CARDIOVASCULAR SYSTEM  Endocardium – endothelial layer of the inner

myocardial surface
Heart Anatomy External Heart: Major Vessels of the Heart
 Approximately the size of your fist (Anterior View)
 Location
 Superior surface of diaphragm Vessels returning blood to the heart include:
 Left of the midline 1. Superior and inferior venae cava
 Anterior to the vertebral column, posterior 2. Right and left pulmonary veins
to the sternum Vessels conveying blood away from the heart
include:
1. Pulmonary trunk, which splits into right and left
pulmonary arteries
2. Ascending aorta (three branches)
a. Brachiocephalic
b. Left common carotid
c. Subclavian arteries

External Heart: Vessels that Supply/Drain the

Heart (Anterior View)

Coverings of the Heart: Anatomy Arteries

 Pericardium – a double-walled sac around the 1. Right and left coronary (in atrioventricular
heart composed of: groove) artery
1. A superficial fibrous pericardium 2. Marginal artery
2. A deep two-layer serous pericardium 3. Circumflex artery
 The parietal layer lines the internal 4. Anterior interventricular artery
surface of the fibrous pericardium
 The visceral layer or epicardium lines
the surface of the heart Veins
3. They are separated by the fluid-filled 5. small cardiac vein
pericardial cavity 6. anterior cardiac vein
Covering of the Heart: Physiology 7. great cardiac vein
 The function of the pericardium:
1. Protects and anchors the heart
2. Prevents overfilling of the heart with blood
3. Allows for the heart to work in a relatively
friction-free environment

External Heart: Major Vessels of the Heart (Posterior View)

Heart Wall
 Epicardium – visceral layer of the serous Vessels returning blood to the heart include:
pericardium
1. Right and left pulmonary veins
 Myocardium – cardiac muscle layer forming
2. Superior and inferior vena cava
the bulk of the heart
 Fibrous skeleton of the heart – Vessels conveying blood away from the heart include:
crisscrossing, interlacing layer of connective 1. Aorta
tissue 2. Right and left pulmonary arteries
 External Heart: Vessels that Supply/Drain the  Left ventricle pumps blood into the aorta
Heart (Posterior View)

Arteries
1. Right coronary artery (in atrioventricular
groove)
2. posterior interventricular artery (in
interventricular groove)
Vein
1. Great cardiac vein
2. posterior vein to left ventricle
3. coronary sinus
4. middle cardiac vein

Pathway of Blood Through the Heart and Lungs

 Right atrium → tricuspid valve → right

ventricle
 right ventricle → pulmonary semilunar valve
→
pulmonary arteries → lungs
 lungs → pulmonary veins → left atrium
 left atrium → bicuspid valve → left
ventricle
Atria of the Heart  left ventricle → aortic semilunar valve →
 Atria are the receiving chambers of the heart aorta
 Each atrium has a protruding auricle  aorta → systemic circulation
 Pectinate muscles mark atrial walls
 Blood enters right atria from superior and
inferior vena cava and coronary sinus
 Blood enters left atria from pulmonary
veins Ventricles of the Heart
 Ventricles are the discharging chambers of
the heart
 Papillary muscles and trabeculae carneae
muscles mark ventricular walls
 Right ventricle pumps blood into the
pulmonary trunk
 Coronary Circulation

Coronary circulation is the functional blood supply

to the heart muscle itself
Collateral routes ensure blood delivery to heart
even if major vessels are occluded

Heart Valves

valves ensure unidirectional blood flow

Heart
through the heart
Atrioventricular (AV) valves lie between the atria
and the ventricles
 AV valves prevent backflow into the atria
when ventricles contract
Chordae tendineae anchor AV valves to papillary
muscles
Semilunar valves prevent backflow of blood into the
ventricles
Aortic semilunar valves lie between the left
ventricle and the aorta
Pulmonary semilunar valve lies between the right Heart Sounds
ventricle and pulmonary trunk

Heart sounds (lub-dup) are associated with closing

of heart valves
 First sound occurs as AV valves close and
signifies beginning of systole (contraction)
 Second sound occurs when SL valves close at
the beginning of ventricular diastole
Cardiac Cycle
(relaxation)

Cardiac cycle refers to all events associated with

blood flow through the heart
 Systole – contraction of the heart muscle
 Diastole – relaxation of heart muscle
Cardiac Output (CO) and Reserve

Cardiac output is the amount of blood pumped by

each ventricle in one minute
  CO is the product of heart rate (HR) and  Angina is accompanied by severe
stroke volume (SV) apprehension and a feeling of impending
 HR is the number of heart beats per death.
minute  Pain is usually retrosternal, deep in the chest
 SV is the amount of blood pumped out behind the upper or middle third of the sternum
by a ventricle with each beat  Discomfort is poorly localized and may radiate
Cardiac reserve is the difference between resting to the neck, jaw, shoulders, and inner aspect of
and maximal CO the upper arms (usually the left arm)
 A feeling of weakness or numbness in the
arms, wrists, and hands, as well as shortness
Functions of the Heart of breath, pallor, diaphoresis, dizziness, or
lightheadedness, and nausea and vomiting,
1. Generating blood pressure may accompany the pain
2. Routing blood: separates pulmonary and systemic  Anxiety may occur with angina
circulations  An important characteristic of anginal pain is
3. Ensuring one-way blood flow: valves that it subsides when the precipitating cause is
4. Regulating blood supply removed or with nitroglycerin
a. Changes in the contraction rate and force Assessment and Diagnostic Methods
match blood delivery to changing  Evaluation of clinical manifestation of pain and
metabolic needs patient history
 Electrogram changes (12-lead ECG), stress
testing, blood tests
ANGINA PECTORIS  Echocardiogram, nuclear scan, or invasive
procedures such as cardiac catheterization
A clinical syndrome characterized by paroxysms of and coronary angiography
pain Medical Management
or a feeling of pressure in the anterior chest. Usually, a  Decrease the oxygen demand of the
result of atherosclerotic heart disease and is myocardium
associated with a significant obstruction of a major  increase oxygen supply
coronary artery. Unstable angina is not associated with  Objectives are met through pharmacologic
the above and may occur at rest. therapy and control of risk factors
 Alternatively, reperfusion procedures may be
Causes:
used to restore the blood supply to the
 insufficient coronary blood flow resulting in an
myocardium. These include PCI procedures
to meet
inadequate supply of the (e.g., percutaneous transluminal coronary
myocardial demand angioplasty [PTCA], intracoronary stents, and
Factors affecting anginal atherectomy) and coronary artery bypass graft
pain:
 Physical exertion (CABG)
 Exposure to cold
 Eating a heavy meal
 Stress or any emotion-provoking situation that
increases blood pressure, heart rate, and
myocardial workload
Factors that trigger angina episodes
 Sudden or excessive exertion
 Exposure to cold
 Tobacco use
 Heavy meals
 Excessive weight
 Some over-the-counter drugs, such as diet
pills, nasal decongestants, or drugs that
increase heart rate and blood pressure
Clinical Manifestation
 Pain varies from a feeling of indigestion to a
choking or heavy sensation in the upper chest
ranging from discomfort to agonizing pain.
 The patient with diabetes mellitus may not
experience severe pain with angina
 AORTIC STENOSIS chambers of the heart as a result of atrial fibrillation, MI,
infective endocarditis, or chronic heart failure

The narrowing of the orifice between the left ventricle

and the aorta. In adults, the stenosis is often a result of
degenerative calcifications, or it may be a result of
rheumatic endocarditis or cusp calcification of unknown
cause.
There is progressive narrowing of the valve orifice over
a period of several years to several decades. The
heart
muscles increase in size (hypertrophy) in response to
all
degrees of obstruction; clinical signs of heart failure
occur when compensatory mechanisms of the heart
fail.
Clinical Manifestation
 Exertional dyspnea
 Orthopnea, paroxysmal nocturnal dyspnea
(PND), and pulmonary edema
 Dizziness and syncope (fainting)
 Angina pectoris
 Blood pressure possibly low but usually normal
 Low pulse pressure (30 mmHg or less)
 Physical examination: loud, rough, systolic
murmur heard over the aortic area; vibration
over the base of the heart
Assessment and Diagnostic Methods
 12-lead ECG and echocardiogram
 Left-sided heart catheterization
Medical and Surgical
Management
 Medications are prescribed to treat
dysrhythmia or left ventricular failure.
 Definitive treatment for aortic stenosis is
surgical replacement of the aortic valve.
 Patients who are symptomatic and are not
surgical candidates may benefit from one- or
two- balloon percutaneous valvuloplasty
procedures.

ARTERIAL EMBOLISM AND ARTERIAL THROMBOSIS

An arterial embolus is a vascular occlusion. It arises

most commonly from thrombi that develop in the
An arterial thrombosis is a slowly developing clot in a
degenerated vessel that can itself occlude an artery.
Thrombi can also become detached and are carried
from the left side of the heart into the arterial system,
where they cause obstruction. The immediate effect
is cessation of distal blood flow. Secondary
vasospasm can contribute to ischemia. Emboli tend
to lodge at arterial bifurcations and areas of
atherosclerotic narrowing (cerebral, mesenteric,
renal, and coronary arteries). Acute thrombosis
frequently occurs in patient with preexisting ischemic
symptoms.
Clinical Manifestations
 The symptoms of arterial emboli depend
primarily on the size of the embolus, the
organ involved, and the state of the collateral
vessels
 Symptoms can generally be described as the
six “ P” s: pain, pallor, pulselessness,
paresthesia, poikilothermia (coldness), and
paralysis.
 The part of the limb below the occlusion is
markedly colder and paler than the part
above as a result of ischemia
Assessment and Diagnostic Methods
 Sudden or acute onset of symptoms and
apparent source for the embolus is diagnostic
 Two-dimensional
transthoracic echocardiography or TEE, chest
x-ray and ECG may reveal underlying cardiac
disease.
 Noninvasive duplex and Doppler
ultrasonography can determine the presence
and extent of underlying atherosclerosis, and
arteriography may be performed.
 ARTERIOSCLEROSIS and ATHEROSCLEROSIS

Arteriosclerosis, or “hardening of the arteries,” is the

most common disease of the arteries. It is a diffuse
process whereby the muscle fibers and the endothelial
lining of the walls of small arteries and arterioles
become thickened
Atherosclerosis primarily affects the intima of the large
and medium-sized arteries, causing changes that
include the accumulation of lipids (atheromas),
calcium,
blood components, carbohydrates, and fibrous tissue
on
the intimal layer of the artery. Although the pathologic
CARDIAC ARREST
process of arteriosclerosis and atherosclerosis differ,
rarely does one occur without the other, and the terms
are used interchangeably. Occurs when the heart ceases to produce an effective
pulse and circulate blood. May be caused by a cardiac
The common direct results of atherosclerosis in the electrical event (i.e., dysrhythmia) such as ventricular
arteries include narrowing (stenosis) of the lumen and fibrillation, progressive profound bradycardia, or when
obstruction by thrombosis, aneurysm, ulceration, and there is no heart rhythm at all (asystole).
rupture; ischemia and necrosis occur if the supply of
blood, nutrients, and oxygen is severely and Cardiac arrest may follow respiratory arrest; it may
permanently disrupted. also occur when electrical activity is present but there
is ineffective cardiac contraction or circulating volume,
Atherosclerosis can develop anywhere in the body but which is called pulseless electrical activity (PEA).
it is most common in bifurcation or branch areas of
blood vessels. PEA can be caused by hypovolemia (e.g., with
excessive bleeding), hypoxia, hypothermia,
Atherosclerotic lesions are of two types: fatty streaks hyperkalemia, massive pulmonary embolism,
(composed of lipids and elongated smooth muscle myocardial infarction, medication overdose (e.g., beta-
cells) and fibrous plaques (predominantly found in the blockers, calcium channel blockers).
abdominal aorta and coronary, popliteal, and internal
carotid arteries). Clinical Manifestation
 Consciousness, pulse, and blood pressure are
Risk Factors lost immediately.
 The use of tobacco products (strongest risk  Ineffective respiratory gasping may occur.
factor)  The pupils of the eyes begin dilating within 45
 High fat intake (suspected risk factor, along seconds.
with high serum cholesterol and blood lipid  Seizures may or may not occur.
levels) The risk of irreversible brain damage and death
 Hypertension increases with every minute from the time that
 Diabetes circulation ceases. The interval varies with the
 Obesity, stress, and lack of exercise age and underlying condition of the patient.
 Elevated C-reactive protein During this period, the diagnosis of cardiac arrest
must be made and measures must be taken
immediately to restore circulation
Clinical Manifestations Management
 Depends on the tissue/organ affected  Initiate immediate cardiopulmonary
 Heart resuscitation (CPR)
 Angina and MI due to coronary  Institute follow-up monitoring once patient is
atherosclerosis resuscitated.
 Brain
 Transient ischemic attacks and stroke due
to cerebrovascular disease
 Peripheral vessels (includes hypertension and
symptoms of aneurysm of the aorta,
renovascular disease, atherosclerotic lesions
of the extremities).
 parts, hepatic engorgement, tachycardia, and
extra heart sounds on physical examination.
Assessment and Diagnostic Methods
 Patient history; rule out other causes of failure
 Echocardiogram, cardiac MRI,
electrocardiogram (ECG), chest x-ray, cardiac
catheterization, and possibly an
endomyocardial biopsy

CARDIOMYOPATHIES

A heart muscle disease associated with cardiac

dysfunction.
Classified according to the structural and
functional abnormalities of the heart muscle:
CORONARY ATHEROSCLEROSIS and CAD
 Dilated cardiomyopathy (DCM) (most
common)
 Hypertrophic cardiomyopathy (HCM) (rare Coronary atherosclerosis is the most common cause of
autosomal dominant condition) cardiovascular disease in the United States and is
 Restrictive or constrictive cardiomyopathy characterized by an abnormal accumulation of lipid or
(RCM) fatty substances and fibrous tissue in the vessel wall.
 Arrhythmogenic right ventricular These substances block or narrow the vessel, reducing
cardiomyopathy (ARVC) blood flow to the myocardium.
 Unclassified cardiomyopathies (different from Atherosclerosis involves a repetitious inflammatory
or have characteristics of more than one of the response to injury of the artery wall and subsequent
other types) alteration in the structural and biochemical properties
A patient may have pathology representing more than of the arterial walls
one of these classifications, such as patient with HCM
Risk Factors (modifiable)
developing dilation and symptoms of DCM.
 Elevated blood pressure
Ischemic cardiomyopathy is a term frequently used to  Hyperglycemia
describe an enlarged heart caused by coronary artery  Metabolic Syndrome
disease (CAD), which is usually accompanied by heart  Obesity
failure.  Physical inactivity
 High blood cholesterol (hyperlipidemia)
Clinical Manifestation
 Cigarette smoking, tobacco
 Presents initially with signs and symptoms of
use Risk Factors (Not modifiable)
heart failure (shortness of breath on exertion,
 Positive family history (a first-degree relative
fatigue).
with cardiovascular disease at age 55 years or
 May also report paroxysmal nocturnal dyspnea
younger for males and at age 65 years or
(PND), cough, and orthopnea
younger for females)
 Other symptoms include fluid retention,
 Age (>45 in men, >55 in women)
peripheral edema, nausea, chest pain,
 Gender (men develop cardiovascular disease
palpitations, dizziness, and syncope with
at an earlier age than do women)
exertion
 Race (higher incidence in African Americans
 With HCM, cardiac arrest (i.e., sudden cardiac
than in Caucasians)
death) may be the initial manifestation in
Clinical Manifestations
young people.
 Symptoms and complications develop
 Systemic venous congestion, jugular vein
according to:
distention, pitting edema of dependent body
1. the location and degree of narrowing of
the arterial lumen;
 2. thrombus formation;  A systolic murmur is heard as a high-pitched,
3. and obstruction of blood flow to the blowing sound at the apex. The pulse may be
myocardium. regular and of good volume, or it may be
 Symptoms include the following irregular as a result of extrasystolic beats or
 Ischemia atrial fibrillation.
 Chest pain: angina pectoris  Doppler echocardiography is used to diagnose
 Atypical symptoms of myocardial ischemia and monitor the progression of mitral
(shortness of breath, nausea, and weakness) regurgitation.
 Myocardial infarction  Transesophageal echocardiography (TEE)
 Dysrhythmias, sudden death provides
Assessment and Diagnostic Methods the best
 Identification of risk factors for coronary heart images of
disease primarily involves taking a thorough the mitral
history, including family history, physical valve
examination (note blood pressure and weight),
and laboratory work (e.g., cholesterol levels
[low-density lipoprotein (LDL) to high-density
lipoprotein (HDL)], glucose).

MITRAL STENOSIS

Mitral stenosis is the progressive thickening and

contracture of the mitral valve leaflets and chordae
tendineae that causes narrowing of the orifice and
progressive obstruction to blood flow from the left
atrium into the left ventricle.
Normally, the mitral valve opening is as wide as three
fingers. In cases of marked stenosis, the opening
narrows to the width of a pencil. The left atrium dilates
MITRAL REGURGITATION (INSUFFICIENCY) and hypertrophies because it has great difficulty
moving blood in to the ventricle and because of the
Mitral regurgitation involves blood flowing back from increased blood volume the atria must now hold.
the left ventricle into the left atrium during systole. Because there is no valve to protect the pulmonary
Often, the edges of the mitral valve leaflets do not veins from the backward flow of blood from the atrium,
close during systole. There is a problem with one or the pulmonary circulation becomes congested. The
more of the leaflets, the chordae tendineae, the resulting high pulmonary pressure can eventually lea
annulus, or papillary muscles. to right ventricular failure
With each beat, the left ventricle forces some blood Clinical Manifestations
back into the left atrium, causing the atrium to dilate
and hypertrophy. This backward flow of blood from the First symptom is often dyspnea on exertion (due to
ventricle eventually causes the lungs to become pulmonary venous hypertension).
congested, which adds strain to the right ventricle, Progressive fatigue (result of low cardiac output), dry
resulting in cardiac failure. cough or wheezing, hemoptysis, palpitations,
Clinical Manifestation orthopnea, paroxysmal nocturnal dyspnea (PND), and
 Chronic mitral regurgitation is often repeated respiratory infections may be noted
asymptomatic; but acute regurgitation (after Weak and often irregular pulse (because of atrial
myocardial infarction [MI]) usually presents as fibrillation) may also be noted
severe heart failure
 Dyspnea, fatigue, and weakness are the most
common symptoms
 Palpitations, shortness of breath on exertion,
and cough from pulmonary congestion also
occur
Assessment and Diagnostic Methods
 MYOCARDITIS

Myocarditis is an inflammatory process involving the

myocardium. When the muscle fibers of the heart are
damaged, life is threatened. Myocarditis usually results
from an infectious process (e.g., viral, bacterial,
rickettsial, fungal, parasitic, metazoal, protozoal,
spirochetal).
It may develop in patients receiving
immunosuppressive therapy or those with infective
endocarditis, Crohn disease, or systemic lupus
erythematosus.
MITRAL VALVE PROLAPSE
Myocarditis can cause heart dilation, thrombi on the
heart wall (mural thrombi), infiltration of circulating
A dysfunction of the mitral valve leaflets that prevents
blood cells around the coronary vessels and between
the mitral valve from closing completely during systole.
the muscle fibers, and degeneration of muscle fibers
Blood then regurgitates from the left ventricle back into
themselves
the left atrium. It occurs more frequently in women
Clinical Manifestations
Clinical Manifestations
 Clinical features depend on the type of
 The syndrome may produce no symptoms or
infection, degree of myocardial damage, and
may progress rapidly and result in sudden
capacity of the myocardium to recover.
death.
 Symptoms may be moderate, mild, or absent.
 Patients may experience symptoms of fatigue,
 patient may report fatigue and dyspnea,
shortness of breath (not correlated with
palpitations, and occasional discomfort in the
activity), lightheadedness, dizziness, syncope,
chest and upper abdomen
palpitations, chest pain, and anxiety.
 Patients may develop severe congestive heart
 Fatigue may be present regardless of the
failure or sustain sudden cardiac death
person’s activity level and amount of rest or
sleep
 During the physical examination, a mitral
(systolic) click is identified. Presence of a click
is an early sign that a valve leaflet is Assessment and Diagnostic Findings
ballooning into the left atrium.  Cardiac enlargement
 A murmur of mitral regurgitation may be heard  Faint heart sounds (especially S1)
if progressive valve leaflet stretching and  Gallop rhythm or
regurgitation have occurred.  a systolic murmur may be found on clinical
 A few patients experience signs and examination
symptoms of heart failure if mitral regurgitation  Cardiac MRI with contrast may be diagnostic
exists and can guide clinicians to sites for
endocardial biopsies