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A. Transesophageal echocardiography
B. MRI of the chest
C. Cardiac enzymes
D. Coronary angiogram
E. Ventilation-perfusion scan
F. Arterial blood gas analysis
Explanation:
This patient is most likely suffering from acute aortic dissection for which a
transesophageal echocardiography or computed tomography of the chest are the
diagnostic studies of choice. Marfan's syndrome predisposes to the development
of aortic dissection. Tearing pain with radiation to the back and a difference in BP
of greater than 30 mmHg between two arms are important clinical clues for aortic
dissection.
MRI is used to establish the diagnosis of aortic dissection when its presentation
is chronic or when there is no hemodynamic instability.
EKG and cardiac enzymes are of great importance when coronary artery disease
is suspected. This patient has no risk factors for CAD and his pain is not typical
of CAD.
Educational Objective:
Transesophageal echocardiography or computed tomography are the diagnostic
studies of choice for suspected aortic dissection.
The left ventricular diastolic pressure is normal in pure mitral stenosis. These
pressures become elevated when there is coexistent mitral regurgitation, aortic
valve disease, systemic hypertension, or coronary artery disease.
Educational Objective:
The hallmark finding of MS is elevated left atrioventricular pressure gradient.
This patient most likely has a left ventricular aneurysm, which is a late
complication of an acute MI. It usually occurs after an anterior wall MI and may
be either asymptomatic, or it may present with congestive heart failure, an
arterial embolism, or sustained ventricular arrhythmias. Precordial examination
may show a double apical beat. Auscultation of the heart may reveal an
additional S3 or S4 and sometimes a murmur of mitral regurgitation is present
due to papillary muscle dysfunction, annular dilatation, or abnormal left
ventricular geometry. Chest x-ray usually shows a characteristic prominence of
the left border of the heart. The EKG shows persistent ST segment elevation.
Ventricular septal defects and papillary muscle rupture may complicate an acute
MI. However, these complications occur much earlier within the first week post
MI and they usually present acutely with a new pansystolic murmur and
cardiogenic shock.
Educational Objective:
LV aneurysm can cause CHF in a patient who sustained an anterior wall MI in
the past. A double apical beat and persistent elevation of the ST segment are
important diagnostic clues.
A. ACE inhibitor
B. Calcium channel blockers
C. Loop diuretics
D. Digoxin
E. Dobutamine
F. Home oxygen therapy
Explanation:
Of all the above-mentioned drugs only ACE inhibitors have been shown to
decrease long-term mortality in patients with ischemic cardiomyopathy and LV
systolic dysfunction. Several randomized and meta analysis studies have proved
this benefit. ACE inhibitors should be considered in all patients with coronary
artery disease who have an EF of less than 40%.
Therapy with digoxin does not improve survival but it provides symptomatic
benefit in patients with systolic dysfunction and sinus rhythm. They are also used
to control ventricular rate in patients of heart failure who have atrial fibrillation.
Use of digoxin has been associated with less hospitalizations and lower health
care costs.
Loop diuretics are very useful in providing symptomatic relief in those patients
with heart failure who have pulmonary or peripheral edema. However, they have
not been shown to improve survival. The only diuretic, which has shown some
survival benefit in patients with severe heart failure, is spironolactone.
Calcium channel blockers have no role in the treatment of CHF and they do not
provide any survival benefit. In fact, they can worsen the peripheral edema by
causing peripheral venous dilatation.
Educational Objective:
Know that ACE inhibitors are the survival improving drugs in congestive heart
failure.
This patient has classic EKG of third degree heart block. In third degree AV
block, no atrial impulses will travel to ventricles. So, atria and ventricles beat
independently and have their respective rates; in this case the atrial rate is
80/min and the ventricular rate is around 30/min. These patients are at very high
risk for sudden cardiac death and they should be admitted in ICU and permanent
pacemaker should be placed as soon as possible. Atropine should always be
made available at the bedside. (Option C).
Option B: An EP study does not need to be done in all patients. This patient has
a coronary artery disease and suffered a conduction block. The EP study does
not change the treatment or the prognosis. EP studies are usually done to
identify the arrhythmia and look for the location of conduction block.
Option D: Observation alone is not indicated for any patient with complete heart
block.
Option E: Starting beta-blockers is the one thing that you can do to kill this
patient immediately; so, obviously it is not the treatment that you would want.
Beta-blockers are contraindicated in all types of heart block.
Educational objective:
Complete heart block is a dangerous condition, which can cause sudden cardiac
death. It requires immediate placement of permanent pacemaker.
A. Diphtheric myocarditis
B. Premature coronary artery disease
C. Trypanosoma cruzi
D. Giant cell myocarditis.
E. Rickettsial myocarditis.
Explanation:
Educational Objective:
Any patient who comes from South America and have findings suggestive of
cardiomyopathy should make you think about Chaga’s disease.
The above patient is most likely suffering from shock secondary to left ventricular
dysfunction. Shock has multiple causes and may result from hypovolemia, sepsis
and cardiac causes. The above patient’s shock may be due to any of the above-
mentioned etiologies and therefore right heart catheterization is essential to
make the diagnosis in this case.
The physical exam findings and the elevated pulmonary capillary wedge
pressure are compatible with left ventricular dysfunction.
In both constrictive pericarditis and pericardial tamponade, right and left sided
diastolic pressures are equal and elevated. In the above patient, his pulmonary
capillary wedge pressure is elevated but not equal to right atrial pressure thus
excluding the diagnosis of pericardial tamponade and constrictive pericarditis.
In cases of septic shock both right atrial pressures and pulmonary capillary
wedge pressure are low.
Educational Objective:
Recognize the clinical features of cardiogenic shock. Elevated PCWP is the most
important finding to concentrate.
A. Acute pericarditis
B. Recurrent ischemia
C. Recurrent infarction
D. Dressler’s syndrome
E. Pulmonary embolism
Explanation:
This patient is most likely suffering from acute pericarditis. Typical findings of
acute pericarditis in this patient include chest pain, worsened by breathing and
improved by leaning forward, presence of a pericardial friction rub and diffuse ST
segment elevation that is concave upwards.
Recurrent ischemia is unlikely as the cause of his chest pain. Ischemic chest
pain is not aggravated by breathing and is not relieved by sitting forward.
Recurrent infarction is unlikely as a cause for his chest pain. Pain in cases of
infarction would be of the ischemic type and CK-MB would also be elevated.
Troponins remain elevated for 1-2 weeks after an acute MI, while CK-MB returns
to normal within 48-72 hours. ST elevation will be convex upwards and is seen in
certain leads, indicating a certain territory, for example either inferior, anterior or
the lateral leads etc.
Educational Objective:
Recognize and differentiate acute pericarditis from other causes of recurrent
chest pain in the setting of an acute MI.
A. Aortic regurgitation
B. Pulmonary regurgitation
C. Mitral stenosis
D. Tricuspid stenosis
E. Aortic stenosis
F. Tricuspid regurgiation
Explanation:
The most likely diagnosis in this patient is aortic regurgitation. This patient has
features of biventricular congestive heart failure secondary to valvular disease.
Presence of collapsing (water-hammer) pulse is a clue for aortic regurgitation
and occurs due to the hyperdynamic circulation and early diastolic run-off. She
has a characteristic murmur of aortic regurgitation that is early diastolic,
decrescendo, high-pitched, blowing best heard in the left third intercostal space.
The murmur is intensified by leaning forward and holding the breath in expiration
(Valsalva).
The murmur of mitral stenosis is a mid-diastolic rumble and it is best heard at the
apex.
The murmur of the aortic stenosis is ejection systolic and best heard at right 2nd
intercostal space.
Educational Objective:
Recognize the clinical features of aortic regurgitation.
A 35-year-old woman who has recently immigrated from Asia presents to the
emergency room with acute onset of dyspnea. She denies any cough, chest
pain, or fever. She has a history of rheumatic heart disease as a teen. On
examination, she has an irregular PR: 97/min; BP: 125/75 mm of Hg;
Temperature: 37.2C(98.9F). Examination of precordium shows tapping apical
impulse. First heart sound is loud and a mid-diastolic rumble is heard at the
apex. Crepitations are present in both lung fields. EKG shows an irregularly,
irregular heart rhythm and the absence of ‘P’ waves. Which of the following is
most likely the cause of abnormal heart rhythm in this patient?
This patient is in congestive heart failure due to atrial fibrillation (the irregularly,
irregular heart rate and absence of ‘P’ waves) which itself is secondary to mitral
stenosis (H/O rheumatic fever, mid diastolic rumble, and loud S1). Left atrial
enlargement that results from mitral stenosis predisposes the patient to the
development of atrial fibrillation. Left atrial enlargement causes atrial fibrillation
by increasing the refractory period as well as the action potential duration and it
is responsible for all cases of atrial fibrillation occurring in the setting of MS.
Left ventricular dilatation and left ventricular hypertrophy do not occur in isolated
MS.
Right atrial dilation is a late finding in the course of MS and it occurs when right
sided heart failure takes place secondary to pulmonary hypertension. Right atrial
dilatation may cause atrial fibrillation also, but in cases of MS, the cause for atrial
fibrillation is usually left atrial dilation that occurs earlier in the course of disease.
Pulmonary HTN itself does not cause atrial fibrillation, but the right atrial
enlargement that results from it, does.
Educational Objective:
Atrial fibrillation in MS is due to left atrial dilatation.
Reduced salt intake only improves symptoms of heart failure and does not
reverse the disease process itself.
Digitalis is most useful in those heart failure patients who have systolic
dysfunction and have rapid ventricular rates due to atrial flutter or atrial
fibrillation. It proves to be useful in these cases by its positive inotropic effect and
negative dromotropic (slowing AV conduction). Use of digitalis has not been
shown to provide any survival advantage in patients with congestive heart failure
and has not been shown to reverse the disease process.
ACE inhibitors have been shown to slow the progression of heart failure but they
don’t reverse the disease process of alcoholic cardiomyopathy. ACE inhibitors
should be given to all patients with heart failure who have systolic dysfunction
unless they are contraindicated or the patients can’t tolerate them.
Cigarette smoking is a risk factor for coronary heart disease and its cessation
should be encouraged in all patients with heart failure. Cessation of cigarette
smoking does not reverse the disease process of alcoholic cardiomyopathy.
Educational Objective:
Know how to diagnose and manage a patient with congestive heart failure due to
alcoholic dilated cardiomyopathy.
34% of people answered this question correctly
A. Early third heart sound and inspiratory increase in jugular venous pulse
B. Water hammer pulse and pistol shot femorals
C. Tapping apex beat and malar flush
D. Pulsus paradoxus and hypotension
E. Pansystolic murmur at left lower sternal border
Explanation:
This patient, most likely, has constrictive pericarditis. The finding of pericardial
calcifications on the chest X-ray is an important clue. The etiology of pericarditis
is probably from her prior history of Tuberculosis. The early third heart sound,
that is also called pericardial knock and the inspiratory increase in the jugular
venous pressure (Kussmaul’s sign), are important physical findings of
constrictive pericarditis. Kussmaul’s sign is also present in right sided heart
failure, severe tricuspid regurgitation, right ventricular infarction and cardiac
tamponade.
Water hammer or collapsing pulse and pistol shot femoral pulses are diagnostic
clues to aortic regurgitation. These physical findings occur due to a
hyperdynamic circulation and early diastolic runoff of aortic insufficiency.
Tapping apex beat and malar flush are important physical findings of mitral
stenosis. Pulsus paradoxus is defined as greater than 10-mmHg fall of the
systolic blood pressure during inspiration.
The need of antibiotic prophylaxis for IE depends on the cardiac abnormality and
the procedure causing bacteremia. Certain cardiac conditions are more
susceptible to endocarditis than others. The risk of bacteremia and the likely
organisms vary according to the procedure being performed. Therefore, the
decision whether or not to prophylax, and the choice of antibiotics, depends both
on the cardiac abnormality and on the procedure.
Cardiac abnormalities are high risk, moderate risk or negligible risk. Antibiotic
regimen is different for GI and GU procedures in high-risk and moderate-risk
patients. Antibiotic prophylaxis is not recommended in moderate-risk patients
with some low-risk procedures. Generally, we can say that prophylaxis is
recommended for high-risk conditions and is optional for moderate-risk
conditions.
Educational Objective:
Patients with artificial pacemakers and defibrillators do not require prophylaxis for
infective endocarditis.
A. Angina pectoris
B. Myocardial infarction
C. Acute pericarditis
D. Aortic dissection
E. Pulmonary embolism
Explanation:
This patient is most likely suffering from aortic dissection. The most frequent
predisposing condition for aortic dissection is hypertension. Sudden onset of
severe tearing pain, with radiation to the back, is a typical presentation of aortic
dissection. The finding of a difference of more than 30 mmHg in the blood
pressure readings between two arms is another important clue for the diagnosis
of aortic dissection.
Pain of IHD usually feels like pressure and it typically radiates to the jaw, left
shoulder or left arm. Pain of angina occurs with exertion and is relieved with rest
and sublingual nitroglycerin. Pain of MI occurs at rest and is not fully relieved by
sublingual nitroglycerin. EKG usually provides evidence for ischemic heart
disease with T-wave inversion in angina pectoris, and ST segment elevation or
ST segment depression in cases of MI. The nature of pain in the above patient
with absent EKG changes makes the diagnosis of angina, or MI, very unlikely.
Pulmonary embolism usually presents with sudden onset of dyspnea, chest pain,
tachycardia, and tachypnea. There is usually a history of risk factors like
immobilization, surgery of hip or femur etc. that predisposes the development of
pulmonary embolism.
Educational Objective:
Suspect aortic dissection as a cause of tearing chest pain in the setting of HTN
and BP difference in the 2 arms.
A. IV lidocaine
B. Defibrillation
C. IV digoxin
D. IV amiodarone
E. Stat echocardiogram
F. STAT check of potassium and magnesium
Explanation:
(Option E): Echo may be done later to assess the heart function but it does not
change the management of ventricular fibrillation. Ventricular arrhythmias are
more prone in patients with ischemic heart disease and in those with low ejection
fractions.
(Option F): When ventricular fibrillation occurs, the first thing is to defibrillate the
patient. Electrolytes and blood gas analysis can be done during the procedure
but should not delay shocking. Ventricular arrhythmias may occur in the
presence of hypokalemia.
Educational objective:
The treatment of ventricular fibrillation is STAT defibrillation with 200-360 joules.
If defibrillation fails, lidocaine or amiodarone (drug of choice) can be loaded and
the patient shocked again. Epinephrine can sensitize the heart and lower the
threshold for conversion.
35% of people answered this question correctly
Urinalysis is within normal limits. What is the most likely cause of the edema in
this patient?
A. Heart failure
B. Liver disease
C. Renal disease
D. Venous insufficiency
E. Side effect of her medications
Explanation:
Liver diseases (Choice B) can cause lower extremity edema, but usually ascites
dominates over peripheral edema, and abnormal laboratory findings
characteristic of liver dysfunction are present (e.g., hypoalbuminemia,
hyperbilirubinemia).
Educational objective:
Dihydropyridine Ca-channel antagonists can cause peripheral edema and
should always be considered in the differential diagnosis of this condition, along
with other causes, such as heart failure, renal disease and venous insufficiency.
A. Penicillin prophylaxis
B. Refer to cardiology for balloon valvotomy
C. Refer to cardiothoracic surgeon for mitral valve replacement
D. Consider anticoagulation
Explanation:
This patient is suffering from rheumatic heart disease with pure mitral stenosis.
Although he is asymptomatic at this stage, his disease is likely to be progressive.
It has been found that prevention of recurrent attacks of rheumatic fever may
slow down the progression of mitral stenosis. Therefore, penicillin prophylaxis
with monthly IM injection of benzathine penicillin is recommended in adolescent
patients in whom the recurrence risk is high. Patients with, or without, carditis
need penicillin prophylaxis, although the recommended duration of prophylaxis is
10 years in the former and 5 years in the latter. Patients with mitral stenosis are
also at high risk for thromboembolism. Anticoagulation is indicated if they have a
history of an embolic event or they have intermittent or chronic atrial fibrillation.
Surgical intervention for mitral stenosis is indicated when these patients develop
symptoms of NYHA functional class III or IV. Balloon valvotomy is the procedure
of choice when there is favorable valve morphology.
Mitral valve replacement is considered to be the last resort for the treatment of
MS because of the high perioperative mortality and morbidity.
Educational Objective:
Know that prevention of recurrent attacks of rheumatic fever with antibiotic
prophylaxis may slow down the progression of mitral stenosis in adolescents.
Asymptomatic MS do not require any treatment except penicillin prophylaxis.
Choice (A): Obtaining cardiac enzymes is incorrect because the patient doesn’t
have any risk factors for an MI. Her ECG changes are secondary to ischemia
and not due to infarction.
Choice (B): TEE is the initial investigation of choice to diagnose suspected aortic
dissection. But it is indicated only after hypertension treatment is initiated.
Choice (E): CT scan of chest also has high sensitivity and specificity and can be
used instead of the transesophageal echo.
Educational Objective:
Antihypertensive management should be the first step in patients with aortic
dissection with hypertension.
A. Electrocardiogram
B. Echocardiography
C. Cardiac catheterization
D. Stress testing
E. MRI
F. Exercise thallium SPECT imaging
Explanation:
Cardiac catheterization is not required for the diagnosis of HCM but it helps to
quantify the pressure gradient and to exclude coexistent coronary artery disease
as a cause of chest pain in older patients.
Educational Objective:
The investigation of choice for the diagnosis of HCM is echocardiography.
Of all the above choices, only ACE inhibitors, aspirin, and beta-blockers have
been shown to reduce mortality after acute MI.
Aspirin has also been shown to be effective and should be given in all patients,
as early as possible in the setting of an acute MI, because it has been shown to
reduce mortality by as much as 30%.
Morphine is an effective analgesic and is used for pain relief in the setting of an
acute MI. Oxygen is useful only when pulse oximetry shows hypoxemia. Its
routine use in all patients of acute MI is not cost effective. Nitrates are used only
for pain relief in the setting of acute MI and they don’t incur any survival
advantage. IV nitrates should be avoided when there is hypotension or evidence
of right ventricular infarction. IV magnesium is indicated only when initial testing
shows low serum magnesium level. Routine use of IV magnesium in all MI
patients does not provide any survival benefit.
Educational Objective:
Aspirin, ACE inhibitors, and beta-blockers have been shown to reduce mortality
in the setting of acute MI.
A. Dilated cardiomyopathy
B. Restrictive cardiomyopathy
C. Hypertrophic cardiomyopathy
D. Cardiac tamponade
E. Constrictive pericarditis
Explanation:
Educational Objective:
Know how to diagnose restrictive cardiomyopathy and how to differentiate it from
other cardiac conditions that may present similarly.
A. Septic embolism
B. Raynaud’s syndrome
C. Norepinephrine
D. Aortic occlusion
E. Thrombosis of forearm vessels
Explanation:
The above presents a case of a patient who is hypotensive and receives fluid
and pressor support. Later, he is found to have all digits blue. The most likely
cause of this patient’s pathology is related to use of norepinephrine.
Norepinephrine is a powerful vasoconstrictor and can lead to decreased blood
supply to both the lower and upper extremity. Norepinephrine is a powerful
pressor drug and frequently used to revive patients in shock. In addition to
decreasing blood supply to the digits, other organs like the kidneys can also be
affected. For this reason, the use of this vasoconstrictor is limited in the ICU.
Patients who have prior atherosclerotic and peripheral vascular disease are most
sensitive to norepinephrine (Option C).
Option A: Emboli to all five digits of the hand is very rare. Embolus in the upper
extremity is very rare and is occasionally related to procedures done in the
brachial artery. Emboli usually affects one or two digits and only the tips of the
finger will be blue. Large emboli will usually affect the entire blood supply to the
radial or ulnar arteries and the bluishness/cyanosis will be visible at the wrist or
forearm. Even a complete occlusion of the radial artery is well tolerated by most
patients.
Option D: Occlusion of the aorta does not produce selective bluishness of the
fingers. Sometimes, occlusion of the subclavian artery can occur in thoracic
outlet syndrome and leads to a cool hand. In this case, the entire hand is cold
and painful, requiring urgent treatment. Occlusion of the aorta generally occurs in
the abdominal area and leads to decreased blood flow to the lower extremities.
Acute aortic occlusion can compromise blood flow to the lower extremities and
abdominal organs.
Option E: Thrombosis of the forearm vessels is very rare and does not present
acutely with a cold hand. Thrombosis of the forearm vessels may be seen in
Buerger’s disease. Buerger’s disease is seen in young males who are heavy
smokers. Digital ischemia and gangrene are common features.
Educational Objective:
Bluish discoloration and cool fingers in the ICU are a common finding after use of
norepinephrine for hypotension.
Atrial flutter, atrial fibrillation and Mobitz type II block are rare arrhythmias
induced by digitalis toxicity.
Atrial tachycardia along with variable degree of AV block is the most important
EKG finding of digitalis toxicity and it has a high specificity for digitalis toxicity.
Educational Objective
Know the electrocardiographic manifestations of digitalis toxicity.
Educational Objective:
Know the physiology of HCM and be able to correctly identify the factors that
increase or decrease the intensity of the murmur in HCM.
(Choice D) Hypokinesia of the inferior wall would be seen in case of inferior wall
myocardial infarction, but clinical presentation of this patient is not suggestive of
myocardial infarction.
(Choice E) Aortic valve vegetation can cause aortic regurgitation, which, if acute,
would not have dilated heart; and, if chronic, would have eccentric hypertrophy of
the heart. Also, patients with infective endocarditis appear sick, and they will
have low to high-grade fevers, chills, or night sweats.
A. Arrhythmia
B. Postural hypotension
C. Situational syncope
D. Seizure
E. Transient ischemic attack (TIA)
Explanation:
Cardiovascular causes like arrhythmia (Choice A) are less likely because there
are no signs of a structural heart disease on the physical examination and
the ECG.
Educational objective:
Situational syncope should be considered in the differential diagnosis of syncopal
episodes. The typical scenario would include a middle age or older male, who
loses his consciousness immediately after urination, or a man who loses his
consciousness during coughing fits.
Severe systolic dysfunction and increased left ventricle size are features of
dilated cardiomyopathy.
Educational Objective:
Understand the presentation of restrictive cardiomyopathy and know its
pathophysiology and hemodynamics
A. Autosomal dominant
B. Autosomal recessive
C. X-linked recessive
D. X-linked dominant
E. Multifactorial
Explanation:
Educational Objective:
HCM follows autosomal dominant inheritance.
A. Start digoxin
B. Start metoprolol
C. Start spironolactone
D. Start verapamil
E. Give IV dobutamine
Explanation:
The most appropriate next pharmacological measure for the treatment of this
patient's CHF is the addition of digoxin to his regimen. Digoxin slows the
ventricular response rate in atrial fibrillation by slowing down AV conduction and
thus increasing the diastolic filling. It also has a beneficial effect in patients of
systolic dysfunction due to its positive inotropic effect. Thus any patient who has
atrial fibrillation and heart failure will benefit from digoxin; it should be considered
over before beta-blockers or calcium channel blockers.
Another next best choice in the management of this patient' which is not given in
the choices would be to anticoagulate the patient, as this is one of the most
important interventions in reducing the morbidity and mortality associated with
atrial fibrillation
Verapamil, as well as metoprolol, will slow down the ventricular response rate by
its negative dromotropic effect but it may worsen systolic dysfunction by its
negative inotropic effect. Beta-blockers are indicated for heart failure patients
who are NYHA class II or III with systolic dysfunction. Beta-blockers are
preferred over the digoxin or calcium channel blockers in patients with coronary
artery disease. Calcium channel blockers are not the best drugs for patients with
heart failure due to their negative inotropic effect.
Educational Objective:
Know how to manage a case of CHF exacerbation due to atrial fibrillation with a
rapid ventricular response. Digoxin is the drug of first choice in this situation.
Although this patient does have ST elevation in the anterior leads, considering
his age, and other features like pupillary dilatation and bleeding from the nose,
cocaine use seems more likely. However, a complete cardiac work up is
mandatory to rule out other cardiac causes for his symptoms. A chest x-ray,
cardiac enzymes and urine toxicology screen would be necessary to make an
accurate diagnosis.
For the same reasons as above, cocaine intoxication would be the most likely
diagnosis. Acute pericarditis would present with diffuse ST elevations (ST
elevations in all the leads) on EKG.
Aortic dissection usually does not cause pupillary dilatation; however, those
patients may have severe chest pain and hypertension,
Educational Objective:
Think of cocaine intoxication in a young patient presenting with chest
pain/myocardial infarction or stroke. Features of cocaine intoxication are cocaine
bugs, agitation, decreased appetite, dilated pupils, elevated or decreased blood
pressure, tachycardia or bradycardia, and sweating.
A. Cor pulmonale
B. Tuberculosis
C. Viral infection
D. Psittacosis
E. Pneumoconiosis
Explanation:
Option A: This patient has no finding suggestive of chronic lung disease, which
would lead to cor pulmonale. Also cor pulmonale would not cause constrictive
pericarditis.
Educational objective:
Tuberculosis is the most common cause of constrictive pericarditis, in immigrant
population. It should be considered in patients with unexplained elevation of JVP
and history of predisposing condition.
A. Observation
B. Atenolol
C. Pacemaker
D. Electrophysiology study
E. Cardiac catheterization
F. Atropine
Explanation:
Option A: First-degree heart block requires no treatment. The heart rate is not
affected and neither bradycardia nor any form of AV block is seen. Atropine,
which is an anticholinergic agent, is never used to treat first-degree heart block.
Atropine increases heart rate.
Option B: Beta-blockers have no role in the treatment of heart block of any form.
Beta-blockers can precipitate and worsen heart block. First-degree heart block
does not affect the heart rate or the force of contraction. Beta-blockers are
generally used as anti-hypertensives, anti anginals and anti arrhythmics.
Educational objective:
First-degree heart block is a completely benign arrhythmia and requires no
treatment.
A. Coxsackie virus
B. Mycobacterium tuberculosis
C. Borrelia burgdorferi
D. Uremia
E. Streptococcal pneumoniae
F. Coronary artery disease
Explanation:
Severe constant pain that localizes over the anterior chest, radiates to the arm,
shoulder, back, epigastrium or neck, is intensified with inspiration, and relieved
by sitting up and leaning forward represents a classic presentation of acute
pericarditis. The pain is often difficult to differentiate from an ischemic pain
because often it is very severe, short, and sometimes has a constricting quality
that radiates either to one or both arms. However, pain which is relieved by
sitting up and leaning forward and is intensified by inspiration or lying supine is
characteristic of acute pericarditis. Acute pericarditis has a very broad differential
diagnosis. But it is most commonly caused by viruses and Coxsackie virus is a
frequent offender. A history of a recent viral illness is common. Other viruses
implicated include echovirus, adenovirus, EBV, and HIV. The classic findings of
pericarditis on EKG are:
1.Diffuse ST segment elevation with upward concavity at ‘J’ point.
2.No new ‘Q’ waves
3.'PR’ segment elevation in aVR with ‘PR’ depression in other leads.
Uremia can cause acute pericarditis and this may represent an indication for
dialysis. The above patient does not have any clue about renal insufficiency.
Educational Objective:
Recognize the clinical presentation of acute pericarditis. Coxsackie-B virus is a
common cause of acute pericarditis.
When someone is having recurrent VT, first thing to do after stabilizing the
patient is to search for underlying cause. This patient, most likely, has an
electrolyte imbalance due to diuretics. Furosemide commonly causes
hypokalemia, which may lead to digoxin toxicity. Therefore, ordering serum
electrolytes and serum digoxin level is the most reasonable approach.
Adding a beta-blocker is a good thing for chronic heart failure but not the next
step in this case.
Educational Objective:
Look for electrolyte abnormalities and correct them in patients with arrhythmias.
An atrial premature beat results from the premature activation of the atria that
originates from a site other than the SA node. EKG shows an early P wave. Atrial
premature beats may be present with underlying heart disease or may even be
present in the absence of any underlying heart disease. They are usually
asymptomatic or can cause palpitations. They may be single or may be seen in
the pattern of bigeminy. Occasionally they may result in supraventricular or less
commonly ventricular arrhythmias.
Treatment is required only when the patient with atrial premature contraction has
disturbing palpitations or supraventricular tachycardia. Precipitating factors like
tobacco, alcohol, or adrenergic agonists need to be identified and corrected
before opting for pharmacological therapy with beta-blockers or calcium channel
blockers. The above patient has precipitating factors that need to be corrected.
He is asymptomatic and does not have supraventricular tachycardia; therefore
there is no need for pharmacological treatment.
Reassurance alone is not appropriate as the identified risk factors for the
development of atrial premature contractions need to be removed.
This patient has no valvular, coronary artery disease or heart failure and
echocardiography is therefore not required.
Holter monitoring is used both for diagnostic and prognostic purposes. In the
above case, diagnosis is already established and his arrhythmia so far is benign.
Therefore, there is no need for Holter monitoring.
Educational Objective:
Tobacco and alcohol are reversible risk factors for the development of atrial
premature beats.
A. IV digoxin.
B. IV verapamil.
C. IV lidocaine.
D. IV procainamide.
E. Cardioversion.
Explanation:
The drugs that slow the AV conduction (digoxin and verapamil) are
contraindicated in patients with atrial fibrillation and Wolff-Parkinson-White
syndrome because they can increase the conduction of impulses through the
accessory pathway, thus leading to malignant arrhythmias and hypotension.
Lidocaine, as well in some cases, may worsen the situation by increasing the
conduction through the AV node. That is why lidocaine is usually not a preferable
drug in this situation.
Educational Objective:
Procainamide or disopyramide are the drugs of choice for Atrial fibrillation in the
context of WPW syndrome. Remember digoxin and calcium channel blockers
should not be used.
A. Electrocardiogram
B. Chest x-ray
C. Coronary angiography
D. Echocardiography
E. No further work-up
Explanation:
Catheterization and angiography (Choice C) can also reveal the structural defect
and assess the severity of the process, but it is invasive; therefore,
echocardiography is employed first.
Educational Objective:
Diastolic and continuous murmurs as well as loud systolic murmurs revealed on
cardiac auscultation should always be investigated using transthoracic Doppler
echocardiography. Midsystolic soft murmurs (grade I-II/IV) in an asymptomatic
young patient are usually benign and need no further work-up.
A. Electro-mechanic dissociation
B. Reentry
C. Full conduction block
D. Increased automaticity
E. Asystole
Explanation:
The most common cause of death in patients with acute myocardial infarction
(MI) is complex ventricular arrhythmia. Acute ischemia creates heterogeneity of
conduction in the myocardium. Areas of partial block of conduction are frequently
formed that predispose the patient to reentrant arrhythmia. Ventricular fibrillation
is a typical example of reentrant arrhythmia. Decline in mortality of patients
hospitalized with acute coronary syndromes is largely attributable to the effective
detection and treatment of reentrant ventricular arrhythmias.
Full conduction block (Choice C) may occur in patients with acute myocardial
infarction, especially inferior wall MI, but it is a less common cause of death.
Educational Objective:
Reentrant ventricular arrhythmia (ventricular fibrillation) is the most common
cause of death in patients with acute myocardial infarction.
A. Pericardial tamponade
B. Pulmonary embolism
C. Rupture of ventricular septum
D. Papillary muscle dysfunction
E. Acute aortic dissection
Explanation:
This patient has classic features of new onset mitral regurgitation. Sudden onset
of shortness of breath (SOB), bibasilar rales, and an 'apical' murmur radiating to
the axilla are quite characteristic of new onset mitral regurgitation. Papillary
muscle dysfunction, or rupture, is the most common cause of MR in this setting.
Ventricular septal rupture has similar features but the murmur is heard at the left
sternal border and would not radiate to the axilla.
Pulmonary embolism (PE) and aortic dissection are completely different from this
presentation. Pulmonary edema is not seen in PE.
Educational Objective:
Recognize the early complications of an acute anterior wall MI.
A. Nitrates should not be given to him within 24 hours of the last dose of sildenafil
B. Nitrates should not be given to him within 12 hours of the last dose of sildenafil
C. The dose of nitrates should be reduced
D. Nitrates can be given safely without any change in the usual nitrate dose
E. The dose of nitrates should be increased
Explanation:
Reduction of the nitrate dose would not protect against the dangerous interaction
with sildenafil and is not the right choice here.
An increase in the nitrates dose, or giving nitrates at the same dose in patients
who are taking sildenafil, is likely to produce substantial vasodilatation resulting
in syncope, MI, or even sudden death.
Educational Objective:
Nitrates are contraindicated when a patient is continuously or intermittently taking
sildenafil (Viagra).
37% of people answered this question correctly
The first line medication for HTN in the general population is either a thiazide
diuretic or beta-blocker. Non-selective beta-blockers are contraindicated in
asthmatics especially if they are steroid dependent or on continuous albuterol.
Stopping the asthma medications is not a good choice here. Use of propranolol
is also contraindicated in this patient.
ACE inhibitors, like enalapril, are the 1st line drugs for diabetics with
hypertension. These are usually 2nd line drugs for the general population.
Educational Objective:
Choose the appropriate initial antihypertensive therapy in a patient with asthma.
HCTZ is the initial drug of choice in patients with chronic persistent asthma.
A. Digoxin
B. Propranolol
C. Lidocaine
D. Quinidine
E. Immediate cardioversion
Explanation:
This patient presents with signs and symptoms suggestive of Grave’s disease -
insomnia, fatigability, weight loss, lid lag, and tremor. Atrial fibrillation is a
common complication of hyperthyroidism. As in other cardiovascular
complications, atrial fibrillation in patients with hyperthyroidism is believed to be
caused by increased sensitivity of beta-adrenoreceptors to sympathetic stimuli.
The best initial choice for these stable patients is a beta-blocker like propranolol.
It not only helps to control the rhythm in tachysystolic atrial fibrillation, but also
diminishes other symptoms of hyperthyroidism.
Educational Objective:
In patients with hyperthyroidism-related tachysystolic atrial fibrillation, a beta-
blocker is the drug of choice.
Educational objective:
It is better to keep systolic pressure < 130 mmHg to slow end-organ damage in
patients with diabetes and chronic renal failure.
Educational Objective:
Always suspect malignant hypertension in patients with very high blood pressure
(>/= 200/140 mmHg). Presence of papilledema on ophthalmoscopy confirms the
diagnosis. The pathologic change responsible for end-organ damage in
malignant hypertension is fibrinoid necrosis of small arterioles.
Q waves do not occur in 30-50% cases of acute infarcts (Non Q wave MI).
The earliest changes of hyperacute ‘T’ waves are frequently not seen in clinical
practice because by the time the patient present they already have ‘ST’
elevation.
Educational Objective:
Know the progression and timeframe of the ECG findings in the setting of an
acute MI. The earliest EKG finding in acute MI is peaked (hyperacute) T waves.
A 60-year-old woman presents to the emergency room for the acute onset of
breathlessness. She has had similar episodes on three prior occasions over the
last few months. Her past medical history is significant for rheumatic fever as a
child. Her vitals are, PR: 115/min and irregularly irregular; BP: 130/70 mm of Hg;
Temperature: 37.1C(98.7F); RR: 14/min. Her apex beat is tapping in quality and
is in left fifth intercostal space just inside the mid-clavicular line. Cardiac
auscultation shows a loud first heart sound and a mid-diastolic rumble best heard
at the apex. Auscultation of her lungs reveals crepitations in both lung fields.
Based on these findings, what is the most likely diagnosis of this patient?
A. Mitral stenosis
B. Mitral regurgitation
C. Tricuspid stenosis
D. Aortic stenosis
E. Aortic insufficiency
Explanation:
This patient most likely suffers from mitral stenosis, which is the most frequent
valvular disease caused by rheumatic heart disease. The presence of a tapping
apex beat, a loud first heart sound, and a mid-diastolic rumble at the apex
suggest the diagnosis of mitral stenosis in this patient. Atrial fibrillation is quite
common in patients with mitral stenosis.
Aortic stenosis, aortic insufficiency, and tricuspid stenosis occur less frequently in
the setting of rheumatic heart disease and the auscultatory findings
in this patient are not compatible with any of these disorders.
The murmur of aortic stenosis occurs in systole (systolic ejection murmur), and
radiates to the neck.
Educational Objective:
Recognize the clinical signs of mitral stenosis, and know how to differentiate it
clinically from other valvulopathies.