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The American College of Cardiology and American Heart Association recommend plant based diets to prevent heart disease.

Arnold Schwarzenegger, Al Gore and a Greta Thunberg are vegan for the environment.

Bernie Sanders just had a heart attack.

Can you eat meat and still care about the environment? Should Bernie go vegan?

Watch the video to see my thoughts.

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Lose weight the right way! Weight loss from a cardiologist: https://youtu.be/qIFydM9nqVs

[learntheheart]

There are three ways to lose weight...learn the right way to do it! A practical, evidence based explanation of how to lose weight explained in my latest YouTube video. Search YouTube.com for Steven Lome. Be sure to subscribe! https://www.instagram.com/p/B1pMTqAJKV5/?igshid=1iyne3egses4s

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Had my 1st Facebook Live event about heart disease prevention/reversal! Some technical glitches but it went well! Follow my Dr Steven Lome Facebook page and check out the first "episode" here: https://www.facebook.com/DrStevenLome/videos/969029659960606/ Next week: Talking to patients about plant based diets https://www.instagram.com/p/Bq-TJZxluyq/?utm_source=ig_tumblr_share&igshid=16yva2o6a4mdt

[orionswisdom]

Ok, so I know that ive said “read this book” several times already. But in all seriousness, if you read ANY of the books I have mentioned on this site, it should be this one. It is the most important out of all the books I have read. Thinking about it, I don’t know why I haven’t read it again! I...

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Here is a case I will never forget. A 45 year old man with reported no prior medical history comes in to the ER screaming of excruciating acute onset substernal chest pains 20 minutes prior to arrival. He says he was fine prior the onset of the chest pain, then suddenly became short of breath and has an “elephant on my chest” with pain down the left arm. He is afebrile with a heart rate of 65, respirations 20, blood pressure 142/72 with normal oxygen saturations. Sublingual nitroglycerin was given 3 times without relief so IV morphine was given and his chest pain eventually subsided. Here is his ECG:

STOP!!!

Lets think about this here...his clinical picture sounds typical for acute MI, right? A little too typical. The ECG shows a little anterior ST elevation. But look closely at the ECG...notice something?

The cath lab is activated for an anterior ST elevation MI. A coronary angiogram showed that his right coronary and circumflex coronary arteries were normal. His left anterior descending (LAD) was...chronically totally occluded consistent with an old remote MI.

OK then. No acute LAD thrombus here like the clinical picture might make us think. Notice those Q waves in the anteroseptal leads V1-V3? That is NOT consistent with acute chest pain for 20 minutes! More like an old anterior MI.

Lets talk about Q waves

The Q wave is the first downward deflection of the QRS complex that occurs before the R wave. It is normal to have small Q waves in most leads. We consider a Q wave pathologic (abnormal) when:

More than 40 ms (1 mm) wide

More than 2 mm deep

More than 25% of the total QRS complex amplitude

Present in leads V1-V3

What does "pathological" mean? This means a certain disease process is present, specifically myocardial infarction, usually old. These Q waves take some time to develop and would NOT be present within 20 minutes of symptom onset. They take at least a few hours to a couple days after an MI to develop and can persisist for lifetime in many cases, especially if coronary revascularization is not performed quickly enough. Here is a comparison of normal Q waves in the inferior leads compared to pathologic Q waves:

Lets review the ECG in an acute MI briefly

Hyperacute T wave changes are the first ECG change during acute MI and are quite transient, so usually missed. Here is an example of hyperacute T waves:

The second change is ST segment elevation at the J point. Here is a picture of an acute anterior ST elevation MI with 5 mm of ST elevation at the J point. They call this "Tombstoning" since the combination of the ST segment and the T wave look like a tombstone:

Eventually the ST elevation resolves and if the infarct completes, a "pathologic" Q wave develops like in our patient's ECG. An old anterior MI would have pathologic Q waves in the anterior precordial leads (V1-V3) and an old inferior MI in the inferior leads (II, III and aVF). 

Frequently we revascularize acute ST elevation MIs quite quickly and Q waves don't develop. The term "Q wave MI" is an old term that used to refer to "transmural" infarctions resulting in Q waves in the ECG.

Here Comes the Twist in the Case

He remained chest pain free and his cardiac enzymes remained normal throughout the hospitalization. A couple hours after the angiogram I was called to check on him due to left groin pain. There was good hematoma there. Odd...I was pretty sure right femoral artery access (not left) was used...so why a left groin hematoma?

A little investigating was done and we found out he DID have a prior history. Actually, this was about coronary angiogram twenty (yes...20) in the past 6 months! Almost every hospital in the area had records of him coming in with chest pains, not relieved with nitroglycerin and then relieved with IV morphine!

We confronted the guy. He admitted that he knew his ECG was abnormal and mimicked an anterior STEMI and he was addicted to IV narcotics! Crazy. But he got the story wrong...he should have said chest pain for 1-2 days in order to truly fit his ECG pattern, not acute onset of chest pain for 20 minutes!

We found out that his initial anterior MI was 6 months ago. Wait! How is there ST segment elevation on his ECG then? Well...thats because his LV angiogram during the cath showed that he had a left ventricular aneurysm!

Here some of the classic findings of left ventricular aneurysm:

Chronic ST segment elevation

Pathologic Q waves

Shape of the ST elevation seen in a LV aneurysm described as "coving".

Here it is again:

Here is what a left ventricular aneurysm looks like. See how the apex is thinned and buldges?

Two side notes

First, there is really no clinical evidence to support this classic teaching of persistent ST elevation after MI being from left ventricular aneurysm. Some studies show that persistent ST elevation correlates more with "dyskinetic" wall motion (myocardium moving outward instead of in during systole) and not necesarrily just with aneurysmal changes.

Second side note. According to the ACC/AHA guidelines for STEMI, to diagnose an anterior ST elevation MI there must be “New ST elevation at the J point in at least 2 contiguous leads of ≥ 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3 and/or of ≥1 mm (0.1 mV) in other contiguous chest leads or the limb leads.” Thus, 1 mm in any 2 contiguous leads EXCEPT leads V2 or V3 where the elevation must be 2 mm in men or 1.5 mm in women. This guy's ECG was borderline for meeting those criteria.

The ECG Dilemma

How could we have figured this out? The ECG has some good Q waves in V1-V3 which is consistent with an OLD anteroseptal MI. His symptoms were quite acute, but he knew all the key words to say. Really, the only way to know for sure the ST elevation on his ECG represents an left ventricular aneurysm is to have clinical history of a prior anterior MI and cardiac imaging showing the aneurysm. So when a guy like him says he has no prior history and has severe chest pains with an ECG like his...the cath lab gets activated...

How about a nice universal electronic medical record (EMR) to prevent this problem?

This patient was "malingering"...attempting to fake his illness for some secondary gain, in his case for IV narcotics. Here is a nice article on malingering and why it is important.

I'll never forget another case I saw during training of fever of unknown origin that was presented in our grand rounds. A guy with recurrent bacteremia of multiple different microorganisms. He had every MRI and CT scan possible as well as a lumbar puncture and transesophageal echocardiogram to exclude endocarditis. Multiple infectious disease specialists were consulted and nobody could figure him out! We found out that he was actually malingering by injecting feces into his IV! Oh my...

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Related Links:

Topic Review: ST Elevation MI

Topic Review: Left Ventricular Aneurysm

References:

1. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric, 6e

Image Reference: CC Patrick J. Lynch and C. Carl Jaffe, Yale University, 2006

By Steven Lome

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From the LearnTheHeart.com Cardiology Blog

So you are on the wards rounding and happen to have one of those cardiology attendings that gets some evil pleasure out of asking questions randomly to students (commonly known as “pimping”). I have seen some attendings get upset if students don’t know the correct answer and basically will send them to the library, tell them to look it up, then come back when they are smarter!

As a medical student, you MUST get these questions right if you are looking to get into a competitive residency/fellowship or just want to avoid embarrassment in front of your peers. Here is a list of the top 50 pimp questions that you may get on a cardiology rotation…know them and impress everyone! Want to really knock everyone’s socks off? I included some “Bonus” tidbits that are interesting and most people don’t know and links for those gunners who want to read more. 

I have organized all of this into general cardiology pimps, physical exam pimps and ECG pimps. This is a lot to know, but 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! 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 patient’s 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 (Boerhaave’s 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 digoxin’s 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 CHA2DS2 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 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, 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).

  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.

BONUS: Another cause of PR depression is “atrial infarction”.

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

Leave a comment on the LearnTheHeart.com blog article “Top 50 Cardiology Pimp Questions”

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New Cardiology and ECG Blog on LearnTheHeart.com for students!

"Eye Popping" Atrial Fibrillation

Not your typical atrial fibrillation case walking through the ER door today. Hold on to your eyeballs here for this case with two major teaching points. A 38 year old obese but otherwise healthy male who complains of palpitations, increasing dyspnea and edema over the past 2 months. He bought online some weight loss medications to “boost metabolism” and has lost 150 pounds in about 3 months on this stuff! Probably not worth it in the long run.

Cardiac Physical Exam…A Waste of Time?

Is the death of the stethoscope near? Why do we even listen to the heart anyway now that we have portable echocardiography? Is it a waste of time? When I was in training to become a cardiologist, I was fortunate enough to be taught by physicians who practiced medicine when physical examination skills were essential in diagnosis. We had multiple physical exam lectures and even a dedicated exam on the topic. W. Proctor Harvey (legendary cardiac auscultation expert) was the idol of our program director.

50 Cardiology Pimp Questions

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

And many more articles! Subscribe to receive new postings by e-mail.

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ECG Quiz on LearnTheHeart.com - more than 200 ECG tracings with detailed answers. Beginner and expert.

To master ECG interpretation takes time and effort, however the LearnTheHeart.com ECG tutorial is designed to be concise and focused on only what you need to know, yet very thorough. Start by reading through the ECG basics and the different parts of the ECG. Once completed, be sure to read through all of the ECG criteria and review pages to learn how to diagnose specific conditions and rhythms such as myocardial infarctions and chamber hypertrophies. Then go through the 100+ practice ECG quizzes below that have detailed explanations and link to the pertinent explanation pages. Then there are ECG cases which test your ECG interpretation skills in the setting of clinical scenarios. Once completed, a thorough understanding of ECG interpretation will be attained. Keep your skills up by signing up for our ECG Blog.

The ECG quizzes on LearnTheHeart.com are organized as below:

Comprehensive ECG Quiz  

From basic 12-lead ECG tracings to the most bizarre expert level tracings, this ECG test is excellent for all levels of ECG interpretation skills. Nearly 200 tracings are currently included each with detailed explanations and links to relevant topic reviews for each ECG.

Expert ECG Quiz

Most challenging and unusual ECG tracings including rare electrophysiologic disorders. Even the ECG gurus of the world will be challenged by some of these tracings!

Beginner ECG Quiz

Simple findings such as the most common rhythm disorders, infarctions, blocks and chamber enlargements.

Heart Blocks ECG Quiz

AV blocks, bundle branch blocks, and sinoatrial exit blocks. Links to comprehensive reviews for all heart block topics are included to enhance the learning experience.

Atrial Arrhythmias ECG Quiz

Atrial fibrillation, atrial flutter, atrial tachycardia, varying SVTs and junctional rhythms. Every derivation of atrial arrhythmias is included with detailed explanations and links to pertinent reviews.

Ventricular Arrhythmias ECG Quiz

Rhythms originating in the ventricles such as ventricular tachycardia (monomorphic and polymorphic), ventricular fibrillation and premature ventricular contractions. Some SVT with aberrancy ECG tracings are included to help enhance the discussion of how to diagnose ventricular tachycardia. Detailed explanation are included with links to the relevant topic reviews.

Infarcts and Ischemia ECG Quiz

Anterior MI ECGs, inferior MI ECGs, posterior MI ECGs and other ischemic ECG changes. All ECGs have detailed explanations and links to relevant topic reviews. Test yourself on these ECG tracings regularly since quick diagnosis is important.

Chamber Enlargement ECG Quiz

Left and right atrial enlargements, left ventricular hypertrophy, right ventricular hypertrophy and more. Detailed explanations and links to topic reviews are included.

Miscellaneous ECG Quiz

Unusual ECG findings such as hyperkalemia, other electrolyte disturbances and rare findings. These include hypothermia and rare electrophysiologic conditions. Detailed explanations are provided with links to topic reviews.

These ECG tests are quite extensive, but it is important to complete all of the tracings to attain a full ECG education. Review then once every few months to keep these ECG principles fresh in your mind. Join the LearnTheHeart.com ECG Blog for regular postings of ECG Cases.

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From LearnTheHeart.com's Twiddler's Syndrome review on the Cardiology Reviews and Definitions page.

Twiddler’s Syndrome occurs when a patient with a permanent pacemaker manipulates the pulse generator usually by turning it multiple times. This results in the leads becoming dislodged and malfunctioning. The manipulation is most frequently done subconsciously in the setting of dementia or during sleeping hours. Chest x-ray is very helpful to make this diagnosis as the leads can be seen twisted.

Treatment includes repositioning of the leads and patient education. Physical restraints may be needed to prevent recurrence. Below is a chest x-ray from a patient with Twiddler's syndrome. Note the twisted leads near the pulse generator. The right ventricular lead has also dislodged into the right atrium.

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From LearnTheHeart.com's Atrial Flutter review

Introduction

Atrial flutter is similar to atrial fibrillation in that the rhythm originates in the atrium and causes a narrow complex tachycardia which has thromboembolic risk. Typical atrial flutter results from a reentrant circuit around the tricuspid valve through the cavo-tricuspid isthmus. This anatomically makes ablation much easier than that of atrial fibrillation which occurs in the pulmonary veins. The atrial rates during atrial flutter vary from 250-350 beats per minutes, slower than the 400-600 beats per minute seen in atrial fibrillation. Frequently, a 2:1 conduction ratio occurs resulting in a ventricular rate of 150 beats per minute.

Pathophysiology

Atrial flutter can described as “typical” (a.k.a. type I) or “atypical” (a.k.a. type II) based on the anatomic location that it originates. Also, “clockwise” or “counterclockwise” atrial flutter is described depending on the direction of the circuit.

Typical atrial flutter is counterclockwise in direction and originates from a reentrant circuit around the tricuspid valve annulus and through the cavo-tricuspid isthmus. This results in negatively directed flutter waves in the inferior leads. At times, the direction of the circuit can reverse causing clockwise atrial flutter from the same anatomical location. This appears as positively directed flutter waves in the inferior leads.

Atypical atrial flutter originates from the left atrium or areas in the right atrium (such as surgical scars) and has a variable appearance on ECG in regards to the flutter waves.

Etiology

The etiology of atrial flutter is similar to that of atrial fibrillation. Identifying the etiology of can not be underemphasized as the treatment of the cause is frequently necessary to eliminate recurrences of atrial flutter. The classic pneumonic “PIRATES” encompases a vast majority of the causes:

Pulmonary embolus, pulmonary disease, post-operative, pericarditis Ischemic heart disease, idiopathic (“lone AF”), intravenous central line (in right atrium) Rheumatic valvular disease (specifically mitral stenosis or mitral regurgitation) Anemia, alcohol (“holiday heart”), advanced age, autonomic tone (vagal mediated AF) Thyroid disease (hyperthyroidism) Elevated blood pressure (hypertension), electrocution Sleep apnea, sepsis, surgery

Historically, hypertension was thought to be the most common cause of atrial flutter, however obstructive sleep apnea is present in about 40% of patients and it is well known that obstructive sleep apnea causes hypertension. The exact proportion of atrial flutter caused directly from obstructive sleep apnea remains unclear.

Diagnosis

Diagnosing atrial flutter is done predominantly on the surface ECG. Sinus P waves are absent. The classic “sawtooth” pattern occurs since the reentrant circuit around the tricuspid valve is large resulting in high amplitude P waves.

Distinguishing between clockwise and counterclockwise atrial flutter was described previously.

The ventricular rate is frequently elevated and regular, the later of which is an important factor allowing to differentiate atrial flutter from atrial fibrillation, however if “variable conduction” of the atrial flutter waves to the ventricles is present, the QRS complexes can be irregularly irregular. Also, multifocal atrial tachycardia can be irregularly irregular.

When the heart rate is significantly elevated (greater than 150 beats per minute), it is frequently difficult to determine atrial flutter from atrial fibrillation, atrial tachycardia, or atrioventricular nodal reentrant tachycardia (AVNRT). In this situation, giving adenosine will transiently slow the ventricular rate unmasking the atrial flutter waves allowing a more definitive diagnosis to be made.

On physical examination the heart rhythm will be frequently tachycardic and at usually regular, however as above may be “irregularly irregular” if variable conduction is present. Findings of congestive heart failure may be present depending on the ventricular rate, duration of atrial flutter and other factors. There will never be an S4 heart sound present during atrial flutter as this heart sound is produced when atrial contraction forces blood into a non-compliant left ventricle. Normal atrial contraction is lost during atrial flutter. 

Diagnosing a left atrial appendage (LAA) thrombus which can result in thromboembolism frequently causing stroke must be done using transesophageal echocardiography (TEE) or cardiac CT (less commonly used). It is important to note that transthoracic echocardiography does not detect left atrial appendage thrombi in the vast majority of patients. TEE findings of a LAA thrombus includes direct visualization of a mobile echodensity within the appendage. The echodensity should move independent of the walls of the atrium which helps to distinguish artifact from thrombus. Pulse wave Doppler can be used in the LAA to determine the flow velocity. A velocity of < 0.4 m/s indicates a higher risk in general of thromboembolism.

Symptoms

The symptoms of atrial flutter relate either to tachycardic heart rate causing palpitations or decreased overall cardiac output (from loss of atrial contraction and fast ventricular rates) resulting in congestive heart failure (see congestive heart failure symptoms). If hypotension is present from a significantly reduced cardiac output, dizziness and even syncope (loss of consciousness) can occur.

Treatment

The approach to the management of AF patients requires the consideration of two distinct areas: Alleviating symptoms of AF and preventing thromboembolism.

Alleviating symptoms

There are two main approaches which can be utilized to alleviate symptoms of AF: A “rate control” strategy or a “rhythm control” strategy.

The AFFIRM trial evaluated using a rate control strategy versus a rhythm control strategy and included a number of patients with atrial flutter in addition to atrial fibrillation. There was no difference in mortality between these approaches and thus an individualized approach is recommended based on the degree of symptoms and the patient’s personal preference. In practice, atrial flutter ablation is commonly utilized in typical atrial flutter since the procedure is much easier than atrial fibrillation ablation with a high success rate and low complication risk.

Rate control

Commonly, controlling the ventricular rate in atrial flutter patients can completely resolve symptoms and no further therapy is needed. This is done using AV blocking medications either intravenously in the acute setting or orally for long-term therapy. Atrial flutter tends to be more difficult to control with AV blocking medications than atrial fibrillation.

Selecting the appropriate AV blocking agent requires the knowledge of other indications and contraindications for these drugs, specifically, knowledge of the left ventricular systolic function is important. AV blocking agents used in atrial flutter include beta-blockers, non-dihydropyridine calcium channel blockers and digoxin.

Beta-blockers (atenolol, metoprolol, carvedilol and others) antagonise beta-receptors (see review of beta-adrenergic blockers) which result in decreasing conduction through the AV node reducing the heart rate in atrial fibrillation patients. Caution is advised in patients with asthma since antagonizing beta-2 receptors can cause bronchospasm. In severe left ventricular systolic dysfunction (reduced ejection fraction), beta-blockers can acutely decrease cardiac output leading to severe hypotension, acute heart failure and even cardiogenic shock. Despite this, beta-blockers are considered safe when used cautiously in this setting.

Non-dihydropyridine calcium channel blockers (diltiazem, verapamil) decrease AV conduction by antagonizing voltage gated calcium channels decreasing intracellular calcium. Since these drugs reduce left ventricular inotropy (contractility) via the same mechanism, they are in general not advised to be used in the setting of left ventricular systolic dysfunction (reduced ejection fraction).

Digoxin blocks the sodium/potassium ATPase pump. The mechanism by which this decreases AV conduction is not clear however is perhaps due to increased vagal tone. Intracellular calcium within the cardiac myocytes is increased by digoxin resulting in increased inotropy (contractility) and thus digoxin is frequently used when AF and left ventricular systolic dysfunction coexist. Digoxin is effective to reduce ventricular rates at rest, however not effective during physical activity and thus it is recommended to use digoxin in combination with a beta-blocker or non-dihydropyridine calcium channel blocker.

Rarely, the above medications are not able to adequately reduce the ventricular rate and AV nodal ablation with permanent pacemaker implantation is needed (see below).

Rhythm control

A rhythm control strategy is employed when rate control is not successful in completely eliminating symptoms from atrial flutter or if the ventricular rate is refractory to the above mentioned AV blocking medications. This can be done using cardioversion, antiarrhythmic drug therapy or ablation.

The term “cardioversion” is used to describe an action taken to restore sinus rhythm. This can be done either electrically by delivering a shock (direct current cardioversion or DCCV) or chemically with certain drugs (class IA, class IC or class III antiarrhythmic drugs).

Once sinus rhythm is restored, antiarrhythmic drug therapy can be utilized to maintain sinus rhythm, especially if the risk of recurrence is high such as in severe left atrial enlargement, severe valvular heart disease or uncontrolled sleep apnea.

Antiarrhythmic drugs used to treat atrial fibrillation include the following:

Class IA (quinidine, procainamide, disopyramide): While class IA drugs are effective to treat atrial flutter, they are not commonly utilized for this purpose due to side-effects and significant pro-arrhythmia except in special situations (atrial flutter with Wolff-Parkinson-White). These agents block cardiac sodium channels and depress phase 0 of the action potential. Procainamide can cause drug-induced lupus erythematosus detected by measuring anti-histone antibodies. Quinidine can cause cinchonism.

Class IB (lidocaine, mexiletine): These ARE NOT effective to treat atrial fibrillation or atrial flutter and are used for ventricular arrhythmias.

Class IC (flecainide, propafenone, moricizine): These drugs are commonly used to maintain sinus rhythm in atrial flutter patients. Significant coronary artery disease is a contraindication to their use as this increases the risk of proarrhythmia and sudden cardiac death. These agents must be used in combination with an AV blocking agent in order to prevent rapid atrial flutter conduction (1:1 conduction) through the AV node resulting in very fast ventricular rates if a breakthrough episode occurs since they also act to increase AV nodal conduction (see Special Situations section). These drugs may be proarrhythmic in the setting of left ventricular hypertrophy (wall thickness > 1.4 cm). Flecainide can be used with a “pill-in-the-pocket” approach. If documented to be successful and safe while hospitalized, flecainide can be used on an as-needed basis in the outpatient setting. Note that propafenone is hepatically cleared (not recommended with liver disease) while flecainide is renally cleared.

Class III (amiodarone, sotalol, bretylium, dofetilide, dronedarone, ibutilide): These drugs are also commonly used in atrial flutter and act by blocking potassium channels. Amiodarone is very effective however amiodarone toxicity is a concern. The half-life of amiodarone is 42 days. Sotalol is proarrhythmic in the setting of left ventricular hypertrophy (wall thickness > 1.4 cm). Amiodarone and dofetilide are preferred in patients with left ventricular systolic dysfunction (reduced ejection fraction). Dronedarone is not safe with systolic heart failure or in the setting of permanent atrial flutter. Bretylium is rarely used.

Atrial flutter ablation can be utilized as an initial rhythm control strategy instead of antiarrhythmic drugs since this procedure is low risk with a high success rate, unlike that of atrial fibrillation where success rates vary and there is a higher complication risk. See the comparison chart below:

*Less commonly atrial fibrillation originates from the right atrium including the superior vena cava or coronary sinus. Atypical atrial flutter may originate from left atrium on occasion, however is less common. **Duration of atrial fibrillation and left atrial volume is main determinant of success rates

Special Situations

1:1 Conduction of Atrial Flutter: When a class IC antiarrhythmic drug is used for atrial flutter, an AV blocking agent must be used simultaneously to avoid a paradoxical increase in ventricular rates. The atrial rate during atrial flutter is between 250-350 beats per minute. At this rate, the AV node is usually refractory long enough to block at least every other beat from conducting to the ventricles. The class IC antiarrhythmic drugs can slow the atrial rate and increase AV nodal conduction as well.

If the atrial rate is slowed, for example, from 300 to 200 beats per minute, the AV node may not be refractory long enough to block any of these atrial impulses. Originally, if 2:1 conduction was occurring with the atrial rate of 300 beats per minute, the ventricular rate would be 150 beats per minute. If the atrial rate is slowed to 200 and 1:1 conduction occurs, the ventricular rate would be faster at 200 beats per minute despite a lower atrial rate.

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From LearnTheHeart.com's Low Voltage ECG Review.

Low voltage is defined as peak-to-peak QRS amplitude of < 5 mm in the limb leads and/or < 10 mm in the precordial leads. Low voltage may be present in the following situations:

Obesity

COPD

Pericardial effusion

Severe hypothyroidism

Subcutaneous emphysema

Massive myocardial damage/infarction

Infiltrative/restrictive diseases such as amyloid cardiomyopathy.

Note: If the gain indicated at the left of the ECG is turned down accidently, the voltage will be falsely low (pseudo-low voltage). The indicator should be set to 10 mm amplitude.

Low Voltage ECG Example 1

Low Voltage ECG Example 2

Low Voltage ECG Example 3

Low Voltage ECG Example 4

Pseudo Low Voltage ECG

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Mitral valve prolapse (Barlow’s disease) is a connective tissue disorder which results in the valve leaflets becoming redundant causing prolapse into the left atrium during systole. This can lead to mitral valve regurgitation. 

Diagnosis of mitral valve prolapse on echocardiography is done by examing the parasternal long-axis view. If the valve leaflets pass the plane of the annulus, then prolapse is present. See the image to the right.

Mitral valve prolapse is usually asymptomatic unless congestive heart failure occurs from mitral regurgitation. The mitral valve prolapse syndrome can be associated with palpitations, chest pains, and panic attacks. The etiology remains unclear however may be due to activation of the sympathetic nervous system.

Mitral valve prolapse produces a mid-systolic click usually followed by a uniform, high-pitched murmur (see image above).  The murmur is actually due to mitral regurgitation that accompanies the MVP, thus it is heard best at the cardiac apex. MVP responds to dynamic auscultation. After sudden standing, preload is decreased and the click moves earlier in systole. With sudden squatting, preload increases and the click moves later in systole.

Mitral valve prolapse is the most common indication for surgical mitral valve repair due to severe mitral valve regurgitation.

The most common segment involved in mitral valve prolapse is termed the P2 segment. The mitral valve structure is complex. The anterior and posterior leaflets have been anatomically separated into 3 segments each (A1, A2, A3 and P1, P2, P3).

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From LearnTheHeart.com Ventricular Septal Defects review.

A ventricular septal defect (VSD) occurs when there is direct communication between the left and right ventricles. This can be a congenital anomaly or acquired as a complication of a myocardial infarction.

Ventricular septal defects are classified as membranous, perimembranous, supracristal (infundibular or subpulmonic) or muscular.

Membranous VSDs are the most common type and originate inferior to the crista supraventricularis, yet still towards the left ventricular outflow tract.

Perimembranous VSDs are also inferior to the crista supraventricularis, however extend into the muscular septum.

Supracristal VSDs occur just beneath the aortic valve at the left ventricular outflow tract. A Venturi effect can occur from the left to right shunt causing the aortic valve leaflet to prolapse into the VSD resulting in significant aortic valve regurgitation.

Muscular VSDs occur in the mid to apical interventricular septum and do not involve cardiac valves.

A Gerbode defect is technically a type of ventricular septal defect, although this results in a left ventricular to right atrial shunt.

Pathophysiology

Significant left to right shunting can occur resulting in a high left ventricular cardiac output. Forward systemic flow can be reduced if the shunt is large resulting in symptoms of congestive heart failure.

The Qp/Qs ratio can be measured during cardiac catheterization or via echocardiography and helps to determine the size of the cardiac shunt. The Qp (flow through the pulmonary vascular bed) is compared to the Qs (flow through the systemic vascular bed). In a normal individual without a cardiac shunt this ratio should be 1, however the pulmonary flow increases significantly compared to systemic flow when a left to right shunt is present. If the Qp/Qs ratio reaches > 2, then clinical symptoms usually manifest.

Physical Examination

A ventricular septal defect produces a holosystolic murmur. Blood abnormally flows from the LV (high pressure) to the RV (low pressure) creating turbulent blood flow and a holosystolic murmur heard best at "Erb's point". The smaller the ventricular septal defect, the louder the murmur. A very small VSD can cause a palpable thrill (vibration on the chest). A small VSD with a loud murmur is called "Maladie de Roger" after the initial describer.

Diagnosis

Diagnosis is predominantly made via echocardiography which directly images the shunt and can can measure important hemodynamic parameters such as cardiac chamber sizes, the Qp/Qs ratio and pulmonary pressures.

Left ventriculography can visualized VSDs as well. During right heart catheterization, oxygen saturations are frequently measured from different cardiac chambers in order to identify left to right shunts. If a ventricular septal defect is present, the oxygen saturation will be markedly higher in the right ventricle due to shunting of well oxygenated blood from the left ventricle to the right ventricle. This diagnostic technique can be helpful when a patient presents after an acute myocardial infarction with pulmonary edema and shock to diagnose an acute ventricular septal defect.

Treatment

There is no specific medical therapy that is recommended in the treatment of a ventricular septal defects. Ventricular septal defects can be closed surgically or percutaneously.

The indications to close a ventricular septal defect include:

Qp/Qs is > 1.5 and there is LV systolic or diastolic dysfunction causing clinical heart failure.

Prior endocarditis on the VSD

Qp/Qs is > 1.5 and the pulmonary pressures are no more than two thirds of systemic pressure.

Qp/Qs is > 2 and there is evidence of volume overload of the LV

Acute VSD after myocardial infarction

If Eisenmenger’s syndrome is present, closure of a VSD is NOT recommended and can be fatal. In this situation, the only remedy is heart-lung transplantation.

References:

1. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine

2. Hurst's the Heart, 13th Edition

Image reference: CC Patrcik J Lynch and C. Carl Jaffe, Yale University, 2006.

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Ebstein’s anomaly is a congenital heart defect in which the tricuspid valve leaflets are abnormally displaced toward the cardiac apex resulting in a small right ventricle and massive enlargement of the right atrium.

Note that if a pregnant mother is taking lithium, the risk of Ebstein's anamaly in the newborn is markedly higher. Also, Ebstein's anomaly is frequently associated with Wolff-Parkinson-White syndrome which can manifest as atrioventricular reentrant tachycardia (AVRT) or atrial fibrillation with pre-excitation. Treatment is emergent cardioversion, procainamide and eventually ablation.

Ebstein's anomaly is associated with atrial septal defects in about 50% of cases.

Tricuspid valve regurgitation can ensue and frequently requires surgical repair. Indications for repair of the Ebstein’s anomaly and associated atrial septal defect (if present) include New York Heart Association Functional Class III or IV symptoms, marked right heart enlargement, cyanosis, and transient ischemic attack (TIA) or stroke.  

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From LearnTheHeart.com Atrial Fibrillation Review.

Treatment - Alleviating symptoms

The approach to the management of atrial fibrillation patients requires the consideration of two distinct areas: Alleviating symptoms of atrial fibrillation and preventing thromboembolism. A summary image is above.

There are two main approaches which can be utilized to alleviate symptoms of atrial fibrillation: A “rate control” strategy or a “rhythm control” strategy.

The AFFIRM trial evaluated using a rate control strategy versus a rhythm control strategy. There was no difference in mortality between these approaches and thus an individualized approach is recommended based on the degree of symptoms and the patient’s personal preference.

Rate control

Commonly, controlling the ventricular rate in atrial fibrillation patients can completely resolve symptoms and no further therapy is needed. This is done using AV blocking medications either intravenously in the acute setting or orally for long-term therapy.

Selecting the appropriate AV blocking agent requires the knowledge of other indications and contraindications for these drugs, specifically, knowledge of the left ventricular systolic function is important. AV blocking agents used in AF include beta-blockers, non-dihydropyridine calcium channel blockers and digoxin.

Rhythm Control

A rhythm control strategy is employed when rate control is not successful in completely eliminating symptoms from atrial fibrillation or if the ventricular rate is refractory to the previously mentioned AV blocking medications. This can be done using cardioversion, antiarrhythmic drug therapy or ablation.

The term “cardioversion” is used to describe an action taken to restore sinus rhythm. This can be done either electrically by delivering a shock (direct current cardioversion or DCCV) or chemically with certain drugs (class IA, class IC or class III antiarrhythmic drugs).

Once sinus rhythm is restored, antiarrhythmic drug therapy can be utilized to maintain sinus rhythm, especially if the risk of recurrence is high such as in severe left atrial enlargement, severe valvular heart disease or uncontrolled sleep apnea.

Antiarrhythmic drugs used to treat atrial fibrillation include the following:

Class IA (quinidine, procainamide, disopyramide)

Class IC (flecainide, propafenone, moricizine)

Class III (amiodarone, sotalol, bretylium, dofetilide, dronedarone, ibutilide)

Atrial Fibrillation Ablation

The indication for atrial fibrillation ablation is symptoms from atrial fibrillation and failure of at least 1 antiarrhythmic drug. An attempt at a second antiarrhythmic drug would also be reasonable.

[learntheheart]

ECG Quiz - What is the clinical diagnosis on the above ECG?

ANSWER:

Pulmonary embolism

The most common ECG finding in the setting of a pulmonary embolism is sinus tachycardia, however the "S1Q3T3" pattern of acute cor pulmonale is classic. This is termed the McGinn-White sign.

A large S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III indicates acute right heart strain. This pattern only occurs in about 10% of people with pulmonary embolisms and is similar to the ECG findings in a left posterior fascicular block (LPFB). Recall that sinus tachycardia is actually the most common ECG finding during a pulmonary embolus.

Pulmonary Embolism (ECG Example 1)

Pulmonary Embolism (ECG Example 2)

Pulmonary Embolism (ECG Example 3)