Pathoma error not corrected in errata?

[johndoe3344]

Page 81, it says regarding mitral valve prolapse, "Click and murmur become louder with squatting (increased systemic resistance decreases left ventricular emptying".

This is incorrect, right? Because MVP and HOCM are the only two murmurs where the sound of the murmur is actually decreased by squatting and increased by standing and Valsalva?

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[ijn]

According to wiki, MVP murmur intensity is increased and murmur duration is decreased by squatting.

"[MVP] is the most common cause of late systolic murmurs. It can be heard best over the apex of the heart, usually preceded by clicks. The most common cause of mitral valve prolapse is "floppy" valve (Barlow's) syndrome. If the prolapse becomes severe enough, mitral regurgitation may occur. Any maneuver that decreases left ventricular volume — such as standing, sitting, Valsalva maneuver, and amyl nitrate inhalation — can produce earlier onset of clicks, longer murmur duration, and decreased murmur intensity. Any maneuver that increases left ventricular volume — such as squatting, elevation of legs, hand grip, and phenylephrine — can delay the onset of clicks, shorten murmur duration, and increase murmur intensity."

 

[johndoe3344]

Not sure where you're quoting from.

http://en.wikipedia.org/wiki/Mitral_valve_prolapse
"In contrast to most other heart murmurs, the murmur of mitral valve prolapse is accentuated by standing and valsalva maneuver (earlier systolic click and longer murmur) and diminished with squatting (later systolic click and shorter murmur). The only other heart murmur that follows this pattern is the murmur of hypertrophic cardiomyopathy."

 

[JRjcu08]

ijn was quoting from Wikipedia: "Systolic heart murmurs"

my source = Uptodate and Lilly's pathophysiology of heart disease (sorry for writing a novel)

MVP and HCM both create systolic murmurs; during systole, ventricles are contracting --> aortic/pulmonary open; mitral/tricuspid closed. The "click" in MVP is from the floppy cusp of the mitral valve going back into the LA, then the murmur starts because there is now backflow into the LA. More backflow (more TPR/ increased arterial pressure) = louder; this is the same as in mitral regurgitation (where MR does not have the click; just a holosystolic murmur). Earlier click in MVP (more pressure on the floppy valve) = longer murmur.

HCM creates a functional aortic stenosis- blood is ejected faster through the aortic valve because the thickened septum has narrowed the outflow tract This pulls down the mitral leaflet and obstructs blood flow into the aorta. Anything that reduces the LV size brings the septum to cover the aortic valve further by increasing the pull on the mitral leaflet, and causes more aortic valve obstruction --> increased intensity of murmur. Anything that increases the LV size increases the distance between the septum and the mitral leaflet by decreasing the pull on the mitral leaflet, causing less aortic valve obstruction --> decreasing the intensity of the murmur.

Standing = same effects as Valsalva
Hand grip = same effects as squatting

Standing- MVP: decreases preload, less tension on chordae tendineae to keep the valve closed, so click is earlier, murmur duration is longer. If during standing, arterial pressure falls and HR increases, the murmur intensity will decrease due to less force of backflow through the valve. HCM: decreased EDV decreases the size of the LV, hypertrophied septum puts stress on the outflow through the aortic valve (more pull on the mitral leaflet) and increases intensity of systolic ejection murmur.

Squatting- MVP: increase in preload and TPR, increased arterial pressure. Delays the click (more resistance on the floppy valve leaflet) and as the MVP worsens, intensity increases because of increased resistance to pull the valve into the LA. HCM: intensity declines because LV volume increases  if the LV increases it takes the stress off the aortic valve because there is less pull by the hypertrophied septum on the mitral leaflet, relieving the outflow obstruction.

Valsalva- MVP: decreased (all of these) preload, RV and LV volume, SV, MAP, PP  increased HR. Intensity of the murmur decreases due to less force of backflow through the valve. Also less EDV means the click comes earlier, just as in "standing" scenario. HCM: increases in intensity because EDV decreases, decreasing the size of LV and putting the stress of hypertrophy back on the aortic valve orifice by pulling the mitral valve leaflet.

Hand grip- MVP: increased TPR, arterial pressure, CO, LV volume and pressure. This is kind of like squatting – Pathoma mentions nothing about hand grip basically ever… but think of it the same way as squatting.
So when Pathoma says the click and murmur become louder with squatting, it is correct, because during squatting there is more resistance to outflow through the valve which accentuates the noises. You'll notice on pg 83 when Pathoma discusses HCM, he just says it creates a functional aortic stenosis; however the murmur is not the same as that of aortic stenosis because the mechanism has to do with the stress of increasing or decreasing the size of the LV.

 

[kaleerkalut]

ijn was quoting from Wikipedia: "Systolic heart murmurs"

my source = Uptodate and Lilly's pathophysiology of heart disease (sorry for writing a novel)

MVP and HCM both create systolic murmurs; during systole, ventricles are contracting --> aortic/pulmonary open; mitral/tricuspid closed. The “click” in MVP is from the floppy cusp of the mitral valve being pushed into the LV, then the murmur starts because there is now backflow into the LV. More backflow (more TPR/ increased arterial pressure) = louder; this is the same as in mitral regurgitation (where MR does not have the click; just a holosystolic murmur). Earlier click in MVP (more pressure on the floppy valve) = longer murmur.

HCM creates a functional aortic stenosis- blood is ejected faster through the aortic valve because the thickened septum has narrowed the outflow tract This pulls down the mitral leaflet and obstructs blood flow into the aorta. Anything that reduces the LV size brings the septum to cover the aortic valve further by increasing the pull on the mitral leaflet, and causes more aortic valve obstruction --> increased intensity of murmur. Anything that increases the LV size increases the distance between the septum and the mitral leaflet by decreasing the pull on the mitral leaflet, causing less aortic valve obstruction --> decreasing the intensity of the murmur.

Standing = same effects as Valsalva
Hand grip = same effects as squatting

Standing- MVP: decreases preload, less tension on chordae tendineae, so click is earlier, murmur duration is longer. If during standing, arterial pressure falls and HR increases, the murmur intensity will decrease due to less force of backflow through the valve. HCM: decreased EDV decreases the size of the LV, hypertrophied septum puts stress on the outflow through the aortic valve (more pull on the mitral leaflet) and increases intensity of systolic ejection murmur.

Squatting- MVP: increase in preload and TPR, increased arterial pressure. Delays the click (more resistance on the floppy valve leaflet) and as the MVP worsens, intensity increases because of increased resistance to outflow. HCM: intensity declines because LV volume increases  if the LV increases it takes the stress off the aortic valve because there is less pull by the hypertrophied septum on the mitral leaflet, relieving the outflow obstruction.

Valsalva- MVP: decreased (all of these) preload, RV and LV volume, SV, MAP, PP  increased HR. Intensity of the murmur decreases due to less force of backflow through the valve. Also less EDV means the click comes earlier, just as in “standing” scenario. HCM: increases in intensity because EDV decreases, decreasing the size of LV and putting the stress of hypertrophy back on the aortic valve orifice by pulling the mitral valve leaflet.

Hand grip- MVP: increased TPR, arterial pressure, CO, LV volume and pressure. This is kind of like squatting – Pathoma mentions nothing about hand grip basically ever… but think of it the same way as squatting.
So when Pathoma says the click and murmur become louder with squatting, it is correct, because during squatting there is more resistance to outflow through the valve which accentuates the noises. You’ll notice on pg 83 when Pathoma discusses HCM, he just says it creates a functional aortic stenosis; however the murmur is not the same as that of aortic stenosis because the mechanism has to do with the stress of increasing or decreasing the size of the LV.

Sorry I didn't read the whole thing but in the first paragraph I think you mean bulges in to LA for MVP right?

 

[JRjcu08]

Sorry I didn't read the whole thing but in the first paragraph I think you mean bulges in to LA for MVP right?

Yes sorry... late at night and I've been studying micro all day... oops

 

[lookmanohands]

Page 81, it says regarding mitral valve prolapse, "Click and murmur become louder with squatting (increased systemic resistance decreases left ventricular emptying".

This is incorrect, right? Because MVP and HOCM are the only two murmurs where the sound of the murmur is actually decreased by squatting and increased by standing and Valsalva?

I agree with you (that Pathoma is wrong). According to First Aid and UWorld (ID 390236), MVP murmurs should DECREASE in intensity with squatting for the reason that you are squeezing your leg muscles so you're increasing preload and volume in the LV. Because you have an large floppy valve in MVP, the enlarged ventricle is more accommodating for an oversized valve to properly close.

So yes, anything that increases blood volume in the LV (ie squatting) will decrease the intensity of MVP for the reason UWorld and it's quoted references say. The explanation for HCM murmurs following a similar pattern is how Jrcu explained (you want to space the mitral valve as far away as possible from the aortic outflow tract through greater blood volume to decrease HCM murmur sounds).

 

[futuredoctor10]

If someone sends this to Dr. Sattar or his team, they will probably correct it promptly...

 

[johndoe3344]

If someone sends this to Dr. Sattar or his team, they will probably correct it promptly...

I just submitted it as a potential errata.

 

[lookmanohands]

ijn was quoting from Wikipedia: "Systolic heart murmurs"

my source = Uptodate and Lilly's pathophysiology of heart disease (sorry for writing a novel)

MVP and HCM both create systolic murmurs; during systole, ventricles are contracting --> aortic/pulmonary open; mitral/tricuspid closed. The "click" in MVP is from the floppy cusp of the mitral valve going back into the LA, then the murmur starts because there is now backflow into the LA. More backflow (more TPR/ increased arterial pressure) = louder; this is the same as in mitral regurgitation (where MR does not have the click; just a holosystolic murmur). Earlier click in MVP (more pressure on the floppy valve) = longer murmur.

HCM creates a functional aortic stenosis- blood is ejected faster through the aortic valve because the thickened septum has narrowed the outflow tract This pulls down the mitral leaflet and obstructs blood flow into the aorta. Anything that reduces the LV size brings the septum to cover the aortic valve further by increasing the pull on the mitral leaflet, and causes more aortic valve obstruction --> increased intensity of murmur. Anything that increases the LV size increases the distance between the septum and the mitral leaflet by decreasing the pull on the mitral leaflet, causing less aortic valve obstruction --> decreasing the intensity of the murmur.

Standing = same effects as Valsalva
Hand grip = same effects as squatting

Standing- MVP: decreases preload, less tension on chordae tendineae to keep the valve closed, so click is earlier, murmur duration is longer. If during standing, arterial pressure falls and HR increases, the murmur intensity will decrease due to less force of backflow through the valve. HCM: decreased EDV decreases the size of the LV, hypertrophied septum puts stress on the outflow through the aortic valve (more pull on the mitral leaflet) and increases intensity of systolic ejection murmur.

Squatting- MVP: increase in preload and TPR, increased arterial pressure. Delays the click (more resistance on the floppy valve leaflet) and as the MVP worsens, intensity increases because of increased resistance to pull the valve into the LA. HCM: intensity declines because LV volume increases  if the LV increases it takes the stress off the aortic valve because there is less pull by the hypertrophied septum on the mitral leaflet, relieving the outflow obstruction.

Valsalva- MVP: decreased (all of these) preload, RV and LV volume, SV, MAP, PP  increased HR. Intensity of the murmur decreases due to less force of backflow through the valve. Also less EDV means the click comes earlier, just as in "standing" scenario. HCM: increases in intensity because EDV decreases, decreasing the size of LV and putting the stress of hypertrophy back on the aortic valve orifice by pulling the mitral valve leaflet.

Hand grip- MVP: increased TPR, arterial pressure, CO, LV volume and pressure. This is kind of like squatting – Pathoma mentions nothing about hand grip basically ever… but think of it the same way as squatting.
So when Pathoma says the click and murmur become louder with squatting, it is correct, because during squatting there is more resistance to outflow through the valve which accentuates the noises. You'll notice on pg 83 when Pathoma discusses HCM, he just says it creates a functional aortic stenosis; however the murmur is not the same as that of aortic stenosis because the mechanism has to do with the stress of increasing or decreasing the size of the LV.

In terms of hand grip vs squatting, your focus should be on 2 different things. Your leg veins are pooling a lot of blood so the effect of increased blood return should be how you think about its effects on murmurs. There's not that much blood pooled up in your arms normally so you should focus on the increase in TPR for hand gripping.

First Aid doesn't mention effects of hand gripping on MVP or HOCM murmurs but in Kaplan Medical USMLE Master the Boards Step 3 (Conrad Fischer does a really good job explaining murmurs and shows up on a google book search), it says that MVP and HOCM murmurs should decrease because an increased TPR means less blood is getting out the LV and greater LV volume as already stated will decrease those 2 types of murmurs. MR on the otherhand will worsen with handgripping as expected

 

[JRjcu08]

I've still been trying to read up on this and figure it out. Most sources just talk about the timing of the click and murmur, not the volume.

The most significant part of MVP is the click; standing and valsalva will decrease LV volume, which makes it more likely that the valve will flop back into the LA. The click is earlier, and because the click is earlier, the murmur is longer. With decreased afterload and decreased ventricular size, there is less of a pressure gradient b/t the LV and LA. If this is the case, and the murmur is longer, it should be quieter.

Squatting/hand grip increase the LV volume, so it takes longer for the pressure against the floppy valve to be significant enough to force it into the LA. The click is later, so the murmur has to be shorter. I think the volume of the murmur has to do with the effect of the increased pressure in the ventricle from increased afterload. If the murmur is shorter, the higher pressure has more force to push the blood back through the valve into the LA which is at a lower pressure. The increased force will make the (shorter) murmur louder.

Maybe I'm totally confusing what is going on, but I also think that the volume is not necessarily as important as the timing when it comes to MVP and position changes.

Will you post Dr. Sataar's response if you get one? He's usually pretty quick at answering emails.

 

[lookmanohands]

If you look at Conrad Fischer's book I mentioned, he also describes the same pattern of murmur sounds that is described in UWorld and First Aid

And the The Cleveland Clinic Intensive Review of Internal Medicine says the same thing pg 781

http://books.google.com/books?id=O9...AKpp-TSDw&ved=0CEAQ6AEwBg#v=onepage&q&f=false

Edit: I looked around some more and every single resource I've come across that has mentioned murmur intensity and MVP all agree (except Pathoma)

 

[johndoe3344]

I will post it if I get a response. Haven't heard anything yet (I submitted it via the website... not sure if that was the right place to do it).

 

[JRjcu08]

If you look at Conrad Fischer's book I mentioned, he also describes the same pattern of murmur sounds that is described in UWorld and First Aid

I did, but he doesn't really describe anything, just a table and a sentence.

Uptodate describes it as (with my notes in italics):
SQUATTING — Squatting from a standing position is associated with a simultaneous increase in venous return (preload) and systemic vascular resistance (afterload) and a rise in arterial pressure. This causes changes in the following murmurs:

Increased intensity of the murmur of mitral regurgitation due to the rise in afterload, which favors the movement of blood in the left ventricle across the insufficient mitral valve rather than entering the systemic circulation across the aortic valve.
In patients with mitral valve prolapse there is a delay in the onset of the click and a shortening of the late systolic murmur. These changes reflect the delay in prolapse induced by the increase in preload. However, as mitral regurgitation becomes more severe, the murmur may increase in intensity with squatting because of the increase in afterload.
So once the valve is partially opened in MVP, the murmur would perform as in MR due to the rise in afterload w/ squatting.

VALSALVA MANEUVER — The hemodynamic changes resulting from a Valsalva maneuver vary with the different phases. Analysis of changes in the intensity and character of the murmur during phase 2 of the Valsalva maneuver is most useful and practical for the differential diagnosis.

During the straining phase, phase 2, there is a decrease in venous return, right and left ventricular volumes, stroke volumes, mean arterial pressure, and pulse pressure; this is associated with a reflex increase in heart rate.

The intensity of flow murmurs, murmurs of aortic and pulmonary stenosis, tricuspid and mitral regurgitation, aortic and pulmonary regurgitation, and mitral and tricuspid stenosis decreases. The volume of the carotid pulse also decreases.
The murmur of hypertrophic cardiomyopathy increases in intensity as the left ventricular outflow size decreases with a decreased venous return. The carotid pulse volume also declines.
In mitral valve prolapse there is an early onset of the click and murmur due to the decrease in left ventricular volume.
Makes no mention here of any volume change in MVP with valsalva... which I think is because valsalva only acts to derease return to heart by increasing the intrathoracic pressure... so valsalva has no effect on afterload, which is what changes the volume of the MVP murmur. Like I said before, I imagine the volume would decrease, just as the volume of MR decreases.

A side note - changes w/ inspiration: "In mitral valve prolapse, the inspiratory decrease in venous return to the left side of the heart reduces left ventricular volume; the murmur and click occur earlier and may diminish." To me, this sounds just like the scenario of standing or valsalva...decreased return/LV volume...earlier click... "may diminish"

Sorry again for writing so much...

 

[lookmanohands]

I've still been trying to read up on this and figure it out. Most sources just talk about the timing of the click and murmur, not the volume.

The most significant part of MVP is the click; standing and valsalva will decrease LV volume, which makes it more likely that the valve will flop back into the LA. The click is earlier, and because the click is earlier, the murmur is longer. With decreased afterload and decreased ventricular size, there is less of a pressure gradient b/t the LV and LA. If this is the case, and the murmur is longer, it should be quieter.

Squatting/hand grip increase the LV volume, so it takes longer for the pressure against the floppy valve to be significant enough to force it into the LA. The click is later, so the murmur has to be shorter. I think the volume of the murmur has to do with the effect of the increased pressure in the ventricle from increased afterload. If the murmur is shorter, the higher pressure has more force to push the blood back through the valve into the LA which is at a lower pressure. The increased force will make the (shorter) murmur louder.

Maybe I'm totally confusing what is going on, but I also think that the volume is not necessarily as important as the timing when it comes to MVP and position changes.

Will you post Dr. Sataar's response if you get one? He's usually pretty quick at answering emails.

I think MVP is all about volume. I agree with your standing and valsalva explaination until your last statement- longer murmur but not necessarily more quieter

With increased volume, you are spacing those papillary muscles further so there is greater tension on the chordae tendinae so the click is later and by that point systole is just about over by the time you're able to get blood into the LA so the murmur decreases in intensity

I agree with your logic but disagree with your final conclusion

 

[JRjcu08]

I think MVP is all about volume. I agree with your standing and valsalva explaination until your last statement- longer murmur but not necessarily more quieter

With increased volume, you are spacing those papillary muscles further so there is greater tension on the chordae tendinae so the click is later and by that point systole is just about over by the time you're able to get blood into the LA so the murmur decreases in intensity

I agree with your logic but disagree with your final conclusion

When I said "volume is not necessarily as important as the timing," I meant volume (loudness) of the murmur, not volume of the ventricle (just to be clear .... also, why can't pathologists use better terminology...too many meanings of 'volume' in one explanation...)
Again, I think the loudness is in the afterload, as I wrote a few minutes ago after more reading. Of the position changes, only squatting/hand grip increase afterload.

 

[lookmanohands]

Sorry I think I put way too much time into this thread. Just know that this is getting tested in UWorld and there is no disagreement between UWorld and First Aid on this (may even be multiple times- they really like heart murmurs)

 

[JRjcu08]

Sorry I think I put way too much time into this thread. Just know that this is getting tested in UWorld and there is no disagreement between UWorld and First Aid on this (may even be multiple times- they really like heart murmurs)

Agreed, so have I, but at least it forced me to review more cardio...I did look up the Uworld explanation in question, and they say: "murmur disappears with squatting because increased preload --> increased LV EDV --> "facilitate proper closure of the otherwise oversized mitral valve leaflets""
I just think that by "disappears" they mean that the click occurs so much later, and the duration of systole doesn't change, there is no virtually no murmur at all, not that it disappears because it is quieter.

 

[lookmanohands]

This will be my last post here. Uworld question ID 1557 explanation for incorrect answers a and c (I think I'm also confused about where this argument headed)

 

[JRjcu08]

This will be my last post here. Uworld question ID 1557 explanation for incorrect answers a and c (I think I'm also confused about where this argument headed)

Sorry, I wasn't aware there was an argument... just trying to clear up what's actually going on in these scenarios.
Question 1557 does not even ask about MVP and the explanations for a and c are as vague as Conrad Fischer's... Reading uptodate or a cardiology textbook is always going to give you a more accurate description/ understanding of the pathology.

I think if there is a question directly asking about MVP, it will be in regards to the timing of the click/ duration of the murmur, while HCM is about the loudness & LV volume/ stretch.

 

[lookmanohands]

Sorry, I wasn't aware there was an argument... just trying to clear up what's actually going on in these scenarios.
Question 1557 does not even ask about MVP and the explanations for a and c are as vague as Conrad Fischer's... Reading uptodate or a cardiology textbook is always going to give you a more accurate description/ understanding of the pathology.

I think if there is a question directly asking about MVP, it will be in regards to the timing of the click/ duration of the murmur, while HCM is about the loudness & LV volume/ stretch.

So I lied; this will be my last post. 1557 was just to illustrate the point that their explaination for MVP murmurs are the same as the other sources (for why it is or in this case, isn't the answer) I agree and it sounds like the murmur questions they've been asking are very straightforward according to my friends. I'm going to kick it into gear for my last week before my exam (today was my day off). Good luck when you eventually take your exam man- you sound more than prepared