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Studying Cardiology
The Cardiology Boards
In the study of cardiology, it is important to fully understand
normal cardiac physiology before learning the pathophysiology of cardiac diseases. Learning is greatly facilitated
by incorporating new information into a preexisting framework of knowledge rather than memorizing the extraneous
facts of cardiology.
Several methods can make the study of cardiology more
interactive and interesting and, in the end, more productive.
A useful study method is to devise examination type multiple choice questions and then formulate in your mind the
framework and logic behind the answer. This method will
help to identify holes in your knowledge which can be filled
in by consulting textbooks, journals, and colleagues. The
advantage of this method is that you develop a questioning attitude that makes your reading of material an active,
searching process rather than a passive, absorptive one.
Another useful study technique is to write all you know
from memory about a specific topic in 30 minutes (time
b. The patient may also have severe coronary artery disease, which is supported by the history of mild angina and
strong risk factors. In a hemodynamically stable patient, the
examination board generally likes to see a progression from
noninvasive to invasive studies and from less expensive to
more expensive studies. Thus, although an exercise sestamibi
stress test would be appropriate if the patients primary problem were coronary artery disease, it would be problematic if
the correct diagnosis was critical aortic stenosis. The old leg
injury may be a problem with an exercise test, but there is
insufficient information to make a definitive judgment about
whether the patient has a good exercise capacity.
c. Electron beam computed tomography is likely to
show coronary calcification, but this information is likely
to be of little clinical value in an elderly patient.
d. If the patients condition were hemodynamically
unstable, an argument could be made for coronary angiography and aortic valve assessment. This would not be the
best initial investigation at this stage but may be indicated
if the patient required aortic valve surgery for critical aortic stenosis or if the severity of the patients aortic valve
disease as assessed echocardiographically was not concordant with his symptoms.
e. Transthoracic echocardiography appears to be the
imaging modality likely to give the most useful clinical
information without significant risk to the patient. Although
a normal brachial pulse does not support the diagnosis of
aortic stenosis, neither does it exclude the possibility in an
elderly patient with likely noncompliant arterial vessels.
Note that the history contains a significant amount of
distracting material, as do histories in real clinical situations: ethnic status, history of cholecystectomy and cataract
surgery, and urinary tract infection.
The core question is Does the candidate understand the
correct management of an elderly, hemodynamically stable
patient with increasing dyspnea on exertion, mild angina,
and a possible presyncopal episode, with physical findings
compatible with aortic stenosis?
Candidates should approach this convoluted question
by understanding that each question on the examination
tests a core competence that generally can be stated in one
sentence.
candidates, 34% to 52%. The results for the 1997 cardiology subspecialty board examination were 66% overall, 71%
for first-time candidates, and 45% for repeat candidates. For
candidates recertifying in internal medicine and cardiology,
the pass rates were 91% and 82%, respectively.
Cardiovascular disease will be the single largest area
tested in the 1999 ABIM Internal Medicine Examination,
accounting for 14% of the questions. Most of the examination questions (about 75%) are based on patient presentations. The settings of the encounters reflect current medical
practice, so most occur in an outpatient or emergency room
setting; the rest occur in an inpatient setting, from an intensive care unit to a long-term-care facility. The majority of
questions require the integration of information from several sources, the prioritization of alternatives, and clinical
judgment to reach a correct conclusion. Few questions
require simple recall of medical facts.
Arrhythmias
A history of aborted sudden death or recurrent syncope
in a young patient or a strong family history of sudden
death should suggest hypertrophic cardiomyopathy,
long QT syndrome, or Brugada syndrome.
Wide complex tachycardia in the setting of structural
heart disease is ventricular tachycardia until proved otherwise.
In patients with atrial fibrillation, look carefully at the
ventricular response to determine whether it is regular
this may signify complete heart block, whereas an excessively fast ventricular response may suggest the
possibility of Wolff-Parkinson-White syndrome.
The presence of sinus bradycardia or the Wenkebach
phenomenon may be a normal finding in an athletic
patient but should be scored for examination purposes.
Digoxin toxicity is an important clinical and ECG diagnosis; be aware of it. Digoxin toxicity is always tested in
some form in most cardiology and internal medicine
examinations. Paroxysmal atrial tachycardia with atrioventricular block and bidirectional ventricular tachycardia (originates from both left and right ventricles) are the
two cardiac rhythms that strongly suggest the diagnosis.
Instead of specifically stating that the patient was taking
digoxin, the clinical history may state that the patient was
taking cardiac medications. Be alert for patients taking
heart failure medications who develop hypokalemia,
because this can precipitate digoxin toxicity.
Chest Pain
When coding myocardial infarctions, ST-segment
elevation is acute myocardial injury and Q waves are
infarction. Watch for posterior infarcts.
Positional or pleuritic chest pain is pericarditis or
pulmonary embolus until proved otherwise.
The best examination strategy for the ECG section of
the cardiology boards is a conservative approach, with
careful coding of significant abnormalities, whereas
debatable answers are best left uncoded. In patients with
wide complex tachycardia, err on the side of coding ventricular tachycardia rather than supraventricular tachycardia with abberant conduction, because coding of the
latter may lead to inappropriate and dangerous clinical
Physical Signs
AF, atrial fibrillation; AR, aortic regurgitation; AS, aortic stenosis; HCM, hypertrophic cardiomyopathy; MR, mitral regurgitation; MS, mitral stenosis;
MVP, mitral valve prolapse; PS, pulmonic stenosis; VPB, ventricular premature beat; VSD, ventricular septal defect.
From J Am Coll Cardiol 32:1486-1588, 1998. By permission of the American College of Cardiology.
Table 5.Factors That Differentiate the Various Causes of Left Ventricular Outflow Tract Obstruction
Valve calcification
Dilated ascending aorta
PP after VPB
Valsalva effect on SM
Murmur of AR
Fourth heart sound
Paradoxic splitting
Ejection click
Maximal thrill and murmur
Carotid pulse
Valvular
Supravalvular
Discrete subvalvular
HOCM
No
Rare
Increased
Decreased
Rare
Uncommon
No
No
1st RIS
Unequal
No
Rare
Increased
Decreased
Sometimes
Uncommon
No
No
2nd RIS
Normal to anacrotic
No
Rare
Decreased
Increased
No
Common
Rather common*
Uncommon or none
4th LIS
Brisk, jerky,
systolic rebound
AR, aortic regurgitation; HOCM, hypertrophic obstructive cardiomyopathy; LIS, left intercostal space; PP, pulse pressure; RIS, right intercostal space; SM,
systolic murmur; VPB, ventricular premature beat.
*Depends on severity.
Modified from Marriott HJL: Bedside Cardiac Diagnosis. JB Lippincott Company, 1993, p 116. By permission of the publisher.
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4.
5.
6.
7.
8.
Acute Pericarditis
Signs:
Fever
Three-component pericardial friction rub that may
disappear when pericardial fluid accumulates
Chronic Constrictive Pericarditis
1. General signs:
Cachexia, jaundice if there is significant liver dysfunction
2. Pulse and blood pressure:
Pulsus paradoxus (more than the normal 10-mm Hg
decrease in arterial pulse pressure on inspiration,
because increased right ventricular filling reduces left
ventricle filling and cardiac output)
Chronic hypotension
3. JVP:
Increased JVP
4.
5.
6.
7.
Cardiac Tamponade
1. General signs:
Tachypnea
Severe anxiety
Pallor
Syncope or near syncope
2. Pulse and blood pressure:
Tachycardia
Pulsus paradoxus
Hypotension
3. JVP:
Markedly increased JVP
Kussmaul sign (common)
Prominent X but absent Y descent
4. Apex beat:
Usually impalpable because of fluid in pericardial
space
5. Auscultation:
Soft heart sounds
6. Lung fields:
Dullness and bronchial breathing at left base because
of compression of the lingula of the lung by the
distended pericardial sac (Ewart sign)
Infective Endocarditis
1. General signs:
Fever
Arthropathy (especially metacarpophalangeal joints,
wrists, elbows, knees, ankles)
2. Hands:
Splinter hemorrhages
3.
4.
5.
6.
7.
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Mitral Stenosis
1. General signs:
Tachypnea
Mitral facies (combination of vasodilatation and
peripheral cyanosis, in severe end-stage mitral
stenosis)
2. Arterial pulse and blood pressure:
Normal or reduced pulse volume due to decreased
cardiac output at late stages
Atrial fibrillation may be present because of left atrial
enlargement
Low blood pressure at late stages of disease
3. JVP:
Usually normal
Prominent A wave if pulmonary hypertension is
present
Loss of the A wave if atrial fibrillation supervenes
4. Precordium:
Tapping apex beat (due to palpable first heart sound)
Right ventricular heave
Palpable second pulmonic sound if pulmonary hypertension is present
Diastolic thrill (rarely present)
5. Auscultation:
Loud first heart sound (indicates that the mitral valve
leaflets are widely separated, yet mobile at the onset
of systole)
Loud second pulmonic sound if pulmonary hypertension is present
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Aortic Regurgitation
1. General signs:
Marfan syndrome in a small number of patients
Ankylosing spondylitis or other seronegative arthropathy
2. Pulse and blood pressure:
The pulse is characteristically collapsing, rapid
upstroke followed by a rapid decline
Wide pulse pressure
3. Neck:
Prominent carotid pulsations (Corrigan sign)
4. Palpation:
Apex beat is characteristically displaced laterally and
hyperkinetic
A diastolic thrill may be felt at the left sternal edge
when the patient sits forward in expiration
5. Auscultation:
Aortic second sound may be soft
A decrescendo high-pitched diastolic murmur beginning immediately after the second heart sound and
extending into diastole (it is loudest at the third and
fourth left intercostal spaces)
A systolic ejection murmur is usually present (due
to associated aortic stenosis or to torrential flow
across a nonstenotic aortic valve)
Aortic stenosis is distinguished from an aortic flow
murmur by the presence of the peripheral signs of
significant aortic stenosis, such as a plateau pulse
Listen for the Austin Flint murmur (a low-pitched
rumbling mid-diastolic murmur audible at the apex
the regurgitant jet from the aortic valve causes the
anterior mitral valve leaflet to shudder); the murmur
is similar to that of mitral stenosis but can be distinguished from mitral stenosis because the first heart
sound is not loud and there is no opening snap
Signs indicating severe chronic aortic regurgitation:
Collapsing pulse
Wide pulse pressure
Long decrescendo diastolic murmur
Left ventricular third heart sound
Soft aortic second sound
Austin Flint murmur
Signs of left ventricular failure
Tricuspid Stenosis
1. JVP:
Increased giant A waves with a slow Y descent
may be seen
2. Auscultation:
Diastolic murmur audible at left sternal edge, accentuated in inspiration, very similar to the murmur of mitral
stenosis except for the site of maximal intensity
Tricuspid stenosis is rare, usually rheumatic in etiology, and is frequently accompanied by mitral
stenosis
No signs of pulmonary hypertension
3. Abdomen:
Presystolic pulsation of the liver caused by forceful
atrial systole
Tricuspid Regurgitation
1. JVP:
Large V waves
JVP is increased if right ventricular failure has occurred
2. Palpation:
Right ventricular heave
3. Auscultation:
A pansystolic murmur maximal at the lower end of
the sternum that increases on inspiration is classic
but may be absent, and the diagnosis must be made
on the basis of peripheral signs alone
4. Abdomen:
Pulsatile, large, tender liver is usually present
Ascites, peripheral edema, and pleural effusions may
occur
5. Legs:
Dilated pulsatile veins
Pulmonary Stenosis
1. General signs:
Peripheral cyanosis (due to low cardiac output)
2. Pulse:
Normal or reduced (because of a low cardiac output)
3. JVP:
Giant A waves because of right atrial hypertrophy;
JVP may be increased because of right heart failure
4. Palpation:
Right ventricular heave
Thrill over the pulmonary area
5. Auscultation:
Murmur may be preceded by an ejection click
Pulmonary Regurgitation
1. Auscultation:
A decrescendo diastolic murmur that is high-pitched
and audible at the left sternal edge is characteristic;
the murmur increases on inspiration
The Graham Steell murmur is functional pulmonary
incompetence due to severe mitral stenosis
Signs of pulmonary hypertension may also be present
2. Note:
If there is no sign of pulmonary hypertension, a
decrescendo diastolic murmur at the left sternal edge
is more likely to be due to aortic regurgitation than
to pulmonary regurgitation.
Hypertrophic Cardiomyopathy
1. Pulse:
Sharp-rising and jerky
Rapid ejection by the hypertrophied ventricle early in
systole is followed by obstruction caused by the displacement of the mitral valve into the outflow tract.
This is very different from the pulse of aortic stenosis
2. JVP:
There usually is a prominent A wave, because of
forceful atrial contraction against a noncompliant
right ventricle
3. Palpation:
Double or triple apical impulse due to presystolic
expansion of the ventricle caused by atrial contraction
4. Auscultation:
Late systolic murmur at the lower left sternal edge and
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3. Auscultation:
If the shunt is of moderate size, a single second heart
sound is heard, but if the shunt is of large size,
reversed splitting of the second heart sound occurs
(a delayed aortic second sound occurs because of
the increased left ventricular stroke volume )
A continuous loud machinery murmur maximal at
the first left intercostal space is usually present
Tetralogy of Fallot
1. Clinical signs:
Central cyanosis is common and occurs because of a
large right-to-left shunt at the ventricular level,
where right and left ventricular pressures are equalized. In addition, the aorta overrides both ventricular outflow tracts and receives a combination of
saturated and desaturated blood
Finger and toe clubbing and polycythemia
Signs of right ventricular enlargement, including a
parasternal right ventricular lift and a thrill at the
left sternal edge
Normal left ventricular impulse
Aortic click
Second heart sound is single (absent second pulmonic
sound)
Pulmonary systolic ejection murmurthe louder and
longer the pulmonary murmur the better, because this
indicates better blood flow through the pulmonary
circulation
No significant murmur across the ventricular septal
defect (no gradient)
Continuous murmur from bronchial collaterals or
associated patent ductus arteriosus
The lungs are protected from pulmonary hypertension
by the pulmonary stenosis (valvular and infundibular)
Oral questions, essay-type questions, and performance of a clinical examination are not part of the
Cardiology Board examination but are required in
many of the examinations of the Royal College of
Physicians.
Most candidates who fail the core questions also fail the
noncore ones.
17
% of questions
12
12
11.5
10.5
9
9
8
7.5
7
4.7
3.3
3
2.5
18
19
20
Notes