How exactly does pulmonary embolism cause gallop rhythm? please help

[Edison]

So in PE, pulmonary vascular resistance is raised, as a result right ventricular systole is prolonged while left ventricular systole remains the same, and hence the splitting of 2nd heart sound into its aortic and pulmonary components. The thing that I don't understand is, why is it that right ventricular systole is prolonged? I just know that it happens. Systole is under the control of action potential propagation; once it's over, the myocardium relaxes; it's not like the ventricles must sqeeze out X% of EDV before they can relax....

Please help and thanks!

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[smq123]

So in PE, pulmonary vascular resistance is raised, as a result right ventricular systole is prolonged while left ventricular systole remains the same, and hence the splitting of 2nd heart sound into its aortic and pulmonary components. The thing that I don't understand is, why is it that right ventricular systole is prolonged? I just know that it happens. Systole is under the control of action potential propagation; once it's over, the myocardium relaxes; it's not like the ventricles must sqeeze out X% of EDV before they can relax...

The way I think of it (maybe it's not correct, but it has worked for me so far) is that the end of systole is when the aortic and pulmonic valves close. If the valves have trouble closing, systole is prolonged. Action potential propagation doesn't necessarily play a role.

In the case of PE, since pulmonary vascular resistance is high, the right ventricle has trouble emptying, and that delays the closure of the pulmonic valve. That's why S2 is split. Valve closure depends on pressure gradients, and not electrical action potentials.

 

[Edison]

Thanks for your reply! I see your logic there; however, if pulmonary vascular resistance is increased, shouldn't the altered pressure gradient on the right side of the heart cause the pulmonic valve to close earlier instead of later? Since the pressure within pulmonary trunk is raised compared to the normal state.

 

[smq123]

Thanks for your reply! I see your logic there; however, if pulmonary vascular resistance is increased, shouldn't the altered pressure gradient on the right side of the heart cause the pulmonic valve to close earlier instead of later? Since the pressure within pulmonary trunk is raised compared to the normal state.

Hmm. I think that the pulmonic valve will still closer more slowly (despite the increased pressure in the pulm. artery) because the pressure in the right ventricle is ALSO higher than normal. Because the right ventricle can't push blood out as quickly as it used to, but more blood is still coming in from the right atrium, the right ventricle is now faced with a higher-than-normal volume load. This still makes the fluid pressure in the ventricle higher than in the pulmonary trunk, and so the valve will close later than usual.

I think.

Can someone correct/confirm/scoff at my poor logic?

 

[OncoCaP]

Thanks for your reply! I see your logic there; however, if pulmonary vascular resistance is increased, shouldn't the altered pressure gradient on the right side of the heart cause the pulmonic valve to close earlier instead of later? Since the pressure within pulmonary trunk is raised compared to the normal state.

I took the info above and provide an explanation below. I don't consider anything not mentioned in the messages above. The following explanation is based only on the fluid-mechanical behavior of check valves, such as those in the heart, and the effect of a higher pulmonary artery pressure. It doesn't consider anything else in this complex organ and could be wrong for non-mechanical reasons or mechanical reasons not related to the basic behavior of a check valve:

It's forward/reverse flow caused by forward/reversed pressure differential that opens/closes check valves like those in the heart. Thus, if the pressure in the pulmonary trunk is raised, that pulmonary valve isn't going to open until later in the contraction of the heart because it's going to take a little bit longer than normal to get to the pressure of the right ventricle above that of the pulmonary trunk. Next, the right ventricle must empty, and this is slower due to the higher resistance to flow caused by the pulmonary embolism (PE). Finally, the pressure in the right ventricle drops below that of the pulmonary trunk, causing (slight) reverse flow to close the pulmonic valve producing a sound, but the sound of the closing pulmonic valve (P2 component of the second heart sound (S2)) is delayed because (a) the valve opened later and (b) the pressure in the right ventricle dropped more slowly. The left ventricle's aortic valve is not affected this same way because the aortic pressure is not similarly elevated and the differential in pulmonary and aortic valve closing sounds produces the gallop.

Hope this helps you out. I really haven't studied the heart that much (I'm a pre-med) and I'm looking at this just from the standpoint of pumps, check valves, pipes, and relative pressures.

 

[deleted29780]

I took the info above and provide an explanation below. I don't consider anything not mentioned in the messages above. The following explanation is based only on the fluid-mechanical behavior of check valves, such as those in the heart

And that is exactly how the heart works, interesting explanation. What matters is being able to remember the split that occurs in PE. The explanation just helps to reinforce it. As such you can always deduce, and not have to remember. And for me thats what matters in learning - deduction and not just memorization.

 

[TheMightyAngus]

So in PE, pulmonary vascular resistance is raised, as a result right ventricular systole is prolonged while left ventricular systole remains the same, and hence the splitting of 2nd heart sound into its aortic and pulmonary components. The thing that I don't understand is, why is it that right ventricular systole is prolonged? I just know that it happens. Systole is under the control of action potential propagation; once it's over, the myocardium relaxes; it's not like the ventricles must sqeeze out X% of EDV before they can relax....

Please help and thanks!

A "gallop rhythm" usually refers to an S3 or S4 heart sound. I think you are asking why S2 splitting is prolonged in PE.

PE causes more blood to back up into the RV. It's takes more time to pump out the extra blood, so closure of the pulmonic valve (P2) occurs later than usual. Systole is prolonged in the right heart.

Let's say the PE is non-life threatening. The LV receives about the same or slightly less blood due to the PE. But the amount of time it takes for it to pump out the blood is the same. Closure of the aortic valve (A2) is normal. Systole is normal in the left heart.

So now systole is prolonged in the right heart but normal in the left heart. P2 closes after A2. S2 splitting is prolonged.

Same thing occurs when you take a deep breath. Hence, the term physiological splitting.

 

[jdh71]

everyone else has covered the delayed emptying thing pretty well . . . a gallop is a ominous sign meaing te right side of the heart is failing produced by all of the blood stuck on the right side of the heart. Although, PE's big enough to cause an s3, s4 will usually kill the patient and it's not likely you'll ever get a chance to hear one.

As an aside . . . had one senior give me a penumonic of sorts for s3, s4.

I believe - s3

Believe me - s4

Say it outloud. That's the rythm, and I've found it helpful ever since. Although, if the heart's rate is racing you won't hear much of anything unless you've been at it for a long time. (Remember NO s4 with A-fib! The surgeons loves to ask you if you heard the s4 in the A-fib patient)

 

[megadon]

Hope this helps you out. I really haven't studied the heart that much (I'm a pre-med) and I'm looking at this just from the standpoint of pumps, check valves, pipes, and relative pressures.

Thanks for the post, I'm also an engineer, mech in fact. Than I did nuclear submarines, so I know about valves. It's a really good way of thinking, but they don't act like classical check valves (check valves are a hinged one flap deal, the pulmonary and aortic and tricuspid, balloon like flap valves). But that thinking will get you through what you need to know, and raise an eyebrow when your anatomy teacher complets jacks up how the mitral valve and tricuspid valve work. I mean jacked it up, it took me sending an email and the course director backing it up to straighten it out. You'll probably find this interesting, what you are hearing when you are measuring blood pressure is water hammer effects from the valves slamming shut.

What you are exactly right in describing is the pressure deal. Once the ventricle pumps out less pressure than is seen in the artery, you get momentary backflow, which inflates the little balloon flaps and shuts them. If the back pressure is high (what you are pumping against, the lungs and embolism), the ventricle empties slower (less gradient) and the pressure in the ventricle remains elevated longer. Thus longer till zero gradient and valve shutting. I had to think about this for a while.

In retrospect, this may have come across as a flamer post, but the comparison to a check valve is pretty darn good!

 

[sylhet]

I took the info above and provide an explanation below. e this helps you out. I really haven't studied the heart that much (I'm a pre-med) and I'm looking at this just from the standpoint of pumps, check valves, pipes, and relative pressures.

this is great. Thanks very very much OncoCap. I was looking for the same ans and finally ended up here. I am lucky that Edison had the same question to ask and everyone participated well and finally you explained very well. You saved me a lot lot of time. Almighty bless you man.

 

[thefritz]

Just like in cor pulomonale, you get RV overload. Acutely, this leads to a dilated RV, a straightened intraventricular septum, and a decreased LV cavity size (leading to the S3 heart sound due to increased filling pressure because of a decrease in volume).

 

[Guero]

everyone else has covered the delayed emptying thing pretty well . . . a gallop is a ominous sign meaing te right side of the heart is failing produced by all of the blood stuck on the right side of the heart. Although, PE's big enough to cause an s3, s4 will usually kill the patient and it's not likely you'll ever get a chance to hear one.

As an aside . . . had one senior give me a penumonic of sorts for s3, s4.

I believe - s3

Believe me - s4

Say it outloud. That's the rythm, and I've found it helpful ever since. Although, if the heart's rate is racing you won't hear much of anything unless you've been at it for a long time. (Remember NO s4 with A-fib! The surgeons loves to ask you if you heard the s4 in the A-fib patient)

Nice! I think I like this one better, though:
[YOUTUBE]QlH6Thr0Ago[/YOUTUBE]

 

[Pons Asinorum]

this is great. Thanks very very much OncoCap. I was looking for the same ans and finally ended up here. I am lucky that Edison had the same question to ask and everyone participated well and finally you explained very well. You saved me a lot lot of time. Almighty bless you man.

OncoCap's last post on SDN was 3.5 years ago.

 

[sylhet]

OncoCap's last post on SDN was 3.5 years ago.

yeah. I wish i could thank him that time. But i find the answer and i thank him now. no harm, right?

 

[sinombre]

yeah. I wish i could thank him that time. But i find the answer and i thank him now. no harm, right?

If he still uses the same email I think he'll get a notification if you PM him. You could try that.

 

[Kaustikos]

OncoCap's last post on SDN was 3.5 years ago.

One does not simply leave SDN. Sure, you log out and close your laptop. You go outside. But just like cocaine; you'll be sitting there one night all alone and realize that the only way to fill that loneliness is through coc-SDN.

 

[Pons Asinorum]

one does not simply leave sdn. Sure, you log out and close your laptop. You go outside. But just like cocaine; you'll be sitting there one night all alone and realize that the only way to fill that loneliness is through coc-sdn.

qft.

 

[Pons Asinorum]

yeah. I wish i could thank him that time. But i find the answer and i thank him now. no harm, right?

Chances of him seeing it? Zero.

Chances of someone who might actually be able to help you in the future putting you on their blocked user list for pointlessly bumping a 6-year-dead conversation? Greater than zero.

 

[Anastomoses]

One does not simply leave SDN. Sure, you log out and close your laptop. You go outside. But just like cocaine; you'll be sitting there one night all alone and realize that the only way to fill that loneliness is through coc-SDN.

this is so much healthier than what some of us would be doing...

qft.

what's qft?

 

[Pons Asinorum]

this is so much healthier than what some of us would be doing...


what's qft?

quite ****ing true

 

[sinombre]

quite ****ing true

I always thought it was "quoted for truth."

I guess they're basically the same.

 

[sylhet]

Chances of him seeing it? Zero.

Chances of someone who might actually be able to help you in the future putting you on their blocked user list for pointlessly bumping a 6-year-dead conversation? Greater than zero.

r u upset man? well than go somewhere else please.

 

[badasshairday]

Just get a CTA, if they can't handle contrst get an echocardiogram. Nobody cares about your gallup. Look for right heart strain on the electrocardiogram and/or tachycardia and/or hypoxia and/or chest pain and/or hemoptysis and/or fever to make the case for imaging study. You will never hear a gallup, or notice it, when you are looking for diagnosis of PE in reality.

 

[Anastomoses]

Just get a CTA, if they can't handle contrst get an echocardiogram. Nobody cares about your gallup. Look for right heart strain on the electrocardiogram and/or tachycardia and/or hypoxia and/or chest pain and/or hemoptysis and/or fever to make the case for imaging study. You will never hear a gallup, or notice it, when you are looking for diagnosis of PE in reality.

Heh, I think you've mistaken some of us for post-Step I students in reality. Reality and the boards...two different ball games.

 

[evilbooyaa]

Heh, I think you've mistaken some of us for post-Step I students in reality. Reality and the boards...two different ball games.

I can all but guarantee that the pathophysiology of why a PE causes gallup rhythm will not be on Step I.

That being said, it was an interesting question posed with a pretty good answer. All this being said, it was asked in 2007 (AKA 6 years ago). To whoever bumped it, please don't necro threads like this, especially not to just thank the person who answered the question 6 years ago. Thanks.

 

[487806]

r u upset man? well than go somewhere else please.

No one's upset. There wasn't a reason for you to necrobump this thread just to thank someone. You could always send them a PM expressing your gratitude.

 

[Kaustikos]

I can all but guarantee that the pathophysiology of why a PE causes gallup rhythm will not be on Step I.

... You serious? Is this a rare topic? Absolutely. But would I be surprised if this showed up on step 1? Not at all. These are the questions meant to make sure you don't get 100% of questions right

 

[evilbooyaa]

There are many, many other obscure questions out there then. The probability of picking something that is relatively obscure in the first place (PE causing a gallup rhythm, without giving you all the other real signs of a PE) and asking about the details behind that process?

Seems unlikely.

 

[Kaustikos]

There are many, many other obscure questions out there then. The probability of picking something that is relatively obscure in the first place (PE causing a gallup rhythm, without giving you all the other real signs of a PE) and asking about the details behind that process?

Seems unlikely.

Oh, then I agree.

But it seems like most questions I get have vignettes dealing with a patient that have symptoms of the disease and a question pertaining to it... The stipulation is you have to actually remove the patient from the question.

A good example is when they asked me about CHF. They didn't say it was decompensated/compensated CHF and the patient was definitely decompensated. And so it asked which was increased...
I put increased cardiac output.

They wanted increased arteriole resistance. Like... I can't really see how my answer was wrong since compensated means increased output. I agree resistance is increased, but COME ON.

 

[Guero]

Oh, then I agree.

But it seems like most questions I get have vignettes dealing with a patient that have symptoms of the disease and a question pertaining to it... The stipulation is you have to actually remove the patient from the question.

A good example is when they asked me about CHF. They didn't say it was decompensated/compensated CHF and the patient was definitely decompensated. And so it asked which was increased...
I put increased cardiac output.

They wanted increased arteriole resistance. Like... I can't really see how my answer was wrong since compensated means increased output. I agree resistance is increased, but COME ON.

I'd be like

 

[45408]

Just get a CTA, if they can't handle contrst get an echocardiogram. Nobody cares about your gallup. Look for right heart strain on the electrocardiogram and/or tachycardia and/or hypoxia and/or chest pain and/or hemoptysis and/or fever to make the case for imaging study. You will never hear a gallup, or notice it, when you are looking for diagnosis of PE in reality.

Pretty much. My first thought when I saw the thread was "I haven't heard an S3 since med school when I was in the sim lab..."

The last time I diagnosed a PE, the progression went like this: post-op pt had a presyncopal episode, remained moderately hypotensive and suddenly required supplemental oxygen just to keep O2 sats >90%, and he was having chest pain. I got an ABG, EKG and CXR. CXR was normal, ABG showed he was hyperventilating, and the EKG showed ST depression. Stat echo showed severe right heart strain, so we put him on a heparin drip and got a CT pulmonary angiogram to confirm the diagnosis.

 

[Guero]

Pretty much. My first thought when I saw the thread was "I haven't heard an S3 since med school when I was in the sim lab..."

The last time I diagnosed a PE, the progression went like this: post-op pt had a presyncopal episode, remained moderately hypotensive and suddenly required supplemental oxygen just to keep O2 sats >90%, and he was having chest pain. I got an ABG, EKG and CXR. CXR was normal, ABG showed he was hyperventilating, and the EKG showed ST depression. Stat echo showed severe right heart strain, so we put him on a heparin drip and got a CT pulmonary angiogram to confirm the diagnosis.

Nice! That seems like a text book case...was it?

 

[45408]

Nice! That seems like a text book case...was it?

More or less. It wasn't exactly a House, MD moment. He was a big setup for such an event (emergency operation, massive transfusion), and the PE was gigantic. He's lucky it didn't kill him...

I've diagnosed more PEs with some non-specific symptoms - low grade persistent tachycardia, mild chest pain, etc - than I have with obvious signs like this guy. I've also found several PEs incidentally (CT abdomen that shows an embolus in an inferior lobe).

 

[Guero]

More or less. It wasn't exactly a House, MD moment. He was a big setup for such an event (emergency operation, massive transfusion), and the PE was gigantic. He's lucky it didn't kill him...

I've diagnosed more PEs with some non-specific symptoms - low grade persistent tachycardia, mild chest pain, etc - than I have with obvious signs like this guy. I've also found several PEs incidentally (CT abdomen that shows an embolus in an inferior lobe).

Hah, definitely not a House, MD moment. I've seen a lot of D-dimers done over here when they have a PE w/u.

That's really cool that you're still finding other pathologies as a surgical resident. I wonder how often you all see pathologies other than those germane to post-op pts (e.g., DVT, PE, SBO).

 

[evilbooyaa]

Pretty much. My first thought when I saw the thread was "I haven't heard an S3 since med school when I was in the sim lab..."

The last time I diagnosed a PE, the progression went like this: post-op pt had a presyncopal episode, remained moderately hypotensive and suddenly required supplemental oxygen just to keep O2 sats >90%, and he was having chest pain. I got an ABG, EKG and CXR. CXR was normal, ABG showed he was hyperventilating, and the EKG showed ST depression. Stat echo showed severe right heart strain, so we put him on a heparin drip and got a CT pulmonary angiogram to confirm the diagnosis.

The patients I've seen diagnosed with a PE in-house(these were only medicine floors) were people with new onset sharp chest pain, tachypnea, and problems with their sats (needing supp. O2). I saw ~ 3 times that these patients were started on a heparin drip while all the other tests were done. 1 of them had a negative CT r/o PE, and he was taken back off the drip.

I imagine with post-op patients, you want to be a little more sure of your diagnosis before you go and anticoag someone like crazy.