General Cardiology Pimps

1. What are the toxicities of amiodarone?

I dare you to look your attending in the eye with a serious face and say BITCH if asked this
question! It is probably not wise to do this unless you are sure they have a good sense of
humor. Remember the mnemonic BITCH to recall the issues with amiodarone
Bradycardia/Blue man syndrome
Interstitial lung disease
Thyroid (hyperthyroid OR hypothyroid)
Corneal/Cutaneous
Hepatic/Hypotension
Another way to remember is Check PFTs, TFTs and LFTs for pulmonary, thyroid and liver
function tests. But really the only monitoring that is done is a TSH level every 6 months as
routine PFTs and LFTs are not recommended.
2. What are the causes of atrial fibrillation?
Remember PIRATES for the causes of atrial fibrillation. This is quite a comprehensive list:
Pulmonary embolism, Pulmonary disease, Post-operative
Ischemic heart disease, Idiopathic (lone atrial fibrillation), IV central line (irritating the
right atrium)
Rheumatic valvular disease (mitral stenosis or regurgitation)
Anemia, alcohol (holiday heart), Age, Autonomic tone (vagal atrial fibrillation)
Thyroid disease (hyperthyroidism)
Elevated blood pressure (hypertension), Electrocution
Sleep apnea, Sepsis, Surgery
3. What are the different types of shock and their treatment?
This picture summarizes it all:

4. What are the causes of congestive heart failure (CHF) exacerbations?
You will very likely get this one. Congestive heart failure (CHF) is the #1 cause of hospital
admission in the US. Whenever a patient comes in with volume overload from CHF, you
must always as the question Why did this patients heart failure get worse. Here are the
reasons from most common to least:
1. Medication non-compliance (not taking diuretics or other medications)
2. Fluid/sodium restriction non-compliance
3. Acute worsening of cardiac output:
Arrhythmia
Ischemia or acute coronary syndrome
Worsening/Progression of cardiomyopathy/valve disease
5. Which medications for systolic congestive heart failure reduce mortality?
Easy...beta-blockers, ACE inhibitors or ARBs, and spironolactone. If ACE inhibitor and
ARB intolerant, then the combination of hydralazine and nitrates are used and reduce
mortality, especially in African Americans. Note that digoxin and diuretics DO NOT reduce
mortality! They are for symptom relief and to prevent heart failure hospitalization only. The
gunners can review Heart Failure here.
6. Which beta-blockers are FDA approved to treat systolic congestive heart
failure?
Not all beta-blockers have clinical trials to support their use in systolic heart failure. Use
these three:
Carvedilol (Coreg)
Bisoprolol
Metoprolol succinate (Toprol) and NOT metoprolol tartrate (Lopressor)
Atenolol, propranolol and the other beta-blockers SHOULD NOT be used in systolic heart
failure.
7. What is the most common cause of right heart failure?
Left heart failure! When anything causes left heart failure (ischemia, valve disease,
cardiomyopathy etc...), the LV pressure increases and transmits back to the lungs causing
pulmonary hypertension. This then strains the right heart and eventually causes right heart
failure. Know the difference between signs/symptoms of left versus right heart failure.
8. A patient comes in with chest pain, what are the 4 life-threatening causes
that should be exclude?
Acute coronary syndrome
Pulmonary embolism
Aortic dissection
Esophageal rupture (Boerhaaves syndrome)
9. What are the signs/symptoms and issues with digoxin toxicity?
This is a good one:
Nausea/Vomiting/Abdominal pain
Weakness/dizziness
Symptoms of arrhythmia
Altered mental status
Vision changes (yellow vision or Xanthopsia)
Digoxin causes EVERY arrhythmia EXCEPT rapidly conducted atrial rhythms (atrial
fibrillation or flutter with a rapid ventricular rate). The classic ECG has the "reverse check"
sign:

The two pathognomonic rhythms in digoxin toxicity are atrial tachycardia with 2:1 block and
bidirectional ventricular tachycardia.
Atrial Tachycardia with 2:1 AV Block ECG Example 1
Atrial Tachycardia with 2:1 AV Block ECG Example 2
Bidirectional Ventricular Tachycardia ECG Example
Reverse with digibind if:
Evidence of end-organ damage (altered mental status, shock liver etc...)
Life threatening arrhythmia
Potassium level > 5.5
Digoxin CAUSES hyperkalemia, but is potentiated by hypokalemia (also hypocalcemia)
Wow...thats a lot to know.
BONUS: The Stone Heart theory. Digoxin toxicity can cause hyperkalemia. Recall that the
treatment for hyperkalemia causing ECG changes is usually intravenous calcium
administration. In the setting of digoxin toxicity and hyperkalemia, giving IV calcium may be
potentially fatal. The massive influx of calcium into myocytes after the IV calcium is given
has been theorized to induce a non-contractile state and has been termed "Stone Heart" (recall
the end-point effect of digoxins actions is to open calcium channels increasing influx into
cells).
BONUS BONUS: Vincent Van Gogh (the artist) was toxic on digoxin (he used the flower
foxglove for a seizure disorder) and this is why he painted everything yellow before he
reportedly commited suicide. Check out this painting of his:

10. What are the FIVE life-threatening complications of aortic dissection?
Coronary dissection, usually the right coronary artery (RCA) causing inferior ST
elevation MI
Carotid dissection causing stroke
Aortic rupture
Cardiac tamponade from rupture into pericardium
Acute aortic valve regurgitation causing cardiogenic shock
11. Which atrial fibrillation patients can we use only aspirin (ASA) for and
who needs full anticoagulation to prevent stroke?
Use the CHA
2
DS
2
Vasc Score:
If 0-1 points then aspirin 81 mg - 325 mg
If > 2 points then full anticoagulation (warfarin, dabigatran, rivaroxiban, apixiban)
Congestive heart failure
Hypertension
Age ( > 65 = 1 point, > 75 = 2 points)
Diabetes
Stroke/TIA (2 points)
Vascular disease (peripheral arterial disease, previous MI, aneurysm aortic atheroma)
NOTE: Female gender is also included in this scoring system = 1 point!
12. What are the different properties of beta-blockers and name specific
drugs?
Cardioselectivity: All beta-blockers act upon both beta-1 and beta-2 receptors. The
Cardioselective beta-blockers act upon beta-1 receptors much more than the beta-2
receptors. For this reason, the cardioselective beta-blockers are safer to use in patients with
asthma or reactive airway diseases.
Lipid solubility: Beta-blockers that are lipid soluble, such as propranolol or metoprolol, can
cross the blood-brain barrier easily. These medications are commonly used for migraine
headaches, stage fright and panic attacks for these reasons.
Intrinsic sympathomimetic activity (ISA): Beta-blockers with ISA only partially
antagonize while actually causing a small degree of activation of the beta receptors. So they
will have some beta-blocking effects, but not to the degree of beta-blockers without ISA.
These are commonly used in younger patients or in athletes where heart rates need to elevate
(allowing overall increased cardiopulmonary effort) in order to compete in sports. Examples
include pindolol and acebutolol.
Membrane stabilization: Stabilizing membranes decreases the propagation of action
potentials. This is also the mechanism that local anesthetics work (lidocaine). Class I
antiarrhythmic drugs possess this characteristic as well. The importance of this is not clear in
clinical medicine in regards to beta-blockers. Perhaps this is partially an explanation for
propranolol treating migraine headaches.


13. What are the side effects and other issues with ACE inhibitors?
Just remember the mneumonic CAPTOPRIL
Cough
Angioedema
Potassium excess
Taste changes
Orthostatic hypotension
Pregnancy contraindication/Pressure drop (hypotension)
Renal failure/Rash
Indomethacin inhibition
Leukopenia (rare)
14. What class of antiarrhythmic drug is ______ in?
Remember what drug is in what class was hard for me, even in fellowship! Now that I use
them all the time I can remember them. Just keep going over them and eventually they will
stick. A more detailed review of antiarrhythmic drugs is here.
Class IA: Queen Amy Proclaims Disos Pyramid = Quinidine, Amiodarone, Procainamide,
Disopyrimide
Class IB: Lidocaine, mexiletine
Class IC: Flecainde, propafenone
Class II: Beta-blockers
Class III: Sotalol, amiodarone (yes...again), dronedarone, dofeilide
Class IV: Calcium channel blockers (diltiazem, verapamil)
Class V: Mechanism unknown
15. How do you diagnose and treat cardiac tamponade?
Becks triad: Hypotension, muffled heart sounds, elevated neck veins
Pulsus paradoxus: Abnormal if > 12 mmHg. Review how to measure here.
Water Bottle Heart: Chest x-ray finding - heart shaped like a canteen
Cardiac tamponade is a CLINICAL diagnosis, not an echocardiographic one, but an echo will
show a pericardial effusion and if the right ventricle is collapsing in diastole, then tamponade
is thought to be present (right ventricle is lowest pressure chamber, so collapses first.
Pressure is lower in diastole than systole).
Treat with IV fluids to increase preload and prevent right ventricular collapse.
Pericardiocentesis is therapeutic.
BONUS: DO NOT rely on analysis of pericardial fluid like we to pleural fluid after
thoracentesis of ascites after paracentesis as the whole transudate or exudate thing is not
validated here.
16. What is the classic triad of symptoms in aortic stenosis?
Angina, Syncope and Dyspnea (from heart failure) is the classic triad.
BONUS: Back in the day aortic valve replacement was not available, so they watched people
with severe aortic stenosis to see how long they live. A classic pimp question is mortality
based on that triad of symptoms if the aortic valve is not replaced. Average life expectancy is:
Dyspnea = 2 years
Syncope = 3 years
Angina = 5 years
This pic shows it all:

17. What is the most common cause of mitral valve stenosis?
By far the most common cause is rheumatic heart valve disease. Gunners read on mitral
stenosis here.
BONUS: Mitral stenosis is in the differential diagnosis of hemoptysis which can occur due to
rupture of a bronchial vein (they call this pulmonary apoplexy).
18. What are the indications for aortic valve replacement (AVR) in aortic
stenosis and aortic regurgitation?
For either aortic regurgitation or stenosis, aortic valve replacement is indicated when
symptoms occur or if the left ventricular systolic function declines, but there is one more
tricky one for aortic regurgitation. AVR is indicated even if the left ventricular ejection
fraction is normal when the end systolic dimension increases to > 55 mm or end diastolic
dimension to > 75 mm on echocardiography.
19. What are the causes of mitral valve regurgitation?
Mitral regurgitation is either organic (actual valve apparatus problem) or functional (dilation
of the annulus).
Organic Mitral Regurgitation Functional Mitral Regurgitation
Myxomatous changes (MVP)
Rheumatic heart disease (RHD)
Endocarditis
Collagen vascular disease
Papillary muscle dysfunction
Mitral annular calcification (MAC)
Spontaneous chordal rupture
Trauma
Ischemic cardiomyopathy
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Left atrial dilation

20. What is the treatment for coronary vasospasm?
DO NOT give beta-blockers!!! So they say this causes unopposed agonism at alpha
receptors since the circulating catecholamines cant act on the beta-receptors if a beta-blocker
is given. The catecholamines decide to go to the alpha receptors and stimulate them which
can worsen vasospasm. Use a non-dihydropyridine calcium channel blocker (i.e. amlodipine).
Maybe the two beta-blockers that also block alpha receptors are OK (carvedilol and
labetalol), but who knows...there is no data on this.
BONUS: Coronary vasospasm can occur with cocaine intoxication, so the same above
principle applies (dont use beta-blockers).
21. Which statin lowers the LDL the most? Which has fewest side-effects?
Rosuvastatin lowers LDL the most. Pravastatin fewest side-effects and safest in liver disease.
Probably not much more to know but for the gunners here is a HMG CoA Reductase inhibitor
review.
22. What are the mechanical complications of myocardial infarction?
Acute ventricular septal defect (VSD)
Acute mitral regurgitation (MR)
Left ventricular free wall rupture
For the gunners read about more complications of MI in the STEMI review.
23. What is the most common cause of aortic valve stenosis in a patient over
the age of 70? Under the age of 70?
Over the age of 70 = senile calcific aortic stenosis
Under the age of 70 = bicuspid aortic valve
24. In a patient with unstable angina or a non-ST elevation MI (NSTEMI),
when should an early invasive strategy be used?
Invasive coronary angiography (an early invasive approach) in unstable angina or non-ST
elevation MI is indicated when:
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
25. What are the absolute and relative contraindications to thrombolytics?
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
26. What are the indications for valve replacement in patients with
endocarditis?
Congestive heart failure from valvular regurgitation
Failure of antibiotic therapy to successfully suppress the infection or infection with
difficult to treat organisms (fungal, Pseudomonas, Brucella, drug-resistant organisms)
Valvular annular abscess
Peripheral embolism of vegetation
Size of vegetation > 1.0 cm
27. What are the common causes of endocarditis?
Streptococcal viridins, Staph aureus, and Enterococcus are the leading three.
BONUS: If Streptococcus bovis endocarditis is associated with colon cancer.
BONUS BONUS: Know the culture negative causes of endocarditis (vegetation on the valve
but no organism growing in blood cultures). These are known as the HACEK organisms:
Haemophilus aphrophilus
Actinobacillus actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae
28. What are the secondary causes of hypertension?
Remember "ABCDEF"
Apnea (obstructive sleep apnea), Acromegaly, Accuracy (incorrect measurement)
Birth control, Bad kidney
Coarctation of the aorta, Cushings syndrome, Conns syndrome, Catecholamines
Drugs (alcohol, nasal decongestants, estrogens)
Endocrine disorders, Erythropoietin
Fibromuscular dysplasia
BONUS: The most common cause of difficult to control hypertension is uncontrolled
obstructive sleep apena followed by renal artery stenosis.
29. Which cardiac biomarker elevates first? Which stays elevated the longest?
Myoglobin elevates first (30 minutes), then troponin and creatine kinase (CK). Troponin
stays high for 7-10 days, but CK for only 3-4 days.

30. What are the three types of cardiomyopathy?
Dilated cardiomyopathy: This results in left ventricular systolic dysfunction and clinical
manifestations of congestive heart failure. Etiologies include viral, alcoholic, idiopathic,
familial and other rare causes.
Hypertrophic cardiomyopathy: Also known as hypertrophic obstructive cardiomyopathy
(HOCM), this results in abnormal hypertrophic changes most commonly in the
interventricular septum with pathologic myocardial disarray. HOCM is familial in about
50% of cases and transmitted in an autosomal dominant fashion. HOCM can result in clinic
heart failure, life-threatening arrhythmias, mitral regurgitation and sudden cardiac death.
Restrictive cardiomyopathy: This results in heart failure related to severe diastolic
dysfunction. Causes include amyloid heart disease, infiltrative disorders, and familial.
Physical Examination Pimps
31. Take a listen to his heart, do you hear the S4 heart sound?
NO YOU DONT!!! The patient is in atrial fibrillation and CANT have an S4 heart sound!
Recall that an S4 happens when the atrium contracts into a non-compliant left ventricle
causing the blood to forcefully strike the left ventricle creating the sound. Patients with atrial
fibrillation DO NOT have any atrial contraction and are not able to have an S4 heart sound.
Dont let your attending trick you...

32. What causes an S3 heart sound versus an S4 heart sound?
An S3 heart sound, a.k.a. the ventricular gallop can be present in systolic heart failure, but
can also be there in normal healthy hearts. The S4 heart sound is almost always pathologic
and can occur in the setting of diastolic heart failure and/or myocardial ischemia.

33. How severe is the aortic stenosis on exam?
There are only 3 ways to tell how severe the aortic stenosis is on physical exam:
1. Timing of the murmur peak (late in systole = severe)
2. The intensity of the S2 heart sound (soft or absent = severe)
3. Pulsus Parvus et Tardus (carotid upstroke weak and late)

34. What are the three causes of a holosystolic murmur?
Mitral regurgitation, tricuspid regurgitation, ventricular septal defect.
BONUS: The Galliveridin phenomenon in aortic stenosis is when the murmur radiates to
the apex and can sound holosystolic mimicking mitral regurgitation. Handgrip maneuvers or
transient arterial occlusion will increase mitral regurgitation and not the aortic stenosis
murmur. Gunners read an aortic stenosis review here.
35. Describe the murmur of aortic regurgitation.
Early diastolic decrescendo. If an actual valve problem caused the aortic regurgitation (i.e.
endocarditis), then the murmur is at the left lower sternal border BUT if it is from dilation of
the aorta (i.e. ascending aortic aneurysm as occurs in Marfans), then the murmur is at the
aortic listening post which is the right upper sternal border. Tricky.
BONUS: The murmur is best heard with the patient leaning forward at end-expiration.
BONUS BONUS: When the aortic regurgitation is severe the murmur is quite short in early
diastole since sooooo much blood leaks back into the left ventricle that the pressure between
the aorta and the LV equalize quickly. Conversely, if mild it takes quite some time for the
pressure to equalize so the murmur is longer (see pic)

36. What is the Austin-Flint murmur?
This is when the aortic regurgitation get strikes the anterior leaflet of the mitral valve in
diastole forcing it partially closed. This kind of creates a mitral stenosis-like picture and a
diastolic rumble at the cardiac apex called the Austin-Flint murmur.
37. What are some of the peripheral signs of aortic regurgitation?
Reel off all of these and people will be staring with their mouths wide open:
Corrigan's pulse: A rapid and forceful distension of the arterial pulse with a quick collapse.
De Musset's sign: Bobbing of the head with each heartbeat (like a bird walking).
Muller's sign: Visible pulsations of the uvula.
Quincke's sign: Capillary pulsations seen on light compression of the nail bed.
Traube's sign: Systolic and diastolic sounds heard over the femoral artery ("pistol shots").
Duroziez's sign: Gradual pressure over the femoral artery leads to a systolic and diastolic
bruit.
Hill's sign: Popliteal systolic blood pressure exceeding brachial systolic blood pressure by 60
mmHg or greater (most sensitive sign for aortic regurgitation).
Shelly's sign: Pulsation of the cervix.
Rosenbach's sign: Hepatic pulsations.
Becker's sign: Visible pulsation of the retinal arterioles.
Gerhardt's sign (aka Sailer's sign): Pulsation of the spleen in the presence of splenomegaly.
Mayne's sign: A decrease in diastolic blood pressure of 15 mmHg when the arm is held
above the head (very non-specific).
Landolfi's sign: Systolic contraction and diastolic dilation of the pupil.
38. What maneuver makes the murmur of hypertrophic obstructive
cardiomyopathy (HOCM) louder?
Valsalva decreases left ventricular filling. In HOCM this allows the very thick
interventricular septum to buldge more into the left ventricular cavity causing more of a left
ventricular outflow tract obstruction, thus making the murmur louder. Much different than the
murmur of aortic stenosis (see pic).

39. What murmur gets louder with inspiration?
Tricuspid regurgitation does. This is called Carvallos sign. Pulmonic regurgitation can
sometimes as well.
BONUS: Severe tricuspid regurgitation causes large V waves in the jugular venous
pulsations from blood leaking back from the right ventricle into the internal jugular during
systole. Also look for a pulsatile liver.
ECG Pimps
First of all, you need to know the basics, like how to diagnose a left and right bundle branch
block, chamber enlargements, axis, heart rate, myocardial infarctions etc... read the ECG
Review here. Below are some of the specific ECG pimp questions that I have run into.
40. What is the most common ECG findings of pulmonary embolus?
Everyone wants to reflexively say S1Q3T3 and if you do, then you are wrong. It is sinus
tachycardia. The S1Q3T3 pattern is the classic finding (see pic below), but sinus tachycardia
is more common.

BONUS: The S1Q3T3 pattern is not just for pulmonary embolism, but for anything that
causes acute right heart strain (can occur in COPD or asthma exacerbations, respiratory
failure etc...) and it is also called the McGinn-White sign.
41. Can you diagnose a myocardial infarction on ECG if there is a left bundle
branch block (LBBB)?
Whoooo hoooo! You are ready for this one! You know that traditionally the answer is no,
ischemia is not readily detected if a left bundle branch block (LBBB) is present, but there are
some means to do this. The Sgarbossa criteria, Chapmans sign, Cabereras sign and also by
examining the T waves in lead V5 and V6. Know these and you will look like a superstar!
Sgarbossa criteria: This is a point scoring system.
1. ST elevation > 1 mm and in the same direction (concordant) with the QRS complex. 5
points
2. ST depression > 1 mm in leads V1, V2, or V3. 3 points
3. ST elevation > 5 mm and in the opposite direction (discordant) with the QRS. 2 points
A score of 3 points is required to diagnose an acute myocardial infarction. Criteria #3 is
under debate as to its usefulness, so basically you need to have either criteria 1 or criteria 2.
Below is an image of ST elevation in V5 and V6 with a LBBB:

Chapmans sign: A notch in the upslope of the R wave in lead I, aVL or V6. This has a low
sensitivity, but a specificity of about 90%. See Chapman sign ECG here.
Cabreras sign: Notching at 40 milliseconds in the upslope of the S wave in lead V3 and V4.
This has a poor sensitivity of 27% for myocardial infarction. See Cabrera's sign ECG here.
T waves in V5 and V6: If upright in these leads when a left bundle branch block is present,
then ischemia is more likely present, although sensitivity is low for this finding.
42. What are the causes of AV dissociation on ECG?
Ventricular tachycardia (VT) and complete heart block (3rd degree AV block)
Here is AV dissociation from VT:

Here is AV dissociation in complete heart block:

BONUS: When AV dissociation is present, this causes the atria to contract at the same time
as the ventricle when the P wave falls on top of the QRS complex. Thus, the atrium is
contracting against a closed mitral/tricuspid valve. This makes blood forcefully go backwards
causing intermittent cannon A waves in the jugular venous waveform.
BONUS BONUS: That huge stretch of the atrium during AV dissociation due to the above
mentioned atrial contraction against closed valves causes release of ANP (atrial natriuretic
peptide) which causes diuresis and thus polyuria! Yes...polyuria can be a symptom of
complete heart block! BAAAMMM!!! Not too many people know this and it will certainly
impress.
43. What are the ECG changes of hyperkalemia and what can you give to
resolve them?
Peaked T waves is the answer most people are looking for. The QRS complex can widen in a
non-specific pattern (not left or right bundle) a.k.a. a non-specific intraventricular
conduction delay. Eventually

44. The patient has 2:1 AV block - How can you tell if it is 2nd degree type I
or 2nd degree type II AV block?
First quick rule: 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 AV block and a pacemaker is probably warranted.
Less quick rule: Exercise the patient. Walk them in the hall or on a treadmill. If it is 2nd
degree type I, the heart rate will increase and you will see prolonging PR intervals until a beat
is dropped. If it is 2nd degree type II, then nothing will happen. You can also give atropine or
do a carotid massage and see what happens.
Here is a pic of 2:1 AV block:

45. What is a _____ wave on the ECG?
Detla wave = Wolff-Parkinson White (short PR interval that is slurred into the QRS complex)

Osborne wave (a.k.a. J wave) = Classically hypothermia, but also hypercalcemia

U wave = hypokalemia

Epsilon wave = Arrhythmogenic right ventricular dysplasia (ARVD) which is RARE

46. What are the causes of ST elevation on ECG besides acute MI?
ECG Causes of ST segment elevation: ELEVATION
Electrolyte abnormalities
Left bundle branch block
Aneurysm of left ventricle
Ventricular hypertrophy
Arrhythmia disease (Brugada syndrome, ventricular tachycardia)
Takotsubo/Treatment (iatrogenic pericarditis)
Injury (myocardial infarction or cardiac contusion)
Osborne waves (hypothermia or hypocalcemia)
Non-atherosclerotic (vasospasm or Prinzmetals angina)
47. What are the ECG findings of a posterior MI?
You better know anterior and inferior MI ECG changes. The posterior MI ECG findings are a
bit more tricky:
ST segment depression (not elevation) in the septal and anterior precordial leads (V1
to V4). This occurs since these ECG leads will see the MI backwards (since the leads
are placed anteriorly, but the myocardial injury is posterior).
The ratio of the R wave to the S wave in leads V1 or V2 is > 1.
ST elevation in the posterior leads of a posterior ECG (leads V7 to V9). Suspicion for
a posterior MI must remain high, especially if inferior ST elevation is also present.
ST elevation in the inferior leads (II, III, and aVF) may be seen if an inferior MI is
also present

48. What are the three irregularly irregular rhythms on ECG?
The three irregularly irregular rhythms are atrial fibrillation, atrial flutter with VARIABLE
conduction and multifocal atrial tachycardia (MAT)

49. What are the causes of a prolonged QT interval?
Electrolyte abnormalities (hypokalemia, hypocalcemia, hypomagnesemia)
Medications (quinolones, macrolides, haloperidol, class IA and class III
antiarrhymics)
Genetic long QT syndromes
Myocardial ischemia
BONUS: Patients with a prolonged QT interval are at risk for Torsades de Points or
polymorphic ventricular tachycardia (see pic). Treat with IV magnesium.

50. How can you distinguish the ECG findings of pericarditis from
myocardial infarction or early repolarization?
The ST elevation that occurs in pericarditis is diffuse meaning in every lead. Acute MI
frequently has reciprocal ST depression and less commonly PR segment depression as is
present in pericarditis.

BONUS: Another cause of PR depression is atrial infarction.
Any other pimp questions you have run into that you think we should know?