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Transcribed by Charles Buchanan Date of the Lecture: 09/24/14

[General Pathology] [Lecture number] – [Hemodynamic and Circulatory Disorders] by Dr.

[Slide 36] – [Outcomes After Formation of a Thrombus]
[Dr. Vernillo] – Alright. Good to see all of you. I’m getting to meet your class. This is the second
of two lectures. I’m Dr. Vernillo and Dr. Curry and I teach the Systemic Pathology course
together so you’re going to be seeing more of us together in that course. And we’re doing
hemodynamic aberrations and blood flow. And we’re going to be talking about a lot of fun things
here. So we’re going to pick up some of the concepts that were introduced at the last lecture and
Dr. Phelan has given me two lectures on hemodynamic aberrations and we’re going to talk about
outcomes after formation of a thrombus. Just as a general recommendation, I write exam
questions every year from scratch every single year. And I do not, even though I do release
exams and you have my questions, don’t expect to find the exact same questions because you
won’t find it. So make sure that you study in advance, you take notes, you don't wait a couple of
days before the podcast because even if that worked for you in other courses, it ain’t gonna work
for you here. So make sure that you take notes. I’m saying this to be constructive. I’m not saying
this to be adversarial or disjunctive. Take notes in class and take notes on the, on the podcast and
throw questions at me because it is why you put me here. I’m here to help you; to learn from your
teacher. Don’t wait a couple of days before the exam and hope that you’ll see an old exam
question and the same choices - you will not. Alright, so there are certain things that repeat
themselves but there are very few that do. I write every single exam every year from scratch with
a blank computer screen in front of my face and the reason I do that is simply put is because your
patients aren’t going to be different, are going to be different, in fact. So you’re going to get Mr.
Smith, and you’re going to see him and a year later, you’re going to have your receptionist call
and you find out that Mr. Smith has developed Leukemia. He’s not the same patient he was a year
ago and you’re not going to get the same exam questions year after year. ~immitating whiny
student ~ “But Dr. Vernillo, thats not fair, we want to pass.” Study, you’ll pass. You’ve got the
-???-, you’re brilliant people. So listen, pay attention. If you want to sleep in here, I’m going to
throw you out of here. So make sure you pay attention. This is not your living room. Ok and
umm, ask questions. Thats why I’m here.
Thrombus is the major form - Thrombus or thrombosis, which we went through last lecture, is
the major cause for myocardial infarction. It’s when the coronary artery becomes blocked.
Three major coronary arteries are…what are they?… You had anatomy?…What are they?…Right
coronary artery, the circumflex, and what’s the big one thats called the widow maker. The LAD -
the left anterior descending coronary artery. What part of the heart does it feed? The left
ventricular wall, good. The free wall of the left ventricle, what else?The apex and what else? The
anterior 2/3, the anterior part of the interventricular septum which separates the right from the left
ventricle. So if that artery is blocked then any and all components of the heart will die. Unless
you can reverse the thrombus and get blood flow in there. Thats why you learn this stuff. So a
thrombus can lyse and you can get blood flow again, until it -???- a drug can lyse it and you
restore blood flow. We’ll talk about that in a few moments. A thrombus can propagate. Last week,
I talked to you about deep venous thrombosis and having it in the iliac vein, and that thing can get
like a snake. So, it breaks off from a thrombus. This is thrombolic diseases in a vein, sticks to the
endothelium in the vein a little higher up towards the heart. It starts to grow again. Breaks off.
Travels a little more. Sticks. Starts to grow. So eventually what you wind up with is basically an
impression of the inside of thats vein. It’s like a snake. It’s called a propagating thrombus. What
happens to that thrombus in that leg vein?

Come on. I’m in the country, its quiet. I hear crickets. What happens to the thrombus? It breaks
off. What do we call that? An embolus. Perfect. Where does the embolus go? Through the iliac
vein and drains into what vein after that? The inferior vena cava (IVC) and the IVC then goes
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
where? Into the right atrium, into the right ventricle. Or to the right atrium and then that
thrombus, that embolus breaks off and goes into the right ventricle.
The veins empty into the right atrium. So now you’ve got something that’s traveling through the
vein, it breaks off and now goes into the right ventricle. And then what does it go into? What
major blood vessel breaks off of the ventricle and goes right into the lungs? The pulmonary who?
Artery. You’ve got a bifurcation point. Left and right pulmonary arteries. The thrombus can sit
right- or the embolus can sit right at that bifurcation point. Any blood going to get into that lung?
If it’s major enough, it won’t. We call that a saddle pulmonary embolus. S-A-D-D-L-E. We call it
a saddle because it looks like a saddle. It sits at the branch point. Where is the blood going to go?
Back to what? to the right ventricle. What happens to the heart? Sudden increased what?
Workload. Will that heart hypertrophy? No. Because you die too quickly for that to happen. What
do we call that? Acute what? Cor pulmonale. Perfect. Good. And what happens to your heart?
Does it keep beating? No. We call that cardiogenic shock. I’m going to go into that with you. Ok.
Good. Thrombi repair, they canalize they try to form new blood vessels and attempt to get blood
flow but thats really a useless response. Most of the time in the vast majority of cases, they
embolize. So when we speak of embolization, most of the time its from arterial emboli. And
we’re going to look at that. But it can also come from veinous emboli in the setting of deep vein
thrombosis (DVT).

[Slide 37] – [Diagram]
[Dr. Vernillo] – Ok so heres an example of deep veinous thrombosis. The patient has surgery.
They’re confined to bed, the blood pools in the iliac vein. We described this. The IVC goes into
the right atrium down into the right ventricle - blocks off the pulmonary artery. You wind up with
embolization to your lung. We’ll talk about that in a few moments. This is what is known as
pulmonary embolus and it comes from deep seated thrombosis - deep veinous thrombosis. Often
do in the setting of stasis. Why would congestive heart failure lead to DVT? Talk to me.
[Student] — (inaudible)
Dr. Vernillo: Good. You’ve got the left side that fails because of what? Hypertension. Nice. And if
the left side fails because of hypertension, right? Where does the blood go? Back into the-right
(i.e. correct). From the left ventricle back into the left atrium into the pulmonary vein. The heart
can’t pump forward efficiently. We call it forward failure - most often due to hypertension. Then
it goes back into the lung. And what is that increased pressure called in the lung? A mechanism of
edema. Talk to me. A mechanism of edema - what do we call that? Increased hydrostatic pressure.
Very nice. And that increased hydrostatic pressure gets into the capillaries that are the walls of the
alveoli. Massive congestion. That which follows congestion is like night that follows day. What is
that? Edema. You get pulmonary edema. Pulmonary edema is the hallmark characteristic of
failure from the left. You have difficulty breathing? Sure you do, unless you’re a fish - you can’t
breathe underwater. Now we go back and we fail the right. The most common cause of right
failure? Failure from the left. Right failure can happen independently of left failure and we call
that? We just discussed it - cor pulmonale. We’ll go into a little more detail on that. Back up on
the right side. We get edema in our legs. We get an enlarged liver. We get an enlarged spleen. We
get distended jugular vein. Those are all the manifestations of right failure. And right failure can
come most frequently from left. Not fun. Not fun at all.
Ok. Just to review some of those salient concepts coming forward.

[Slide 38] – [Outcomes After Formation of a Thrombus]
[Dr. Vernillo] – Ok. Now you have something called cardiomyopathy. Cardiomyopathy is a
heterogeneous group of disorders in which there’s a central feature thats called ventricular
hypertrophy and it has a genetic basis. So why would thrombosis be more likely, in a setting of
cardiomyopathy, where you have left ventricular hypertrophy. Same reason you would have the
likelihood of a thrombus where you would have left ventricular hypertrophy, where you would
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
have failing left heart, in the setting of hypertension. Why would a thrombus more than likely
form with left ventricular hypertrophy? Is that an efficient pump? Is it pumping blood forward
efficiently? No. So blood is backing up where? In the left ventricle? So if its not backing up and
its not moving forward, is there some stasis of blood flow there? And what would that predispose
to? Thrombus. Again. Once you understand these concepts, they keep repeating.
Endocarditis is inflammation. We’ll talk a lot more about that. It is inflammation of the valves of
the heart and it’s inflammation of the vessels of the heart. And it can be inflammation of the heart
wall. Why would inflammatory disease of the heart predispose to thrombosis? Thats it!
Inflammation. Platelets. Remember we spoke about the myocardium when it’s infarcted? Platelets
stick there because your body is trying to get rid of the dead heart. It’s inflammation and you get
thrombosis. Good. Not so good for the patient who has this.

[Slide 39] – [Venous Thrombosis
(Deep Venous Thrombosis)]
[Dr. Vernillo] – This is veinous thrombosis. This is deep veinous thrombosis. We spoke a moment
ago about heart failure. Heart failure can lead to back up of blood. Left to right back up of blood
in the veins. Deep veinous thrombosis and then that can embolize and go to what organ?
What side are we on? Deep veinous thrombosis. What side are we on? The veinous side, which is
the - so if that breaks off and embolizes, where does it go to? Come on, back, breaks off,
embolizes, goes back up to the inferior vena cava and goes back to…your right side. And then it
blocks off what artery? The pulmonary artery. And that leads to acute cor pulmonale in some
cases. Sometimes, however, the embolus isn’t that big. And you survive. We’ll talk about that in a
moment. In fact, all of you sitting here are throwing emboli into your lung. But none of you are
infarcting your lung. We’ll explain that. Prolonged bed rest, immobilization - these things cause
stasis of blood in the leg veins, leading to deep veinous thrombosis. Cancer can make blood more
coagulable. Makes it viscid. Makes it thick. Makes it more likely to clot. Virchow’s postulates
include turbulence, stasis, and hypercoagulability of blood and they predispose to thrombosis.

[Slide 40] – [Circulatory Disorders]
[Dr. Vernillo] – So we’ll take a look at embolism, which is related to thrombosis. We spoke about
embolism. Most of it is arterial. And DVT’s can be veinous. So it can be arterial
thromboembolism, veinous thromboembolism. But the vast majority of cases - embolism is from
pre-existing arterial thrombi.

[Slide 41] – [Embolism]
[Dr. Vernillo] – And emboli are not bright. Emboli are very dumb. Emboli, in fact, go with the
flow. They don’t sit down there and think “I’m gonna go here, and I’m gonna go there.” They go
wherever blood flows.
They’re not very smart. So i’ll get a student I’m talking to who IS smart who is not using, as they
say in Brooklyn, his or her “kidneys,” and I’ll say to them “we’ve got a thrombus on the wall of
the left ventricle and it breaks off. Where does it go? And someone says to me “back into the
lung?” Lets think about this for a moment. An embolus is nothing more than a little pencil dot.
It’s a little, itty bitty, puny ass fragment that comes off the thrombus. What do you think is the
likelihood that that thing is going to go back up into your lung where blood is coming back down
on top of you this way. Is it gonna go against a gradient like that? No, of course not. It’s going to
break off and it’s going to go with the flow. Go downstream through the aorta. Go upstream to the
carotid. It’s going to go with the flow. Thats what emboli do. So you go up to Buffalo, and you
visit Niagara Falls and you’re drunk as a skunk. And you’re standing at the bottom of the falls
and you say to your friends on the top of the falls “watch me, I’m going to swim up against the
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
falls.” You cant do that, and neither can an embolus. Alright. Now, emboli for the most part come
in a number of flavors. Most commonly, thromboemboli and preexisting thrombi and most of the
time arterial thrombi.

[Slide 42] – [Types of Emboli]
[Dr. Vernillo] – That’s the most common form of embolization, but all of these things listed here
represent other forms of emboli. So you can have gas that gets into your blood stream- which is
called Caissons Disease/decompression sickness if you sea dive. If you seadive…sharks. But,
anyways. You go down, you come up quickly. Amniotic fluid, if there, is an obstetric
complication where amniotic fluid can get into a vein and actually lead to death.
Fat emboli are also forms of emboli that get into veins. Bone marrow emboli get into veins.
Tumor emboli can get into both veins or arteries. They erode vessels. Then they break off. So
anything which breaks off and travels, be it from a tumor, be it from bone marrow, be it from fat,
be it from gas, be it from amniotic fluid - all of those things represent emboli. The most common
form of an embolus is from a thrombus and thats listed on the top as the most common form of it.
And go away, leave me alone for today. Stop it. OK. Now you’re being difficult. Lets try it again.
Thank you. I didn’t want you to do that. It’s not the fault of the computer. It’s the fault of me. Ok.

[Slide 43] – [Pulmonary Embolism]
[Dr. Vernillo] – Now we mentioned pulmonary embolus. Ok. You have a deep DVT. Deep vein
thrombosis. It breaks off, embolizes, goes into the bifurcation point and it occupies the
bifurcation point, such that the left and right pulmonary arteries don’t get any blood and neither
do your lungs. So thats acute cor pulmonale. We call it a saddle embolus because the embolus sits
at the bifurcation point and blocks off the right and left pulmonary artery. Very much like a
cowboy who’s sitting on a horse? His left and right legs represent the left and right pulmonary
artery. And he’s sitting in a saddle - that represents the bifurcation point. So this is called the
saddle embolus. And it is uniformly fatal and rapidly so.
Pulmonary infarction happens when you have necrosis of the lung. Now listen to this mein kind
(my child) . You have little emboli that get throughout the pulmonary artery. You’re throwing
them out right now. They’re getting into your blood stream. They're getting into your lung. Why
don’t you necrose your lung? Because the embolus says “I like him or her and I’m not looking to
do him or her any harm?” Come on, talk to me. What do we know about the anatomy of the lung
in terms of blood supply?
[Student] - inaudible
[Dr. Vernillo] – They’re smaller and the fact that they're smaller means that they’re going to do
less damage than one that get stuck over here like a saddle embolus. So thats certainly part of it
and you’re absolutely right. But what else contributes to the fact that you don’t get necrosis and
it’s the more important piece of this. Go ahead.
[Student] - does it get shunted…
[Dr. Vernillo] – What do you mean by shunted?
[Student] - Like if it goes through the artery…
[Dr. Vernillo] – I’m not so sure of that, but that’s an interesting thought. Give me something that’s
more pedestrian. More fundamental than that. Go ahead. Well, capillaries represent a meshwork.
What do you know about the lung. Does it have one arterial circulation or two? So you have the
pulmonary arteries, right. What is the other arterial circulation? You had anatomy right? Did you
have this in anatomy? Yes or no, be honest with me. If you didn’t have it, then I’m teaching it to
you. If you did…shame on you, I should electrocute you with my shock buzzer. Where’s the-what
is the other artery called? Did you have this in anatomy or not? Am I speaking Sanskrit over here?
Did you have this in anatomy? Good. We’re going to have a good time in this course, you and
me. So, the bronchial artery. And the bronchial artery takes its origin from the aorta. So if you
block a small branch of the pulmonary artery with an embolus -It’s small. It doesn’t cause much
damage because not only is it smaller but to add to what your colleague said, in that respect,
you’ve got blood coming out of the bronchial artery DVT and it is getting into the lung, it’s
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
going to rescue you. So even if there is a small embolus at a branch point of the pulmonary artery,
the bronchial artery is going to put blood in the lung and prevent it from necrosis. Most of the
time - unless you happen to be a congestive heart failure patient, you’re a chronically controlled
diabetic and you don't have the greatest circulation, that bronchial artery is not going to rescue
you. And then that lung is going to be dead and red. We call it a red infarction and that’s seen
typically in organs that have a dual blood supply. We’ll talk about that in a few moments. Ok.

[Slide 44] – [Saddle Embolism Picture]
[Dr. Vernillo] – Alright, fun and games. This is a saddle embolus. Look at this sucker. This broke
off from an embolus in a deep leg vein and all of this blob here - that is sitting on the bifurcation
point, and here’s your right, your left pulmonary artery completely occluded by this mess. This
looks like a 1950s horror show - “The Embolus That Took Over Cleveland”. I mean, this thing is
blocking major bloodflow. No wonder you get acute cor pulmonale and you die suddenly. You’re
not getting any blood into your lung. It suddenly comes back on your right heart, you’re going
into sudden arrhythmia and die.

[Slide 45] – [Arterial Emboli]
[Dr. Vernillo] – Ok now arterial emboli are interesting. One of my students said to me, one year,
“what’s a destination organ?” This is a student that didn't pay attention. Destination organs are
organs that receive arterial emboli. The destination is the organ that receives the embolus. Or,
another way of saying this is that the embolus is destined for those sites. 75% of the time, the
destination organ, the organ that receives arterial embolus is the leg. 75% of the time. Why do
you think that might be? Ok, so you got an aorta. Where do you see atherosclerosis, most often?
In the abdominal aorta is exactly right. And because you have atherosclerosis in the abdominal
aorta, what do we know about atherosclerotic plaques? They favor the formation of thrombi. So,
now you’ve got this big atherosclerotic plaque in an abdominal aorta with a thrombus on top of it.
Sitting on top of this schmutz. A word that I will use frequently in pathology. It means “junk.”
Because that’s what plaque is. And this thrombus is sitting on top of this plaque, in the abdominal
aorta. Where is it going to embolize to? What happens to the abdominal aorta? What does it
branch of into? Femoral arteries and branches there of the… you said it …iliac and the…and
smaller branches to include the popliteal. These things feed your legs. So because the abdominal
aorta is the most common site for atherosclerosis and plaques in general are thrombogenic, that
thrombus at that site can break off and embolize and go right to the aorta and into its branches
and pick off your leg. And if you’re diabetic, thats why you wind up with the complications of
amputations for exactly that same reason. Because if you’re diabetic and you don’t control your
disease, atherosclerosis starts sooner and it is more extensive in the diabetic than the non-
diabetic.This is what you’re going to be seeing. This stuff is not make believe. It’s like Judge
Judy again - real cases, real people. They don’t make it any more real than this -I wish they

The brain, in terms of being a destination organ-
(referring to his computer) What are you connecting to? I don’t want you to connect to anything.
Get the hell out of here.
Now, the brain is ten percent. Believe it or not, 10% of arterial emboli. And you tell me 10% but
suddenly so many people have strokes - from emboli. Emboli - 10% go to the brain. Or we see so
many people with strokes. So what would cause a stroke in other cases, if it were not an embolus
that come from the heart?
[Student] - Embolus formed in the brain?
[Dr. Vernillo] - Good, now you’re using your kidneys. You’re absolutely right. Unless its formed
in the brain. Which means that if you have atherosclerotic disease, it is all over you in your
arteries. Your medium ones, and your large ones. So your cerebral arteries already have plaques
in there. They don't need an embolus to go there and cause a stroke. Why, a thrombus can form
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
right there on top of the plaque inside of a brain artery and cause your brain to die and give you
an infarction. Absolutely right.

So the most common source for arterial emboli, then, is your heart. A mural thrombus that breaks
off. Or a diseased valve where there is inflammation. But most commonly, the mural thrombi that
form in your heart and aorta and they break off and they get into the systemic arterial circulation
and travel they do. 75% of the time to the leg is emboli. 10% of the time to the brain is
embolying. Testing,kidney, much less in heart, rarer in hens teeth (?no clue?).

[Slide 46] – [Circulatory Disorders]
[Dr. Vernillo] – Most of the time when people have infarctions, its thrombosis. If I give you a
question on the exam, don’t tell me it’s an embolus that gives you an MI - I’ll shoot you.
Thrombosis. Pay attention.

[Slide 47] – [Infarction]
[Dr. Vernillo] – You’re brilliant people. Im amazed though - and I tell students this all the time.
(Mimicking student) I dont have time. I was a dentist in my former life too. I still am. I went into
academics because I’m insane. And I love what I do, but I went into academics. This is the only
way that is going to pamper and feed me, water and feed me and make me happy. They put me
outside in public and I’m a danger to society. So they keep me here. But what you need to
understand is that a lot of what we are teaching you is stuff that you are going to have in practice.
Patients are going to come in. And I always say (in nagging voice) “Well I was going to be a
cardiologist but I don’t know. And I was going to be a liver disease specialist.” Why are we
teaching you all this. I don’t want you to be a cardiologist any more than I am but lets think about
this. Here’s a little nugget for you. If you speak to the cardiologist about that patients teeth that
you’re going to remove, did you ever stop to realize that both you and the cardiologist are treating
the same patient? And therefore you need to have a dialogue with the cardiologist so you can
understand what’s going on with the patients heart. But that cardiologist needs a dialogue from
you on what your doing. You’re both teaching each other here. It’s not one versus the other here.
It’s both of you. So that’s why you need to understand something about a disease process.

Infarction is necrosis. What type of necrosis? Infarction of the heart - what type of necrosis?
[Student] - Coagulative-
[Dr. Vernillo] – Coagulative. Thank you. Where is it liquifcative?
[Class] - The brain
[Dr. Vernillo] – Yes. Can you have liquifactive necrosis in an organ other than your brain? Yes
you can. So if you have infarction of a kidney, and you have death of tiss-you (tissue) as the
British would call it - and then you have infection on that dead tissue, it will liquify and you can
have liquifactive necrosis over preceding coagulative necrosis. But the brain, for whatever reason
or reasons it may be, there is never coagulative. It just dies and becomes liquifactive. Who knows,
who cares, thats the way it is. Ok. And they can heal. If you live long enough they can heal with
scarring. So when we get into the conferences, I’m going to ask you to look at a chart so you can
better understand what changes took place in that heart provided you live long enough. You have
to have enough time to scar.

[Slide 48] – [Common Sites of Infarction from Arterial Emboli]
[Dr. Vernillo] – common sites of infarction. Well there they are, from arterial emboli. Your brain,
your eyeballs - you can go blind. Your kidney, you can go into renal failure. Yeah. The arteries in
your leg. You can wind up with a gangrenous leg and lose the leg in your foot. This is not fun
stuff. If you think of a malignancy as being destructive, which it is. This is not malignancy, but I
dare say that if you have heart disease, you are dealing with a disease that is just as pernicious,
just as destructive, just as malignant as cancer is. It’ll take you down piece, by piece, by piece, by
piece until there is absolutely nothing left of you or very little of it. Once this thing starts, your
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
hope-the hope is that you can stop it from getting worse. It’s a very wicked disease. Heart disease
is no fun.

[Slide 49] – [Gross and Microscopic Descriptions of Infarcts]
[Dr. Vernillo] – Pale infarcts. Dr. Phelan puts this in. These are her slides. I don’t know why she
puts them in. She puts them in because she wants you to know some terms and it’s good. You can
have infarcts that are pale or white. The British call them anemic infarcts. Or you can have
infarcts that are red. Lets take a look at these fun things shall we?

[Slide 50] – [Gross and Microscopic Descriptions of Infarcts]– SKIP

[Slide 51] – [Spleen, Heart and Lung Pictures]
[Dr. Vernillo] – Heres the spleen. Now, in organs that have a blood supply, one major artery,
okay? That goes into that organ, the coronary artery that goes into the heart, the splenic artery
thats in your spleen. One artery, if that gets blocked and you have coagulative necrosis and thus
infarction - the infarct is typically white. So this is an infarct that I’m pointing to right there. See
that? That’s dead. Thats deader than a doornail - Charles Dickens Christmas Carol and so was
Marley. And here we have the heart. It’s dead. Thats an infarction.Well look at the lung. What
color is that? We call that a hemorrhagic or red infarction. You see that classically in organs that
have a double blood supply. Again, you infarct a part of your pulmonary artery,it dies but the
bronchial artery tries to rescue you so it pumps blood into the area that is dead. Does it rescue
you? Sometimes it doesn’t and you wind up with an infarcted lung that looks red. That’s what
you’re seeing in the lower panel and that’s a red infarct. Alright.

[Slide 52] – [Coagulative Necrosis of Cardiac Muscle]
[Dr. Vernillo] – See how all this fun stuff comes together. It’s a real party. Now coagulative
necrosis of cardiac muscle. Lets take a look at that. What are these things up here? So you've had
an infarction. Now, little piece of information for you that you’ll readily understand because I
know you will. If you block blood from coming into the heart - if you form a thrombus in a
coronary artery and, all of a sudden, the heart is not getting blood, it’s not getting oxygen - What
is the first thing that’s likely to happen to the heart? You going to contract? Oh, come on… I
know you know. Why are you so shy on me? Is the heart going to contract if no blood is coming
in there? No. Because the fibers are saying “where’s my oxygen, where’s my nutrients. I’m not
happy”. So they get very testy. They get irritable. And they don’t contract efficiently. What do we
call that. Arrhythmia. The most common outcome following an MI is ventricular
arrhythmia.Remember that. Now if you die suddenly, and you haven't had a preexisting
infarction, will you see anything under a light microscope? Will the heart tissue look different?
Will it look the same? Will it show any changes? It will? You die suddenly, because why?- go
ahead, go with it. Because….Well there’s no hypertrophy, right -but there’s no time to do
anything. You die suddenly. You’re not going to see anything. One of my professors in grad
school had once said to me that there are four dimensions to pathology. There’s depth, width,
length and the dimension of time. Philosophical in some ways, but in actuality, that’s true. You
need a certain amount of time to pass before that heart actually undergoes those changes. If you
die suddenly, you’re not going to see anything. You’re not going to see squat. It’s going to look
like a normal heart muscle - unless you had a preexisting infarction at some point. But if you
didn’t, you’re not going to see anything. What are those things? I get a blockage in my coronary
artery now. I’m two to three days away from that and I’m still alive. What are those things?…
What is it?…Flea shit? What is this? Talk to me. Is the heart alive or dead? It’s an infarction boys
and girls. Is it alive or dead?
[Class] - Dead
[Dr. Vernillo] – Now if it’s dead, what does my immune system do with dead tissue?
[Class] - Get rid of it.
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
[Dr. Vernillo] –Absolutely, how does it get rid of it? Inflammation- perfect! What are those
things? 2-3 days later - those are PMN’s. How do you think they got there? They take a bus on
First Avenue? How’d they get there? Through the bloodstream..All this is is an inflammatory
response. You cut your finger and it swells, and 2 or 3 days later, you’re going to have PMN’s in
your finger. Those PMN’s are doing their job. What are they doing there? Cleaning things up is a
perfect answer. These are perfectly phagocytic cells. So are macrophages. They come in later if
you live long enough. But these PMNs are trying to digest those dead fibers. That’s what they’re
doing there. Is that a happy heart? No it’s not. You can die of an arrhythmia at any time. But that’s
an immune response to injury and it's no different than what happens in your finger if you cut it.
But when it happens in your heart, it isn’t such a bargain.

Ok, now. Take a look at these fibers here. Now, you notice how these fibers look? They’re kind of
packed together? Look at this one. You see this white area here? You got some white areas in
here. Whats happening to these fibers? Well they’re dying alright, but what else is happening to
them. That’s a good answer but what else is happening to them? Is this inflammation? What
happens with inflammation. Redness, yeah you have death of tissue. I mean, philosophically and
clinically speaking, immunity is at your own expense. When you try to heal from something, at
some extent, it’s injury to you. I mean, this is really the conflict of immunity generally. So if you
wind up with inflammation, right? You’re going to have redness. You remember the classic signs
of inflammation? Remember..redness heat, calor, dolor, and if you have lack of function - lacitude
functionalis (heads up,definitely not Latin: defectu functio) What is this? Swelling! Edema! And
when you cut your finger, what is you body trying to do? Your finger is swollen, can you move it
well? No because your body is saying “don’t move it stupid. I’m trying to heal you.” That’s its
response. To protect you. But the edema here is spreading those fibers farther apart. And that’s
causing disruption of these fibers which sets the stage for arrythmia. You’re never free of a threat
from this. Thats why you’re going to see these patients on anti-arrythmic drugs. You learning
pharmacology now? Soon you will.

[Slide 53] – [Septic Infarct]
[Dr. Vernillo] – Septic infarcts are infarcts caused by bacteria. You can get necrosis of tissue. The
tissue dies. Uhh, you inhale (?) back to when you were a sick person, you can get infarctions in
your lung if you get enough pneumonias or are immunologically compromised - your lung can
die from septic infections. What is the difference between bacteremia and sepsis? Absolutely
right. Sepsis is systemic. Bacteremia is- I’m getting bacteremia right now just gabbing to you all
over here. You brush your teeth, you get bacteremia. You know, you talk you get bacteremia but
you don’t die from sepsis. (I think he meant to say you do’t get sepsis) Sepsis is multi system
organ failure from infection. That’s sepsis. And you can see it in all different kinds of settings.
Sepsis in the lung can cause infarction. And the most common cause of death- parenthetically,
I’m going to be teaching you a lot about this next term in Leukemia - is sepsis. Thats the most
common reason people die in leukemia.

[Slide 54] – [Examples of Infarcts in Specific Locations]
[Dr. Vernillo] – Ok, Dr. Phelan put this slide together and I looked at her like “Dr. Phelan, why
the hell are you repeating infarction 25x there?” But she just got happy with this. But obviously,
whenever you block an artery, the heart, the lung, the intestine, the spleen - it’s an infarction.
You’re blockin' an artery. On the right side, when you have deep veinous thrombosis (DVT), why
do we call that a pulmonary infarct? That’s on the veinous side. Why are we calling it a
pulmonary infarct if an infarction is due to the blocking of an artery? Because what happens in
DVT? What are you blocking? The pulmonary artery. That’s infarction in the lung. Good.

[Slide 55] – [Myocardial Infarcts (MI/Myocardial Infarction/Heart Attack)]
[Dr. Vernillo] – Now, myocardial infarcts come in two flavors. Listen carefully, two flavors. In
the vast majority of cases, in the vast majority of cases, infarctions are transmural. They go
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
through the entire wall. From the endocardial surface facing the chamber, through the myocardial
surface and all the way up the epicardial surface. The coronary arteries enter the epicardial
surface and deliver blood to the heart. So transmural infarction is through the whole wall.
Through the whole wall. The subendocardial myocardial infarction is not throughout the whole
wall. It’s roughly 1/2 to 1/3 of it. Now that can happen, the subendocardial myocardial infarction,
right beneath the endocardium lining the chamber. When you have an infarction and you block
the coronary artery, where would death begin first in the wall? Would it begin at the
epicardial surface where the coronary arteries are putting oxygen in there. Or would it occur at
the endothelial surface beneath the ventricle? Farthest away from where the coronary arteries are
delivering the blood? Epicardial area or subendocardial area? Subendocardial area. So when
infarction start, they start in the subendocardial region of the myocardium, just beneath the
endothelium lining the chamber of the heart. There’s a small area of heart, however, that remains
viable even though it’s dying. There’s like a rim of tissue, or tiss-you if you will, where that area
is still viable. And that’s because there is still blood and oxygen in the chamber. And it passively
diffuses into the myocardium so it keeps a very thin rim of tissue alive. But the rest of it begins to
die and it progresses throughout the whole wall. So that in the majority of the cases they are
transmural. Now, subendothelial myocardial infarction can happen, for example, if blood flow is
resumed. Remember I spoke to you about the outcomes of thrombosis? You can lyse a thrombus.
Sometimes when you have a thrombus, if you give a person an aspirin, even if it is completely
occluded- the coronary artery, that aspirin can cause thrombolysis. It can lyse that thrombus and
restore blood flow. So if Uncle Joe is, you know, smoking himself into a frenzy and suddenly he
gets chest pain and he hits the floor - remember a myocardial infarction is known commonly as a
heart attack- you give Joe the aspirin, assuming he is conscious. You don’t go putting something
inside someones mouth when they’re unconscious because you’ll kill ‘em. But while he’s alive,
you give him aspirin. How do you give him the aspirin? Chew it and swallow it. “It’s up to you
Uncle Joe, whatever you want to do.” What do you want to do? You know this, come on. You
hear the sound of horses hooves outside your window, you know this is how I was taught, you
think the obvious. Think horses. Don’t think yak. Usually, the obvious answer works. What
would you give to Uncle Joe? Would you tell him to swallow it? Chew it, because you want to
disseminate the drug more rapidly into his system. Break it up. Ok.
So if you do that, that aspirin may actually cause that clot to break off. And then you start to get
blood flow going back into that myocardium. So even if some of it has died, you restore that
blood flow -the rest of the heart muscle might live and you end up with subendocardial MI. Is that
benign? No. You can still die from a subendocardial myocardial infarction. You don’t have to
have the whole wall dead. Have 1/3 or 1/2 of it dead - that’s enough to kill you but most of the
time they are transmural. One last point. Infarctions are left sided events in the heart because they
are arterial events. You’ve blocked off the coronary artery, and you wind up with a dead heart
muscle. right ventricular infarctions are typically rare. You don’t see them very often. You may
see infarctions on the right side 1,2,3% of the cases. And when they do exist, they are typically
from extension from the left. So if you have an infarction on the left, that dead tissue, that
schmutz, just goes over to the right side and the right side dies along with it. Most of the time,
right ventricular infarcts aren’t common unless they extend from the left. Ok.

[Slide 56] – [Pulmonary Infarcts]
[Dr. Vernillo] – Now we mentioned pulmonary infarcts and here we go. You have a medium sized
pulmonary artery. And you have bronchial arteries. Thats your dual circulation in the lung, we
mentioned. And if you block off that little branch, your colleague said -what was your name
again? Kate- So Katie said depending on where that embolus winds up, and students, I learn
names. Now I’m not good at learning everyones name because how many of you are there in a
class? 5000 maybe? So I can’t remember all of your names, but I do make it an effort to
remember as many as I can because sometimes I forget my own, but that’s ok. I usually make
more room for yours. And it’s always funny when I get in an elevator and I talk to a student and I
say “hey how ya’ doing Joe” or “Hey, how ya doing Alice?” and all of a sudden they go ~pats
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
around for ID~ and they’re looking for their badge. “I don't have my badge on. How the hell does
he know my name?” I remembered you. For better or for worse I remembered you. Now. The
pulmonary artery tries to rescue you. Ok. Sometimes it does, sometimes it doesn’t. If it doesn’t,
your heart, your lung dies, you get- your bronchial artery tries to rescue you and sometimes if it
cant rescue you when you have blockage in some branch of the pulmonary artery, the lung can die
and you get an infarction. Sometimes it doesn’t. Sometimes the bronchial circulation wins the

[Slide 57] – [Cerebral Infarcts]
[Dr. Vernillo] – We mentioned cerebral infarctions. Liquifactive necrosis. We call this a stroke,
we call this a cerbrovascular accident and the British call it…They call it stroke, but they also call
it something else. Apoplexy - A-P-O-P-L-E-X-Y. Stroke. Same thing. Now Look at that. Cerebral
infarcts. You've got no trouble understanding that an embolus from a mural thrombus in the heart
wall can break off, travel to the brain and give you a stroke 10% of the time. But we also
discussed a few moments ago - and this gentleman and I were discussing…your name? Bobby
was discussing “yeah, it can happen right here in your brain.” Because if you've got
atherosclerosis, you can form a thrombus right there on top of that plaque in your cerebral artery.
You don’t need an embolus or mural thrombus in your heart to make it over here. You can die
right here when you form an embolus - a thrombus on top of a plaque. And you block off the
artery and you get liquifactive necrosis of your brain. What happens to a blood vessel in either
case, be it an embolic event or thrombotic event? Either thromboembolic event or a thrombotic
event. What happens to that vessel. What does your body want to do to that clot, that
intravascular clot, that pathological clot? What does your body want to do with it? Get rid of it.
How does it get rid of it? Excuse me? Say. Inflammation. OK. What? You’re close. What makes
inflammation? Cells. What do they release? Oh. So now these enzymes are trying to- good -
they’re trying to digest that clot. Do they just digest the clot? No. What do they also digest? The
wall itself. What do you think happens to that wall? It gets weaker. It may dilate like a balloon.
We call that what? An aneurysm. Nice. Or, it may not dilate, but it just might outright rupture. By
the way, now you’ve got blood in your brain - thats called a hemorrhagic stroke.

Now why would ischemia cause a cerebral infarction? That’s not a thromboembolic event. I
mean…you can have plaques, yes. You can have narrowed arteries or stenosis, but why would
ischemia cause an infarction? What is ischemia, by definition? Not lack of blood. But hypo
perfusion of blood. Now if it’s really severe -ischemia- are you getting enough blood? Not much.
Are you getting enough nutrients? Not much. What can happen to some of those heart cells? They
die. So in severe ischemia, you can get infarction. In the absence of thrombus. Because if it’s that
severe, then you don’t have enough blood flow and that can kill the cells. Pretty nasty stuff. And
of course, you’ve learned in general pathology, it was mentioned again the liquifactive necrosis in
the brain. It’s a pretty awful disease.

[Slide 58] – [Circulatory Disorders]
[Dr. Vernillo] – What are the risk factors for cardiovascular disease? Smoking. Why smoking?
Chemical injury to the endothelium. The hypothesis is that injury to the endothelium initiates
atherosclerosis, and atherosclerotic plaques are thrombogenic. And why are they?
[Student] - Because they're rough and platelets adhere to them.
[Dr. Vernillo] – Nice. The body tries to get rid of them. There’s inflammation. There’s the release
of enzymes. The plaque cracks and fissures and platelets stick there. Why else? What other factor
would cause platelets to stick to the plaque?
[Student] — Cholesterol?
[Dr. Vernillo] – Good. Well, cholesterol makes up part of the plaque. We’re going to be talking
about that in greater detail at the conferences. Turbulence. Why turbulence? Right. You’ve got a
plaque that’s sitting out in the lumen now. Blood is flowing over that plaque. It’s like a rock in a
stream. So you now have blood that’s moving over that plaque and that flow is no longer nice
Transcribed by Charles Buchanan Date of the Lecture: 09/24/14
physiological laminar flow. It’s turbulent. It predisposes to thrombosis. Plaques are highly
thrombogenic. Ok.