Coronary Artery Disease

Advanced Pathophysiology-Giner > Unit 3

Cardiovascular Disorders
Cardiovascular disorders are prevalent in primary care. Many of the
disorders develop over several years, due to the risk factors to
which individuals have been exposed. For each disorder covered in
this unit, a discussion of risk factors will be included. For the
concepts covered below, clinical application of each disease will be
provided so that students can understand the importance of
pathophysiology in diagnosing and treating the disease.
Prerequisite knowledge:
For this content, you should have a basic knowledge of cardiac
anatomy; know the differences between the right and left sides of
the heart, in terms of structure and function. You should also
possess solid knowledge of the unidirectional blood flow through the
heart. For example, deoxygenated blood arrives to the right side of
the heart, travels to the pulmonary arteries to release CO2 and pick
up oxygen. At this point, the oxygenated blood is carried from the
lungs through the pulmonary veins to the left side of the heart
where it eventually reaches the aorta to carry oxygenated blood out
to the body organs. The cellular physiology related to cardiac
contraction is another important basic concept to know, as
electrolytes (sodium, potassium and calcium) play a major role in
muscle contraction. Finally, the concepts of preload, afterload, and
contractility are essential to understand, as all of these can be
affected in some way when a person has cardiovascular disease.
CAD, myocardial ischemia, and MI form a pathophysiologic
continuum that impairs the pumping ability of the heart by depriving
the heart muscle of blood-borne oxygen and nutrients.

Blood flows between the heart and lungs in the following way:
1. 1. From the body to the heart
Oxygen-poor blood enters the heart through the superior and inferior
vena cava, which are two large veins. The blood then goes to the right
atrium, then to the right ventricle.
2. 2. From the heart to the lungs
The right ventricle pumps blood to the lungs through the pulmonary
artery. The pulmonary artery splits into two main branches, one for each
lung.
3. 3. From the lungs to the heart
The blood picks up oxygen in the lungs and returns to the heart through
the pulmonary veins. The blood then goes to the left atrium, then to the
left ventricle.
4. 4. From the heart to the body
The left ventricle pumps blood to the rest of the body through the aorta.
The pulmonary circulation system is a network of arteries, veins,
and lymphatics that exchange blood and other fluids between the
heart and lungs.

What is Coronary Artery Disease (CAD)?

CAD is considered the leading cause of death in the United States
(U.S.). It is the result of longstanding atherosclerosis. Atherosclerosis
begins with damage to the endothelium. It is the endothelium, under
normal functioning that maintains balance between the
vasoconstrictive and vasodilation actions, prevents platelets from
aggregating and control of the production of fibrin. When the
endothelium becomes damaged, our familiar inflammatory
processes occur. Macrophages attach to the endothelium, setting up
phagocytosis; plaque formation and vasoconstriction also occurs
marking the beginning of atherosclerosis. The plaque lesions located
in the vessels become enlarged which allows the plaque to progress
within the enlarged vessel lumen. The plaque lesion disrupts normal
blood flow and causes thrombus formation which can be triggered
by cardiac risk factors such as elevated LDL, cholesterol, smoking
and diabetes. So, why is this a problem? Well, the plaque takes
decades to develop in the coronary arteries. With mild disease,
blood flow can get through the arteries and the patient is
asymptomatic. Overtime, this build up can lead to narrowing which
results in decreased oxygen supply. When atherosclerosis reaches a
clinically significant level, the patient will begin to experience
angina. Further progression of the disease will result in acute
coronary syndrome (ACS), formerly known as myocardial infarction
(MI).

Coronary Artery Disease

Let’s take a look at the following video, which describes the
process in greater detail.
What is Coronary Artery Disease?
The major risk factor for the development of CAD is
family history. There is a 50% higher risk for
individuals to develop heart disease if they have a first degree
relative (especially father) or sibling who has suffered from ACS or
premature cardiac death (< age 55 years). Lifestyle also impacts
risk, especially tobacco use and even secondhand smoke exposure.
It is always important for the NP to stress smoking cessation with all
patients who smoke tobacco, in order to decrease the patient’s risk
for CAD. Sedentary lifestyle will also increase one’s risk for
developing CAD. Physical inactivity can lead to overweight (BMI 25–
29.9) or obesity (BMI 30 and above). Male gender, hypertension,
Elevated total cholesterol, elevated low-density lipoprotein (LDL),
and/or decreased high-density lipoprotein (HDL) are also risk factors,
as well as diabetes mellitus.
C.G., a 47-year old male presents to the primary care clinic with
complaints of chest pain that occurs when he is working out at the
gym. He describes the pain as substernal chest pressure that
radiates to the left arm.
He indicates that the pain and pressure subside once he is home,
has showered and is resting. He has not had any other associated
symptoms including dyspnea, diaphoresis or nausea and vomiting.
He also tells the NP that his father died of a heart attack at the age
of 54 years old. He does report a previous medical history (PMH) of
hypertension (HTN) and indicates that he has been taking
metoprolol (Lopressor) for the last two years.
He has a 30-pack-year history of smoking. He reports today that he
would like to take measures to stop smoking. He also indicates that
he has been eating a low-fat diet since he started working out 2
months ago.
The NP conducts an exam and the subjective and objective findings
reveal the following:
Vital signs: BP 144/94; HR 84; RR 20; afebrile; Height: 5’9”; Weight:
187 lbs.; BMI: 27.6
Subjective Objective
Chest pain on exertion Hypertensive
Radiation to the left Overweight
arm
Relieved with rest
PMH: HTN, smoking
Family History:
Premature cardiac
death in father at, age
54

The patient’s major symptom is chest pain on exertion that is

relieved by rest.
Let’s work through this patient case logically to determine the
pathophysiological causes of his symptoms, what put him at risk,
and what his final diagnosis might be. Myocardial ischemia is the
cause of his chest pain. Ischemia occurs when the heart’s oxygen
demand exceeds supply. For this patient, he experienced his chest
pain during exercise. Ischemia occurred because of the narrowing
of at least one coronary artery by atherosclerotic plaques. The result
is the narrowing of the diameter of the coronary artery. This reduces
oxygenated blood flow through the artery that leads to an
insufficient oxygen supply to the heart. Adenosine is also released
that stimulates sympathetic nerve fibers that causes atrial and
ventricular contraction. In addition, sympathetic stimulation occurs
at the upper thoracic dorsal roots of the spinal cord that leads to the
arm pain.
C.G. has several risk factors contributing to the development of
CAD:
1) male
2) family history of CAD
3) hypertension
4) smoking
Through analysis of the patient presentation, past medical history
(PMH) and risk factors, a diagnosis of CAD should strongly be
suspected and further testing to assess the extent of the patient’s
disease including electrocardiogram (ECG), cardiac enzymes &
troponin, lipids, and cardiac stress test. In most cases, the patient
will be referred to and co-managed by a cardiologist. Treatment will
include both non-pharmacological and pharmacological
management of the disease.

Heart Failure
Advanced Pathophysiology-Giner > Unit 3
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Increased preload indicates more volume in the ventricles, thus

increasing the amount of blood ejected.
Preload is the amount of stretch on the ventricles caused by the
amount of volume. The more volume, the more stretch. Conditions
that would cause less volume with a resulting decreased preload is
hemorrhage, cardiac tamponade and dehydration.
Hypertension causes constriction, thus immediately increasing the
amount of pressure the ventricle has to pump against to move blood
from the ventricle.
Pulmonary hypertension is the most common cause of right sided
heart failure, as blood backs up to the right ventricle due to
resistance of blood flow into the pulmonary artery.

Heart Failure
Heart failure is a very complex disease state that can be the result
of structural or functional impairment of the heart, which then leads
to the heart’s impaired ability to fill or eject sufficient amounts of
blood out to the body. Let’s review some basic concepts related to
this disease:

 Cardiac Output (CO): The amount of blood that the heart

pumps in 1 minute. CO is also known as cardiac contractility.
 CO Formula: CO=heart rate (HR) x stroke volume (SV).
 SV: The volume of blood pumped out of the left ventricle
during each systolic cardiac contraction.
  Afterload: The force, or load, which the heart must contract
against in order to pump blood. Afterload is also known as
systemic vascular resistance (SVR).
 Preload: The amount of stretch that the cardiac muscle
exhibits at the end of ventricular filling.

Not all patients present with the same signs and symptoms of heart
failure and symptoms are dependent upon which side of the heart is
affected. Let’s discuss the difference.
Right-sided Heart Failure

 Right ventricle
 superior vena cava (preload)
 pulmonary artery (afterload)

Let’s shift to right heart failure (Cor Pulmonale). This is defined as

the inability of the right ventricle to provide adequate blood flow
into the pulmonary circulation. Causes of right heart failure include:
1) pulmonary disease that causes pulmonary hypertension. This is
the most common cause; 2) right ventricular myocardial infarction
(MI), which weakens the cardiac muscle; 3) right ventricular
hypertrophy (secondary to cardiac damage); 4) tricuspid valve
damage (causing backflow of the blood into the right atrium or right
ventricle after ejection); 5) secondary failure as a result of left heart
failure due to the build-up of pressure in the damage left ventricle.
Since pulmonary hypertension is the most common cause of right-
sided heart failure, it will be used to outline the disease process.
Again, keep in mind that regardless of the cause of right heart
failure, the overall process outlined here will be the same.
High pulmonary vascular pressure (increased afterload) will cause
an increased right ventricular contraction force in order to eject the
blood. Overtime, this will reduce the ejection fraction and the right
ventricle will be unable to eject the normal amount of blood. This
will increase the amount of blood remaining in the right ventricle
and, as a result, increase right ventricular preload, resulting in the
inability for the right atrium to eject the normal amount of blood into
the right ventricle. This will increase the amount of blood remaining
in the right atrium and, therefore, increase right atrial preload. This
causes the back-up of blood volume and pressure in the vena cava
and systemic veins. Jugular vein distension is characteristic of right
heart failure. Because of the large volume of blood flow through the
liver and spleen, these areas become engorged, resulting in
hepatosplenomegaly. Increased pressure will force fluid from the
systemic capillaries into the peripheral tissues, essentially flooding
those areas and resulting in peripheral edema. Unresolved right
heart failure will increase pressure on the left side of the heart,
contributing to left heart failure as well. Again, this will result in a
biventricular heart failure.

Left-sided Heart Failure

 Left ventricle
 Pulmonary vein (preload)
 Aorta (afterload)

High systemic vascular resistance, or increased afterload, will

increase the left ventricular contraction force in order to eject the
blood from the left ventricle. Over time, this will reduce the patient’s
ejection fraction and the left ventricle will be unable to eject normal
a normal amount of blood. This results in an increased amount of
blood remaining in the left ventricle. As a result, left ventricular
preload will be increased, impeding the left atrium from ejecting the
normal amount of blood into the left ventricle. This will eventually
cause the blood volume in the pulmonary veins. Pressure will also
be increased in the pulmonary veins. This increased pressure will
force fluid from the pulmonary capillaries into the pulmonary
tissues, which essentially floods those areas. The result is
pulmonary edema and dyspnea. If left ventricular heart failure is
unresolved, volume and pressure will continue to build until it
reaches the right side of the heart, contributing to right heart failure
as well. In this case, the condition becomes a biventricular heart
failure. Disease processes that increase left ventricular afterload
include hypertension and aortic valve disorders.
Right-sided Left-sided
 Jugular vein  Increased left ventricular
distention afterload
 Hepatosplenomegaly  Decreased ejection fraction
 Peripheral edema  Increased left ventricular
 CorPulmonale preload
  Tricuspid valve  Pulmonary edema
damage  Dyspnea

High Output Heart Failure

A patient can also have high-

output failure (HOF). This is the inability of the heart to pump
enough amounts of blood to meet the circulatory needs of the body,
despite normal blood volume and cardiac contractility. Several
diverse conditions can lead to HOF. In contrast to left and right heart
failure, where the heart is unable to effectively increase its output,
the heart can in HOF to at least, for a while, increase its output.
Unfortunately, though, even with increased cardiac output, the
metabolic needs of the body are not met. Some of the causes and
processes involved in HOF are discussed here. As presented earlier
in this module, anemia, regardless of type, ultimately impair oxygen
delivery to the tissues.
Nutritional deficiencies, especially of the vitamin thiamine,
decreases cardiac muscle function and output, which impairs
oxygen delivery to the tissues. Hyperthyroidism, fever and sepsis
increase basal metabolic rate which leads to increased tissue
oxygenation demands. As conditions like these result in increased
oxygen demand, the supply of oxygen is simply not there, which
leads to a hypoxic condition. This activates the sympathetic
response. The catecholamines, epinephrine and norepinephrine, are
released, which increases the heart rate and stroke volume to
increase cardiac output. In HOF, the heart cannot keep up with all of
the body’s demand for oxygen nor maintain an extended increased
heart rate and stroke volume in an attempt to supply the body with
the oxygen that it needs. Over time, HOF can deplete the cardiac
muscle reserve and lead to low-output heart failure. Consider the
patients that you may have encountered in your nursing practice.
Many individuals are being treated for multiple conditions like the
ones stated above that demands increased oxygen.

Compensated vs. Decompensated Heart

Failure

The main difference between compensated and decompensated

heart failure is the severity of symptoms and whether medical
attention is needed:
 Compensated heart failure
Symptoms are stable or absent, and the heart is working well enough
that the body can adjust. People with compensated heart failure may not
have fluid buildup in their legs and feet, and they can breathe without
trouble.
 Decompensated heart failure
Symptoms are worse and require medical attention. Symptoms include:
 Shortness of breath, also known as dyspnea

 Wheezing
 Edema
 Coughing at night
 Congestion in the lungs
 Fatigue
 Reduced exercise tolerance
 Increasing breathlessness on exertion
 Abnormal heart rhythms (arrhythmias)
Decompensated heart failure can occur suddenly without a prior
diagnosis, or it may be the result of worsening symptoms in
someone who already has heart failure.
Stages of Heart Failure
When diagnosing heart failure and determining the patient’s
treatment plan, the NP must consider the stage and classification of
heart failure using the American College of Cardiology/American
Heart Association’s (ACC/AHA) current clinical practice guideline on
the management of heart failure. Diagnosis and treatment of heart
failure always requires identification of its stage and classification.
They are identified below:
Stages of Heart Failure
Stage A: Patients at risk for heart failure who have not yet
developed structural heart changes (i.e. those with diabetes, those
with coronary disease without prior infarct).
Stage B: Are patients with structural heart disease (i.e. reduced
ejection fraction, left ventricular hypertrophy, chamber
enlargement) who have not yet developed symptoms of heart
failure.
Stage C: Patients who have developed clinical heart failure.
Stage D: Patients with refractory heart failure that require
advanced intervention (for example, the need for a biventricular
pacemaker, left ventricular assist device, or heart transplant).

Classes of Heart Failure

Class I: there is no limitation of physical activity; Ordinary physical
activity does not cause symptoms of HF.
Class II: there is a slight limitation of physical activity. The patient
is comfortable at rest, but ordinary physical activity results in
symptoms of HF.
Class III: there is marked limitation of physical activity. The patient
is comfortable at rest, but less than ordinary activity causes
symptoms of HF.
Class IV: The patient is unable to carry on any physical activity
without symptoms of HF, or they have symptoms of HF at rest.
Now, let’s compare the stages and classification system. Patients
with heart failure can progress through the four stages of heart
failure as their condition worsens. Once a stage has been reached,
the person can never go back to the prior stage. In other words, the
damage to the heart cannot be reversed. This is not the case with
the NYHA classification that focuses entirely on patient symptoms.
Patients may move between Class 1 and Class IV as symptoms can
be improved through treatment with medications. While a patient
may be in a certain stage of heart failure, they symptoms exhibited
within that stage can be managed and improved.

Heart Valve Disorders

Aortic Stenosis & Aortic Regurgitation

Here we actually see the LV, or left ventricle, contacting into the aorta,
and the red arrow's looking at the aortic valve, which is actually not
opening very much if you can see that. So this is aortic stenosis. What
is aortic stenosis? Very basically, it's having a tight aortic valve so not
enough blood can get through. You'll see our label here, the LV, the left
ventricle, and then I'll label the aorta here. Blood normally flows from
the LV through the aortic valve into the aorta, and then supplies the
rest of the body. So, to take you through the progression of blood flow,
you have blood that returns to the left atrium from the lungs, goes into
the left ventricle through the mitral valve, leaves through the aorta,
and then goes and oxygenates tissue in the rest of the body. Now, if it
can't get from the left ventricle to the aorta due to something such as
aortic stenosis, then you're going to have blood backed up in the left
ventricle, and you're going to have problems profusing, or supplying,
enough blood and enough oxygen to the rest of the body's tissues.
Let's talk about some of the major causes of aortic stenosis. The first
thing we want to talk about is having a bicuspid aortic valve. This a
congenital condition, meaning you're born with it, and this means that
you only have two cusps to the aortic valve. Let's demonstrate this
here. Normally, the aortic valve has three cusps. I'm going to label
those one, two and three. But a certain portion of the population
actually has a congenital bicuspid aortic valve, only having one and
two cusps. The reason why a bicuspid aortic valve is more likely to get
aortic stenosis or is more likely to become stenotic, is because you
actually have two cusps doing the work of three, and so these bicuspid
valves actually get damaged quicker and can become calcified over
time, and are thus more likely to become stenotic and more likely to do
so at an earlier age. Another cause of aortic stenosis is age-related
calcification. As you get older, the valve actually calcifies and gets
hardened, and can actually obstruct, or stop, the valves from opening
all the way and causing a stenosis. The risk factors for having
calcification of the aortic valve are very similar to the process of
coronary artery disease. So when we talk about risk factors for this, we
talk about things such as smoking, high blood pressure, or
hypertension, hyperlipidemia, or high cholesterol, and diabetes
mellitus. Another cause of aortic stenosis could be rheumatic fever.
Generally, the mitral valve is more commonly affected, but the disease
process of rheumatic fever and rheumatic heart disease can actually
affect the aortic valve as well. The way that you can remember the
signs and symptoms of aortic stenosis is with the acronym SAD. S
stands for syncope, meaning fainting. A stands for angina, which is a
type of chest pain. And dyspnea, meaning shortness of breath. Other
things that you can look for are things like pulsus parvus et tardus.
Now, this sounds kind of funny and kind of weird, but all it means is
that you have a small or weak pulse, parvus meaning small, and tardus
meaning like tardy, slow. So it's a small or weak pulse that is slow to
rise, because if you think of blood coming out of a very tight valve,
you're not going to have the normal rise in pressure that you normally
do, that you feel when you're feeling someone's pulse. Another thing
that may occur is LVH, or left ventricular hypertrophy. What you can do
on physical exam is you can actually palpate what's called the PMI, or
the point of maximal impulse. This should normally be in the fifth
intercostal space in the midclavicular line, so similar to what we call
the mitral area when you're auscultating, or listening with a
stethoscope. In people with LVH, this PMI can actually move medially,
or towards the sternum, and that would be a sign of left ventricular
hypertrophy, meaning the muscle has kind of gotten thicker. Another
thing that you can see in aortic stenosis is MAHA, or microangiopathic
hemolytic anemia. What happens here is that red blood cells actually
get sheared as they go across the really tight valve, and so the cells
are actually broken apart and you can get an anemia that shows red
blood cells that have kind of been broken apart, and that's due to the
aortic stenosis. Finally, you get a systolic ejection murmur on
auscultation, and this systolic ejection murmur is best heard in the
aortic area, or the right upper sternal border, and that may or may not
have an ejection sound as the valve pops open. So, to explain the
angina real quick, angina is basically chest pain that is related to
ischemia, or lack of oxygen. There are kind of two good reasons why
you get angina in someone who has aortic stenosis. Someone may
have pre-existing coronary artery disease or they may have left
ventricular hypertrophy. With coronary artery disease, we'll draw an
artery here, or a coronary artery, one of the arteries that supplies the
heart. Here in this orange we'll draw a plaque that's kind of pushing
into the lumen, or the inside of the artery, where the blood flows. If we
say that this plaque is occluding, or blocking, 65% of the artery, when
someone has aortic stenosis and can't get enough blood out, this
blockage that is actually 65% may feel like a 75% blockage and cause
chest pain to become apparent or cause more chest pain. In someone
with left ventricular hypertrophy, this is when the heart becomes more
muscular, and so you have increased muscle mass and you have an
increased oxygen demand from the tissue. If you have an increased
oxygen demand and you can't meet that demand because you have
aortic stenosis, you can get chest pain. Now, let's talk about the
opposite of aortic stenosis, and that'll be aortic regurgitation. What you
can see here is I've labeled the aorta for you and the left ventricle, and
what the arrow's pointing to is actually regurgitation of blood flow. You
can see that part of the valve is actually kind of just flopping there
from all this blood coming back into the left ventricle. That's aortic
regurgitation. This is kind of a floppy aortic valve. Here we'll label the
LV, the left ventricle, the LA, the left atrium, the aorta, and you'll see
that normally the blood goes out of the aorta into the rest of the body
like we showed before. But in the case of aortic regurgitation, when the
heart is supposed to be relaxing and filling with blood from the atrium,
the blood can actually come back through the aortic valve and into the
left ventricle, when really that valve should be shut and not letting any
blood back. So the flow of blood would be normally from the left atrium
to the left ventricle, and then out of the aortic valve to the aorta and to
the rest of the body. But here, blood is actually coming back from the
aorta into the left ventricle through the regurgitant aortic valve. Let's
talk about some causes of aortic regurgitation. One way that this
occurs is when you get a widening, or aneurysmal change. An
aneurysm is really just a ballooning or an out-pouching of a vessel, so
widening or aneurysmal change of the aortic annulus. The annulus is
really just a ring of fibrous tissue that surrounds the aortic valve. Any
time that becomes widened, the valve area becomes widened and the
valve can't close as well. This happens in conditions such as tertiary
syphilis, or some of the connective tissue disorders such as Marfan
Syndrome and Ehlers-Danlos, which are both disorders relating to
collagen, which is a connective tissue protein in the body used for
structural support of blood vessels and other things. Another reason
that this can occur, aortic regurgitation, is due to endocarditis. You can
get an infection of the valve that can lead to the formation of a
vegetation and this big ball of platelets and bacteria that can actually
stop a valve from closing effectively. Finally, rheumatic fever. As we've
already seen, rheumatic fever normally affects the mitral valve, but it
can easily affect the aortic valve as well. Let's talk about some signs
and symptoms of aortic regurgitation. Patients may experience fatigue.
This is because all the blood that's being pumped out to the aorta is
not exactly staying there. Some of it may come back into the heart.
They may have syncope for similar reasons. Shortness of breath and
palpitations. Other things that you may want to look for on physical
exam or when you take a blood pressure would be something called
wide pulse pressure. The pulse pressure, let me just define that for
you. The pulse pressure is the difference between the systolic blood
pressure, SBP, and the diastolic blood pressure, DBP. Let's go ahead
and draw this for a second. Here you're going to see the aorta, and
then we'll make the valve, an open valve, an open aortic valve, in
white. When blood comes through, this is at a systolic pressure of 120
millimeters of mercury. That's the blood getting ejected from the heart.
Now, when the heart goes to relax and the valve closes as a result of
the elastic recoil of the aorta against a closed valve, the pressure in
the system actually stays pretty high, around 80 millimeters of
mercury. A normal systolic over diastolic blood pressure would be
something like 120 millimeters of mercury over 80 millimeters of
mercury. If this aortic valve was regurgitant, and a lot of blood backed
through, you wouldn't be able to maintain that normal pressure of
about 80, which is due to the elasticity and recoil of the aorta on a
closed aortic valve, but now you would have something like about 50,
because that blood would be flowing back through that aortic valve. In
addition, because more blood is flowing back into the left ventricle, this
actually increases what's called the pre-load, or how much blood that
ventricle is filled with. Then due to something called Frank–Starling's
law, or Frank–Starling's curve, if you have increased pre-load, the heart
actually contracts harder and better to put out all of that blood that it's
receiving, and so that systolic blood pressure will actually increase. So
if you have an increase in pre-load, you're no longer going to have that
120 millimeters of mercury, but now maybe 140 millimeters of
mercury. So you went from a pressure of, let's say, 120/80 to about
140/50, which is going to increase your pulse pressure. Another thing
that you may notice on physical exam is left ventricular dilatation, and
this can be recognized through a couple of different things. You can see
this on echocardiography or you can have an S3, an extra heart sound,
which signifies volume overload. The blood is getting too much volume
back from the aorta when it's not supposed to. This may also displace
the point of maximal impulse. When we talked about left ventricular
hypertrophy earlier, the PMI would actually move medially towards the
sternum, but in a case where the heart is volume overloaded, it will
actually move laterally, and possibly inferiorly. An aortic regurgitation
can be heard on auscultation as an early diastolic murmur along the
left sternal border.

Mitral Regurgitation & Mitral Valve

Prolapse
So now let's talk about mitral regurgitation. So all that really means is
that the mitral valve, the valve between the left atrium and left
ventricle, is "floppy." So you'll see here that I'm going to mark off the
LV or left ventricle, and then I'm going to show you the normal path it
takes out of the aortic valve to the aorta and the rest of the body. But
in mitral regurgitation, blood actually goes back into the left atrium.
And then blood can actually back up from there into the pulmonary
system. And so, you'll see I'm drawing these lines from the pulmonary
veins that usually come from the lungs, but blood is going to get
backed up from the left atrium to these pulmonary veins and back to
the lungs that I'm drawing right here. So the normal path of blood
would be from the left ventricle, to the aorta, and out to the rest of the
body. But with mitral regurgitation, you actually have blood that goes
from the left ventricle to the left atrium and then can back up in the
lungs or pulmonary system, which can cause some symptoms. So now
you'll see here is actually an echocardiogram of someone with mitral
regurgitation, and what you'll notice is the blue flash back into the left
atrium when the heart contracts. So normally when the heart
contracts, blood should go out through the aorta, into the rest of the
body, but here you'll see that blue flash, and that blue flash means
that blood is actually coming back into the left atrium, indicating mitral
regurgitation. So what I want to do is talk about the major causes of
mitral regurgitation, and now there are a lot of them, so I'll try and
focus on some of the major ones and then give you some other ones as
well. So one of the first things is anything that leads to dilatation of the
left ventricle or left ventricle dilatation can actually stretch the heart
and cause the mitral valve to no longer come together appropriately,
and that will lead to mitral regurgitation. So you'll see that I'm drawing
here these arrows outward, kind of signifying enlargement of the left
ventricle, and you'll notice that if that cavity enlarges, so does the
mitral valve, and it can no longer close effectively. So things that lead
to left ventricular dilatation would be a remodeling process, which is
something that you would see occurring after a myocardial infarction,
so remodeling post MI, and that's really just the heart taking on a
different shape to try and compensate for problems after having a
heart attack. Another thing would be dilated cardiomyopathy. And so,
this is an inherent disease of the heart muscle that can cause the heart
to become dilated, and this can actually be broken down into ischemic
and nonischemic causes. So if someone has coronary artery disease for
a while, this can actually happen, and the heart can become dilated to
compensate for that, but it can also be a genetically-acquired disease
or it can occur from things like alcohol or toxins. Another cause of
mitral regurgitation would be rheumatic fever or rheumatic heart
disease, and mitral regurgitation is actually the early lesion of
rheumatic fever. Remember that the later lesion is mitral stenosis, and
that occurs after you've had multiple bouts of rheumatic fever. Another
cause is endocarditis. So you can get an infection of the valves, leading
to a vegetation or something that builds up on the valve and doesn't
allow it to close effectively. And another cause would be something like
papillary muscle dysfunction or rupture, and this also goes along with
chordae tendineae rupture or dysfunction, because those two are
connected, and you'll see what I mean in a second. So let's scroll up a
little bit, and we'll come back to that papillary muscle or chordae
dysfunction. And the last cause would be calcification of the valve or
around the valve that may not allow it to close effectively. So let's go
back to the papillary muscle and chordae tendineae dysfunction so
that I can show you what I mean here. So you'll see on this diagram,
that's really kind of a cut through the left ventricle, that the blue things
are the papillary muscles, and the gray strings are the chordae
tendineae. And so, these are really just an anchoring system for the
valves, to make sure that they can open and close effectively. And I
just realized that I spelled tendineae wrong, so I'll fix that right now.
And you can see that the chordae are actually attached to the mitral
valve. And let me just label these things for you. So left atrium here
and aorta here, and we're in the left ventricle there. So you can see if a
papillary muscle ruptures or one of the chordae ruptures that you'll
actually have a leaflet of the valve that may just be flailing around.
And so, the mechanism of opening and closing becomes pretty
inefficient. So now let's talk about some signs and symptoms of mitral
regurgitation. So you can actually have acute mitral regurgitation or
chronic mitral regurgitation, which is more what we're talking about
here, but an important cause of an acute mitral regurgitation, where
the heart has no time to compensate, would be something like a
papillary muscle rupture, and this could occur after something like a
heart attack. For chronic mitral regurgitation, this would be something
along the lines of a dilated left ventricle due to chronic coronary artery
disease. So you'll see I write dilated ischemic cardiomyopathy there.
Now, back to the papillary muscle rupture. If something like this
happens acutely, the heart has no time to adapt to these pressure
changes, and so you get what you call flash pulmonary edema or acute
pulmonary edema, and the person may go into congestive heart
failure. And so, this is a medical emergency, and this needs to be
treated right away. Now, for something like the dilated ischemic
cardiomyopathy, or any other major cause of chronic mitral
regurgitation, where there's been time to adjust to these pressures,
you'll see things like fatigue and shortness of breath and maybe some
pulmonary congestion or edema but not this rapidly developing type
that we saw in the acute mitral regurgitation. Other things that you
may be able to see are signs of left atrial enlargement, which you may
be able to see on an EKG or in an echo, and then on auscultation, or
when you listen with your stethoscope, you should be able to hear a
holosystolic murmur at the apex or in the mitral region, which is in the
fifth intercostal space in the midclavicular line. So now let's talk about
mitral valve prolapse. So mitral valve prolapse is when the valve
actually billows or bulges into the left atrium. And mitral valve prolapse
itself actually doesn't usually lead to a murmur, but if the valve then
becomes dysfunctional, you can actually get the murmur of mitral
regurgitation. So if you notice I'm going to zoom into the heart down
here, and you'll see I'm drawing the chordae attached to the papillary
muscles, and then I'm going to erase one of the valves here, one of the
normal valves, and show you what it looks like when mitral valve
prolapse has occurred. And so, here you'll see that little hump, and it's
like this valve has kind of ballooned into the left atrium. And I'm
drawing an arrow to that now. Now if you'll see here, you can see I've
labeled the left atrium, the left ventricle, and the aorta, and during
systole, when the left ventricle contracts and blood should be going
out of the aorta, you'll see that one of the cusps of the mitral valve
actually comes into the left atrium a little bit, and you can see I put an
arrow next to that. So let's talk about the causes of mitral valve
prolapse. The major causes, one of them is actually idiopathic,
meaning we don't really know what causes it. Another cause is when
this mitral valve prolapse actually occurs secondary to a connective
tissue disorder, and a connective tissue disorder means exactly what it
sounds like. You have a problem in making proper connective tissues
which make up some of your arteries and some of the tissue in the
body. And so, certain conditions like Marfan syndrome or Ehlers-Danlos
actually can cause mitral valve prolapse. So some signs and symptoms
of mitral valve prolapse. Well, this is kind of a tough one. So many
people are asymptomatic and may just have been told by their doctor
at one point that they had a funny sound when the doctor listened to
their heart. But there's another group of people that actually have
some symptoms that the medical community has labeled the mitral
valve prolapse syndrome. And there's some debate as to whether or
not this is actually a real syndrome, but what this consists of is some
atypical chest pain, meaning it's not anginal in character, meaning it's
not the typical pain that you get with coronary artery disease or
blockages of the arteries. These people also complain of palpitations or
the feeling that their heart is beating either extra fast or extra forceful,
and then also some shortness of breath and some dizziness or
syncope. And syncope is just fainting. And the way that we can identify
this condition with auscultation is that we hear a mid systolic click, and
then if it has progressed into valve dysfunction, you'll actually hear the
murmur of mitral regurgitation following this mid systolic click, but the
mid systolic click is a classic sign for mitral valve prolapse. And one
other important thing to know is that mitral valve prolapse actually
puts you at an increased risk for a couple of things, such as infective
endocarditis. So remember, this valve is not totally normal, and so it's
slightly more likely that bacteria can actually colonize and infect this
valve. In addition, mitral valve prolapse may predispose these people
to certain arrhythmias, and then, like we said before, it can actually
progress to mitral regurgitation. And so, that can cause some more
problems.

Mitral Valve Stenosis

So what you're looking at here is an ultrasound, or what they call an
"echo," of the heart, and you can see the four different chambers and
you'll see I've labeled the left ventricle and the left atrium, and what
you'll notice is that the arrow is pointing to the valve in between the
left ventricle and left atrium, which is the mitral valve, and that valve is
actually not opening. When that valve is really tight or doesn't open,
that is what's called mitral stenosis. So like I said, mitral stenosis is
when you basically have a tight mitral valve. Now what I'm going to do
is I'm going to draw a little set of lungs here, and kind of briefly take
you through how blood flows from the right heart through the lungs,
and then from the lungs, and now I'm drawing back to the left heart,
and so those arrows are going to the pulmonary veins, which go into
the left atrium, which I'm marking off here, LA, and then the left
ventricle, LV. And that, that I'm circling right now, is the mitral valve.
The progression of blood is left atrium to left ventricle, out the aorta,
and to the rest of the body. And of course that blood into the left
atrium, like we just said, was from the lungs. Now if the blood can't get
from the left atrium to the left ventricle, it is going to back up in the
left atrium and the lungs, everything that was before it. Let's talk
about some of the causes of mitral stenosis. What causes this valve to
be tight? Well, you can have what's called rheumatic fever, or more
specifically, rheumatic heart disease when it affects the heart. So
another cause can actually be what's called endocarditis, and that's
really an inflammation or an infection of the actual valve. These are
are some of the major causes of mitral stenosis. There are obviously
others, but I want to keep you focused on the major ones. So what
causes rheumatic fever? It's actually a pretty specific bacteria, and it's
part of a group called "group A streptococcus." We can actually
abbreviate that "GAS," Group A Streptococcus, and what we're really
talking about here is a specific bacteria called streptococcus pyogenes.
This bacteria is actually what just causes strep throat. So what'll
happen is someone gets a strep pyogenes infection, or a pharyngitis,
meaning a throat infection, and two to three weeks later, if it's not
treated correctly, the person can actually present with some pain in
their joints, or arthralgias, heart problems, like a new heart murmur,
some skin problems, and a bunch of other symptoms, but for the most
part, the joints, the skin, and for our sake, the heart problems are what
we really want to focus on. Now the mechanism behind why this
infection by this bacteria actually causes heart problems is called
"molecular mimicry," and what happens is here, if you see I draw this
antigen, this green antigen, as a triangle, and then this red antibody,
and so the antigen is really going to be part of the bacteria that our
body's immune system is going to respond to with an antibody, but
what happens is some of the antigens that this particular type of bug,
strep pyogenes, puts out are actually very similar to some of the
normal antigens or components of the tissue of the heart valves. So
what can happen is when you actually form an antibody response to
the particular infection, those antibodies can actually go ahead and
attack the heart. The reason why you get all the other symptoms are
because those antigens are also found in those parts of the body, so
the joints, the skin, and other things. Now the early lesion of rheumatic
heart disease is mitral regurgitation, but the late lesion, meaning when
you've had repeated bouts of this rheumatic heart disease, or of this
infection with strep pyogenes, you actually get mitral stenosis, which is
what we're talking about now. Mitral stenosis is characteristic for
rheumatic heart disease. So really what I'm trying to say is that a strep
pyogenes infection itself, the bacteria itself does not cause the heart
problems, it's actually our body's immune system responding to that
infection that causes the heart problems. So let's talk about
endocarditis now, which we said is an inflammation or infection of the
heart valves. Now, I'm going to write "infective" here because there
are other rare, more rare, types of endocarditis, but for the most part,
this is usually infective endocarditis, when it has something to do with
an infection, either by a bacteria or a fungus or a virus. So there are
kind of different ways that this can happen. You can get an infection of
a completely normal valve and the way that this happens is you
actually have a bacteria that's really bad, and so it's bad enough that it
can infect a normal valve. This is something like staph aureus. Now,
you can also have an infection of a previously damaged valve, so if
someone already had some damage to their valves, a bacteria that's
not as bad may be able to actually cause this problem. This is often
seen with normal flora in the mouth, or bacteria that normally colonize
in the mouth, such as strep viridans, and that's actually a class of
bacteria, but these bacteria are just in the mouth, and so this is
actually why some people can get infections of their valves after
having work done at the dentist, because they actually become
bacteremic, or have these bacteria in their blood after their teeth and
mouth have been manipulated. The last type is when someone has a
prosthesis, or a prosthetic valve, has had a valve replacement in the
past, and these are characteristically caused by staph epidermidis, or
staph epi. These like to form little layers on prosthetic valves that allow
them to survive and cause problems, or endocarditis. In addition, the
worst bacteria usually cause what we call "acute bacterial
endocarditis." The less virulent bacteria usually cause what we call
"sub-acute bacterial endocarditis," and you should just remember that
this infective endocarditis can be caused by bacteria, viruses, and a
little bit more rare, but can happen, fungi. Now let's talk about the
signs and symptoms associated with mitral stenosis. Now granted,
these may be based on the mechanism, or how it was caused, so if you
have something like endocarditis as a result of an infection, the person
may have typical signs of an infection, like fever, chills, and elevated
white blood cell count, stuff like that, but for signs and symptoms of
mitral stenosis, specifically we're going to talk about signs and
symptoms relating to the heart and cardiac physiology. If we go back
to our drawing of the lungs, which then return oxygenated blood to the
left atrium, which then goes through the mitral valve to the left
ventricle, and then to the body through the aorta, we can see that if
blood backs up, you don't have as much output of blood to the body,
so you can get fatigued, you can be short of breath because blood is
backing up into the lungs, you can have exercise intolerance because
you can't get enough blood to the body to profuse or to adequately
oxygenate your tissues, give you enough oxygen, or you can have a
cough, again, because you're backing up blood into the lungs. Some
signs that you may be able to see on echo, or with your physical exam,
or maybe on an EKG, would be signs of left atrial enlargement,
because if blood is backing up into the left atrium. You can have
pulmonary congestion, or edema. And then you would also have a
characteristic auscultatory finding, or finding that you hear when you
listen with a stethoscope, and that would be a diastolic rumble. Now,
there's also another characteristic finding that occurs just before that
diastolic rumble. Do you happen to remember what it is? It's an
opening snap, and if you forget any of these symptoms, just remember
that if you stop bloodflow from the left atrium to the left ventricle, it
backs up into the lungs, and then you can kind of regenerate what kind
of symptoms and signs that someone may present with when they
have mitral stenosis.
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