the nephron, and stimulation bypioglitazone results in increased sodium reabsorption. This is the same channel via whichaldosterone mediates its effects on sodium retention. Fluid retention can occur in 4-6% ofpatients on thiazolidinediones, but most of these patients likely have underlying heart failure.This patient's history of a myocardial infarct that was not followed by catheterization, as well asthe presence of an S3 on physical exam, are highly suggestive of underlying heart failure.Given that the aldosterone channel is involved in mediating the sodium retention, treatmentwith an aldosterone inhibitor such as spironolactone may be particularly effective in removingthe excess fluid.

(Choice A) Fluid overload is not associated with statin medications such as atorvastatin. Themost common side effects of statins include hepatotoxicity and muscle injury.

(Choice B) Glyburide is a sulfonylurea medication and as such its most common side effect ishypoglycemia.

(Choice C) ACE inhibitors or ARBs such as losartan are a key component of heart failuretherapy and would not be expected to induce pulmonary edema in patients with underlyingheart failure.

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(Choice D) There is no increased risk of fluid retention with metformin. However, metforminshould be used with caution in patients with heart failure since lactic acidosis can result shouldthe patient become hemodynamically unstable.

Educational objective:The thiazolidinedione medications can result in fluid retention via PPAR- agonist effects onthe renal collecting tubule resulting in sodium reabsorption. This effect is usually seen inpatients with underlying heart failure.


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A 70-year-old Caucasian man is brought to the emergency room by his wife after an episodeof syncope while working in his garden. His wife says that he has always been physicallyactive, but complained of increased fatigability lately. His past medical history is significant fordiabetes mellitus type-2 and gout. His only current medication is glyburide. His blood pressureis 100/80 mmHg, and heart rate is 90/min. Physical examination is significant for a harshcrescendo-decrescendo type murmur that is heard at the base of the heart and radiates to thecarotids. ECG reveals left ventricular hypertrophy and secondary ST segment and T wavechanges. Echocardiography shows concentric left ventricular hypertrophy with severecalcification of the aortic valve. The aortic valve area is 0.78 cm2, and the trans-valvulargradient is 50 mmHg. Which of the following is the best statement about this patient'scondition?

A. The onset of symptoms minimally, if at all, affects the prognosis. B. Conservative treatment should be tried before offering an intervention. C. Balloon valvulotomy is preferred due to low procedural morbidity. D. Balloon valvulotomy is preferred due to better long-term prognosis.

E. Aortic valve replacement is associated with marked reduction in mortality.

Explanation:

This patient presents with symptomatic aortic stenosis. An aortic valve area of less than 1.0cm2 is considered severe stenosis. The onset of symptoms markedly affects the prognosis inpatients with aortic stenosis (Choice A); therefore, prompt intervention is recommended inpatients who have cardinal symptoms of aortic stenosis (dyspnea of heart failure, anginal pain,and syncope). Aortic valve replacement is associated with marked reduction in symptoms andmortality in patients with symptomatic aortic stenosis, and is considered the treatment ofchoice.

(Choices C and D) Balloon valvulotomy is associated with high procedural morbidity andtransient efficacy. It is considered only in selected clinical settings (e.g. patients withhemodynamic instability or significant comorbidities).

(Choice B) Conservative treatment has little role in the management of patients with aorticstenosis, because most medical interventions can destabilize the patients (e.g. diuretics orvasodilators).

Educational Objective: Aortic valve replacement is associated with marked reduction in symptoms and mortality inpatients with symptomatic aortic stenosis, and is considered the treatment of choice.


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A 72-year-old Caucasian man is brought to the emergency department (ED) after having anepisode of syncope during a family meeting. His granddaughter states that in the last couple ofmonths he has been having frequent episodes of dizziness, which are sometimesaccompanied by confusion, and are not related to physical activity or changes in position. Thepatient lives at home, has a history of coronary artery disease and hypertension, and does notuse tobacco or drink alcohol. His medications include aspirin, enalapril, metoprolol, andisosorbide mononitrate. While in the ED, his symptoms are progressively getting better. Thephysical examination reveals a heart rate of 45/min, a blood pressure of 90/50 mmHg, andrespiratory rate of 14/min. No other important clinical findings are noticed. He is fully alert andoriented, and there are no focal neurologic findings. An EKG shows a constant PR interval of0.18 ms and a normal QT interval, but the QRS complexes are lost on every third beat. Whichof the following is the most appropriate course of action?

A. Administer intravenous atropine. B. Observe and admit. C. Place an external pacemaker.

D. Place a transvenous pacemaker. E. Place the patient on telemetry or Holter monitor for 24-48 hours.

Explanation:

This patient has Mobitz II, second-degree atrioventricular (AV) Block. In comparison to MobitzI, second-degree AV Block (Wenckebach's), the PR does not prolong progressively, but QRScomplexes are suddenly lost. Mobitz II AV Block can cause dizziness, episodes of syncope, ortransient altered mental status, thus explaining the symptoms of the patient. Because Mobitz IIcan progress to third-degree AV Block, it needs to be managed with a permanent pacemaker.Even if the patient is asymptomatic, the AHA/ACC (American Heart Association/AmericanCollege of Cardiology) consensus advises the use of a permanent pacemaker insertedthrough a venous access.

(Choice B) It would be unsafe to manage a patient with this condition without a pacemaker.Observation is not an option.

(Choice A) Atropine will increase the heart rate, worsening the heart block. Atropine is usuallyindicated for sinus bradycardia; in that case, QRS complexes will not be lost.

(Choice C) An external pacemaker will only be a temporary solution and may require sedationof the patient. It is generally used for acute rate control, not for this chronic condition.

(Choice E) A Holter monitor or telemetry is not needed at this point to evaluate the cause ofthe syncope if Mobitz II is treated appropriately.

Educational Objective:Mobitz II second-degree AV Block is diagnosed when the EKG shows bradycardia withpreservation of the PR interval, accompanied by periodic loss of QRS complexes. This

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condition is an indication for permanent cardiac pacemaker insertion.


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A 27-year-old woman is brought to the emergency department because of a 4-hour history ofsubsternal chest pain. She has not had nausea, vomiting or shortness of breath. She smokedcrack cocaine shortly prior to her episode of chest pain. She has a history of intravenous druguse. She has no family history of premature coronary artery disease. She does not take anymedications and has no known drug allergies. Her temperature is 37.8 C (100 F), bloodpressure is 204/102 mm Hg, pulse is 102/min, and respirations are 18/min. She appears thin,anxious, and agitated. Cardiac examination shows normal heart sounds. The lungs are clearto auscultation. An ECG shows a sinus tachycardia but is otherwise unremarkable. An x-rayfilm of the chest shows no abnormalities, and the initial set of cardiac enzymes is normal.

Item 1 of 2

Which of the following is the most appropriate next step in management?

A. Anticoagulation with low-molecular-weight heparin B. Cardiac catheterization C. High-dose ibuprofen

D. Intravenous lorazepam E. Intravenous metoprolol

Explanation:

Chest pain in patients who have recently taken cocaine is common and caused by severalfactors, including increased myocardial oxygen demand, vasoconstriction, and aprothrombotic state (secondary to platelet activation). Patients who have recently takencocaine have an increased rate of myocardial infarction and aortic dissection, and the risk ofthese complications is highest in the first hours after drug use.

For the most part, management of patient with cocaine related chest pain is similar to chestpain in the general population. One key difference is that cocaine-related chest pain patientsshould be treated early with benzodiazepines. Benzodiazepines (e.g. lorazepam) candecrease anxiety and agitation associated with cocaine use. Because the cardiovascularmanifestations of cocaine use are intimately associated with its neuropsychiatric effects,benzodiazepines may indirectly decrease myocardial ischemia by resolving associatedhypertension and tachycardia.

(Choice A) Anticoagulation with heparin should only be performed if there is evidence ofmyocardial infarction in the form of positive cardiac biomarkers or abnormal ECG findings.

(Choice B) Emergent cardiac catheterization should be performed if the patient has evidenceof ST elevation on ECG.

(Choice C) Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen should only be

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used in cases of chest pain with a suspected musculoskeletal etiology. Musculoskeletal chestpain is typically a diagnosis of exclusion.

(Choice E) Although beta-blockers are used in the management of myocardial infarction inthe general population, they should be avoided in patients with recent cocaine use to preventcoronary vasospasm caused by unopposed alpha stimulation.

Educational objective:Management of cocaine-related chest pain is similar to management of chest pain in thegeneral population with a few key exceptions. Benzodiazepines should be given early to thesepatients to decrease neuropsychiatric manifestations of cocaine use and thereby improvehypertension and tachycardia. In addition, beta-blockers should be avoided in patients withcocaine-related chest pain to avoid causing coronary vasospasm.


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Item 2 of 2

In spite of initial treatment measures, the patient continues to have chest pain. Her bloodpressure is 216/112 mm Hg and pulse is 103/min. Which of the following is the mostappropriate pharmacotherapy for this patient's hypertension?

A. Intravenous loop diuretics B. Intravenous metoprolol C. Intravenous morphine

D. Intravenous phentolamine E. Oral angiotensin converting enzyme inhibitors

Explanation:

Benzodiazepines often improve tachycardia and hypertension in patients with cocaine-relatedchest pain to the degree that myocardial ischemia is lessened. However, this patient ispersistently hypertensive and more aggressive blood pressure treatment is thereforeindicated. Phentolamine is an alpha-antagonist which is a frequently used option formanagement of persistent hypertension after cocaine use. Phentolamine also decreasescoronary vasospasm, which may be a precipitating factor for myocardial ischemia in patientswith recent cocaine use. Phentolamine may be helpful for management of hypertensiveemergency in patients with any cause of increased sympathetic activity, which would alsoinclude pheochromocytoma. Alternative options for blood pressure management in this casewould include nitroglycerine and nitroprusside.

(Choice A) Loop diuretics are typically used more as a treatment for volume overload asopposed to hypertension, and there is no evidence that this patient is fluid overloaded.

(Choice B) Beta-blockers such as metoprolol should be avoided in patients with recentcocaine use because they can result in unopposed alpha effects with subsequent coronaryvasospasm.

(Choice C) Benzodiazepinesnot opioidsare typically the treatment of choice formanaging the neuropsychiatric effects of cocaine use.

(Choice E) ACE inhibitors may be indicated before discharge from the hospital if the patienthas had a myocardial infarction, but they are not used to acutely lower blood pressure duringinitial evaluation.

Educational objective:In patients with cocaine-related chest pain, more aggressive management of hypertension isindicated when blood pressure does not improve with benzodiazepines. Phentolamine isparticularly effective and additionally decreases coronary artery vasospasm, althoughnitroprusside and nitroglycerine are also reasonable options. Beta-blockers should beavoided.

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56% of people answered this question correctly; 3/19/2011 Item 29 of 38


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A 62-year-old Caucasian man comes to the emergency department (ED) and complains ofcrushing substernal chest pain. The pain started one hour ago while he was shoveling snow onhis driveway. At the onset of his pain, he took nitroglycerin sublingually, but the pain did not getany better and he was taken to the ED by his son. He has a history of coronary artery disease,hypertension, hyperlipidemia, and osteoarthritis. He is on daily aspirin, metoprolol, lisinopril,atorvastatin, and naproxen as needed. In the ED, his electrocardiogram reveals a normalsinus rhythm with no acute ST-T wave changes. He is given morphine for his pain, started onnitroglycerin drip, and admitted to the telemetry floor. The next day, an adenosine thalliumstress test reveals a moderate size reversible perfusion defect in the lateral wall of the leftventricle. Which of the following coronary vessels is most likely to have a significant occlusion?

A. Left circumflex coronary artery B. Left anterior descending coronary artery C. Left main coronary artery D. Right coronary artery

Explanation:

In all patients with known or suspected coronary artery disease, exercise or pharmacologicalstress testing with radionuclide myocardial perfusion imaging (thallium or technetium-99m) isuseful for confirming the diagnoses and for risk stratification. The pharmacologic stress agents(adenosine and dipyridamole) act by producing coronary vasodilatation and increasing thecoronary flow rate and velocity. In normal coronary vessels, the resulting vasodilation increasesthe blood flow; however, in areas with severe stenosis, there is already a compensatorymicrovascular dilatation at rest to maintain normal blood flow, so no further increase in the flowoccurs. The resulting heterogenous blood flow due to the stenotic or occluded region isdetected by radionuclide imaging studies as a perfusion defect. After establishing thepresence of a defect, the next step is to localize the affected myocardial region in order toidentify the culprit vessel.

All coronary arteries supply a specific region of the ventricle. In this case, the patient'sadenosine thallium stress test revealed a perfusion defect in the lateral wall of the left ventricle.The culprit vessel is most probably the left circumflex artery, which runs laterally in