Podcast Episode 93: Murmurs Made Incredibly Easy (Part 3 of 5) – Pulmonary Valve Stenosis and Regurgitation

The Audio PANCE and PANRE Physician Assistant Board Review Podcast

Welcome to episode 93 of the Audio PANCE and PANRE physician assistant/associate board review podcast.

Today is part three of this extraordinary five-part series with Joe Gilboy PA-C, all about cardiac murmurs. In this week’s episode of the Audio PANCE and PANRE podcast, we continue our discussion of cardiac murmurs with a focus on the pulmonic valve.

We’ll talk about the different types of murmurs (stenosis and regurgitation) that can occur with the pulmonic valve and how to differentiate them from other types of murmurs. If you haven’t already, make sure to listen to our previous podcast episode where we covered the aortic valve murmurs and mitral valve murmurs.

The Pulmonic Valve

Pulmonic valve stenosis (PVS) and pulmonic valve regurgitation (PVR) are two common heart valve diseases. PVS is a narrowing of the pulmonic valve, while PVR is leakage of blood back through the pulmonic valve. Both conditions can lead to significant heart problems if left untreated.

Pulmonic valve stenosis

PVS is the most common congenital heart disease, affecting approximately 1 in 1000 people. It can lead to right heart failure and/or pulmonary hypertension (high blood pressure in the lung arteries). PVS is caused by an abnormally thickened pulmonic valve or localized stenosis which means that it has a narrowing of the valve. Pulmonic valve stenosis has several different causes including:

• Congenital heart disease – this means that the abnormal valve was present from birth but is often undiagnosed until adulthood. For example, children with Down’s syndrome or Noonan syndrome are more likely to have an undiagnosed congenital heart defect such as PVS. It commonly is a component of tetralogy of Fallot.
• Cocaine use in pregnancy – research has shown that there is a link between the use of cocaine in pregnant women and children with PVS, particularly if it is used close to the time of conception or later stages of pregnancy.
• Infection during pregnancy can cause an inflammatory response which may lead to heart problems for the baby.
• Autoimmune disease – PVS is sometimes associated with other autoimmune diseases, such as lupus.

Symptoms of PVS can vary depending on the type of stenosis that is present and how much it has advanced. Mild cases may not cause any symptoms at all; however, it is common for patients to experience breathlessness, fatigue, chest pain, and palpitations.

Heart sounds include increased splitting of S2 and a harsh crescendo-decrescendo ejection murmur heard best at the left parasternal 2nd or 4th intercostal space when the patient leans forward; the murmur grows louder immediately with Valsalva release and with inspiration.

People with PVS may need to take some medication to ease their symptoms. For example, diuretics can help remove excess fluid; beta-blockers reduce the workload on the heart and therefore lower blood pressure and heart rate, and long-acting calcium channel blockers can reduce the force of contraction of the heart’s left ventricle.

Pulmonary valve replacement is an effective treatment for severe PVS, which involves surgically implanting a new pulmonary valve to replace the defective one. Because the valve only affects the blood flow through one part of the heart, this surgery can often be carried out using minimally invasive techniques.

For milder cases of PVS that do not cause symptoms then medication or exercise may be prescribed instead. Regular exercise helps to strengthen the left ventricle (the main pumping chamber) which is important for people with PVS. For more information, view our lesson on pulmonary stenosis.

Pulmonic valve regurgitation

Pulmonic valve regurgitation is leakage of blood back through the pulmonic valve.

It can lead to right-sided heart failure and/or pulmonary hypertension (high blood pressure in the lung arteries). This means that it has a leakage of the valve.

It can be caused by any condition that impairs cardiac function, including pulmonary hypertension (the most common cause), chronic obstructive pulmonary disease (COPD), left ventricular hypertrophy (LVH), and heart failure (HF).

Although 5-8% of the general population has PVR, it is more common in COPD and other respiratory diseases, such as bronchiectasis.

Pulmonary valve regurgitation is an important determinant of functional class and quality of life among patients with chronic obstructive pulmonary disease (COPD), who have a higher incidence of this valvular disease than the general population. It appears to be more frequent than traditionally thought and its impact on patient survival is greater than previously estimated.

Heart sounds when PR is due to pulmonary hypertension include a high-pitched, early diastolic decrescendo murmur that begins with P2 and ends before S1 and that radiates toward the mid-right sternal edge; it is heard best at the left upper sternal border while the patient holds the breath at end-expiration and sits upright.

The murmur of PR without pulmonary hypertension is shorter, lower-pitched, and begins after P2.

Treatment is directed at the cause; valve replacement is usually not needed.

Podcast Episode 93: Murmurs Made Incredibly Easy (Part 3 of 5) – Pulmonary Valve Stenosis and Regurgitation

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Welcome back, everybody. This is Joe Gilboy PA-C, and I work with Stephen Pasquini PA-C at Smarty PANCE. Today, we will cover the dreaded two words that all PA students hate. What are these dreaded words?

Heart murmurs

We’ve covered the aortic valve. We’ve covered the mitral valve. Who’s the next one up?

The pulmonic valve

Okay. So, let’s erase everything we memorized in school.

Most of you are chuckling right now and saying Joe, it’s already erased, right? I’m sure it is.

So, let’s do it my way. I want you to pull back and forget everything you already know.

What’s the pulmonary valve supposed to do on a typical day? Let’s think about this. The right ventricle contracts and the pulmonic valve is supposed to open up. Then, that deoxygenated blood goes out to the pulmonary vasculature.

And then, on a normal day, the pulmonic valve closes during diastole to keep the blood out in the pulmonary area, and then that deoxygenated blood becomes oxygenated.

So, that diagram that you see in the books where the blood is blue, deoxygenated, then becomes oxygenated and red. And then it comes back to the pulmonary vein and back to the left atria, left ventricle, and up to the rest of the body, it goes. So that’s a nice normal day.

And where is the pulmonic valve located? Well, there’s only one valve on the right. That’s the aortic valve. Everybody else is on the left. So, where is the pulmonic valve? The left upper sternal border.

Pulmonary Stenosis

Okay, I want you to stop and just pull back and think, just think, and stop memorizing.

So, I have this stenotic pulmonary valve, and it’s hard to open up.

When am I supposed to open up? During systole. Does a stenotic pulmonic valve open up easily during systole? No, it has a hard time. So, when are you having difficulty with this valve? During systole. Because during diastole, it’s supposed to close. That’s what it wants to do. It wants to stay closed.

So, I don’t have a problem during diastole. I have a problem with systole. So, pulmonary stenosis is going to be a systolic ejection murmur.

So, here’s my question to you. Where’s the blood flow supposed to go? It’s supposed to go to the pulmonary area. Alright, stop and think about this for a second.

I’ve got a lack of blood flow to my pulmonary area. Lack of it. How is your oxygenation now? It’s pretty poor. So how are you going to present? I will be short of breath.

Imagine I go to walk up a flight of steps. I’m walking down the aisle in Costco. I’m completely tanked out. I am short of breath – I lack so much oxygenation I become syncopal; maybe I lack so much oxygen to my heart I have angina. You’ve got a lack of oxygenated blood because the right ventricle can’t get that blood past that valve.

And now, let’s pull back. Remember from the last podcast that S1 is the date between the mitral and the tricuspid valve, and S2is the date with the aorta and pulmonary valve.

Hi, I’m pulmonary stenosis, and I’m taking longer to open up. How’s your S2?

Well, I’m kind of late to the date. Yes, you are because you’re taking longer to open up. So how is your S2 in pulmonic stenosis? It’s split!

Do you now see what the split S2 means? Either I’m aortic stenosis or pulmonic stenosis – someone’s late to the date because it’s taking longer to open up.

Now that I know I have a split S2, I need more information to determine if this is aortic or pulmonic stenosis. But imagine (on the exam) they give you a split S2, and I’m on the right side – that’s aortic.

Now imagine having a split S2, and I’m on the left? Oh, that’s pulmonic. And now give this some thought. Okay, you’ve got this stenotic pulmonic valve, and I can’t get blood out. So, of course, I’m short of breath.

Can I ask you a question? Just give this some thought. Ready?

Hi, you have a stenotic pulmonic valve. Where’s the blood flow back up to? The right ventricle!

OK, so you’re the right ventricle. What are you going to do with all this extra blood? I’m going to dilate, and I’m going to get right ventricular hypertrophy.

And now imagine, if you can, that right ventricle gets bigger and bigger and bigger – stretching, stretching, stretching, stretching, stretching, stretching your right ventricle wall. Can I ask you a question? Can I bust those wires in the right ventricular wall? Yes, I can!

Welcome to right bundle branch block. So, could I get a right bundle branch block with pulmonary stenosis? Yes, I can.

• I get right ventricular hypertrophy.
• I get right axis deviation on EKG. That makes sense.
• And then I’m going to bust that wall wide open. And we’re going to bust the wires from the hypertrophy, and I get right bundle branch block.

And that’s precisely what we see with pulmonary stenosis.

So, pulmonary stenosis.

• I see the shortness of breath, angina, and I can see myself having syncope.
• I’ve got a split S2 because I’m late for the date
• I have a systolic ejection murmur, and it’s going to be on the left upper sternal border, not the right upper sternal border (as in aortic stenosis).

Imagine you are given a question, and the patient has a systolic ejection murmur on the left side of the sternal border. There is a split S2, and the patient is short of breath. Maybe they are lacking so much blood flow they get syncopal.

What’s the diagnosis? You have all the information you need. It’s pulmonic stenosis!

Now let’s make the murmur sound louder.

Okay, back to our first podcast on murmurs. What’s the maneuver that makes all the blood flow go back home? Squatting, squatting is a party. So, if I bring more blood flow back home, just laminar flow physics, the more blood flow I have against the murmur, the louder it sounds – so squatting. That’s a party, and squatting makes the murmur of pulmonic stenosis sound louder.

Remember this: Inspiration, right = Louder and Expiration, left = louder. Inspiration right => Expiration => left

The pulmonic valve is on the right side, so inspiration will make the murmur of pulmonic stenosis sound louder, and the murmur of pulmonic stenosis would go away with expiration.

What are low-volume maneuvers? Standing and Valsalva. So, if I stand or Valsalva, the murmur of pulmonic stenosis goes away.

So, let’s recap once again:

• I have a systolic ejection murmur left upper sternal border.
• Blood flow goes back to the right ventricle, and it dilates. I get right ventricular hypertrophy.
• I’m going to get right bundle branch block because I stretched the wires.
• Inspiration is going to make it sound louder. Expiration is going to make it go away.
• Standing and Valsalva are low-volume maneuvers, and it goes away.
• Handgrip challenges the aortic valve and does not affect the murmur of pulmonary stenosis.

Pulmonary regurgitation

Okay, so let’s just stop and think about this for a second.

Regurgitation – come and get goes you please, I could care less, my doors are always open. I’ve got regurgitation, and I have an open door, and I can come and go as I please.

So now think about it. During systole, should I be open? Yeah. But diastole, am I supposed to be closed? Oh, yes, I am.

But remember, in pulmonary regurgitation, you’re coming and going as you please. You’re supposed to be closed, but you’re not. So, this is a diastolic murmur, and it’s going to go from the left upper sternal border down to the apex. That’s just physics.

Can I ask you a question? That blood flow, where was it? Well, Joe, it was out in the lungs. Exactly. And so now what are you doing? I’m taking blood flow away from our lungs.

Is anybody late to the date? No, not at all. So that’s going to be okay.

So, it will be a diastolic murmur, and it will decrease. It will be loud in the beginning, and then, of course, as the right ventricle fills up, it’s going to sound less. So, it’s going to be considered a diastolic, decrescendo murmur.

But now I want you to stop and think about this because this is where a lot of the test questions come from.

Okay, so I have to blow through the pulmonic valve, right? Yeah. Okay, so let me think about this.

So, I have to push so hard push against the pulmonic valve that it blows open. So, I could see how right ventricular hypertrophy could cause that.

What does your right ventricle push against? It’s the pulmonary vascular.

I’m going to get pulmonary hypertension. See it? Who’s going to push hard against pulmonary hypertension? You’re like, oh, it’s the pulmonary valve on the right side. Is it built for high blood pressures? Yes, or no? And the answer is no.

So, you tell me if I get right ventricular hypertrophy due to pulmonary hypertension, I may blow my pulmonic valve? That’s precisely what’s going to occur.

What’s the most common cause of pulmonary regurgitation? Pulmonary hypertension because my right ventricle will hypertrophy, and I have to push harder. Exactly. The most common cause of pulmonary regurgitation is pulmonary hypertension.

Now, we can get to this argument of what causes pulmonary hypertension. CHF is a common cause.

Everybody’s on Adderall. What’s one of the side effects of Adderall? Pulmonary hypertension. And then here you are the pulmonary valve fighting, Adderall, and you’re like, Dude, that’s pulmonary hypertension out there. I have to push harder. Then you get right ventricular hypertrophy. And then what could I eventually get blowing through the valve? Pulmonary regurgitation!

What are the most common things that we see in people on Adderall? Pulmonary hypertension and pulmonary regurgitation.

So, when I start to fill in that right ventricular, and it hypertrophies due to all that pulmonary hypertension, I will push hard against your pulmonary valve. I can push so hard that I push right through it. Then what do you get? Pulmonary regulation.

Pulmonic valve disorders recap

Who was pulmonary stenosis? That was a systolic ejection murmur left upper sternal border, right ventricular hypertrophy, right bundle branch block.

This could be congenital. We see with tetralogy of Fallot.

And then we saw pulmonary regurgitation. What was that? It was a diastolic crescendo/decrescendo murmur. As the right ventricle filled up, it started tailing off, henceforth the word decrescendo.

Remember, what caused me to blow through my pulmonary valve? The right ventricle got so big that it just blew through because the pressure was so high. And remember, I’m the pulmonary valve. I’m not built for high blood pressure.

What was my right ventricle fighting the whole time? Pulmonary Hypertension. So, who was that? Well, that could be the Adderall. That could be the Fen-Phen. And then here’s the point. I don’t want you to forget.

Can I ask you a question? Who’s the vasoconstrictor everywhere?

What is nicotine? Nicotine is a drug. What is it? A vasoconstrictor? Where does it vasoconstrict? Everywhere! Who has the highest incidence of hypertension? Smokers!

What is the most common cause of coronary disease? Vasoconstricting and smoking.

What is a risk factor for peripheral vascular disease? Smoking.

I lack blood flow to my fingers and now my toes so much that they lack blood flow. They lack blood flow so much that they can’t grow. What’s clubbing, smoking! And now who saw the vasoconstriction? First, folks?

Your lungs? Yeah. What do you think you have as a smoker with COPD, and you’re going to go, oh, wait a second, Joe? I have pulmonary hypertension! Entirely correct.

Wait a second, Joe; then you’re telling me I get right into ventricular hypertrophy smoking? That’s exactly right. Then I can stretch my walls and get right bundle branch block? 100% correct. Then I can blow through my tricuspid and pulmonic valve with my pulmonary hypertension. Exactly.

What is the most common cause for pulmonic regurgitation or tricuspid regurgitation? Regurgitation blew through because the right ventricle got so big? Hmm. Smoking, COPD! Now, does everybody see the bigger picture?

So, imagine the exam question where a patient presents with a murmur at the right upper sternal border? There’s only one person up there at the right upper sternal border, and that’s the aortic valve.

Now, if they tell you the murmur is at the left sternal border, that’s everybody else. Now I need some more information.

• Is it systolic or diastolic?
• Does it get better with inspiration => right or expiration => left?
• Squatting is a party, so that’s just everybody and anybody.
• Handgrip challenges the aortic valve.
• Valsalva and squatting are low-volume maneuvers, and that makes everything go away.

Try to make sense of this, and if you do, you will always answer heart murmur questions the best way.

I still remember being in PA school at Duke, and I still remember memorizing all the buzzwords and all this stuff. And I remember my first year in the ER. I couldn’t tell you what murmur I was hearing on the physical exam.

And now that I have stepped back and taken the time to learn the pathophysiology, I can appreciate how the cardiologist calls this a two, or three, or four, five, or six systolic ejection murmur. I really can understand where they’re coming from. I hope one day that you too can appreciate that as well.

So once again, it’s been an honor and, as always, a pleasure to speak to everybody out there in the PA podcast world.

Please be healthy, please be good, and whatever you guys do. Try to make sense of things.

Take care, Joe.

Transcribed for your reading enjoyment by https://otter.ai and Stephen Pasquini PA-C

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