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Level 1 Content for the Alternative PANRE: Cardiology

CME4Life Synapse By May 27, 2022April 24th, 2024No Comments
Level 1 Content for the Alternative PANRE: Cardiology

Welcome to part one of the Alternative PANRE study resource from CME4LIFE. This blog post is going to focus on topics that are relevant to the boards, and we’re going to focus on the red light content.

Now, what do you mean by red light? Level one content. Remember ladies and gentlemen, the NCCPA said, in the upcoming alternative PANRE, there’s level one, level two and level three type content. You have to know information at different depths of knowledge, where level one means you need to recognize the most likely diagnosis, using signs, symptoms, and risks, and refer appropriately. So level one, you don’t have to know everything. You don’t even have to know the preliminary tests. You have to go, “Oh shoot, I think this is something really bad” and get the proper referral.

Now, as part of this series, we’re just going to review the red light content. Now, what do you mean by red light? To me, red light is level one content. At CME4LIFE, we’re calling it red, yellow, green. Red is level one content, yellow is level two, and green is level three.

Now, I know that imitation is the highest form of flattery, and we have had other educational companies contact us, ask us if they could use that model as well. And absolutely, it’s our goal to help people learn, whether you’re learning through us or any other educational resource. Your job is to prepare for your boards appropriately, crush your boards, and go back to helping people.

So today, I just want to talk about the red light content of cardiology. And this is part one. We will do 14 blog posts that only cover red light content. These are, once again, the types of medical diseases that you have to recognize the most likely diagnosis based on the signs or symptoms and the risk factors, so signs, symptoms, and risks.

When it comes to cardiology, there are topics that we need to know just as far to say, “Holy cow, I really think that’s what’s going on here.” So we need to know valvular heart disease. That means mitral insufficiency, mitral valve prolapse, and aortic stenosis. We need to know bundle branch blocks, heart blocks, and sick sinus syndrome, ileac artery occlusion, pericardial effusions, Prinzmetal angina, aneurysms, which are thoracic or abdominal, endocarditis, cardiogenic shock, diastolic heart failure, and HOCM. That’s hypertrophic obstructive cardiomyopathy.

So my whole goal here in this blog post is to really give you the skinny, give you pearls on each one of those.

Valvular Heart Disease

We’re going to start with valvular heart disease. Now, the cool thing about this is, when you look at the valves they’re talking about, they’re left-sided heart valves. So like mitral insufficiency or aortic stenosis, these are the valvular heart problems on the left side of your heart. And that makes sense because that’s really the high-pressure center. The right side is very low pressure, very low degrees of murmur.

In teaching our board review courses, I say in South Vietnam there are MIAs. What does that mean, John? So our major systolic murmurs are MIAS. MI, which is mitral insufficiency. AS is aortic stenosis. So these valvular heart problems are both systolic in nature. And the cool thing about them is they both have very specific radiation patterns. Aortic stenosis loves to radiate to the carotids, where mitral insufficiency likes to radiate to the axilla. So common denominators are they’re both systolic murmurs, they both have a radiation pattern. Aortic stenosis goes to the carotids. Mitral insufficiency loves to radiate to your axilla.

Now, aortic stenosis, think of the letter A, where the letter A goes up and down. So the murmur of aortic stenosis, crescendo decrescendo. The murmur of mitral insufficiency, think of the letter I. Okay, that second letter of mitral insufficiency, it’s holosystolic. Okay, so mitral insufficiency, aortic stenosis. Now, the signs and symptoms. The major signs of any valvular heart problem is traditionally CHF. And CHF always presents with shortness of breath. This typically is going to be someone who’s short of breath with a murmur. Now to understand that aortic stenosis, if they’re put under a situation where their heart races, they could have a syncopal episode.

So valvular heart disease will either present with shortness of breath and by far that will be the overwhelming majority of patients. CHF also presents shortness of breath. Remember that. So valvular heart disease will eventually damage the heart and put them into congestive heart failure.

Please remember, this is a huge thing, and it’s almost an eye-opener for a number of people who come to our live curriculum. It’s that CHF is not a disease, it’s a symptom of a disease. It’s like you wouldn’t diagnose someone with a fever, because something always causes the fever. I need to know what’s causing it. You wouldn’t diagnose someone with anemia, because something’s always causing the anemia. It’s the same thing with CHF. Something is always causing it. It’s a symptom of a disease. We need to know underlying pathology, and valvular heart disease is indeed one of them.

So, once again, the most common presentation of valvular heart disease is CHF with shortness of breath. Or aortic stenosis can present with syncope when their heart races. Now on the question, they’d have to give that to you.

Hypertrophic Obstructive Cardiomyopathy

Now a good understanding, for the rest of your life, is anybody who has something bad happen to them, like they pass out when their heart is racing, it’s cardiac and you need an echocardiogram. Now, that could be a kid, that could be a geriatric patient. What do you mean by kid, John? Well, if you have a kid running to first base and all of a sudden, they have a syncopal episode, their heart was racing and you have to think of something bad, like hypertrophic obstructive cardiomyopathy.

Now, hold on a second. Hypertrophic obstructive cardiomyopathy is one of the red light things that you need to know for your boards. So let’s compare and contrast them. HOCM is the number one cause of sudden death in anyone under the age of 35. So this is someone who, when their heart is racing, they have a syncopal episode. Now, HOCM also has a systolic murmur that’s very similar to aortic stenosis. Crescendo, decrescendo but it doesn’t radiate to the carotids, okay? So HOCM is traditionally younger than 35. Aortic stenosis is normally older people, but a younger person could have aortic stenosis, I guess. Not common, but it’s possible. Both of those patients need echocardiograms.

So if it’s a kid that has an unresponsive episode when their heart’s racing. John, what’s going to make a kid’s heart race? Well it’s traditionally during a temper tantrum or during feeding. You need to do an echo.

Heart Blocks

Next, we’re going to talk about heart blocks, and that has to do with bundle branch blocks, heart blocks themselves, and sick sinus syndrome. So bundle branch blocks would be very tricky to describe in a blog post. We have a video series that has an EKG curriculum that walks you through this in detail. Just understand that a left bundle branch block could be the presentation of a big heart attack. Now a big heart attacks are known as STEMIs, ST segment elevation myocardial infarction.

Remember you have three blood clots that are catastrophic that you have to know for your boards. And we’ll talk about them in the series, but it’s definitely talked about in the videos in the live curriculum. The three blood clots are heart attack, stroke, and a pulmonary embolism. Cool. Now to understand what you need to know for your boards, you have to understand that two of them are arterial, one is venous. So heart attack and stroke are arterial, PE is venous. That’s beautiful.

Also understand that you have big ones and small ones in all the categories. You have a big heart attack, which is called a STEMI. You have a small heart attack, which is called the non-STEMI. You have a big stroke, which is a CVA. You have a small stroke, which is a TIA. Then you have big PEs and small PEs. The big PEs present predominantly with shortness of breath. The small PEs present predominantly with pleuritic chest pain.

If a left bundle branch block is new or presumably new, we have to immediately get our supervising doc, especially in the light of chest pain. A new right bundle branch block suggests pulmonary disease, like a PE. So bundle branch blocks are an EKG finding only. Now, if they look sick, they look sick, and that’s why we get consultation.

This is kind of interesting, where you have three kinds of heart blocks: first degree, second degree and third degree. Why did they put them in these categories? Well, a first degree heart block has a long PR interval, but 100% of the impulses get through. Every time the atria beats, the ventricular gets stimulated. Now, a third degree heart block, no impulses get through, none. That’s why it’s a third degree. Now second degree, some get through and some don’t. It’s intermittent.

Now, as you know, there are two types of type two heart blocks. You have a type one and a type two. So you have Mobitz type one and a Mobitz type two. And this has really to do with anatomy, where the Wenkebach, or the Mobitz II type one, is a blockage at the AV node. Where, if it’s a Mobitz II type two, that’s a heart block down at the bundle of His. It’s a little bit lower. That anatomy is pointed out in our pharmacology section because you have to understand that our vagus nerve, and the vagus nerve is the leash of the heart, and if you stimulate the vagus nerve, the heart’s going to go slower. Well, that innervates the heart at the AV node. So, atropine works on that vagus nerve, and atropine is then very effective for Wenkebachs or Mobitz II type ones.

How will you know if someone has a heart block? Well, understand, ladies and gentlemen, you do not need to know the EKG criteria of a heart block anymore. You have to know the probable diagnosis based on signs, symptoms and risk factors. So these people will present with slow heart rates. They’re going to be bradycardic. If you have someone who’s bradycardic and symptomatic, and their heart rate’s in the low 40s, 30s, you have to go, “Holy crap. I think they have a heart block” and get consultations. We don’t need to know first line treatment anymore. That’s the cool thing.

Sick Sinus Syndrome

Now sick sinus syndrome, this is also known as Tachy-Brady syndrome, where the patient will have episodes where their heart races about 150, 160 and then have episodes of pauses, five, six, seven, eight second pauses. Once again, they’ll typically present with some kind of syncopal episode or near syncopal episode. They’ll have episodes where the heart’s racing or the heart’s going brady. That’s when we would consult our doc and say, “Hey, I think I got a sick sinus syndrome.”

Ileac Artery Occlusion

Next is ileac artery occlusion. So the ileac artery, that would be from an arterial thrombus and, ladies and gentlemen, whenever blood is cut off to an organ that has nerve innervation, the pain is agonizing. Pain out of proportion to exam is what we like to talk about. This would be someone who has a cold pulseless leg, and they have a big fat blood clot. They will be agonizing in pain. So if someone comes in with a cold, pale leg with no pulses, we race to get our supervising docs and or vascular surgery.

Pericardial Effusion

Now, something that’s interesting about pericardial effusion and pneumothorax. To compare and contrast them, you have a substance in a space that it shouldn’t. So pericardial effusion, you have fluid in a space that shouldn’t be there. If you have a pneumothorax, you have air in a space that shouldn’t be there. Now, you have pericardial effusion, which is just fluid in the wrong space. Pneumothorax, air in the wrong space.

Now, you can have the catastrophe of that. The catastrophe of pericardial effusion is pericardial tamponade. It’s causing the heart to be squished and they’re sick, just like you can have a tension pneumothorax that’s causing the mediastinal structures to get squished and they’re losing their blood pressure. So the sequelae of both of them are an obstructive-like shock, where you have to fix them with a needle. With tension pneumothorax, you do a needle decompression. If it’s a pericardial effusion that’s now in tamponade, we would put a needle known as a pericardiocentesis.

So pericardial effusion, oftentimes, they present with what’s called Beck’s triad. That is muffled heart sounds, hypotension, and JVD. Now, I’m going to say this again because I think this is really important. On the boards in the past, anytime you have two diseases that are similar, it makes it very easy for test writers to write a question about that. The murmur of aortic stenosis and HOCM is very similar, crescendo, decrescendo, so it’s very easy for them to write questions about it.

It is classic on the boards in the past and in advanced trauma life support to ask a question comparing and contrasting pericardial tamponade and tension pneumothorax. It’s a classic question. You know why? Because they both have a thoracic trauma traditionally, and they both have JVD and hypotension. So pericardial effusion, just to understand that the trachea is going to be midline, and they’re going to have really clear lungs. There’s no asymmetrical lung findings with pericardial effusions. So if you have someone who has JVD and hypotension and clear lungs, that’s pericardial effusion.

Prinzmetal Angina

Prinzmetal is also known as variant angina. They look exactly like a STEMI, which means they’ll come in with chest pain and they’ll have all the looks of someone having a big, fat heart attack. Now, they’re going to have ST-segment elevations on their EKG in the lead that that vessel is pointing towards. Again, that’s talked about in detail in our EKG curriculum. And I taught EKGs for my whole career, last 18 years, and I’ve really simplified it.

On my YouTube channel, you’ll see a bunch of videos on the topic that we put up for free because we want you to learn. We want people to learn. When people learn, they’re better providers. And when there are better providers out there, our profession’s stronger and more people are helped.

Prinzmetal angina looks just like a STEMI. And when you have a STEMI, the primary focus removing that blood clot. They’re dying, and their heart is dying. We’ve got to stop that blood clot from getting bigger and try to get it out of there. And it’s either by getting them to a cath lab or by using thrombolytics.

Now, with Prinzmetal, it’s not a blood clot. It’s vasospasm. They look exactly the same, but it’s vasospasm. What typically happens is you have someone who’s got really bad pain, they get a little bit of Nitro or morphine, and their pain goes completely away. And then you do an EKG, it goes completely back to normal. If you have someone who that has occurred with, we immediately talk to an interventional cardiologist and say, “Hey, this is what happened.” They will take them to the cath lab and see if there’s indeed a clot there. If not, these people are typically treated with a calcium channel blocker.

But you don’t have to know that. You have to know that this is someone who looks like a STEMI and their EKG is very ominous. Remember, a STEMI is ST-segment elevation myocardial infarction. So the only way we can diagnose a STEMI is via an EKG. That’s it. These people will have a really, really ugly looking EKG and, all of a sudden, it goes completely back to normal. That’s suggestive of Prinzmetal. We get help.


Next is aneurysms, thoracic or abdominal. Remember, if you have an aneurysm, that’s a ballooning out of an artery. Now, once it tears, that’s a dissection. So you can have an aneurysm in the thoracic aorta or the abdominal aorta. The big thing here, ladies and gentlemen, they cannot ask you a question about this, and this is also very important to clinical practice. It’s going to come on very abruptly, bam, out of nowhere. They have to say acute onset.

Anytime you have a bursting of a blood vessel, like a subarachnoid hemorrhage, it’s acute in onset, to the point where there’s only one acute headache. That’s subarachnoid. If they say anything about an acute headache, it can only be a subarachnoid hemorrhage. Sinusitis is gradual. Migraine’s gradual. Tension is gradual. Cluster is gradual. The only acute headache is subarachnoid.

Now, with a triple A, that is agonizing pain going to the back. Most of them had a history of smoking at some point. Thoracic dissections, this is acute onset of chest pain. It does like to radiate to the back between the scapulae. At times, they can have asymmetrical blood pressures. And at times, they can have neurological symptoms. So this is going to be acute onset of chest or abdominal pain, typically radiating to the back.


Now, endocarditis can become subacute endocarditis or acute endocarditis, just depending on the germen, how they get infected. So endocarditis is infection of the heart valves. Now, these people love to shoot septic emboli, and there are four classic septic emboli. The Roth spots go to the retina. Roth spots are retina, so it’s an embolic phenomenon that goes to the retina. Splinter hemorrhages goes to the fingernails, and I think that’s pretty self-explanatory because they kind of look like splinters.

What I teach at our live courses is that, if I ask you why did OJ Simpson get off from killing his wife, you’d say, “Well, if the glove don’t fit, you must acquit.” So OJ, you’re thinking of the hand and glove. OJ, those are two names of the hand findings of endocarditis, and that’s Osler’s nodes and Janeway lesions. Osler’s nodes, ouch; the Osler’s hurt. The Janeway don’t.

So we have four findings of endocarditis, Roth’s spots, splinter hemorrhages, Osler’s nodes and Janeway lesions. One is in the eye, and three of them are on the hand. Now, we’re clearly in an era where IV drug use is really high. It makes me think this is going to be more likely of a question they ask on our upcoming boards. Now, we look for the physical exam findings such as track marks.

The endocarditis that’s subacute, that’s typically from dental procedure or anything that enters bacteria into the system. And these are people with artificial heart valves. So if they ask a question that has an artificial heart valve, endocarditis, and the thought that that valve can become infected has got to go very high on your list of concerns. And typically, we do an TEE and blood cultures.

Cardiogenic Shock

Next is cardiogenic shock. Guys, it’s very simple, okay? CHF is right heart failure and left heart failure. Now typically, congestive heart failure has a combination of both left and right together. Now, left heart failure, their lungs are filled with fluid and they’re very short of breath. Right heart failure, the roads that lead to the heart are the superior and inferior vena cava. So if you back up pressure, they’re going to have JVD. And if you back up pressure going south down the inferior vena cava, they’re going to have hepatojugular reflux, ascites, and edema.

Now, cardiogenic shock is just CHF with hypotension. My experience working in emergency medicine, hospital medicine ICU is cardiogenic shock, the mortality is very high. If I have someone who comes in in CHF and hypotensive, it’s really very difficult to treat. To me, cardiogenic shock is as sinister as Reynold’s pentad.

Well, what’s Reynold’s pentad, John? It’s Charcot’s triad that’s in shock. Wait, what’s Charcot’s triad? Charcot’s triad is the triad of jaundice, right upper quadrant pain, and fever. So it’s a common bile duct stone, and they’re infected. If they get septic, they’ll get hypotensive and have altered mental status. So I’m saying the cardiogenic shock is as sick as Reynold’s pentad. Very, very difficult to treat.

Diastolic Heart Failure

Next is diastolic heart failure. Here is the deal. When someone presents with heart failure, we absolutely need an echocardiogram. That is critically important. Someone who’s got CHF, I need to know what their ejection fraction is, and I need to know what their valves are. That’s really important. If you’re a clinician reading this, any time you see a patient with CHF, your gut response should be, “What’s their ejection fraction?” You should always ask that question. It’s like a left bundle branch block. You should always ask if it’s new or old.

Remember, normal ejection fraction is about 60 to 65 percent, meaning that if your heart and your left ventricle gets about 100 ccs of blood and then, every beat, it squirts out 65 mLs, your ejection fraction is 65 percent. That would be normal.

If you’ve got someone who’s got CHF and a normal ejection fraction, the bottom line is we don’t know what to do with that. There is very little information and data, random control trials and meta-analysis of people with diastolic heart failure, so it’s tricky to know what to do with, even by a cardiologist perspective. So we refer that.


Folks, that is the red light cardiology content for the boards. So, how do we proceed in our studies? Well, if you’re like me, I listen and I learn very well from listening. I’m going to be very aggressive in getting the red light podcasts on, so you can learn while you drive. If you’re taking alternative PANRE, you need to be prepared.

We don’t know what the testing’s going to be like. We don’t know what the questions will be like. We don’t know what the fail rate’s going to be. We don’t know how inconvenient it’s going to be in your life. There are a lot of variables.

Now, to truly support the NCCPA and what they’re doing, this is good stuff clinically. They’re not asking us to know all the crazy stuff they have in the past. This is a new era of PA education. So the stuff that I’m teaching you, the red light content, this will be good for you whether you’re dermatology, psychiatry or ortho. And it’ll allow you to jump to another field of medicine if you want to. My hope is this is helpful for you.

Good luck. Keep studying.

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