Source: Lome is a cardiologist at the Community Hospital of the Monterey Peninsula.
Disclosures: Lome reports no relevant financial disclosures.
March 05, 2014
17 min read

50 Cardiology Pimp Questions

Source: Lome is a cardiologist at the Community Hospital of the Monterey Peninsula.
Disclosures: Lome reports no relevant financial disclosures.
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Steven Lome

As a medical student rounding on the wards, you might happen to have one of those cardiology attendings who gets some evil pleasure out of asking questions randomly to students ― commonly known as “pimping.”

Some attendings get upset if students don’t know the correct answer, then basically send them to the library, tell them to look it up and to come back when they are smarter.

If you are looking to get into a competitive residency or fellowship, or just want to avoid embarrassment in front of your peers, you really want to get these questions right. Below is a list of the top 50 “pimp” questions you may encounter on a cardiology rotation. Know them, and impress everyone. For those of you gunners who want to knock everyone’s socks off, interesting “bonus” tidbits that most people don’t know and additional links are included.

The material is organized into General Cardiology Pimps, Physical Exam Pimps and ECG Pimps. This is a lot to know, but it should prepare you well.

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. Though it is probably not wise to do this unless you are sure he or she has 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)

Another way to remember is “Check PFTs, TFTs and LFTs” for pulmonary function tests, thyroid function tests and liver function tests. But really, the only monitoring that is done is a thyroid-stimulating hormone, or TSH, level every 6 months as routine PFTs and LFTs are not recommended.

2. What are the causes of atrial fibrillation?

Remember the mnemonic 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 treatments?

This picture summarizes it all:

4. What are the causes of congestive heart failure exacerbations?

You will very likely get this one. Congestive heart failure, or CHF, is the number one cause of hospital admission in the United States. Whenever an individual comes in with volume overload from CHF, you must always as the question: “Why did this patient’s heart failure get worse?” The reasons are listed below, from most to least common:

  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 or progression of cardiomyopathy or valve disease.

5. Which medications for systolic congestive heart failure reduce mortality?

This one is easy. Beta-blockers, angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) and spironolactone. If a patient cannot tolerate ACE inhibitors or ARBs, the combination of hydralazine and nitrates are used — and also 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. For you gunners, the Congestive Heart Failure - Systolic Topic Review provides an in-depth summary from pathophysiology to treatment.

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:

  1. Carvedilol (Coreg)
  2. Bisoprolol
  3. 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 is the most common cause of right heart failure. When anything causes left heart failure — ischemia, valve disease, cardiomyopathy, etc — the left ventricular 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 vs. right heart failure.

8. A patient comes in with chest pain; what are the four life-threatening causes that should be excluded?

  1. Acute coronary syndrome
  2. Pulmonary embolism
  3. Aortic dissection
  4. Esophageal rupture (Boerhaave’s syndrome)

9. What are the signs/symptoms and issues with digoxin toxicity?

  • 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.

Reverse with digibind if any of the following present:

  • Evidence of end-organ damage (altered mental status, shock liver, etc.)
  • Life threatening arrhythmia
  • Potassium level > 5.5 mEq/L

Digoxin causes hyperkalemia, but is potentiated by hypokalemia (also hypocalcemia).

(Well, that sure is a lot to know.)

Bonus: Let’s review what is known as 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 could be fatal potentially. The massive influx of calcium into myocytes after the IV calcium is given has been theorized to induce a noncontractile state termed “Stone Heart.” Remember the end-point effect of digoxin’s actions is to open calcium channels increasing influx into cells.

Bonus bonus: The artist Vincent Van Gogh was toxic on digoxin — he used the flower foxglove for a seizure disorder — and this is why he painted everything yellow before reportedly committing suicide.

10. What are the five life-threatening complications of aortic dissection?

  1. Coronary dissection (usually the right coronary artery, or RCA) causing inferior ST segment elevation MI
  2. Carotid dissection causing stroke
  3. Aortic rupture
  4. Cardiac tamponade from rupture into pericardium
  5. Acute aortic valve regurgitation causing cardiogenic shock

11. Which atrial fibrillation patients would receive only aspirin (ASA) and which would require full anticoagulation to prevent stroke?

Based on the CHA2DS2 VASc Score, patients with 0-1 points would receive aspirin 81 mg-325 mg, and  those with > 2 points would receive full anticoagulation (warfarin, dabigatran, rivaroxiban, apixiban).

CHA2DS2 stands for (Congestive heart failure, Hypertension, Age ( > 65 = 1 point, > 75 = 2 points), Diabetes, previous Stroke/transient ischemic attack (2 points). VASc stands for vascular disease (peripheral arterial disease, previous myocardial infarction, aortic atheroma).

Note: Sex category (female gender), also included in this scoring system, equals 1 point.

12. What are the different properties of beta-blockers? 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 whose heart rates require elevation (allowing overall increased cardiopulmonary effort) to compete in sports. Examples include pindolol and acebutolol.

Membrane stabilization: Stabilizing membranes decreases the propagation of action potentials. This is also the mechanism by which local anesthetics (lidocaine) work. Class I antiarrhythmic drugs possess this characteristic, as well. The importance of this is not clear in clinical medicine regarding beta-blockers. Perhaps this is partially an explanation for using propranolol to treat migraine headaches.

13. What are the side effects and other issues with ACE inhibitors?

Just remember the mnemonic “CAPTOPRIL”

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?

Remembering what drug was in which 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 Diso’s 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?

Beck’s 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. 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 the lowest pressure chamber, so it 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 do with pleural fluid after thoracentesis of ascites after paracentesis, as the whole “transudate or exudate” issue 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 would live. A classic pimp question is, what 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 image 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)
Collagen vascular disease
Papillary muscle dysfunction
Mitral annular calcification (MAC)
Spontaneous chordal rupture
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 can’t 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 (don’t 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, Cushing’s syndrome, Conn’s 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 DON’T!!! The patient is in atrial fibrillation and CAN’T 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. Don’t 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 Marfan’s), 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 “Carvallo’s 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, Chapman’s sign, Caberera’s 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:

Chapman’s 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.

Cabrera’s 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 Prinzmetal’s 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.

Any other pimp questions you have run into that you think we should know?

- by Steven Lome