How to navigate the likelihood ratios for mitral regurgitation presented by the physical exam, particularly auscultation, are the focus of this episode of AP Cardiology with host Andrew Perry, MD, joined by Shreyas Venkataraman, MBBS, of Washington University School of Medicine in St. Louis and its Barnes-Jewish Hospital.
A transcript of the podcast episode follows:
Perry: Hi, everyone. Andrew here. Today is a continuation of the physical exam series with Shreyas Venkataraman, an internal medicine resident at Barnes-Jewish Hospital in St. Louis. You will remember Shreyas from a previous episode discussing the physical exam related to aortic stenosis. Today we will be focusing on mitral regurgitation.
This episode is supported by the Thinklabs One digital stethoscope…
If you haven’t listened to the prior episode on aortic stenosis, I would recommend going back and listening to the first part where we discussed likelihood ratios, as we will be using those in our discussion today. I learned a lot in preparing for this episode and I hope you do too while listening to it.
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Venkataraman: Hey, Andrew. Today we’re going to be talking about an evidence-based physical diagnosis of mitral regurgitation.
Perry: This episode is going to refer to likelihood ratios as a way to help you increase or decrease your probability of having the diagnosis of mitral regurgitation. For a review of that, we would direct you back to the previous episode of the physical exam series on aortic stenosis.
Venkataraman: All right, let’s jump right in. Today we have a 59-year-old male with a past medical history of diabetes who is a former smoker and today he presents to your clinic with subacute dyspnea for the last 3 weeks. He says that he’s not able to do any work. When we ask him what kind of work he does, he is involved in a moving company. He does a lot of physical work moving stuff and is also involved in being a handyman on the side, so he feels that he’s not able to really do any of the work he used to be able to do and it’s really affecting the quality of his life. What do you think about this patient we have today, Andrew?
Perry: Yeah. As a cardiologist in training, I see a middle-aged gentleman with diabetes, smoking history, coming in with shortness of breath. Part of the pyramid of dyspnea that we learn about is cardiac causes. There are many other causes that can cause shortness of breath, but if I’m seeing this kind of patient I’m wondering whether this person’s having heart failure or whether they’re having a valve problem primarily causing their shortness of breath. Additionally, this person may be having ischemia driving their shortness of breath, but that’s a bit of a more atypical presentation.
Venkataraman: When we do see a patient for whom we’re suspecting to have mitral regurgitation, I think it’s imperative for us to distinguish between acute and chronic types of mitral regurgitation, because they have vastly different presenting features. Also, symptoms are important in these patients, because they play a critical role in determining who gets an intervention and when they get an intervention. So that’s another reason to pay attention to symptoms. Why we say this is because although symptoms haven’t been studied extensively from a likelihood ratio perspective, they do play a significant role in the clinical care of patients.
Perry: What you’ve talked about here, the difference between acute and chronic types of mitral regurgitation, acute MR can be a very dramatic presentation. The patients are very dyspneic, including at rest, so they can be hypotensive, sometimes in shock. In contrast, the patients who present with more chronic types of mitral regurgitation, they’re having more of a subacute to a chronic progression of shortness of breath and fatigue, and they may or may not have heart failure symptoms on presentation. How about we talk about our patient’s physical exam, Shreyas?
Venkataraman: All right. We first measure his pulse. We see that he has a normal pulse at 85 beats per minute. His blood pressure is relatively normal at 110 by 80. That’s been his baseline. He’s satting at around 95% on room air. But on inspection we actually see that his apical impulse is displaced, and when we make him lie down at 45 degrees he has elevated neck veins on the right side.
Perry: Shreyas, what do you think about that physical exam?
Venkataraman: I do notice that he has a displaced apical impulse, and that in combination with an elevated neck vein on the right does suggest to me that he has a large heart, and a large heart in the presence of heart failure. I think that would be the first thing I take from this. But having said that, I’m just wondering, how do neck veins really correlate with left-sided pressures, Andrew? Don’t they actually tell us about right-sided pressures?
Perry: Yeah. In this patient — and we’re doing an episode on mitral regurgitation here and so we’re thinking about more how MR can influence left atrial pressure — we can detect a displaced apical impulse when we palpate, and second, we detect elevated neck veins on inspection. These really are not direct measures for left atrial pressure.
Now, the elevated neck veins are a sign for right atrial pressure, and a common cause of right heart failure and elevated right heart pressures is left heart failure and elevated left-sided pressures, which can be seen and associated with mitral regurgitation. When you have a jugular venous pressure elevation, the probability of having an elevated left atrial pressure has a likelihood ratio of 3.9, while having a negative finding, meaning that you don’t find any jugular venous pressure, really doesn’t have a significant impact on your post-test probability for having an elevated left atrial pressure.
Venkataraman: All right. From what I understand, although we are looking at right-sided pressures, it gives us an insight into how well the overall heart is functioning. Is that correct?
Perry: Yes, that’s correct.
Venkataraman: Perfect. Okay. You said a likelihood ratio of 3.9. That’s around a 20% increase, so not too significant, but something we can work with.
Perry: As you’re palpating this person’s heart, you can feel that it’s displaced. What do we know about the relationship between a displaced apical impulse or the characteristics of apical impulse and their relationship to an elevated left atrial pressure?
Venkataraman: We do have evidence to support the role of the apical impulse playing a role in us understanding a patient’s wedge pressures, so in this study, patients were supine and their apical impulse was palpated lateral to the midclavicular line, and what they saw was if it was palpated lateral to the midclavicular line, it usually correlated with a wedge pressure of more than 12.
This particular finding had a positive likelihood ratio of 5.8. That’s pretty big in the larger scheme of things, given until now we haven’t had a likelihood ratio this high, so that’s somewhere around 35%. But in contrast, if we do not have this finding it is not really useful and we can’t really make any judgments or conclusions about the patient’s capillary wedge pressure. The presence does help us, but the absence, not so much. But given this patient’s findings, what else would you look for in a patient like this, Andrew?
Perry: When we’re talking about their apical impulse, there is something to be said that we can feel the type of their apical impulse, so not just the placement. If they have a hyperkinetic and a sustained impulse, like we had mentioned in the previous episode on aortic stenosis, you can get a prolonged sustained apical impulse. Having a sustained apical impulse can increase your likelihood ratio by 11.2, which increases your post-test probability of greater than 50%. Furthermore, the absence of having a hyperkinetic apical movement decreases that risk with a likelihood of 0.3.
Venkataraman: All right. Another thing that we notice is that in patients with severe mitral regurgitation, ventricular contraction causes a backward jet of blood into the left atrium, which then essentially lifts the heart, which is then felt as a sustained movement to the person examining the patient. How this helps us as clinicians is essentially when we do palpate patients’ hearts and we do see that there is a prolonged and sustained apical impulse, this directly correlates with the severity of the mitral regurgitation, which is really interesting because essentially what this means is the longer you can feel the heart, the more severe the mitral regurgitation is.
Perry: Yeah. It’s pretty interesting, and additionally, mitral regurgitation, chronically and over long periods of time, this can cause elevated pulmonary pressures. So while we’re palpating we should palpate for the P2, and this is when the pulmonic valve is closing. So if we’re having high pulmonary pressures, we can get a palpable P2 with that high force causing the closure of the pulmonic valve.
However, if we don’t feel a palpable P2, then this really drops the likelihood of having elevated pulmonary vascular pressures with a negative likelihood ratio of 0.05. That dramatically reduces your probability by over 50% of at least having elevated pulmonary wedge pressures, which if you’re having severe chronic mitral regurgitation, you’re probably going to have some elevation in your pulmonary pressures.
Venkataraman: Another thing we could possibly see or feel is a palpable S3, which is seen in most conditions with a rapid ventricular filling, so these are the things we would feel for, so that is quite a bit of information. Let’s quickly review what we talked about until now before we move on.
The first thing we talked about was monitoring of symptoms is extremely important. Why I say that is, although we do not have numbers that help us determine which symptoms are more important, they play a very useful role clinically because it helps us in determining the time of intervention. Following that, another very useful thing we can do for patients with mitral regurgitation is palpate the heart.
Why palpate the heart? Because, one, it helps us determine pulmonary wedge pressures, where if we do feel a laterally displaced apical impulse, it increases the likelihood of elevated wedge pressures by around 30%. And most interestingly, if we also feel — or don’t feel, rather — a P2, this markedly reduces the risk of having elevated wedge pressures, so this is wedge pressures.
Another reason we would need to palpate the heart is to potentially know how severe the mitral regurgitation is before we send the patient for an echo, where a sustained apical impulse closely correlates with the severity of mitral regurgitation, with a correlation coefficient of 93%, which is very, very strong. Having said all of these things, you know, we do have to give you a disclaimer. None of these findings are specific for mitral regurgitation. But having said that, it’s very useful in detecting an elevated left atrial pressure or findings of heart failure with its associated findings.
Perry: That’s to say that patients with mitral regurgitation commonly are found to have heart failure and commonly found to have elevated pulmonary pressure. So really, these bits about the physical exam that we’ve talked about so far are looking for these secondary effects from the mitral regurgitation.
Venkataraman: Yes. All right, so now we’re going to be listening to the murmur.
[HEART BEATING]
Venkataraman: All right, so what I heard was an S1. It was very non-characteristic if you’d ask me, but what I did hear was a soft S2 and a very characteristic murmur. I felt it was a soft blowing type of a murmur, and with regard to timing I would think it was holosystolic. So that is one thing we see. But also, we further see that this murmur radiates to his axilla and is most prominent near his apex.
Perry: Yeah, very good. This is a soft holosystolic blowing type of murmur radiated to the axilla. This is kind of your classic textbook example of mitral regurgitation. I think here we’ll play an example of the aortic stenosis murmur that you can hear to contrast with what you just heard for the mitral regurgitation.
[HEART BEATING]
Perry: Back to the murmur that we had for mitral regurgitation, the one notable thing that we don’t hear is having a loud S1, and that’s associated with a prolapse.
Venkataraman: Let’s hear that again.
[HEART BEATING]
Venkataraman: It’s interesting that you would say we do not hear a loud S1, Andrew, because Tei et al. studied the intensity of S1 using two-dimensional echocardiography to determine the types of mitral valve prolapse. And what they saw was a loud S1 usually correlated with an early prolapse of the mitral valve, but many mitral regurgitation patients had normal or a soft S1. That’s S1. So Andrew, what are your thoughts about S2 and S3?
Perry: For S2 you can have a wide physiologically-split S2, and that can be seen in mitral regurgitation, but this hasn’t been studied as extensively as it has been in pulmonary stenosis. Now S3, the presence, that’s going to direct us towards having a patient who has an elevated left filling pressure with a positive likelihood ratio of 3.9, while its absence isn’t a useful likelihood ratio.
This finding can be suggestive of having severe mitral regurgitation, but important to note that an S3 is more specific for just having heart failure in general. And a common cause of heart failure and a commonly-found condition in heart failure is having mitral regurgitation. So really, like that piece of information doesn’t provide a lot of useful information to me as to the presence or absence or the severity of mitral regurgitation.
Venkataraman: Right. We did reiterate that we heard a holosystolic blowing type of murmur that radiated to his axilla. What are your thoughts on that?
Perry: The characteristic of this murmur, soft blowing holosystolic, if it’s heard in the mitral area, meaning the mid-left thorax, fifth intercostal space, the likelihood of MR is slightly increased with a likelihood ratio of 3.9. That’s somewhere around 25%. In the absence of a murmur, that significantly reduces the probability of MR with a likelihood ratio of 0.12. Really, that’s to say not hearing the murmur is more useful to say that there’s not MR than hearing the murmur is to say that there is MR.
Venkataraman: Another thing is that the murmur is usually very high in frequency and usually radiates to the axilla. A louder murmur is usually associated with an increased severity, where when you do hear a louder murmur the positive likelihood ratio of having a severe type of MR is 4.4, which is an increase of 25%. This correlation coefficient is 0.67, which is not as strong as palpating the heart, but it does help our overall diagnostic approach.
Having said that, this finding has a negative likelihood ratio of 0.2, so it decreases, or rather, the absence of hearing an increased severity of a murmur decreases the risk by around 45% and its absence could decrease the probability of potentially having a moderate or severe type of mitral regurgitation.
Perry: Okay. Let’s go back to our patient and say that we hear this type of murmur, and then we do a hand grip on the patient. If this patient has significant mitral regurgitation, what would be the expected change in the quality and sound of this patient’s murmur?
Venkataraman: When comes to a hand grip, what we try to do with the hand grip is essentially increase the patient’s afterload. And by increasing the patient afterload, we decrease the ability of blood to go through this particular tract. And by doing this, there is an increase in regurgitant flow via the mitral regurgitant lesion.
In summary, when we do hear an increase in the severity of the murmur after a handgrip, there is an increased likelihood of mitral regurgitation. This finding has a positive likelihood ratio of 5.8, which is somewhere around 35%. But having said that, the absence of an increase following a handgrip does not help us much because of non-significant negative likelihood ratio values.
Another thing that’s historically been used is amyl nitrate, which is used for echoes, which is rarely used in the clinical setting right now. But what that does is decrease afterload, and by decreasing afterload, the blood is more likely to go through the aortic valve rather than the mitral regurgitation lesion. And this causes the mitral regurgitation murmur to become softer. This finding is associated with a positive likelihood ratio of 10.5, which is quite high, and again, a negative finding does not help us much.
Perry: Currently we don’t use amyl nitrate inhalation, but we could use something like sodium nitroprusside. Or if the patient’s undergoing general anesthesia, both of these things and others will decrease the patient’s afterload and so the severity of the murmur may decrease because of that.
One other thing to note about when we’re auscultating taking these patients is that in the situation where patients may have mitral valve prolapse, this can present as a late systolic murmur.
That’s to say that the prolapse of the valve doesn’t occur immediately at the beginning of systole, but that maybe midway through systole or later in systole, with the increase in LV pressures, finally the valve will prolapse backwards, meaning that it buckles back into the left atrium and then opens up and causes a mitral regurgitation. So you can have situations where you don’t have a holosystolic murmur but rather a late systolic murmur, and you may hear an opening click associated with the prolapse.
Venkataraman: Do keep in mind that these likelihood ratios are fairly modest, but these are the only findings we have. All right, so we did go through a lot of content there. Let’s briefly review what we have learned about auscultating patients with mitral regurgitation.
What we do know is louder murmurs are associated with an increased severity of mitral regurgitation, and this increases the probability around 25%. Also, maneuvers like the handgrip that increase the severity of the murmur increase the likelihood of mitral regurgitation by around 30%. Also, another possible maneuver that we can use is using afterload-reducing agents like sodium nitroprusside, which decrease the afterload and increase the likelihood ratio by around 50%, which is a huge increase. We’ve primarily been discussing findings with chronic mitral regurgitation. Andrew, how do these findings change in somebody with acute mitral regurgitation?
Perry: Acute mitral regurgitation may develop in scenarios such as papillary muscle rupture from ischemia, like during a heart attack, or a leaflet perforation from endocarditis. These patients may present with no detectable murmur, or when you listen to them they have a very soft murmur, and the reason behind this relates to the fact how murmurs relate to differences in pressure, and in this situation, the difference in pressure between the left ventricle and the left atrium.
In acute new onset mitral regurgitation, the left atrium is normal-sized and noncompliant. During systole, the left ventricle ejects blood into the left atrium and there’s a rapid equalization of pressures, so the regurgitant volume may be smaller than that seen in chronic mitral regurgitation, because the left atrium has not been stretched out from years of regurgitant flow, so the left atrium cannot handle that volume and it goes into the pulmonary veins, causing pulmonary venous congestion and dyspnea as a result.
The pearl to remember is that you need to have a high clinical suspicion for severe acute mitral regurgitation because you may not detect a murmur. The patient’s going to be very tachypneic and very tachycardic. You need to make that clear to the echocardiographer, because the typical methods for assessing mitral regurgitation by echocardiography, such as effective regurgitant orifice area or vena contracta, may be inaccurate.
I was involved in a case where the initial color Doppler really underestimated the mitral regurgitation, as did the effective regurgitant orifice, but when you looked at the continuous wave Doppler, it showed a very dense regurgitant jet and there was pulmonary vein flow reversal.
That might be a bit much, but suffice it to say that because of the issues with chronicity and having an acute mitral regurgitation, you can be tricked in your physical exam for not detecting the typical signs of severe mitral regurgitation.
Venkataraman: Wonderful. All right. We learned quite a bit about mitral regurgitation, right from how symptoms can be important for us to treat patients, right down to how severity can be determined by palpating somebody’s heart as well as listening to the severity of their murmur.
Perry: Yep, very good. Great discussion. Thanks for listening, and we’ll see you next time.
This episode was sponsored in part by Thinklabs, the creators of the Thinklabs One digital stethoscope.
Andrew Perry, MD, is a cardiology fellow at the University of Washington Medical Center in Seattle.
Source: MedicalNewsToday.com
