Official Step 1 HY Cardiology Concepts & Discussion Thread

[Mr. Mojo Risin]

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Feel free to use this thread to discuss HY Cardio concepts. Good luck to everyone!

Links to the other HY subject threads:

Biochemistry: http://forums.studentdoctor.net/thr...y-biochem-concepts-discussion-thread.1115421/

Endocrinology: http://forums.studentdoctor.net/thr...crinology-concepts-discussion-thread.1115426/

Gastroenterology: http://forums.studentdoctor.net/thr...nterology-concepts-discussion-thread.1115427/

Hematology/Oncology: http://forums.studentdoctor.net/thr...-oncology-concepts-discussion-thread.1115428/

Immunology: http://forums.studentdoctor.net/thr...mmunology-concepts-discussion-thread.1115423/

Microbiology: http://forums.studentdoctor.net/thr...-microbio-concepts-discussion-thread.1115422/

MSK/Skin/Connective Tissue: http://forums.studentdoctor.net/thr...ve-tissue-concepts-discussion-thread.1115430/

Neurology: http://forums.studentdoctor.net/thr...neurology-concepts-discussion-thread.1115431/

Psychiatry: http://forums.studentdoctor.net/thr...sychiatry-concepts-discussion-thread.1115432/

Renal: http://forums.studentdoctor.net/threads/official-step-1-hy-renal-concepts-discussion-thread.1115433/

Reproductive: http://forums.studentdoctor.net/thr...roductive-concepts-discussion-thread.1115434/

Respiratory: http://forums.studentdoctor.net/thr...spiratory-concepts-discussion-thread.1115435/

 

[faisal 2000]

which diseases other than thoracic outlet syndrome and takayasu arteritis can cause Pulseless in upper extremity?
thoracic outlet syndrome affects ulnar nerve and subclavien artery and result in absence of radial pulse (ipsilateral)
takayasu arteritis involve aortic arch at branches point and basically leads to pulseless in upper extremity

 

[dfib slim]

Coarctation of the aorta proximal to the ductus like in Turner syndrome.
Certain type of aortic dissection, I forget which one.

 

[dfib slim]

Which antiarrhythmic can cause your skin to turn blue?

 

[seminoma]

Which antiarrhythmic can cause your skin to turn blue?

Amiodarone

 

[seminoma]

Besides hydralazine and methyldopa, name two antihypertensives that are used in pregnancy.

 

[dfib slim]

Besides hydralazine and methyldopa, name two antihypertensives that are used in pregnancy.

Uh.. labetalol and amlodipine? Definitely not RAAS drugs.

 

[seminoma]

Uh.. labetalol and amlodipine? Definitely not RAAS drugs.

Yep! FA says nifedipine, but amlodipine works too.

 

[dfib slim]

Medical treatment for A Fib with WPW?

 

[pathologyDO]

Medical treatment for A Fib with WPW?

amiodarone?

 

[dfib slim]

amiodarone?

Negative, that will put them into VF/VT. Slowing down the AV pathway allowing for the accessory pathway to propagate.

 

[pathologyDO]

Negative, that will put them into VF/VT. Slowing down the AV pathway allowing for the accessory pathway to propagate.

radiofrequency ablation therapy?

 

[dfib slim]

radiofrequency ablation therapy?

Medical treatment i.e. Drugs

 

[pathologyDO]

Medical treatment i.e. Drugs

Thanks for clarifying.

Honestly I thought since amiodarone has properties of so many classes (basically class I-IV) of antiarrhythmics that it would also work to slow down the refractory stage of the accessory pathway as well.

Hints? Having trouble with this one.

 

[dfib slim]

Thanks for clarifying.

Honestly I thought since amiodarone has properties of so many classes (basically class I-IV) of antiarrhythmics that it would also work to slow down the refractory stage of the accessory pathway as well.

Hints? Having trouble with this one.

Can also cause lupus-like syndrome

 

[pathologyDO]

Can also cause lupus-like syndrome

Ah hah. Procainamide.

Could you explain why the class IA would be used in this case?

 

[dfib slim]

Ah hah. Procainamide.

Could you explain why the class IA would be used in this case?

My guess would be the antimuscarinic effects causing shortened PR interval. Anything that prolongs the PR interval, such as beta blockers, calcium channel blockers, or amiodarone, would be contraindicated.

 

[pathologyDO]

My guess would be the antimuscarinic effects causing shortened PR interval. Anything that prolongs the PR interval, such as beta blockers, calcium channel blockers, or amiodarone, would be contraindicated.

Hmm I guess that makes sense? Did you get your answer to this question from FA?

According to this medscape article http://emedicine.medscape.com/article/159222-treatment#aw2aab6b6b3

"Class Ia drugs (eg, quinidine) and class Ic drugs (eg, flecainide, propafenone) slow conduction velocity in the AP and prolong the AP refractory period in the bypass tract.

Amiodarone, dofetilide, and sotalol prolong refractoriness in myocardial tissue, including AV bypass tracts."

So those medications are apparently also indicated for use in WPW with A Fib in addition to procainamide.

And then they go on to say...

"Procainamide is no longer available in an oral formulation and is typically only used during EPS or in the emergency department (ED) or cardiac intensive care unit (ICU) setting."

 

[faisal 2000]

Medical treatment for A Fib with WPW?

we have to decrease activity of av node , so there are 3 strategies to do that: ca channel blocker,digitalis and Na channel blocker
from uptodate ;

"For patients with acute symptomatic orthodromic AVRT who are hemodynamically stable, our approach is as follows (table 1) (see 'Acute termination of orthodromic AVRT' above):
•We recommend initial treatment with one or more vagal maneuvers rather than pharmacologic therapy (Grade 1B).
•If vagal maneuvers are ineffective, pharmacologic therapy with an AV nodal blocking agent (ie, adenosine, verapamil, beta blockers) should be instituted. We suggest intravenous adenosine rather than intravenous verapamil as the initial choice based on its efficacy and short half life (Grade 2B).
•If adenosine is ineffective, we proceed with intravenous verapamil as the second line agent. If orthodromic AVRT persists, intravenous procainamide, beta blockers approved for intravenous administration (propranolol, metoprolol, and esmolol), and digoxin are additional therapeutic options.
●For patients with acute symptomatic antidromic AVRT who are hemodynamically stable, we treat with intravenous procainamide in an effort to terminate the tachycardia or, if the tachycardia persists, slow the ventricular response. (See 'Acute termination of antidromic AVRT' above.)"

 

[dfib slim]

If you block the AV node they can go into VT/VF

Also from uptodate

For patients with acute symptomatic preexcited atrial fibrillation (AF) who are hemodynamically stable, our approach is as follows (see 'Acute treatment of atrial fibrillation with preexcitation' above):



•We suggest initial medical therapy for rhythm control versus rate control (Grade 2C). This is based on the greater ease of controlling the ventricular rate in sinus rhythm. While there is no clear first line medication for rhythm control, options include ibutilide and procainamide.



•For all patients with preexcited AF, we recommend NOT using standard AV nodal blocking medications (ie, beta blockers, non-dihydropyridine calcium channel blockers [verapamil and diltiazem], digoxin, adenosine, and amiodarone) (Grade 1A). Blocking the AV node may result in increased conduction of atrial impulses to the ventricle by way of the accessory pathway, increasing the ventricular rate and potentially resulting in hemodynamic instability. (See'Avoidance of AV nodal blockers' above.)

 

[pathologyDO]

If you block the AV node they can go into VT/VF

Also from uptodate

For patients with acute symptomatic preexcited atrial fibrillation (AF) who are hemodynamically stable, our approach is as follows (see 'Acute treatment of atrial fibrillation with preexcitation' above):



•We suggest initial medical therapy for rhythm control versus rate control (Grade 2C). This is based on the greater ease of controlling the ventricular rate in sinus rhythm. While there is no clear first line medication for rhythm control, options include ibutilide and procainamide.



•For all patients with preexcited AF, we recommend NOT using standard AV nodal blocking medications (ie, beta blockers, non-dihydropyridine calcium channel blockers [verapamil and diltiazem], digoxin, adenosine, and amiodarone) (Grade 1A). Blocking the AV node may result in increased conduction of atrial impulses to the ventricle by way of the accessory pathway, increasing the ventricular rate and potentially resulting in hemodynamic instability. (See'Avoidance of AV nodal blockers' above.)

Oh nice, I like this answer. Thanks. Are you a 2nd year or are you in your clinical years? Interested to know if you bought uptodate during pre-clinical years

 

[dfib slim]

I'm a second year at a DO school. They give us free access to Uptodate the entire 4 years.

 

[pathologyDO]

I'm a second year at a DO school. They give us free access to Uptodate the entire 4 years.

Nice.

Alright so back to the topic.. procainamide (or ibutilide) is the tx of choice for WPW with A Fib because it doesn't slow AV nodal conduction, but does slow the accessory pathway through the bundle of Kent. Got it.

This was a good concept to cover. Thanks again

 

[scoKraz4]

Coarctation of the aorta proximal to the ductus like in Turner syndrome.
Certain type of aortic dissection, I forget which one.

Coarctation proximal to ductus would cause bounding pulses in upper extremity and possibly pulseless in lower extremity

 

[dfib slim]

Coarctation proximal to ductus would cause bounding pulses in upper extremity and possibly pulseless in lower extremity

I meant proximal to the left subclavian which is technically proximal to the ductus right? 😛

 

[seminoma]

FA Antianginal errata? FA15 page 305 says beta blockers have will have "no effect" or "decrease" EDV. Shouldn't beta-blockers increase EDV? They decrease HR --> increase diastolic time --> increase filling. They also decrease inotropy --> decrease EF --> increase EDV.

 

[smarts1]

Just throwing in a calculation question. 🙂

If someone has an O2 consumption of 1000 ml/min with an O2 content of the arterioles of 200 ml/L of blood and a venous O2 content of 150 mL/L, what is the cardiac output?

If the heart rate is 60 beats/min and the ESV is 40 mL, what is the ejection fraction?

 

[seminoma]

Just throwing in a calculation question. 🙂

If someone has an O2 consumption of 1000 ml/min with an O2 content of the arterioles of 200 ml/L of blood and a venous O2 content of 150 mL/L, what is the cardiac output?

If the heart rate is 60 beats/min and the ESV is 40 mL, what is the ejection fraction?

CO = 1000/(200-150) = 20.

I don't know how to calculate EF from HR and ESV..? Is there a way?

 

[smarts1]

CO = 1000/(200-150) = 20.

I don't know how to calculate EF from HR and ESV..? Is there a way?

Oh I should have been clear... The second question also depends on your answer and info in the first question.

 

[faisal 2000]

CO = 1000/(200-150) = 20.

I don't know how to calculate EF from HR

c.o=s.v×h.r
= 20000ml/min(c.o) /60

 

[smarts1]

c.o=s.v×h.r
= 20000ml/min(c.o) /60

Well that gives you the stroke volume... So you'll need to calculate EF now. 🙂

 

[faisal 2000]

E.d.v=s.v+e.d.v= 33+40 = 73
e.f=33/73=0.45 --- 45%ejected per ventricular systole

 

[syoung]

FA Antianginal errata? FA15 page 305 says beta blockers have will have "no effect" or "decrease" EDV. Shouldn't beta-blockers increase EDV? They decrease HR --> increase diastolic time --> increase filling. They also decrease inotropy --> decrease EF --> increase EDV.

From FA14:

So maybe it was saying when used in combo w/ nitrates? I agree w/ what you said about beta-blockers.

 

[seminoma]

From FA14:
View attachment 188667
So maybe it was saying when used in combo w/ nitrates? I agree w/ what you said about beta-blockers.

Yeah, I think the FA14 table is correct. Here's the table from FA15.

 

[seminoma]

Firecracker says that the chronic stage of mitral regurg is LA dilation and LA increase in compliance. Can someone explain the increase in compliance? I thought that the LA would dilate + hypertrophy just like in mitral stenosis == higher pressures (lower compliance) due to the hypertrophy.

Mitral stenosis: opening snap followed by an early mid-diastolic rumbling, most often due to chronic rheumatic fever


Stenosis → left atrial dilation and hypertrophy → atrial fibrillation → stasis with thrombus formation → possible embolization


Left-atrial dilation and hypertrophy → compresses esophagus → dysphagia for solids


Mitral regurgitation: holosystolic high pitched "blowing" murmur, heard loudest at the apex, radiates to the axilla.


Acute: regurgitation results in increased left atrium pressures and pulmonary congestion

Chronic: left atrium compensates to the increased volume by dilating and increasing compliance → increased incidence of fibrillation rhythms

 

[faisal 2000]

is there any disease Causes difference in blood Pressure in the both arms (eg., hypertension in R/ arm while normal blood Pressure in L / arm )

 

[seminoma]

is there any disease Causes difference in blood Pressure in the both arms (eg., hypertension in R/ arm while normal blood Pressure in L / arm )

Coarctation, Takayasu, possibly dissection.

 

[faisal 2000]

Coarctation, Takayasu, possibly dissection.

coaractation causes differences in upper (hypertension) and lower(hypotension) not right and left

 

[dfib slim]

coaractation causes differences in upper (hypertension) and lower(hypotension) not right and left

Unless the coarctation is proximal to the left subclavian.

 

[seminoma]

coaractation causes differences in upper (hypertension) and lower(hypotension) not right and left

Depends where the coarctation is.

 

[pd1112]

Can someone explain the finding of a loud S1 in the presence of ASD? I understand the wide, fixed S2 split, but FA also mentions a loud S1.

 

[IndiaInk567]

is there any disease Causes difference in blood Pressure in the both arms (eg., hypertension in R/ arm while normal blood Pressure in L / arm )

Subcalvian stenosis: http://www.medscape.com/viewarticle/729129_3

 

[Instatewaiter]

is there any disease Causes difference in blood Pressure in the both arms (eg., hypertension in R/ arm while normal blood Pressure in L / arm )

Don't forget Atherosclerosis of the subclavians
Coarctation
Takayasus
Aortic Dissection

Edit- someone beat me to it

 

[seminoma]

Can someone explain the finding of a loud S1 in the presence of ASD? I understand the wide, fixed S2 split, but FA also mentions a loud S1.

S1 = AV valves closing. With ASD there is a relative RV volume overload leading to increased tricuspid excursion (into the RA) during ventricular systole. More excursion of the valve = louder sound. Now, you might be wondering "well, if there's more volume in the RV causing more excursion of the TV and a louder T1, then shouldn't there be less volume in the LV and therefore a softer M1?". That's a logical connection to make, however in a normal heart there isn't excessive excursion of the mitral valve into the LA and the relatively lower LV volume in ASD doesn't significantly "soften" the M1 sound. Recall that in a normal heart M1 is louder than T1 so the combination of increasing the intensity of T1 (as in ASD) and negligibly softening M1, you are getting a louder overall S1.

If that doesn't make sense try thinking of it like this: Imagine you are listening to music with your earphones, but only your left earphone is in (and your right earphone is on the desk or something). Also imagine that your sound balance is shifted all the way to the left (so your right earbud is silent even if you were to put it in your ear). Now, adjust the sound balance a little bit to the right (thus softening the left earbud and giving some sound to the right earbud). Now put the rightearbud into your right ear. Now you have both earbuds in. Is the net sound going to be louder or softer? Definitely going to be louder even though you softened the left earbud.

Edit: If it wasn't clear, T1 = tricuspid sound, M1 = mitral sound. And left earbud = MV.

 

[Slade009]

Here's one:

A 60-year old man with stable angina is being treated with Atenolol and Aspirin. He reports that over the last week, his symptoms have been worsening. His physician decides to add a new medication to his regimen. Several days later, he presents with severe dizziness. On physical examination his blood pressure is 100/70 mmHg and his heart rate is 38 beats per minute. Which of the following medications was most likely administered?

A. Nifedipine
B. Captopril
C. Verapamil
D. Isosorbide Dinitrate
E. Prazosin

 

[pathologyDO]

Here's one:

A 60-year old man with stable angina is being treated with Atenolol and Aspirin. He reports that over the last week, his symptoms have been worsening. His physician decides to add a new medication to his regimen. Several days later, he presents with severe dizziness. On physical examination his blood pressure is 100/70 mmHg and his heart rate is 38 beats per minute. Which of the following medications was mot likely administered?

A. Nifedipine
B. Captopril
C. Verapamil
D. Isosorbide Dinitrate
E. Prazosin

Either C or A because they're Ca2+ channel blockers that when added with a beta-blocker could decrease HR substantially. My best guess here is verapamil because it is a cardioselective CCB, and thus would have a smaller effect on blood pressure than iono/chronotropy of the heart like we are seeing in this case, and is associated with more side effects than nifedipine when used in combo with a beta blocker.

So I'm going with C. Verapamil

 

[Mr. Mojo Risin]

Either C or A because they're Ca2+ channel blockers that when added with a beta-blocker could decrease HR substantially. My best guess here is nifedipine, because it is associated with a very rapid drop in blood pressure and patients may feel dizzy or lightheaded upon starting its use.

So final answer is A. Nifedipine

Hm, honestly I was leaning more to verapamil due to double whammy effect on sinus nodal activity (verapamil: cardiac > vascular). Nifedipine (DHP CCB) is similar in effect to nitrates, whereas verapamil (Non-DHP CCB) is similar in effect to beta-blockers. Double sinus nodal depression --> really low HR.

I'm referring to pg. 305 in FA 2015.

 

[Slade009]

Either C or A because they're Ca2+ channel blockers that when added with a beta-blocker could decrease HR substantially. My best guess here is verapamil because it is a cardioselective CCB, and thus would have a smaller effect on blood pressure than iono/chronotropy of the heart like we are seeing in this case, and is associated with more side effects than nifedipine when used in combo with a beta blocker.
So I'm going with C. Verapamil

Hm, honestly I was leaning more to verapamil due to double whammy effect on sinus nodal activity (verapamil: cardiac > vascular). Nifedipine (DHP CCB) is similar in effect to nitrates, whereas verapamil (Non-DHP CCB) is similar in effect to beta-blockers. Double sinus nodal depression --> really low HR.

I'm referring to pg. 305 in FA 2015.

Good job. Correct it's C.

Nifedipine is a DHP CCB with minimal effects on the SA node and cardiac conduction. It acts predominately as a vasodilator and can cause a reflex increase in heart rate. It would be unlikely to cause synergistic slowing of the SA node firing rate when combined with a B-blocker. The rest all cause a Reflex Tachycardia.
The trick here is to focus on the Heart Rate. People tend to look at the word Dizzy and think Nitrates right away or confused when seeing Nifedipine and forget that this is given predominantly for Hypertension.

 

[pathologyDO]

Hm, honestly I was leaning more to verapamil due to double whammy effect on sinus nodal activity (verapamil: cardiac > vascular). Nifedipine (DHP CCB) is similar in effect to nitrates, whereas verapamil (Non-DHP CCB) is similar in effect to beta-blockers. Double sinus nodal depression --> really low HR.

I'm referring to pg. 305 in FA 2015.

Yeah I changed my answer quickly after posting that original, was hoping the edit was fast enough lol

 

[theTruth_97]

Could anyone list like the main electrolyte abnormalities and their associations with EKG changes? The only ones that I can think of are hyperkalemia with high T wave and hypercalcemia with short QT (well at least that is what I think both of those are associated with). Any help would be really appreciated!