ECG Pearls

The three irregularly irregularly irregular rhythms are atrial fibrillation, atrial flutter with variable
conduction and multifocal atrial tachycardia (similar to wandering atrial pacemaker).

AV dissociation occurs in complete heart block (3rd degree AV block) and ventricular tachycardia.

Treat a wide-complex tachycardia like ventricular tachycardia until proven otherwise. Use the
Brugada criteria to distinguish ventricular tachycardia from SVT with aberrancy.

If no P waves can be seen and the QRS complexes are irregularly irregular, then atrial fibrillation is
present.

ST segment elevation from pericarditis is diffuse (all leads except aVR and V1) and concave
upward.

PR segment depression can be from acute pericarditis or an atrial infarction.

Diffuse T wave inversion is stage III of the ECG changes in pericarditis.

Pericarditis can be distinguished from early repolarization by the ratio of the T wave to the ST
elevation. If the ratio is > 4, then early repolarization is present (the ST elevation is < 25% of the T
wave amplitude).

The ST elevation from early repolarization resolves with exercise while that of pericarditis does
not.

Acute myocardial infarction can be diagnosed on an ECG in the setting of a left bundle branch
block (LBBB) on occasion using Sgarbossa Criteria or identifying Chapmans sign or Cabreras sign.

The causes of the R wave in lead V1 greater in amplitude than the S wave include right bundle
branch block, posterior myocardial infarction, WPW type A, right ventricular hypertrophy,
ventricular tachycardia with right bundle morphology and isolated posterior wall hypertrophy
occurring in Duchennes muscular dystrophy.

An Epsilon wave in lead V1 occurs in Arrhythmogenic Right Ventricular Dysplasia (ARVD) and is
described as a grassy knoll appearance just after the QRS complex.

An Osborne wave classically occurs in the setting of hypothermia and is seen as a spike at the end
of the QRS complex. An Osborne wave can also occur from hypercalcemia.

Hypercalcemia shortens the QT interval.

Dextrocardia shows negative QRS complex in lead I with negative P and T wave in this lead. There
is low voltage in leads V4 through V6 (unlike limb lead reversal which has normal voltage in these
leads, but negative QRS in lead I).

Hypokalemia causes U waves in the ECG seen as a positive wave just after the T wave.

Hyperkalemia causes peaked T waves initially, then an intraventricular conduction delay with a
widened QRS complex, then bradycardia and eventually a sine wave pattern ensues.

Hyperacute T waves are large and broadly shaped occurring in the first few minutes of an acute
myocardial infarction.

Delta waves occur in Wolff-Parkinson-White Syndrome

Hypertrophic Obstructive Cardiomyopathy (HOCM) is characterized by sharp, dagger-like Q waves

in the lateral leads in the setting of left ventricular hypertrophy.

The most common ECG finding of an acute pulmonary embolism is sinus tachycardia, however
the classic finding is an S wave in lead I, Q wave in lead III and inverted T waves in lead III (S1Q3T3
pattern).

A bifascicular block is a combination of a right bundle branch block with a left anterior or
posterior fascicular block.

A trifascicular block is a bifascicular block with a first degree AV block.

2:1 AV block is a form of second degree AV block that can be type I or type II. If the PR interval of
the conducted beat is prolonged AND the QRS complex is narrow, then it is most likely second
degree type I AV nodal block (Wenckebach). Alternatively, if the PR interval is normal and the QRS
duration is prolonged, then it is most likely second degree type II

Carotid massage, atropine administration or exercise can help determine if 2:1 AV block is from
second degree type I or second degree type II AV block (see 2:1 AV block review).

A posterior wall MI shows ST depression, not elevation in leads V1 and V2 with an R:S ratio
greater that 1 in lead V1.

Blocked premature atrial contractions occurring in a pattern of bigeminy can mimic sinus
bradycardia.

Coarse fibrillatory waves can be seen during atrial fibrillation.

Clockwise atrial flutter causes positively deflected P waves in the inferior leads while
counterclockwise atrial flutter causes negative deflected P waves in the inferior leads.

Multifocal atrial tachycardia (MAT) requires 3 different P wave morphologies in 1 ECG with a QRS
complex rate of > 100.

Wandering atrial pacemaker (WAP) requires 3 different P wave morphologies in 1 ECG with a
QRS complex rate of < 100.

Idioventricular rhythms meet criteria for ventricular tachycardia, but have a heart rate of < 100.

Massive left atrial enlargement causes a notch in the P wave and is termed P-mitrale

A left ventricular aneurysm results in chronic ST elevation in the anterior precordial leads.

Low voltage on the ECG can be caused by obesity, COPD, pericardial effusion, severe
hypothyroidism, subcutaneous emphysema, massive myocardial damage/infarction, or
infiltrative/restrictive diseases such as amyloid cardiomyopathy.

Electrical alternans occurs when every other QRS complex has varying amplitudes and is from the
heart swaying within a large pericardial effusion.

Sinus arrhythmia requires a variation of at least 120 milliseconds of the PP interval.

A prolonged QT interval from hypocalcemia has a lengthened ST segment, then normal

appearing T wave.

Wellens phenomenon occurs from a proximal left anterior descending subtotal occlusion and has
2 types. Type I is deep inverted T waves in the precordial leads and type II is biphasic T waves in V1
through V3.

Digoxin can cause ST depression appearing as a reverse tick or reverse check.

Bidirectional ventricular tachycardia occurs when every other beat has a different QRS
morphology and each morphology meets VT criteria. This is caused most commonly by digoxin
toxicity.

Atrial tachycardia with 2:1 AV block is a common rhythm in the setting of digoxin toxicity.

An acute intracranial process (hemorrhage, trauma, carotid endarterectomy etc...) can cause
dramatic T wave inversions and a prolonged QT interval on the ECG.

Ostium primum atrial septal defects cause an incomplete right bundle branch block with left axis
deviation. Ostium secundum atrial septal defects cause an incomplete right bundle branch block
with right axis deviation.

Cardiology Physical Examination Pearls

A S4 heart sound CANNOT be present during atrial fibrillation (atrial kick is required).

A S3 heart sound CANNOT be present in the setting of severe mitral stenosis.

A S3 heart sound can be present in athletes, pregnant females and other young healthy
individuals.

A S3 heart sound can indicate severe systolic heart failure.

A S4 heart sound is always pathologic and can indicate diastolic heart failure, left ventricular
hypertrophy or active myocardial ischemia.

Factors that increase the intensity of the S1 heart sound include short PR interval, fast heart rate
and mild mitral stenosis.

Factors that decrease the intensity of the S1 heart sound include long PR interval, slow heart rate
and severe mitral stenosis.

A fixed split S2 heart sound can be from an atrial septal defect.

A paradoxically split S2 heart sound can be caused by aortic stenosis, hypertrophic obstructive
cardiomyopathy or a left bundle branch block.

A widened split S2 heart sound can be caused by severe mitral regurgitation, pulmonic stenosis or
a right bundle branch block.

Large systolic jugular venous pulsations can be from V waves due to severe tricuspid
regurgitation.

A holosystolic murmur at the left lower sternal border louder with inspiration is due to tricuspid
regurgitation (Carvallos sign).

The aortic stenosis murmur can radiate to the cardiac apex where it sounds holosystolic and can
mimic the murmur of mitral regurgitation (Galiveriden phenomenon).

The three physical exam findings that correlate with severity of aortic stenosis include the timing
of the murmur peak in systole (late peak is severe), the intensity of the S2 heart sound (soft or
absent is severe) and pulsus parvus et tardus.

The late diastolic crescendo portion of a mitral stenosis murmur disappears when atrial fibrillation
is present due to the loss of the atrial kick.

The murmur of aortic regurgitation is located at the right upper sternal border (aortic post) ONLY
if the etiology is aortic root dilation. If valve leaflet pathology is the cause then the murmur is
heard at the left lower sternal border.

The best position to hear the murmur of aortic regurgitation is to have the patient lean forward
and listen after a forced, held expiration.

As aortic regurgitation worsens, the murmur becomes shorter in early diastole due to the aortic
and left ventricular pressure equalizing more quickly.

The two murmurs that can be heard in the patients back are mitral regurgitation and coarctation
of the aorta.

The Austin-Flint murmur is a diastolic rumble at the cardiac apex in a patient with aortic
regurgitation and occurs from the regurgitant jet striking the anterior mitral leaflet.

There are multiple peripheral physical exam findings in patients with severe aortic regurgitation
due to the high stroke volume (see Aortic Regurgitation Review)

When the mitral regurgitant jet is eccentrically directed posterior (anterior leaflet involvement),
the murmur radiates to the back. When directed anterior (posterior leaflet involvement), the
murmur radiates to the cardiac base.

The murmur of mitral regurgitation increases with handgrip and transient arterial occlusion since
these maneuvers increase afterload.

The earlier the opening snap in a patient with mitral stenosis, the more severe it is due to higher
left atrial pressures forcing the valve open immediately in early diastole.

The murmur of a small ventricular septal defect (VSD) is very loud a frequently associated with a
thrill. This murmur is referred to as maladie de Roger

The murmur of an atrial septal defect is a systolic, crescendo-decrescendo murmur at the

pulmonic listening post due to increased pulmonic valve flow. There is frequently a fixed splitting
of the S2 heart sound.

The murmur of a patent ductus arteriosus is continuous throughout systole and diastole since the
aortic pressure (normally 120/80) is ALWAYS higher than the pulmonary artery pressure (normally
25/10) in both systole and diastole.

A right ventricular heave can be present from severe pulmonary hypertension.

Cannon A waves can be seen in the jugular venous pulsations when the atrium contracts at the
same time as the ventricle (against a closed tricuspid valve) which occurs in the setting of AV
dissociation (complete heart block or ventricular tachycardia).

Roth spots, Janeway lesions and splinter hemorrhages are all peripheral signs of endocarditis.

Unequal radial pulses can be a sign of aortic dissection (with subclavian artery compression) OR
from atherosclerotic subclavian arm occlusion.

Always check blood pressure in both arms in acute chest pain patients to help diagnose aortic
dissection (will be markedly lower in one arm, usually the left, if the subclavian artery is involved).

Cardiac Pharmacology Pearls

Cardioselective beta-blockers act on beta-1 more than beta-2 and thus will not trigger or worsen
asthma as much as non-cardioselective beta-blockers.

Carvedilol and labetalol are non-selective beta-blockers that also block alpha-1 receptors

Propranolol and metoprolol are the most common lipid soluble beta-blockers and can be used to
treat anxiety, migraine headaches, tremor and stage fright.

The antidote for beta-blocker overdose is glucagon and inotropes (i.e. dobutamine).

Alpha blockers can cause severe first dose hypotension potentially resulting in syncope, thus they
are frequently given a night before bedtime.

ACE inhibitors can cause angioedema which may be life-threatening.

ACE inhibitors can cause hyperkalemia and renal failure. The should be stopped if the creatinine
increases to > 2.5 and/or the potassium to > 5.5.

ACE inhibitors can cause a dry cough thought to be related to the inhibition of bradykinin
breakdown (resulting in bradykinin accumulation).

Angiotensin receptor blockers (ARBs) are the preferred drug in patients who are not able to
tolerate ACE inhibitors due to a cough.

The only dihydropyridine calcium channel blocker that has been shown to be safe in the setting of
systolic heart failure is amlodipine.

Non-dihydropyridine calcium channel blockers must be used cautiously in patients with systolic
heart failure due to their negative inotropic effects.

Amiodarone can cause liver failure (monitor LFTs), either hyper or hypothyroid (monitor TFTs) and
pulmonary fibrosis (monitor PFTs).

Amiodarone can cause blue man syndrome resulting in bluish discoloration of the skin.

Amiodarone intravenously can cause dramatic hypotension due to the solvents used in the drug
preparation.

Amiodarone can cause ocular problems including sudden blindness on rare occasions.

Amiodarone and dofetilide are the only two antiarrhythmic drugs safe to use in the setting of left
ventricular systolic dysfunction.

Amiodarone is only FDA approved for the treatment of ventricular tachycardia and NOT atrial
fibrillation, although it is commonly used for this indication.

Dronedarone is similar to amiodarone, but without the iodine component. This results in less
toxicity, however somewhat less efficacy.

Procainamide is used in the setting of Wolff-Parkinson-White syndrome and atrial fibrillation.

Procainamide and hydralazine can cause drug-induced lupus erythematosus which can be
diagnosed by measuring anti-histone antibodies.

Quinidine can cause cinchonism.

Disopyramide is used to treat vagally mediated atrial fibrillation and hypertrophic obstructive
cardiomyopathy.

Disopyramide has strong anti-cholinergic properties.

Lidocaine toxicity can cause seizures and is used intravenously only for the treatment of
ventricular arrhythmias.

Mexiletine is an orally available class 1B antiarrhythmic drug similar to lidocaine and can be used
to treat ventricular tachycardia.

Sotalol has beta-blocker properties, can be used to treat atrial fibrillation and/or ventricular
tachycardia and can prolong the QT interval.

Sotalol must be initiated in the inpatient setting in individuals at high risk for QT prolongation to
monitor the QT interval and for proarrhythmia.

Sotalol exhibits reverse use-dependence meaning at faster heart rates (when potassium
channels are being used more), the antiarrhythmic effect is less. The antiarrhythmic effect is

greater when heart rates are slow.

Flecainide and propafenone (class IC antiarrhythmic drugs) must be used with an AV blocking
drug (beta-blocker or non-dihydropyridine calcium channel blocker) in order to prevent 1:1
conduction of atrial flutter which can be life-threatening.

Hydralazine can cause a reflex tachycardia and thus an AV blocking drug should be used
simultaneously.

Minoxidil is a direct arterial vasodilator like hydralazine used in medicine to treat hypertension,
however is also used over-the-counter to promote hair growth (Rogaine).

The combination of hydralazine and a long-acting nitrate (isosorbide mononitrate or isosorbide

dinitrate) has similar hemodynamic effects compared to ACE inhibitors (reduced afterload by
hydralazine and reduced preload by nitrates). This combination is used in the setting of systolic
heart failure when ACE inhibitors and ARBs are not able to be tolerated.

Tachyphylaxis can occur with nitrates (tolerance) when used 24 hours/day, thus they are
recommended for intermittent use. For example, nitroglycerine patches are put on in the
morning and taken off in the evening to allow a nitrate free period.

Nitrates are contraindicated within 24 hours of sildenafil or 48 hours of vardenafil/tadalafil due to

severe hypotension that can occur with the combination.

Eplerenone is an aldosterone antagonist (like spironolactone) that does not cause gynecomastia,
unlike other drugs in this category.

Digoxin toxicity presents with nausea, vomiting, abdominal pain, visual disturbances, and
symptoms of arrhythmia.

Digoxin toxicity can cause ANY arrhythmia EXCEPT rapidly conducted atrial arrhythmias (like atrial
flutter with a fast ventricular response).

Three typical digoxin toxic rhythms are: Atrial fibrillation with a slow ventricular response, atrial
tachycardia with 2:1 block and bidirectional ventricular tachycardia.

Hypokalemia and hypercalcemia potentiate digoxin toxicity.

Since digoxin acts by blockage of the sodium/potassium ATPase pump, digoxin toxicity can result
in hyperkalemia.

Calcium should NOT be given intravenously when the potassium is high related to digoxin toxicity
as this theoretically could cause serious arrhythmia since hypercalcemia potentiates the actions of
digoxin (end-point of digoxin mechanism is opening Ca channels allowing increased Ca influx,
this IV calcium markedly would increase Ca inclux). There is little evidence to support this theory.

Digoxin toxicity can cause xanthopsia or yellowing of the vision which the artist Vincent Van
Gogh was thought to suffer from toward the end of his life (he was using Foxglove to treat a
seizure disorder).

Ethacrynic acid is the only loop diuretic that does not have a sulfa component and is safe to use in
the setting of a severe sulfa allergy.

The only three beta-blockers FDA approved to treat systolic heart failure are metoprolol succinate
(NOT metoprolol tartrate), carvedilol, and bisoprolol.

Ticlopidine was shown to cause thrombotic thrombocytopenic purpura (TTP) and thus is not used
to a large extent any further.

Prasugrel is contraindicated in patients with a prior TIA or stroke.

Apixaban showed superiority in a head-to-head trial against warfarin in patients with atrial
fibrillation in regards to stroke prevention and mortality.

Dabigatran is an orally available direct thrombin inhibitor used to prevent thromboembolism in

atrial fibrillation and can cause significant GI upset.

Thiazide diuretics can cause hyponatremia, hypokalemia and sun sensitivity.

Nesiritide is a b-type natriuretic peptide (BNP) analog which is used intravenously in acute
decompensated heart failure, however has not shown a mortality benefit in clinical trials.

Ivabradine is an If channel antagonists used in Europe to treat heart failure patients when their
heart rate is > 70 beats per minute (clinical benefit shown in this subgroup).

Rosuvastatin has the greatest LDL reduction and HDL raising of the HMG-CoA reductase
inhibitors.

Pravastatin is the safest HMG-CoA reductase inhibitor in the setting of liver disease.

The rate of liver failure in patients taking HMG-CoA reductase inhibitors is the same as the rate of
liver failure in patients NOT taking HMG-CoA reductase inhibitors.

HMG-CoA reductase inhibitors have been loosely associated with increased risk of diabetes,
proteinuria and memory loss.

Lovastatin interacts with cyclosporine (raises levels) and for this reason was historically used in
transplant patients in order to reduce the dose of cyclosporine needed (due to the high cost of
cyclosporine).

HMG-CoA reductase inhibitors (statins) frequently cause myalgias (muscle aches), but rarely
cause rhabdomyolysis (about 1 in 10,000).

The first HMG-CoA reductase inhibitor discovered was mevastatin in the fungus Penicillium
citrinum, however it caused liver cancer in lab animals. Lovastatin was then isolated from
Aspergillus terrus. The in vivo actions of these drugs is thought to be antibacterial (like penicillin),
creating interest in research into possible infectious etiologies to the atherosclerotic properties
(statins of pleiotropic effects beyond their cholesterol lowering, the etiology of which remains
unclear).

Using coenzyme Q10 and replacing vitamin D in those deficient has been thought to potentially
help reduce statin induced myalgias.

General Cardiology Pearls

Platypnea is shortness of breath that occurs when sitting up relieved while laying supine (opposite
of orthopnea) and occurs in the setting of pulmonary arteriovenous malformations
(hepatopulmonary syndrome) or a left atrial myxoma.

The classic triad of symptoms from aortic stenosis is dyspnea on exertion, angina on exertion and
syncope on exertion.

The survival in patients with symptomatic severe aortic stenosis who do not undergo aortic valve
replacement is 2, 3 and 5 years in patients who present with dyspnea, syncope and angina
respectively.

Aortic valve replacement is indicated in severe aortic stenosis when symptoms develop or left
ventricular systolic dysfunction occurs.

Aortic stenosis is associated with small intestinal angiodysplasia which can cause GI bleeding. This
is termed Heydes syndrome and resolves after aortic valve replacement. The mechanism is
thought to be related to shearing of the Von Willebrand factor as blood courses through the
stenotic aortic valve.

Transcatheter aortic valve replacement (TAVR) is indicated in high risk surgical patients with severe
symptomatic aortic stenosis.

The mean pressure gradient and the aortic valve area are the two measurements used on
echocardiography to determine the severity aortic stenosis.

Severe aortic valve regurgitation causes multiple peripheral signs due to the high stroke volume
present in this condition (see Aortic Regurgitation review).

Aortic regurgitation and other high output states (sepsis, hyperthyroidism, arteriovenous
malformations as occurs in Pagets disease) cause a widened pulse pressure.

Functional mitral regurgitation occurs when the mitral annulus is dilated, usually from left
ventricular enlargement. This results in a centrally-directed regurgitant jet.

Organic mitral regurgitation occurs when there is a problem with the mitral valve leaflets
themselves. If an anterior leaflet problem is present, the regurgitant jet is directed posteriorly. If a
posterior leaflet problem is present, the regurgitant jet is directed anteriorly.

The ejection fraction in a patient with severe mitral regurgitation should be 65% or greater. If
less than 65%, then left ventricular systolic dysfunction may be present possible due to the mitral
regurgitation itself.

The most common cause of mitral valve stenosis is rheumatic valvular disease (accounts for 99%
of cases in the United States).

The Wilkins echocardiographic score is used to determine if a person with rheumatic mitral valve
stenosis is a candidate for percutaneous mitral balloon valvotomy.

Tricuspid regurgitation rarely requires surgical intervention, however can be indicated when
severe and causing symptoms of right heart failure refractory to medical management.

The CHADS 2 Vasc score or the CHADS 2 score are used to determine thromboembolic risk in
patients in atrial fibrillation and helps to determine whether aspirin or full anticoagulation should
be used.

The causes of atrial fibrillation can be remembered with the mnemonic PIRATES.

When deciding upon an AV blocking agent to slow down the heart rates from atrial fibrillation, it
is important to know the ejection fraction as non-dihydropyridine calcium channel blockers such
as diltiazem should be avoided if the systolic function is reduced.

Conditions that cause shock (hypotension) and pulmonary edema include acute mitral
regurgitation and acute ventricular septal defects.

Avoid beta-blockers or use those with alpha blocking properties in patients with coronary
vasospasm to avoid unopposed alpha agonism which can cause vasoconstriction and worsen
the vasospasm.

ACE inhibitors/ARBs and beta-blockers need to be titrated up slowly to their goal doses in
patients with systolic heart failure in order to achieve the greatest benefit.

The most common causes of heart failure exacerbations include medication non-compliance,
fluid/sodium restriction non-compliance, arrhythmia, ischemia and progression of the primary
disease process.

Treat a wide QRS complex tachycardia like ventricular tachycardia until proven otherwise.

The TIMI Risk Score should be used to predict outcomes in patients presenting with potential
anginal symptoms.

Below are high risk features that would warrant an early invasive strategy in patients with
unstable angina or non-ST elevation myocardial infarction:

1. Increased cardiac biomarkers (troponin, CK-MB)

2. New ST segment depression
3. Signs or symptoms of congestive heart failure (rales on examination, hypoxia with pulmonary
edema on chest x-ray)
4. Hemodynamic instability
5. Sustained ventricular tachycardia or ventricular fibrillation
6. Recent coronary intervention within 6 months
7. Prior coronary artery bypass grafting
8. High TIMI risk score

9. Reduced left ventricular systolic function (EF < 40%)

10. Recurrent angina at rest or with low level activity
11. High risk findings from non-invasive testing

Absolute contraindications to thrombolytic therapy include:

1. Prior intracranial hemorrhage

2. Ischemic stroke within 3 months
3. Known cerebrovascular abnormality such as aneurysm or arteriovenous malformation
4. Known malignant intracranial tumor
5. Significant closed head trauma or facial trauma within 3 months

Relative contraindications to thrombolytic therapy include:

1. Uncontrolled hypertension (blood pressure > 180/110) either currently or in the past
2. Intracranial abnormality not listed as absolute contraindication (i.e. benign intracranial tumor).
3. Ischemic stroke > 3 months prior
4. Bleeding within 2-4 weeks (excluded menses)
5. Traumatic or prolonged cardiopulmonary resuscitation (CPR)
6. Major surgery within 3 weeks
7. Pregnancy
8. Current use of anticoagulants
9. Non-compressible vascular puncture
10. Dementia