explain the murmur maneuvers. please!

[Zoom-Zoom]

Hey peeps, so Ive got a few days before Step 1 and after spending some time on heart murmurs I seem to understand less now than I did before...i'm confused.

Can someone please succinctly explain how the different maneuvers (standing, squatting, valsalva) affects the various murmurs? I get the inspiration/expiration thing...goljan does a good job with that. I really don't get the difference, especially on the left heart, between expiration and valsalva. Does prolonged expiration (valsalva) reduce preload to the left heart?

I'de really like a source that clearly states "valsava does X to preload, squatting does Y, etc" and then for each murmur, "made worse with more preload", etc. If you have a source or don't mind explaining, i'de really appreciate it.

Also, if anyone has a link to a site that explains the effects of stenosis/regurg on those pressure diagrams, I'de love that also.

Thanks,
Zoom

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[ScubaStarved]

Type these fast so someone please correct me if I've erred or oversimplified:

For the purposes of Step1, left heart murmurs basically shouldn't change with breathing. (Expiration dose cause some increased preload.) Right heart murmurs obviously do.

For left heart murmurs, first master an understanding of preload changes (before adding afterload).
Inc preload = squatting, lying, valsalva
Dec preload = standing

HCM and AS are affected "oppositely" by preload.
HCM is softer with increased preload because the dynamic outflow obstruction is less severe --> IV septum is further from MV leaflet with larger ventricular volumes. Therefore, lying and squatting will DECREASE HCM murmur. Standing will accentuate. (Beta blockers help in part by increasing diastolic filling time.)
AS is louder with increased preload because you have greater turbulence at the stenotic valve. Therefore, squatting and lying will INCREASE AS murmur. Standing will diminish it.

(Mitral valve click may be decreased by increased preload. Something to do with redundant tissue that is corrected by increased EDVolumes. This is not Step1 relevant either, IMO.)

 

[Zoom-Zoom]

Type these fast so someone please correct me if I've erred or oversimplified:

For the purposes of Step1, left heart murmurs basically shouldn't change with breathing. (Expiration dose cause some increased preload.) Right heart murmurs obviously do.

For left heart murmurs, first master an understanding of preload changes (before worrying about afterload, valsalva and handgrip).
Inc preload = squatting, lying
Dec preload = standing

HCM and AS are affected "oppositely" by preload.
HCM is softer with increased preload because the dynamic outflow obstruction is less severe --> IV septum is further from MV leaflet with larger ventricular volumes. Therefore, lying and squatting will DECREASE HCM murmur. Standing will accentuate. (Beta blockers help in part by increasing diastolic filling time.)
AS is louder with increased preload because you have greater turbulence at the stenotic valve. Therefore, squatting and lying will INCREASE AS murmur. Standing will diminish it.

(Mitral valve click may be decreased by increased preload. Something to do with redundant tissue that is corrected by increased EDVolumes. This is not Step1 relevant either, IMO.)

Thanks, that makes sense. I don't really get how squatting - i'm assuming this raises arterial pressures - affects preload rather than afterload. I'd assume it'd change preload to the right heart if anything, or maybe it's both?

Anyway that relieves my stress a little bit. UWorld has all these questions about the S1 to Click interval with MVP and stuff like that... but I agree that this shouldn't really be Step 1 material...

 

[Zoom-Zoom]

nevermind, i think i get it. FA explains squatting in terms of resistance but it makes sense that contracting muscles would pump venous flow up to the heart. Am I safe to assume this would increase preload on both sides of the heart?

As far as valsalva is concerned...this is definitely step 1 stuff, at least it was on my physio shelf. Am I ok to assume for step 1 purposes that valsalva is equivalent to standing?

 

[hyrule]

squatting + handgrip = same thing.. increase afterload
Valsalva: think of it in terms of intrathoracic pressure... +ive intrathoracic pressure --> so you decrease preload


MV prolapse: Location of mid-systolic click
-Anxiety: closer to SI b/c of decreased preload... heart is pumping too fast
- Squatting/Handgrip: closer to S2 because blood staying in heart longer

 

[ScubaStarved]

nevermind, i think i get it. FA explains squatting in terms of resistance but it makes sense that contracting muscles would pump venous flow up to the heart. Am I safe to assume this would increase preload on both sides of the heart?

As far as valsalva is concerned...this is definitely step 1 stuff, at least it was on my physio shelf. Am I ok to assume for step 1 purposes that valsalva is equivalent to standing?

Unless thinking about TOF, it's my opinion that simplicity is key for step 1 murmurs (and for IM shelf and step 2 for that matter).

As far as anything I've seen, squatting has the same effect on HCM as does lying down. You can worry about which veins and arteries are compressed if you want, I guess. But for me, squatting = increased preload (unless they ask specifics about TOF compensation).

As for valsalva, I agree it is step 1 testable. I only meant to say you should walk before you run. Valsalva classically increases HCM murmur (and decreases AS). I don't fully understand the mechanism so didn't go into it. It is complex and has several stages. In its last phase, it increases parasympathetic outflow (and can be used to ablate SVT) and may increase preload at that time? I edited my above post to include it in causes of increased preload, in any event.

Mitral valve click variation is garbage IMO. Learn it if you want. If it appeared on step 1 I'd be very, very surprised.

 

[hyrule]

Unless thinking about TOF, it's my opinion that simplicity is key for step 1 murmurs (and for IM shelf and step 2 for that matter).

As far as anything I've seen, squatting has the same effect on HCM as does lying down. You can worry about which veins and arteries are compressed if you want, I guess. But for me, squatting = increased preload (unless they ask specifics about TOF compensation).

As for valsalva, I agree it is step 1 testable. I only meant to say you should walk before you run. Valsalva classically increases HCM murmur (and decreases AS). I don't fully understand the mechanism so didn't go into it. It is complex and has several stages. In its last phase, it increases parasympathetic outflow (and can be used to ablate SVT) and may increase preload at that time? I edited my above post to include it in causes of increased preload, in any event.

Mitral valve click variation is garbage IMO. Learn it if you want. If it appeared on step 1 I'd be very, very surprised.

I didn't think so either. But Goljan mentioned that it had appeared on previous tests.

 

[Day man]

for MVP, i read about this method of thinking about it, and haven't had trouble memorizing crap about it anymore:

click alway will only occur at a certain diameter of heart/ventricles, at a point where the LV has already pushed with some force to expel blood into the aorta during systole. so if the LV has some increased preload, it takes just a little bit longer for it to expel all that blood and reach the 'click volume', so the mid sys click moves away from S1. Decrease the preload-->less blood to push out-->'click volume' is reached earlier and is closer to S1.

i straight up forget where i read this, but i really think i did. maybe someone incepted me. who the heck knows anymore...saturday night and i'm posting about a damn MVP method haha.