DISORDERS OF

CARDIOVASCULAR SYSTEM

By
Saleet Abdullah
Lecturer KMU-IHS, Swabi
 Objectives

• Explain Coronary Artery Diseases

• Explain the myocardial ischemia
• Explain the pathophysiological changes in patients with ischemic
heart diseases.
• Discuss the myocardial infarction
 Coronary Artery Disease
Coronary artery disease (CAD) is the most prevalent type of
cardiovascular disease. For this reason, it is important for
nurses to become familiar with the various types of coronary
artery conditions and the methods for assessing, preventing,
and treating these disorders medically and surgically.
 Coronary Artery Disease
CORONARY ATHEROSCLEROSIS:
• The term atherosclerosis, which comes from the Greek words atheros (“gruel” or
“paste”) and sclerosis (“hardness”).
• The most common heart disease in the United States is atherosclerosis, which is
an abnormal accumulation of lipid, or fatty,substances and fibrous tissue in the
vessel wall.
• These substances create blockages or narrow the vessel in a way that reduces
bloodflow to the myocardium.
• Although authorities disagree about how atherosclerosis begins, they agree that
atherosclerosis is a progressive disease that can be curtailed and, in some
cases,reversed.
 Coronary Artery Disease
Pathophysiology:
• Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima
of the arterial wall.
• The continued development of atherosclerosis involvesan inflammatory
response.
• T lymphocytes and monocytes (that become macrophages) infiltrate the area
to ingest the lipids and then die; this causes smooth muscle cells within the
vessel to proliferate and form a fibrous cap over the dead fatty core.
• These deposits, called atheromas or plaques, protrude into the lumen of the
vessel, narrowing it and obstructing blood flow.
 Coronary Artery Disease
• If the fibrous cap of the plaque is thick and the lipid pool remains
relatively stable, it can resist the stress from blood flow and vessel
movement.
• If the cap is thin, the lipid core may grow, causing it to rupture and
hemorrhage into the plaque, allowing a thrombus to develop.
• The thrombus may obstruct blood flow, leading to sudden cardiac
death or an acute myocardial infarction (MI),which is the death of
heart tissue.
 Coronary Artery Disease
• The anatomic structure of the coronary arteries makes them particularly
susceptible to the mechanisms of atherosclerosis.
• As they twist and turn as they supply blood to the heart, creating sites
susceptible to atheroma development.
• Although heart disease is most often caused by atherosclerosis of the coronary
arteries, other phenomena decrease blood flow to the heart.
• Examples include vasospasm (sudden constriction or narrowing) of a coronary
artery, myocardial trauma from internal or external forces, structural disease,
congenital anomalies, decreased oxygen supply (eg, from acute blood loss,
anemia, or low blood pressure).
Coronary Artery Disease
Coronary Artery Disease
Coronary Artery Disease
Coronary Artery Disease
Coronary Artery Disease
Coronary Artery Disease
 Coronary Artery Disease
Clinical Manifestations:
• Coronary atherosclerosis produces symptoms and complications
according to the location and degree of narrowing of the arterial
lumen, thrombus formation, and obstruction of blood flow to the
myocardium.
• This impediment to blood flow is usually progressive, causing an
inadequate blood supply that deprives the muscle cells of oxygen
needed for their survival. The condition is knownas ischemia.
 Coronary Artery Disease
ANGINA PECTORIS:
• Angina pectoris is a sypmtom usually characterized by episodes of
pain or pressure in the anterior chest.
• The cause is usually insufficient coronary blood flow.
• The insufficient flow results in a decreased oxygen supply to meet an
increased myocardial demand for oxygen in response to physical
exertion or emotional stress.
• In other words, the need for oxygen exceeds the supply.
• The severity of angina is based on the precipitating activity and its
effect on the activities of daily living.
Coronary Artery Disease
Coronary Artery Disease
 Coronary Artery Disease
Pathophysiology:
Angina is usually caused by atherosclerotic disease. Almost in variably,
angina is associated with a significant obstruction of a major coronary
artery.
Several factors are associated with typical anginal pain:
• Physical exertion, which can precipitate an attack by increasing
myocardial oxygen demand.
• Exposure to cold, which can cause vasoconstriction and an elevated
blood pressure, with increased oxygen demand.
 Coronary Artery Disease
• Eating a heavy meal, which increases the blood flow to the
mesenteric area for digestion, there by reducing the blood supply
available to the heart muscle (In a severely compromised heart,
shunting of blood for digestion can be suf-ficient to induce anginal
pain.)
• Stress or any emotion-provoking situation, causing the release of
adrenaline and increasing blood pressure, which may accelerate the
heart rate and increase the myocardial workload.
 Coronary Artery Disease
Clinical Manifestations:
• Ischemia of the heart muscle may produce pain.
• The pain is often felt deep in the chest behind the upper or middle
third of the sternum (retrosternal area). Typically, the pain or
discomfort is poorly localized and may radiate to the neck, jaw,
shoulders, and inner aspects of the upper arms, usually the left arm.
• A feeling of weakness or numbness in the arms, wrists, and hands
may accompany the pain, as may shortness of breath,pallor,
diaphoresis, dizziness or lightheadedness, and nausea and vomiting.
 MYOCARDIAL INFARCTION
Myocardial Infarction:
• MI refers to the process by which areas of myocardial cells in the
heart are permanently destroyed.
Causes:
• Like unstable angina, MI is usually caused by reduced blood flow in
a coronary artery due to atherosclerosis and occlusion of an artery by
an embolus or thrombus.
• Because unstable angina and acute MI are consideredto be the
same process but different points along a continuum, the term acute
coronary syndrome (ACS) may be used for these diagnoses.
 MYOCARDIAL INFARCTION
• Other causes of an MI include vasospasm (sudden constriction or
narrowing) of a coronary artery; decreased oxygen supply (eg, from
acute blood loss, anemia, or low blood pressure); and increased
demand for oxygen (eg, from a rapid heart rate, thyrotoxicosis, or
ingestion of cocaine).
• In each case, a profound imbalance exists between myocardial oxygen
supply and demand.
 MYOCARDIAL INFARCTION
Pathophysiology:
• Coronary occlusion, heart attack, and MI are terms used
synonymously, but the preferred term is MI. The area of infarction
takes time to develop.
• As the cells are deprived of oxygen, ischemia develops, cellular injury
occurs, and over time, the lack of oxygen results in infarction, or the
death of cells.
• The expression “time is muscle” reflects the urgency of appropriate
treatment to improve patient outcomes.
MYOCARDIAL INFARCTION
Clinical Manifestations
 MYOCARDIAL INFARCTION
Assessment and Diagnostic Findings
• Diagnosis of MI is generally based on the presenting symptoms, the
ECG, and laboratory test results (eg, serial serum enzyme values).
• The prognosis depends on the severity of coronary artery obstruction
and the extent of myocardial damage.
• Physical examination is always conducted, but the examination alone
is insufficient to confirm the diagnosis.
 MYOCARDIAL INFARCTION
PATIENT HISTORY:
The patient history has two parts: the description of the presenting symptom
(eg, pain) and the history of previous illnesses and family health history,
particularly of heart disease. Previous history should also include information
about the patient’s risk factors for heart disease.
ELECTROCARDIOGRAM:
The ECG provides information that assists in diagnosing acute MI. It should be
obtained within 10 minutes from the time a patient reports pain or arrives in
the emergency department. By monitoring the ECG over time, the location,
evolution, and resolution of an MI can be identified and monitored.
 MYOCARDIAL INFARCTION
• The ECG changes that occur with an MI are seen in the leads that
view the involved surface of the heart. The classic ECG changes are T-
wave inversion, ST-segment elevation, and development of an
abnormal Q wave.
• Because infarction evolves over time, the ECG also changes over
time. The first ECG signs of an acute MI are from myocardial ischemia
and injury.
• Myocardial injury causes the T wave to become enlarged and
symmetric.
• As the area of injury becomes ischemic, myocardial repolarization is
altered and delayed, causing the T wave to invert.
MYOCARDIAL INFARCTION
 MYOCARDIAL INFARCTION
ECHOCARDIOGRAM:
The echocardiogram is used to evaluate ventricular function. It may be
used to assist in diagnosing an MI, especially when theECG is non
diagnostic. The echocardiogram can detect hypokinetic and akinetic
wall motion and can determine the ejection fraction.
Normal Ejection Fraction is 55%-70%.
LABORATORY TESTS:
Historically, laboratory tests used to diagnose an MI included creatine
kinase (CK). These tests are based on the release of cellular contents
into the circulation when myocardial cells die.
 MYOCARDIAL INFARCTION
Creatine Kinase:
There are three CK isoenzymes: CK-MM (skeletal muscle), CK-MB (heart
muscle),and CK-BB (brain tissue). CK-MB is the cardiac-specific
isoenzyme; CK-MB is found mainly in cardiac cells and therefore rises
only when there has been damage to these cells.
 MYOCARDIAL INFARCTION
Troponin:
• Troponin, a protein found in the myocardium, regulates the
myocardial contractile process.
• There are three isomers of troponin (C, I, and T). Because of the
smaller size of this protein and the increased specificity of the
troponins I and T for cardiac muscle, these tests are used more
frequently to identify myocardial injury (unstable angina or acute MI).
• The increase in the level of troponin in the serum starts and peaks at
approximately the same time as CK-MB. However, it remains elevated
for a longer period,often up to 3 weeks, and it therefore cannot be
used to identify subsequent extension or expansion of an MI.
MYOCARDIAL INFARCTION
Acquired Valvular Disorders
 Acquired Valvular Disorders
• The valves of the heart control the flow of blood through the heart
into the pulmonary artery and aorta by opening and closing in
response to the blood pressure changes as the heart contracts and
relaxes through the cardiac cycle.
• When any of the heart valves do not close or open properly, blood
flow is affected.
• When valves do not close completely, blood flows backward through
the valve in a process called regurgitation.
• When valves do not open completely, a condition called stenosis, the
flow of blood through the valve is reduced.
 Acquired Valvular Disorders
MITRAL REGURGITATION:
Mitral regurgitation involves blood flowing back from the left ventricle into
the left atrium during systole. Often, the margins of the mitral valve cannot
close during systole.
• Pathophysiology:
Mitral regurgitation may be caused by problems with one or more of the
leaflets, the chordae tendineae, the annulus, or the papillary muscles.
• A mitral valve leaflet may shorten or tear. The chordae tendineae may
elongate, shorten, or tear.
• The annulus may be stretched by heart enlargement or deformed by
calcification.
• The papillary muscle may rupture, stretch, or be pulled out of position by
changes in the ventricular wall .
Acquired Valvular Disorders
Regardless ofthe cause,
blood regurgitates back
into the atrium during
systole.

With each beat of the

Mitral regurgitation
left ventricle, some of
ultimately involves the lungs
and the right ventricle. the blood is forced back
into the left atrium.

As a result, the lungs become Because this blood is added to the

blood that is beginning to flow in
congested, eventually adding
from the lungs, the left atrium must
extra strain on the right stretch. It eventually hypertrophies
ventricle. and dilates.

The backward flow of blood from

the ventricle diminishes the volume
of blood flowing into the atrium
from the lungs.
 Acquired Valvular Disorders
Clinical Manifestations:
• Dyspnea,
• fatigue,
• weakness .
• Palpitations,
• shortness of breath on exertion,
• cough from pulmonarycongestion also occur.
 Acquired Valvular Disorders
MITRAL STENOSIS:
Mitral stenosis is an obstruction of blood flowing from the left atrium into the
left ventricle.
Pathophysiology:
• Normally, the mitral valve opening is as wide as the diameter of three
fingers.
• In cases of marked stenosis, the opening narrows to the width of a pencil.
• The left atrium has great difficulty moving blood into the ventricle because
of the increased resistance of the narrowed orifice; it dilates (stretches) and
hypertrophies (thickens) because of the increased blood volume it holds.
 Acquired Valvular Disorders
• Because there is no valve to protect the pulmonary veins from the
backward flow of blood from the atrium, the pulmonary circulation
becomes congested.
• As a result, the right ventricle must contract against an abnormally
high pulmonary arterial pressure and is subjected to excessive strain.
Eventually, the right ventricle fails.
 Acquired Valvular Disorders
Clinical Manifestations:
• The first symptom of mitral stenosis is often breathing difficulty (ie,
dyspnea) on exertion as a result of pulmonary venous hypertension.
• Patients with mitral stenosis are likely to show progressive fatigue as a
result of low cardiac output. They may expectorate blood (ie,
hemoptysis), cough, and experience repeated respiratory infections.
 Acquired Valvular Disorders

AORTIC REGURGITATION:
Aortic regurgitation is the flow of blood back into the left ventricle from
the aorta during diastole.
Causes:
• It may be caused by inflammatory lesions that deform the leaflets of
the aortic valve,preventing them from completely closing the aortic
valve orifice.
• This valvular defect also may result from endocarditis, congenital
abnormalities, diseases such as syphilis, a dissecting aneurysm that
causes dilation or tearing of the ascending aorta.
 Acquired Valvular Disorders
Pathophysiology:
• In aortic regurgitation, blood from the aorta returns to the left
ventricle during diastole in addition to the blood normally delivered
by the left atrium.
• The left ventricle dilates, trying to accommodate the increased
volume of blood.
• It also hypertrophies,trying to increase muscle strength to expel more
blood with above normal force—raising systolic blood pressure.
• The arteries attempt to compensate for the higher pressures by reflex
vasodilation; the peripheral arterioles relax, reducing peripheral
resistance and diastolic blood pressure.
 Acquired Valvular Disorders
Clinical Manifestations:
• Aortic insufficiency develops without symptoms in most patients.
• Some patients are aware of a forceful heartbeat, especially in the
head or neck.
• Progressive signs and symptoms of left ventricular failure include
breathing difficulties (eg, orthopnea, paroxysmal nocturnal dyspnea),
especially at night.
 Acquired Valvular Disorders
AORTIC STENOSIS:
Aortic valve stenosis is narrowing of the orifice between the left
ventricle and the aorta.
In adults, the stenosis may involve congenital leaflet malformations or
an abnormal number of leaflets (ie, one or two rather than three), or it
may result from rheumatic endocarditis or cusp calcification of
unknown cause.
The leafletsof the aortic valve may fuse.
 Acquired Valvular Disorders
Pathophysiology:
• There is progressive narrowing of the valve orifice, usually over a
period of several years to several decades.
• The left ventricle overcomes the obstruction to circulation by
contracting more slowly but with greater energy than normal, forcibly
squeezing the blood through the very small orifice.
• The obstruction to left ventricular outflow increases pressure on the
left ventricle, which results in thickening of the muscle wall.
• The heart muscle hypertrophies. When these compensatory
mechanisms of the heart begin to fail, clinical signs and symptoms
develop.
 Acquired Valvular Disorders
Clinical Manifestations:
• Many patients with aortic stenosis are asymptomatic.
• After symptoms develop, patients usually first have exertional
dyspnea, caused by left ventricular failure.
• Other signs are dizziness and syncope because of reduced blood flow
to the brain.
• Angina pectoris is a frequent symptom that results from the increased
oxygen demands of the hypertrophied left ventricle, the decreased
time in diastole for myocardial perfusion, and the decreased blood
flow into the coronary arteries.
 Infectious Diseases of the Heart
INFECTIVE ENDOCARDITIS:
• Infective endocarditis is an infection of the valves and endothelial
surface of the heart.
• Endocarditis usually develops in people with cardiac structural defects
(eg, valve disorders). I
• nfective endocarditis is more common in older people, probably
because of decreased immunologic response to infection and the
metabolic alterations associated with aging.
• There is a high incidence of staphylococcal endocarditis among
IV/injection drug users who most commonly have infections of the
right heart valves
 Infectious Diseases of the Heart
Pathophysiology:
• Infective endocarditis is most often caused by direct invasion of the
endocardium by a microbe (eg, streptococci, enterococci, pneumococci,
staphylococci).
• The infection usually causes deformity of the valve leaflets, but it may
affect other cardiac structures such as the chordae tendineae.
• Patients at higher risk for infective endocarditis are those with
prosthetic heart valves, a history of endocarditis.
 Infectious Diseases of the Heart
• Hospital-acquired endocarditis occurs most often in patients with
debilitating disease, those with indwelling catheters, and those
receiving prolonged intravenous or antibiotic therapy.
• Patients receiving immunosuppressive medications or corticosteroids
may develop fungal endocarditis
 Infectious Diseases of the Heart
Clinical Manifestations:
• The signs and symptoms develop from the toxic effect of the
infection, from destruction of the heart valves, and from embolization
of fragments of vegetative growths on the heart.
• The heart murmurs that are characteristic of valvular stenosis,
regurgitation, or both become audible on auscultation and, in some
patients, even detectable as thrills on palpation.
 References

• pathophysiology concepts of altered health states(eighth-edition)

• Bruner Med & Surgical.