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Cardiology Facts and Pearls


By Steven Lome

ECG Pearls - Cardiac Physical Exam Pearls - Cardiac Pharmacology Pearls - General Cardiology Pearls

The Cardiology Facts and Pearl’s section provides concise tidbits of information
essential to know about each major cardiology topic. From must-know facts about
common cardiac conditions to important rare cardiac findings, this summary is an
essential quick review for the student learning cardiology.

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.

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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
Chapman’s sign or Cabrera’s 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 Duchenne’s 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.

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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.

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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.

Wellen’s 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.

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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 (Carvallo’s 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 patient’s back are mitral regurgitation and
coarctation of the aorta.

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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.

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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.

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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.

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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

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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.

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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 “Heyde’s 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.

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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 Paget’s 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 Wilkin’s 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.

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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:

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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

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