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Pathology 2B HEART (DR.

GACASAN)

the heart, this comprises 1.4 of the total number of cells. But amazingly,
if you look at the volume, yung 25% na yun, occupies 90% of the volume
of the heart. So that is the cardiac myocytes.
Myocardium also has sarcomere, which is the functional
intracellular contractile unit of the heart. Contained substances are
myosin and actin responsible for the movement you have studied in
physiology. It also has troponin and tropomyosin. Troponin particularly
is released when there is damage to the myocardium kaya nirerequest
natin yan pagdating sa MI specifically Troponin I and Troponin T kasi
they are coming from myocytes. Ang CK-MB it is also requested but it is
not as specific as Troponin I and Troponin T. Pag mataas ang Troponin I
and T, alam mong puso yan. Pag mataas and CK-MB, you can have false
positive because of lysis of muscles somewhere else. But we still utilize
all of them.
The sarcomere gives the striated appearance of cardiac muscle
cells.
In comparison when it comes to the weight, hearts of males
are heavier than that of females. What we have right now in the values
are of Caucasians. Remember that our patients are mostly Asian or
Filipinos so you might see lighter organs. It doesn’t mean na abnormal
siya. It’s in our race that we have smaller organs compared to
Caucasians kaya pwede yung weight mas mababa kesa dun sa list na
meron tayo.
Generally, females have 250-300g weight of their heart. Males
have higher, 300-350g. But emotionally, weight of the heart varies from In the atrium, there are some atrial cells with specific atrial
males to females. But anatomic wise, males have heavier hearts. granules. Meron silang content na ANP which is concerned about certain
Regarding the thickness of the ventricles, there is a difference physiologic changes and processes like vasodilatation and the like. So
between the right and the left ventricle. We know that the left ventricle these are the roles of ANP.
has a thicker diameter as compared to the right ventricle. Why? Because
it supplies the systemic organs and it needs a thicker muscle to be able
to do that. So left ventricle is 1.3 to 1.5 cm and right ventricle is 0.3 to
0.5 cm. Why do we need to know this? To know if there is hypertrophy.
Kasi you will be given autopsy results, walang diagnosis yun, description
lang. So kung dinescribe jan, na the left ventricle is 3.5 cm then you
know that it is higher than normal then you are dealing with
hypertrophy. Your diagnosis will be left ventricular hypertrophy. We will
be looking at the different causes of hypertrophy later on.

It also has intercalated disks, which mediate functional


integration of cardiac myocytes.
It also has gap junctions that facilitates synchronous myocytes
contraction. Eto yung mga spaces wherein ions can pass through.
Exchange of ions from one cell to another passess through the gap
junction. So nagfafacilitate siya ng exchange ng ion so thereby metabolic
functions kasi nagkakaroon ng facilitation.

Component of the heart are endocardium, myocardium and


epicardium.
When regards to the myocardium, it is composed of cardiac
myocytes. If you look at the percentage of the total number of cells of

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Pathology 2B HEART (DR. GACASAN)

This is a picture of a normal myocardium. As you can see, it


has nuclei and striations. If you are looking underneath a microscope, Very important also is the blood supply. We have coronary
you must be able to demonstrate the presence of striation. The loss of arteries and epicardial arteries.
that as well as the loss of nuclei would mean that this muscle has These 3 are considered to be the major epicardial coronary
undergone coagulation necrosis. Meaning the cells are dead already. arteries supplying most of the different areas of the heart.
We have the Left Anterior Descending artery which supplies:
1. Apex
2. Anterior wall of LV
3. Anterior 2/3 of IV septum
Let Circumflex Artery
1. Lateral wall of LV
Right Coronary Artery
1. RV wall
2. Posterobasal wall of LV
rd
3. Posterior 3 of IV septum
Why is this important? Because you might be given clinical
case protocols. Example they did an echocardiography and it was found
out that the left anterior descending artery was occluded for about 80%,
or there is thrombus in the left circumflex artery. You can be asked
which part of the heart is or maybe affected. So nagcocorelate yan
dapat. We have to know these coronary arteries in order to locate what
Normally, we have conducting myocytes. These are the ones particular part can be affected and if you know that you will be able to
that regulate rate and rhythm. Kaya nga sa PD, pag physical do something about it.
examination, meron regular rate and regular rhythm. Meron din
irregular depending on your observation and when you do your
auscultation on the heart of patients.
The different myocytes that are responsible for that are the
following. The SA node, AV Node, Bundle of His which branches out to
right and left bundle branches.
There is also participation of the autonomic nervous system.
This one controls rate of firing of the SA node that will initiate or trigger
the start of the cardiac cycle

Look at this normal coronary artery, it is clean looking meaning


without atherosclerosis, obstruction and thrombus. Also there is no
calcification on the wall. What is the disease that has medial calcfiic
condition you have learned in patho A? Monckeberg sclerosis which is
not shown in this picture.

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Pathology 2B HEART (DR. GACASAN)

There are 3 types of pathologic changes in the valves. It can be


damage to collagen that weakens the leaflets so meron kang
insufficiency. May insufficient valve, regurgitant valve and weak valve
because of the problem in collagen.
Yung number 2 and 3, tumitigas naman ito. There is nodular
calcification or there can be fibrotic thickening. Calcification means
Now we have valves which maintain unidirectional blood flow. there is deposits of calcium. Fibrosis can be secondary to injury that has
We have 2 semilunar and 2 atrioventricular valves. Which of these are happened before and lead to fibrosis. In these 2 conditions, you have
found on the left side and which are on the right side? stenotic valves.
Aortic  Left
Pulmonic  Right
Mitral  Left
Tricuspid  Right

These are the components of the valves. We have fibrosa,


spongiosa, ventricularis/atrialis and endothelial covering. So yung inner
lining ng heart natin ay endothelium just like blood vessels. Let’s review the normal blood flow. This is supposedly a one-
way traffic. It is not 2-way traffic and it should be closed. If you breath
in, oxygen comes into your lungs and there’s gonna be blood gas
exchange. At the level of alveolar wall, the oxygen will be taken out by
the RBCs. This blood coming from the lungs will be taken into the left
side of the heart, which is the left atrium. It will pass to the mitral valve
going into the left ventricle. From the left ventricle, it will pass through
the aortic valve, aorta and then distributed to the different systemic
organs to deliver nutrients and oxygen. These things will be utilized by
the cells and eventually you will have products of metabolism like
carbon dioxide. The blood will be collected again and will be taken back
into the heart but this time on the right side. From the systemic organs,
it will be deposited into the right atrium passes through the tricuspid
valve going to the right ventricle. It will pass through the pulmonic valve,
pulmonic artery and goes for another cycle of oxygenation in the lungs.
So remember that this is a closed system and a one-way
traffic. Any distraction in any place, there’s gonna be a problem and will
We look at the normal heart valves like aortic and tricuspid affect the heart.
valves. Tricuspid valve has papillary muscles and chordae tendinae.

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Pathology 2B HEART (DR. GACASAN)

Regurgitant flow, what do we mean by this? If you have


incompetent valve for example. Supposedly, during diastole, it is the
time to fill up the heart with blood kasi during diastole, nagrerelax then
papasok ang blood. During systole, the moment when the ventricle
contracts, the blood is extruded out of the heart. But if you have
regurgitant or insufficient tricuspid or mitral valve for example, during
systole, bumabalik yung blood sa atrium. According to physiology,
nagshushutoff dapat yung mga valves during systole or hindi dapat
bumabalik ang blood sa atrium. If the valve is insufficient, malambot
siya. It’s like a swing door, when you pass through it, diba pabalik balik
siya ganun pag insufficient. Pag matigas ang valve, it is like a door that
has not been opened for 20 years, mahirap buksan. This time, in
regurgitant flow, it is like a swing door. During Diastole, the valve will
Before we go into the different pathology of the heart, let’s open up, there will be filling up of blood. During systole, dapat extrude
out ang blood and magcclose or shut off ang AV valve so that no blood
look into what’s gonna happen into your heart when you get older.
will be going to the atrium. But what happens in regurgitant flow?
There is increase in epicardial fat and reduced in left
ventricular cavity. Why is there decreased in left ventricular cavity in During systole, certain amount of blood goes back to the atrium and
older individual? If you get older, there is deposition of atherosclerotic certain amount will also go out. During diastole, more blood is being
plaque in the aorta adding to the workload of the heart. There will be pushed to the ventricle because there is remaining blood and then
concentric hypertrophy or inward hypertrophy because of the increase another batch will come in. The result of this will be dilated
hypertrophy.
pressure that it has to overcome.
Next would be shunted flow. Dito pumapasok ngayun yung
There are also calcifications and Lambl excrescences which are
small masses found along the closure line of the valves because of mga congenital anomalies. We have VSD for example. There is a hole in
organized thrombi that are deposited in the valves. the heart. Parents told you that “may butas po ang puso ng anak ko”
You also expect to have fewer myocytes, collagenized, amyloid that was seen during examination. Where is the hole? In between the
and lipofuschin deposition. Lipofuschin pigment is a product of lipid right and left ventricle, right and left atrium or it can bebetween the
pulmonary artery and aorta, or it can be combination of all these things
metabolism that’s why in older individual you have more of this.
Constant exposure to lipids later on you will have metabolic processes together. So there is shunting of flow. Pwedeng left to right or right to
and brown pigments will be produced and they are deposited not just in left. Supposedly, the one on the left is oxygenated blood and on the
the heart but in other organs as well. There is what we call brown right is the unoxygenated blood. When we say left to right shunt
atrophy wherein the heart is small and it has a lot of lipofuschin pigment binabawasan mo ang oxygenated blood kasi sinasama mo siya sa
deposited in it. unoxygenated. When we say right to left, cinocombine mo yung
oxygenated sa unoxygenated. Magkasama ang supply, oxygen and waste
product.
Next are disorders of cardiac conduction. We have mentioned
conducting myocytes. If there is a problem in the SA node or in the right
and left bundle branches, what will happen? Flow of electrical impulse in
the heart is not coordinated so that’s the time that you will have
arrhythmia, ventricular tachycardia and all these changes or problems in
the movement of the heart.
Lastly, disruption of continuity of the circulatory system.
Example stab wound and abdominal aorta was hit. There is a hole and
blood comes out of the abdominal cavity. That is a disruption in the
continuity of the circulatory system. It was mentioned a while ago that
heart has a closed system and it is not going out. But any disruption in
Now we go to different mechanisms of heart impairment. First that closed system could affect. The function of the heart.
is pump failure. There is poor contractile function here or there is
inability to relax. It’s either nahihirapan siyang magcontract or masyado
siyang matigas or makapal that there is a problem in the relaxation.
Second is obstruction to flow. What can cause the
obstruction? There can be presence of thrombus anywhere else or
emboli, tumor, sclerosis, atherosclerotic etc. Pwede ring outside that
could encroach on the abdominal aorta for example, that is a form of
obstruction.

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Pathology 2B HEART (DR. GACASAN)

because when we say systolic, contraction. When we say diastolic, we


refer to filling up

Now let’s look into the heart failure. Heart failure or rather Due to increased mechanical work, we have pressure and
wise known as Congestive Heart Failure is the inability to pump blood in volume overload. When we say pressure overload there is an increase in
relation to the need of the body. Hindi kayang masupplyan and nag fail pressure that has to be overcome by the heart. Example, when you were
na ang heart. There is a vast need but the heart could not supply it and a kid, you don’t have atherosclerosis yet depending on the lifestyle as
that is a failing heart. Before a heart fails, lalaki muna yan or what we well as genetics. Some of us will have bigger atheroma and that is a form
call Hypertrophy. of obstruction. That is something that needs to be overcome by this
These are the mechanisms that you have studied in physiology particular side of the heart in order to deliver enough supply to the
that maintains arterial pressure and perfusion. We have Frank-starling different organs system. Since may bara, what does a particular part of
law. This is concerned about the enhanced functional activity of the the heart should do? It has work harder to be able to overcome that
sarcomere. The more you stretch the muscle, the harder would be the pressure. By doing that, there will be hypertrophy or increase in the cell
contraction . So if you fill up the heart (ventricle) with more blood, size because there is also an increase in cellular organelles. There is
malakas din ang palo niya. But there is a limit to that. Frank-starling says, inward hypertrophy, there is smaller caliber of the ventricle. If you look
like a rubber band, if you stretch it the first time, bitawan mo, malakas at the top view, there is concentric hypertrophy, lumiliit ang chamber
ang pitik. The second time, you stretch it, medyo malakas padin. Pag because of the thickened wall of the ventricle. What are the other
nistretch mo pa ng todong todo, medyo humihina na. Pag nistretch mo causes? Systemic hypertension due to some other problems. Same
pa ng todo, its either mapigtas or lupaypay na siya. And that happens in thing will happen that there will be a pressure overload and eventually
the heart also. You stretch it the first time, there will be adaptation concentric hypertrophy.
which is hypertrophy and the force will be greater. But if you keep on On the other hand, if you are dealing with dilated hypertrophy
stressing that, it’s gonna fail and that’s the time that you will have heart or volume overload. It was mentioned a while ago that if you have
failure. regurgitant flow or severely stenotic valve for example na hindi na siya
Next we have myocardial structural changes but of course, makabalik it is the same process that will happen that during diastole,
dadami syempre ang mitochondria to adapt to the changes and the blood will flow to the ventricles and during systole, some blood will go
other cellular organelles. to the atrium. Repeated cycle of that, what will happen? There will be
Activation of neurohumoral systems like norepinephrine, dilatation because you are filling it up with more and more blood. But
RAAS, ANP (Atrial Natriuretic Peptide). dilated and concentric are both hypertrophy. In concentric hypertrophy,
lumiit ang chamber while in dilated hypertrophy, lumaki ang chamber.
Both the these hypertrophy can go into failure. If you look at these
microscopically, you will see hypertrophic cardiac myocytes. They may
differ grossly but microscopically, they will look the same that they have
bigger myocytes and a undergo failure later on.
So there is increase protein synthesis, sarcomere and
mitochondria. Also there is enlarged nuclei that’s why you have
hypertrophy.

Heart failure can result from systolic dysfunction where in


there is progressive deterioration of myocardial contractile function
Why does hypertrophy leads to failure? Because cells are
becoming enlarged, so the need also increases. The heart now cannot

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Pathology 2B HEART (DR. GACASAN)

cope because the capillaries are not increased so there is And there are extracardiac effects. So it is not only the heart
decompensation. Heart is vulnerable to decompensation and there is that has changes, also other organs. We have 3 organ system that are
trouble of failure. affected in a left-sided heart failure (Lungs, Kidneys and Brain).
Remember this to compare left side from the right side or from a
biventricular which is a combination of the two. You should know the
different manifestations that are associated with left, right or
biventricular heart failure.

The picture above is an example of concentric hypertrophy.


Makapal masyado ang kanyang ventricle. How will you say that it is For the lungs, it is heavy and wet. When we say edema, it is
thick? You should know the normal thickness. left sided. Effusion is for the right-sided. If you see both, then you are
dealing with a biventricular failure.
So we have here, transudate, widened alveolar septa, edema
in the alveolar spaces and presence of the heart failure cells. Heart
failure cells are macrophages containing hemosiderin. They do not come
from the heart, they are there because of the cardiac problem. They are
just called heart failure cells because they are related to heart failure but
these are resident macrophages in the lungs that has engulfed
hemosiderin because of the breakdown of RBCs.
Clinical manifestations. You have dyspneic patients or
nahihirapan huminga or difficulty of breathing. Orthopnea or needs 2 to
These are the causes of left-sided heart failure. 3 pillows or sometimes sitting down or cannot sleep or lying down flat
on bed. Paroxysmal nocturnal dysnea or biglang nagigising ang patient
kasi feeling niya nalulunod siya, that can be a sign of left-sided heart
failure.

What do we see in the heart? It depends on the disease


process. Most of the time, dilated hypertrophy is observed.

So in the kidneys, there is decreased renal perfusion that will


stimulate the RAAS and cause retention of salt and water.
Pre-renal azotemia is the one that contributes to pulmonary
edema. Azotemia differs from uremia. Both of them have increase in

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Pathology 2B HEART (DR. GACASAN)

BUN and creatinine. But in azotemia, it doesn’t have clinical


manifestations while uremia, it has.

Changes again depends on the cause. Hypertrophy and


dilatation of right atrium and ventricle can be observed here.

In the brain, there is cerebral hypoxia that will lead to hypoxic


encephalopathy. You will have irritable patients, they have loss of
attention span, restlessness, stupor or you might have a patient with
coma

As compared with the left sided, more tissues are affected


here because in extracardia effects, we have the involvement of the liver
and portal system, kidneys, brain, pleural and pericardial spaces and
subcutaneous tissue. Now it is not the lung per se that is affected but
the spaces. That’s what we are talking about a while ago that pag
effusion right sided, pag edema, left sided.
Left-sided heart failure is clinically divided into systolic and
diastolic failure.

Let’s now go to the right-sided heart failure. Commonly it is a In the liver and portal system, hepatosplenomgaly can be
consequence of a left-sided heart failure. Pag ganyan ang scenario, observed. So when you palpate patients, liver and spleen is enlarged.
biventricular na yan because the primary problem is left-sided and then
eventually right-sided heart failure. But there are times that you have
pure right sided heart failure, meaning there’s no problem with the
heart to begin with. There is chronic severe pulmonary hypertension or
chronic cor pulmonale which is the only reason why there will be a pure
right sided heart failure.

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Pathology 2B HEART (DR. GACASAN)

In the kidneys, this time, the fluid retention is responsible for


the peripheral edema or bipedal edema or pitting edema. Pitting edema
can be grade 1, grade 2 etc. They can also have Anasarca which is a
generalized edema. And lastly they also have azotemia. Now let’s go to the congenital heart diseases. There are 3
general classifications of congenital heart disease:
1. Left to right
2. Right to left
3. Coarctation of the aorta
Why is there congenital heart diseases? Because of faulty
th
embryogenesis. 3th to 8 week is important because that’s the time
that the heart is being born. So any teratogens, infections that could
affect the mother can infect the embryo that is growing there and have
an effect on the heart.
Congenital heart disease is the most common heart disease in
children and the most common among these is Ventricular Septal Defect
(VSD) wherein there is a hole between the right and the left ventricle.
For the brain, it is the same with the left-sided HF. But with
regards to the spaces, we have effusions. In the lungs, you can have
compression atelectasis because of the effusion.

For the subcutaneous tissue, as mentioned, there is edema or


anasarca.
What are the etiologic agents, scenario as well as
pathogenesis? We have genetic abnormalities. Also genetic factors like
in Trisomy 21. We have learned in Patho 2A that Trisomy 21 is
associated with congenital anomalies.
Environmental factors as we have mentioned we have rubella
This refers to the biventricular failure that we have mentioned infection and teratogens.
earlier. And that’s it for the heart failure. When it comes to nutritional factors, obstetricians are very
mindful about this giving all the necessary nutritional support to the
mother.
Lastly, maternal factors (age). You have learned that Down
Syndrome (trisomy 21) is associated with increased maternal age and
thereby it is also associated with congenital heart disease.

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Pathology 2B HEART (DR. GACASAN)

there is decompensation, the initially left to right will become right to


left shunt. So that’s the time that you will have cyanosis because pag
nagkaroon na ng reversal of shunt, dun palang magkakaroon ng
cyanosis. Again, Eisenmenger syndrome, initially blood from the left side
to the right then dilate ng dilate hanggang sa magkaroon ng right
ventricular hypertrophy and then eventually magffailure then there will
be reversal of shunt (right to left)

These are the possible affected genes in congenital heart


diseases. You just go through that and we will not go into the details of
knowing all these.

These are the different congenital heart diseases under left to


right shunt. All of Ds are left to right shunt plus Patent Foramen Ovale.

These are the major classifications of congenital heart disease.

In ASD, there is an abnormal opening in the interatrial septum.


This is asymptomatic until adulthood and there are 3 types. Most
common is the secundum.

Let’s go now to the first classification, the left to right shunt. It


is also known as Late Cyanotic Heart Disease. There is no cyanosis to
begin with unless there is increase in demand. We have mentioned
earlier that in left to right shunt, babawasan lang yung oxygenated
blood. So yung dinidistribute mo, kulang. When the demand do not
increase, the body can cope or the heart can cope. But if there is
increase in demand, that’s the time that manifestations will come in. For
example, we have a case 17 year old, male. When he was young, it was
not observed that he has a problem pertaining to the heart. But when
he became teenager, he started playing basketball so there was an
increase in demand or madali na siya mapagod or worse, mahihimatay.
That’s because there is already increase in demand and unknowingly, he
has left to right shunt like in ASD (Atrial Septal Defect). It’s good if it was
found out early because if not, his heart can go into failure without the
benefit of being seen. So that’s late cyanotic heart disease. So these table shows the location of different ASD and their
There is such a thing as Eisenmenger syndrome or complex. associated anomalies. Congenital heart anomaly can be a single anomaly
This is like a reversal of shunt. Parang end-point ng left to right. When

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Pathology 2B HEART (DR. GACASAN)

or a combination of congenital heart anomalies depending on the


defect.

This picture shows ASD. You can see that there’s a hole in the
This VSD is the second type of left to right shunt. There is a
atrium.
hole in the interventricular septum. There is incomplete closure of
interventricular septum. This is the most common congenital cardiac
anomaly and most associated with other defects.

Later on, if ASD is not corrected, you can have reversal of


shunt of Eisenmenger syndrome.

VSD also has 3 types. Membranous is the most common.

ASD is usually asymptomatic until the age of 30, with murmur.


Surgical closure can be done and with low mortality. According to
cardiovascular surgeons, this is the most commonly repaired congenital They don’t repair VSDs at once because smaller VSDs can close
heart anomaly. spontaneously. Bigger VSDs are the ones being repaired.

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Pathology 2B HEART (DR. GACASAN)

PDA is the connection between the pulmonary artery and the This is an example of AVSD. There are 2 separate holes in the
aorta. During the time that you are inside your mother’s womb, it was atrium and ventricle but other cases you can have 1 big hole.
open. When you are born, it will spontaneously close normally. But
there are times that it stays open, so that is now the Patent Ductus
Arteriosus. But there are times that we intentionally keep it open
because there’s a need for the child to have that open if he or she has
other congenital anomalies.

PDA has machinery-like murmur. If you want to keep it open,


you can give Prostaglandin E to preserve the patency. Then we have PFO. There’s a small hole from an open hole in
the atrial septum at the oval fossa. Maliit lang siya compared to ASD.

Next is AVSD. This is a combination of atrioventricular septal


defect. It can be separate or one big hole nvolving the atrium and the Then we have the right to left shunts. This is called Cyanotic
ventricle. There are 2 types and greater than 1/3 is associated with Congenital Heart Disease, with cyanosis and paradoxical embolism
Down Syndrome. wherein emboli from the peripheral veins do not pass through the lungs
and go to the systemic circulation. Diba pag galling sa peripheral system,
ang balik niyan sa right side of the heart tapos pupunta dapat sa lungs?
This time, since you have connection between the right and left side of

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Pathology 2B HEART (DR. GACASAN)

the heart, there’s gonna be a paradoxical embolism. Natatapos siya to


the left side then it will be distributed to the different organ system and
that is paradoxical embolism.

The consequence depend on the severity of the subpulmonic


stenosis. If mild, they call it Pink Tetralogy. If severe, classic tetralogy.
Boot-shaped heart on x-ray and they repair this surgically.

All those with Ts are right to left shunts. Diba dun sa left to
right, all those with D, eto naman sa right to left, lahat ng nagsstart sa T.
Tetralogy of fallot is the most common. We also have problematic
transposition of great arteries. The rest are the uncommon ones.

TOF. As the name imply, there are 4 components. There is One problematic case would be Transposition of Great
embryological anterosuperior displacement of infundibular septum. Arteries because there is switching of where the aorta arises as well as
the pulmonary artery. There is abnormal formation of truncal and
aortopulmonary septa. This is incompatible with life without shunt
because we said a while ago that the circulatory system is a one-way
traffic.

There are 4 components:


1. VSD
2. Overriding of the Aorta on the VSD
3. Pulmonic Stenosis
- Which is the reason for the classification of mild
to severe TOF
- It determines the severity of TOF
4. Right Ventricular Hypertrophy.
If with PDA  PENTALOGY OF FALLOT Normally, the aorta should arise from the left ventricle and the
pulmonic artery should arise from the right ventricle. What happens in
the TOG is the aorta arises from the right ventricle and the pulmonary
artery arises from the left ventricle. What will happen is the blood
coming from the lungs will go to the left side which is the left atrium
then left ventricle then to the pulmonary trunk with is connected to the
lungs so puro oxygenated blood ang nanjan.

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Pathology 2B HEART (DR. GACASAN)

From the systemic organs, blood will go to the right side of the
heart meaning to the right atrium then right ventricle then aorta which
is connected to the systemic circulation so puro unoxygenated naman
yung andito.
In short, nagging two-way traffic na siya. They are not
connected with each other. Will it help the patient to survive? NO! The
patient will die. So there is a need for shunt because in the absence of
that, if the baby will be born, he or she will be dead.

Tricuspid atresia. So atretic meaning may occlusion na yan.

Fortunately, most of them will have VSD, ASD, PDA. VSD and
ASD are stable shunt while PDA is unstable shunt. Kasi mas malaki ang
butas ng VSD and ASD compared sa PDA kaya mas stable siya.
Most patients die within first months so you must do
reparative operation here but the problem is you cannot do it right away
because you have a very young baby. You need to build up the nutrition
and if you have congenital anomaly, expect that there are other TAPVC. There is no pulmonary vein directly connected to left
anomalies or genetic problems. So most of the time, a lot of these atrium.
babies born without being corrected.

This will not be discussed. Just read this on the book. The third classification is obstructive congenital anomalies. We
have 3 here: Coarctation of aorta, pulmonary stenosis & atresia and
aortic stenosis & atresia.

In COA, there is narrowing or constriction in the aorta. This is


more common in males than in females and frequently associated with

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Pathology 2B HEART (DR. GACASAN)

Turner Syndrome. What is Turner Syndrome? Is it found in males or in


females? In females. There is webbing of the neck and absence of
secondary sexual characteristics.
There are 2 types of COA. There is infantile and there is adult.
In infantile, there is tubular hypoplasia of aortic arch with PDA. The adult
type is without PDA.

Stenosis and atresia. These are obstructive because matigas


ang valve or walang butas.

How does it look schematically? There is narrowing of the


aorta. Here, the diameter of the aorta is smaller. If there will be a
hypertrophy, what kind is it? Pressure overload hypertrophy.
What do they do with this? Cut it off and repair them.

Aortic stenosis and atresia. This one is associated with


hypoplastic left heart syndrome.

If with PDA, lower half of the body with cyanosis. If without


PDA there is hypertension on the upper extremities, weak pulse & low These are the clinical manifestations. So those are the
BP on the lower extremities and notchings or erosions in the ribs congenital heart diseases which are common in children.
undersurfaces.

Clinically, you will get to hear systolic murmur, thrill on Now let’s go to the common problems in adult  ISCHEMIC
palpation, cardiomegaly will be observed on x-ray or echocardiography. HEART DISEASE.
Surgical resection is a form of management in this patient.

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Pathology 2B HEART (DR. GACASAN)

Ischemic heart disease or coronary heart disease or coronary they are still symptomatic at rest. Higher risk lang yung mga maliliit na
artery disease. This is secondary to ischemia. plaques to develop thrombosis.
Ischemia is most commonly due to atherosclerotic coronary
arterial obstruction.

There is acute plaque change so there is a risk of developing


Myocardial Infarction (MI). We say that if plaque is big, di siya madali
natitinag kasi matigas na siya. If flow if blood is greater, it is not easily
There are 4 syndromes here. Angina pectoris which has 3 dislodged.
types, myocardial infarction, chronic IHD with heart failure associated But if pressure rises and plaque was dislodged or disrupted, in
with previous MI or other cardiac disease and then we have sudden patho 2A, we said that this is a form of injury. With injury, inflammation
cardiac death. ensues. So what will happen? Influx of white blood cells. On the side of
hemodynamics process, endothelial cell is disrupted and this will
stimulate coagulation process. Initially platelet plug formation or
primary hemostatic plug so you will form thrombus. It can be quite big
that it can occlude the whole thing. So coagulation process and
inflammatory process happens and also coronary thrombosis.
In small arteries, arterioles and capillaries, what happens?
Initial is vasoconstriction. So you have a thrombus, there is
vasoconstriction and that one is occluded. In 20-40 minutes you have to
recanalize that or else, your patient will have coagulation necrosis and
Let’s talk first of ischemic heart diseases. There is insufficient that is irreversible. When you get to see a patient in the emergency
coronary perfusion relative to myocardial demand. This is due to the room, you must be able to recognize if you are dealing with an intending
following: infarction or crescendo angina. What will you do? ECG, request for
1. Atherosclerosis Troponin I and CK-MB. In ECG you will see changes that will give you a
2. Variable degrees of acute atheromatous plaque change clue that you are dealing with a cardiac problem. If that happens, give
3. Thrombosis antithrombolytic agent to get rid of that then recanalize that to
4. Vasospasm reperfuse the area of injury.

Angina Pectoris is a symptom complex of Ischemic Heart


If 75% of more ang obstruction, there is symptoms that is Disease. There is recurrent substernal or precordial discomfort and this
exercise induced. So if there is activity, manifestations will be seen. If is caused by transient ischemia (15 secs to 15 mins). Mabilis lang yan.
dormant or walang ginagawa, no manifestations. Pag nagpahinga ang patient and okay siya, it is stable.
If obstruction is 90%, even at rest, there is already
manifestations.
One lecturer mentioned that those smaller plaques are more
at risk of being disrupted so more common to develop thrombosis
because they are easily dislodged. Those bigger plaques are harder but

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Pathology 2B HEART (DR. GACASAN)

We have here the 3 patterns. Stable (typical), Prinzmetal


(variant) and Unstable or the Premyocardial (Crescendo)

Unstable or Crescendo Angina. There is progressively


increasing frequency. This occurs at rest or even with lower levels of
physical activity. This is more prolonged and considered as preinfarction
angina. You need to be quick because with this one your cells are not yet
necrotic. Pag lumampas ka, MI na yun.

This is what we call heart attack. Can occur in any age so this is
not exclusive to older people because even young patient can have this.
Stable of Typical is the most common. There is imbalance in Example are call center agents with different lifestyle can go to MI.
coronary perfusion secondary to atherosclerosis relative to myocardial Women are protected during reproductive age because they have
demand. This can be relieved by rest or nitroglycerin. The cause of this is estrogen. But the moment that women menopaused, they are now the
atherosclerosis and there will be a problem with the balance of coronary same with men that are at risk.
perfusion.

The typical cause of MI is coronary artery occlusion. There are


also plaque change, thrombi formation, vasospasm, and occlusion of the
Prinzmetal or Variant Angina. This is uncommon. The cause of lumen. Those are the usual causes (about 90%).
this is due to coronary spasm. Atherosclerosis was not a cause here and
mas nakakatakot to. They give lifetime vasodilators (nitroglycerin, Ca
channel blockers) to this patient to relieve spasm.
This one occurs at rest and tha change in ECG is elevated ST
segment and there is transmural ischemia.

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Pathology 2B HEART (DR. GACASAN)

If subendocardial, non-ST elevation infarcts. It involved the


But 10% of the cases, there is no typical pathology. What are inner 1/3 to ½ of ventricular wall.
the causes of MI here? Vasospasm. Example is emotional excitement. Sa
sobrang tuwa, walang medication tapos nagspasm, ayun nag MI. O kaya
sobrang nalungkot tapos sobrang down, biglang sumikip ang dibdib ayun
nag MI. So pag alam mong ganun, give lifetime vasodilators.
Next cause is emboli coming from other parts of the body. And
lastly ischemia without detectable coronary atherosclerosis and
thrombosis.

Microscopically, there is coagulation necrosis. These are


frequencies of site of infarction depende dun sa sinusupplyan. Most
common is LAD (Left Anterior Descending Artery) (40-50%) which
supplies apex, anterior and part of the septum. Next is RCA (Right
Coronary Artery) and LCX (Left Circumflex Artery)

Vital time is 20 – 40 minutes. If you go beyond that, it will be


irreversible. The irreversible injury occurs first in the subendocardial
region and it can be transmural later on.

Most are transmural meaning it involves full or near full


thickness of ventricular wall and there is ST elevation infarcts.

Grossly not apparent if <12 hours. Pag may namatay na


patient and you were thinking of MI, di mo pa siya makikita grossly. If
you immerse the heart in triphenyltetrazolium chloride (TTCT), it will
stain the uninfarcted with brick red and pale the infarcted area.
The typical coagulative necrosis will be seen in 6-12 hours.
Wavy fibers at the periphery can be seen initially which is an indication
of an early myocardial infarction.

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Pathology 2B HEART (DR. GACASAN)

The infarct can extend beyond the original borders and that is
what you call Extension.

So here you can see the area of infarction. You can see there
hemorrhage on the surrounding area. Yung nasa baba mas matagal na
yan because you have scar formation already.

Reperfusion can be done by doing the following. Thrombolysis.


Sa ER aspect palang bibigay mo na yan. Pag need din ng angioplasty at
pwede pa, it can be done. Pag di na kaya ng angioplasty, you do you
bypass or CABG.

Microscopically, initially pwedeng hemorrhage lang which can


be secondary to myocardial infarction. And then you will have acute
inflammatory infiltration wherein you have neutrophils and that’s the
time that you will also see coagulation necrosis and loss of nuclei, loss of This is a picture of a heart that has undergone CABG but
striation but you can still see the outline of cardiac muscle cells. eventually succumb to death.

Macrophage will replace the neutrophils in 3-7 days. In 1-2


weeks’ time, there is granulation tissue formation. There is formation of Other terms we have reperfusion injury. Nareperfuse mo but
new blood vessels, proliferation of collagen and fibroblasts. Maximum in eventually it can create another problem.
the first 2 weeks. Scarring in 6 weeks’ time.

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Pathology 2B HEART (DR. GACASAN)

Stunned myocardium is a reversible cardiac failure recovering


after several days.
Hibernating myocardium has lowered metabolism and
function.

We should know these clinical features. th


I don’t think that this is still in your book (Robbins 8 edition).
1. Rapid weak pulse
C-reactive protein. This is an acute phase reactant. This can predict the
2. Diaphoretic
risk of MI. If >3 mg/L, patient is in highest risk. If 1-3 mg/L, moderate
- Cold clammy perspiration
risk.
3. Dyspnea
Don’t forget ECG. Others are done by higher centers but ECG
There are certain patients that are asymptomatic about 10-
should be a basic one.
15% of them especially elderly and diabetic patients.

Complication of MI. Arrhythmias is within 24 hours, common


scenario. Others can be chronic or after a while.
Laboratory wise, Troponin I and Troponin T are the most
sensitive and specific. CK-MB is specific but not that sensitive as
Troponin I and T. Both of them will be increasing in 2-4 hours. CK-MB
peaks earlier at 24 hours while Troponin I and T peaks at 48 hours. And
lastly, Troponin I and T stays in the system longer than CK-MB.
But why do we need to request both of them? Pwede yan for
initial diagnosis and following up your patient. Example Na-ICU ang
patient mo. After 3 days gusto mo malaman kung okay na siya or kung
th
may new MI evolving. I will request for CK-MB on the 4 day kasi kung
Ruptures can happen if large area is affected. You can have
mataas padin ang CK-MB, may bagong MI na madidiscover jan. Pag
rupture of the myocardium.
bumaba na yan, you expect Troponin I to be still elevated in 7-10 days,
th th
no problem with that. But if CK-MB mo ay mataas padin on the 4 – 5
day, most probably may bago ka jan and you have to monitor your
patient closely. Another example, pumunta sayo ang patient after a
th
week or pang 8 day kasi may naramdaman siyang sakit sa dibdib nung
nakaraan pero di niya pinansin then ngayung nagkaoras siya, pumunta
siya sayo. Tapos nakita mo na Troponin I is elevated and CK-MB is not.
So meaning, nagkaroon siya ng MI during that time so you have to
manage your patient.

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Pathology 2B HEART (DR. GACASAN)

The heart is enlarged and heavy. There is atherosclerosis.


Microscopically, you see hypertrophy, subendocardial vacuoles and
scars.

This is an example of rupture. Leading to a sudden gush of


blood out into the pericardium leading to cardiac tamponade that can
kill a patient.
For chronic stage, we have aneurysm. There is dilatation in the
wall of the myocardium.

Sudden Cardiac Death on the other hand is secondary to lethal


arrhythmia. Most common trigger is acute myocardial ischemia. If you
do autopsy in these cases, there is marked coronary atherosclerosis in 1
or more of the major vessels. This is associated with heritable
The risk of specific post infarct complication depends on the conditions.
following.

There is such a thing as ventricular remodeling wherein the


non-infarcted region undergoes hypertrophy and dilatation. Parang
nagaadapt siya.

Now we have Chronic Ischemic Heart Disease often in elderly.


There is a progressive heart failure here. This has previous MI attacks or
Anginal attacks which are on and off.

Jomero M. Cleofe RN Page 20


Pathology 2B HEART (DR. GACASAN)

With regards to pulmonary hypertensive heart disease it can


be acute or chronic. Earlier we talked about chronic severe pulmonary
hypertension, that is the chronic cor pulmonale.
Acute cor pulmonale is when there is a massive pulmonary
embolism. You will have dilated right ventricular wall without
hypertrophy.

Hypertensive heart disease. There are 2 types: Systemic and


pulmonary. In systemic, the left side is affected. In pulmonary, the right
sided part is affected.

With regards to systemic, there is left ventricular hypertrophy


(Concentric) and hypertension. These 2 are your criteria that need to be
fulfilled to say that this is Systemic Hypertensive Heart Disease.

In pulmonary hypertensive heart disease, you have core


pulmonale, right ventricular hypertrophy, dilatation and there is a
potential failure here.

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Pathology 2B HEART (DR. GACASAN)

We can also have mitral stenosis and insufficiency. Mitral


Valvular heart disease, we only have 2. It can either be stenosis is most commonly associated with RHD. In RHD, the most
stenotic or insufficient. common affected is the mitral valve and next would be the aortic valve.
Stenotic meaning matigas. There is a failure of the valve to
open completely. Or it can be very stenotic that it will not close
anymore.
Insufficiency. There is regurgitation or incompetent valve.
There is failure of the valve to close completely. This will allow reversed
flow. Remember that hindi lang dito ang reversed flow, it can also
happen in severe stenosis wherein nagshorten na yung papillary muscles
mo na hindi na siya makapagclose which can happen in Chronic
Rheumatic Heart Disease

Also we have aortic stenosis or insufficiency.

We go now to rheumatic heart disease. Rheumatic fever is the


acute phase. This is immune mediated, multi-systemic and its preceding
event is Group A Streptococcal Pharyngitis but it is not the one causing
problem in the heart, it is the immune reaction to this condition that’s
causing it.

This is calcific aortic stenosis. Masyadong matigas na hindi na


siya mabuksan.

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Pathology 2B HEART (DR. GACASAN)

There are antibodies directed against M proteins of Strep. that


cross react with self-antigens in the heart kaya nagkakaroon ka ng
valvular disease, myocardial disease and all the layers of the heart can
be affected here.
In addition, CD4+ T cells specific for strep peptides also react
with self-proteins in the heart that will activate macrophages. This is a picture of bread and butter pericarditis.

What do we see? Aschoff bodies which are swollen


eosinophilic collagen surrounded by lymphocytes and Anitschkow cells This is an example of Verrucae bodies or the vegetations along
otherwise known as Caterpillar Cells. Pag nakakita ka ng Anitschkow, the closure lines. In cases of chronic RHD, nagkakaroon ka ng fusion ng
pathognomonic yan for rheumatic fever but Aschoff body is a very chordae tendinae as well as broadening or fibrosis of papillary muscles
characteristic of rheumatic disease also. so nagkakaroon problem sa closure or opening of the valve.
Diffuse inflammation and Aschoff bodies maybe found in all
the layers of the heart: epicardium, endocardium and myocardium.

They also have this bread and butter pericarditis. Pag


nagpalaman ka ng butter in between 2 pieces of bread then you lift it
up, there are strands of butter, that’s how it looks like, the bread and Microscopically, this is Aschoff nodule or Aschoff bodies.
butter pericarditis.
Vegetations or verrucae are seen along the lines of closure.
They have these MacCallum plaques which are irregular thickenings.

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Pathology 2B HEART (DR. GACASAN)

1 major 2 minor plus this definite evidence  Rheumatic


Fever.

In higher magnification, you have eosinophilic collagen with


mononuclear cells When RHD becomes chronic, that’s the time that you will have
stenosis and fibrosis leading to fish mouth or buttonhole stenosis.

This is an example of fish mouth stenosis.

These are the Anitskow or caterpillar cell. Mukha siyang


caterpillar because the chromatin material ay parang nastretch.

Aside from RHD, we have instances that we affect the


endocardium. We have another disease known as Infective Endocarditis.
This is said to be the most serious composed of bulky friable vegetation.
Since this is infective, may bacteria siya. It can be acute or subacute.

This is the Jones criteria. Should be that there is a definite


evidence of Strep infection here. Serologically, you can determine that
there is a previous infection or you can also have the ASO titer.
2 major plus this definite evidence  you have this Rheumatic
Fever.

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Pathology 2B HEART (DR. GACASAN)

To compare acute from subacute. Acute is destructive, seen in


previously normal heart, secondary to highly virulent organism and
We have here a picture of infective endocarditis. Anjan yung
death occurs within days to weeks.
bulky vegations. You should take that out, gawa ka ng gram stain, meron
Subacute on the other hand is insidious. To begin with, there is
kang microorganism, then do culture and sensitivity and it will be
already a problem with the heart. Low virulent organisms here. They
positive.
recover with appropriate treatment.

Microscopically, this is what we see. Bacterial colonies that


mixed with inflammatory infiltrates. Basta evidence of inflammatory
process anu yung pwedeng mga makikita dun? Pwedeng granulation So ang mga organisms, we have Strep viridans common in
tissue, inflammatory cell infiltrates. In addition we have bacterial subacute. Then we also have Staph aureus in the acute infective
colonies. We can also see calcifications in certain stages. endocarditis. Then you have other organisms yung mga Haemophilus
hacek so you have to check on that also.

Fever is the most consistent sign. Some will have just flu-like
This is another view showing us the same thing. syndrome yun pala meron nang endocarditis. Murmurs are present in
90% of patients.

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Pathology 2B HEART (DR. GACASAN)

You have to check on this Duke Criteria to provide assessment


of Infective Endocarditis.

Like in this one, may vegetation jan. If you have that


underneath, that’s a characteristic of LSE.

Then we have the Non-bacterial Thrombotic Endocarditis


(NBTE). Also called Marantic endocarditis which is associated with
debilitating conditions like malignancies, Trosseau syndrome and
endocaridal trauma. Trosseau syndrome is migratory thrombophlebitis
that can have condition in the heart which is in the form of NBTE.

Carcinoid Heart Disease. This is associated with the syndrome


of carcinoid like flushing of skin, cramps, nausea, vomiting and diarrhea.
So what do we see here? There is fibrous thickening of the inside surface
of the cardiac chambers.

This is an example of NBTE. Meron kang vegetations as you


can see here in Marantic endocarditis.

Libman-Sacks Endocarditis (LSE). This is the one associated


with SLE, binaliktad lang LSE  SLE. There is one particular characteristic
of this. Pag pinutol mo yung connection ng valves, pag tiningnan mo sa
ilalim you also see the vegetations there.

Let’s dwell more with this Cardiomyopathies. We mentioned


earlier that there are 3 Cardiomyopathies. These are myocardial

Jomero M. Cleofe RN Page 26


Pathology 2B HEART (DR. GACASAN)

problems. The primary is confined to the heart, secondary is involved in


systemic disorder.

These are the 3 types of cardiomyopathies. There are only 2


dysfunctions here. It can either be diastolic dysfunction or systolic
dysfunction.
Dilated cardiomyopathy is the only one with systolic Then we have Hypertrophic cardiomyopathy. This has diastolic
dysfunction. Yung D, hindi siya D rin or diastolic. S siya  Systolic dysfunction.
The other 2 which are Hypertrophic and restrictive both have
diastolic cardiomyopathy. HRD. HR  Diastolic.

This one has the “banana like” configuration of the chamber


not the heart per se but it’s the inside of the heart or the chamber. This
one has concentric hypertrophy.

Dilated cardiomyopathy. We said that this has systolic


dysfunction. These are the causes of it: genetic, myocarditis, alcohol &
other toxins and childbirth.

Restrictive cardiomyopathy. Diastolic din and dysfunction nito.


Unaffected ang systolic function. Commonly, there is amyloid deposition
or iron deposition so nagkakaroon ka ng infiltration of these different
materials or substances.
This is how it looks like.

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Pathology 2B HEART (DR. GACASAN)

This is a table showing us the differences among the 3. So in


restrictive, there is amyloidosis and hemochromatosis.
This is a picture of iron deposition. Still, restrictive
cardiomyopathy. So microscopically, if there is amyloid or iron, it is
restrictive cardiomyopathy. If none, it is dilated or hypertrophic
cardiomyopathy so you have to check on the history.

Eventhough they differ grossly, microscopically, they are the


same. This is a cross-sectional view. Malaki ang mga cardiac muscle cells. Another problem in the myocardium is Myocarditis. Most
commonly caused by viral infection. Most common is Coxackieviruses A
and B & other entroviruses. There is broad clinical spectrum.

In pericardial diseases, it can be Pericardial effusion or


Hemopericardium. The normal is 30-50 ml dapat ang lamang fluid ng
pericardial space. Pag nagincrease yan beyond, you have effusion or
This is a picture of amyloid deposition so this is restrictive
ascites.
cardiomyopathy.
If there is rapid accumulation up to 300 ml, there is cardiac
tamponade.
Assignment: Know the normal pleural fluid, peritoneal fluid.

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Pathology 2B HEART (DR. GACASAN)

Hemorrhagic. Tatlo lang yan. If not cardiac surgery or trauma,


it can be malignancy or tuberculosis. The same thing holds true for
pleural effusion. Pag ka bloody ang pleural effusion mo, think of 2
things. Is it malignant condition or tuberculosis?

Acute pericarditis. Serous is usually in rheumatic fever, SLE,


scleroderma, tumors and uremia. Nagkakaroon ka ng serous pericarditis
jan sa mga yan.

Purulent material is present and this is infectious ofcourse.

Fibrinous and Serofibrinous. Is seen in acute MI, uremia, chest


radiation, RF, SLE and trauma. Serous in combination with fibrin ito or di Microscopically, it depends on the cause. If purulent, then you
kaya ay puro fibrin protein material. have a lot of neutrophils, inflammatory reactions. Others, you will see
fibrin if fibrinous.

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Pathology 2B HEART (DR. GACASAN)

Noncardiac neoplasm, common parin ito just like in the lungs


and liver and even in other organs. These are metastatic tumors.

There is such a thing as Chronic or Healed pericarditis. There


are 3 types.

This one is tumor emboli in the heart.

Lastly, we have the cardiac tumors. Myxoma is the most


common primary tumor and it is the wrecking ball effect.

This is a picture of lymphoma cells in the heart.

But in children, Rhabdomyoma is the most common primary


heart tumor in infants and children.

These are other tumors.

Jomero M. Cleofe RN Page 30