CARDIOVASCULAR SYSTEM:
 The heart is a hollow, muscular organ located in the center of the
thorax, where it occupies the space between the lungs (mediastinum)
and rests on the diaphragm.
 the weight and size of the heart are influenced by age, gender, body
weight, extent of physical exercise and conditioning, and heart disease.
The heart pumps blood to the tissues, supplying them with oxygen and
other nutrients
 The heart is composed of three layers. The inner layer, or
endocardium, consists of endothelial tissue and lines the inside of the
heart and valves. The middle layer, or myocardium, is made up of
muscle fibers and is responsible for the pumping action. The exterior
layer of the heart is called the epicardium
 The heart is encased in a thin, fibrous sac called the pericardium,
which is composed of two layers. Adhering to the epicardium is the
visceral pericardium. Enveloping the visceral pericardium is the
parietal pericardium, a tough fibrous tissue that attaches to the great
vessels, diaphragm, sternum, and vertebral column and supports the
heart in the mediastinum. The space between these two layers
(pericardial space) is normally filled with about 20 mL of fluid, which
lubricates the surface of the heart and reduces friction during systole
 Heart Chambers: The pumping action of the heart is accomplished
by the rhythmic relaxation and contraction of the muscular walls of its
two top chambers (atria) and two bottom chambers (ventricles).
During the relaxation phase, called diastole, all four chambers relax
simultaneously, which allows the ventricles to fill in preparation for
contraction. Diastole is commonly referred to as the period of
ventricular filling. Systole refers to the events in the heart during
contraction of the atria and the ventricles. Unlike diastole, atrial and
ventricular systole are not simultaneous events. Atrial systole occurs
first, just at the end of diastole, followed by ventricular systole. This
synchronization allows the ventricles to fill completely prior to
ejection of blood from these chambers.
 The right side of the heart, made up of the right atrium and right
ventricle, distributes venous blood (deoxygenated blood) to the lungs
via the pulmonary artery (pulmonary circulation) for oxygenation. The
pulmonary artery is the only artery in the body that carries
deoxygenated blood. The right atrium receives venous blood returning
to the heart from the superior vena cava (head, neck, and upper
extremities), inferior vena cava (trunk and lower extremities), and
coronary sinus (coronary circulation). The left side of the heart,
composed of the left atrium and left ventricle, distributes oxygenated
blood to the remainder of the body via the aorta (systemic circulation).
The left atrium receives oxygenated blood from the pulmonary
circulation via four pulmonary veins
 Both the sinoatrial (SA) node (the primary pacemaker of the heart) and
the atrioventricular (AV) node (the secondary pacemaker of the heart)
are composed of nodal cells. The SA node is located at the junction of
the superior vena cava and the right atrium. The SA node in a normal
resting adult heart has an inherent firing rate of 60 to 100 impulses per
minute; however, the rate changes in response to the metabolic
demands of the body
 This exchange of ions creates a positively charged intracellular space
and a negatively charged extracellular space that characterizes the
period known as depolarization. Once depolarization is complete, the
exchange of ions reverts to its resting state; this period is known as
repolarization.The repeated cycle of depolarization and repolarization
is called the cardiac action potential
CARDIAC CYCLE:
 The number of cardiac cycles completed in a minute depends on the
heart rate.During diastole, all four heart chambers are relaxed. As a
result, the AV valves are open and the semilunar valves are closed.
Pressures in all of the chambers are the lowest during diastole, which
facilitates ventricular filling. Venous blood returns to the right atrium
from the superior and inferior vena cava, then into the right ventricle.
On the left side, oxygenated blood returns from the lungs via the four
pulmonary veins into the left atrium and ventricle.Toward the end of
this diastolic period, atrial systole occurs as the atrial muscles contract
in response to an electrical impulse initiated by the SA node. Atrial
systole increases the pressure inside the atria, ejecting the remaining
blood into the ventricles.At this point, ventricular systole begins in
response to propagation of the electrical impulse that began in the SA
node some milliseconds earlier.Beginning with ventricular systole, the
pressure inside the ventricles rapidly increases, forcing the AV valves
to close. As a result, blood ceases to flow from the atria into the
ventricles, and regurgitation (backflow) of blood into the atria is
 prevented. The rapid increase in pressure inside the right and left
ventricles forces the pulmonic and aortic valves to open, and blood is
ejected into the pulmonary artery and aorta, respectively. The exit of
blood is at first rapid; then, as the pressure in each ventricle and its
corresponding artery equalizes, the flow of blood gradually decreases.
At the end of systole, pressure within the right and left ventricles
rapidly decreases. As a result, pulmonary arterial and aortic pressures
decrease, causing closure of the semilunar valves. These events mark
the onset of diastole, and the cardiac cycle is repeated.
 Cardiac output refers to the total amount of blood ejected by one of
the ventricles in liters per minute.
 Stroke volume is the amount of blood ejected from one of the
ventricles per heartbeat.
 Baroreceptors are specialized nerve cells located in the aortic arch
and in both right and left internal carotid arteries The baroreceptors are
sensitive to changes in blood pressure (BP). During significant
elevations in BP (hypertension), these cells increase their rate of
discharge, transmitting impulses to the cerebral medulla. This action
initiates parasympathetic activity and inhibits sympathetic response,
lowering the heart rate and the BP. The opposite is true during
hypotension (low BP). Less baroreceptor stimulation during periods of
hypotension prompts a decrease in parasympathetic activity and
enhances sympathetic responses. These compensatory mechanisms
attempt to elevate the BP through vasoconstriction and increased heart
rate
 Preload refers to the degree of stretch of the ventricular cardiac
muscle fibers at the end of diastole. The end of diastole is the period
when filling volume in the ventricles is the highest and the degree of
stretch on the muscle fibers is the greatest. The volume of blood within
the ventricle at the end of diastole determines preload, which directly
affects stroke volume. Preload is decreased by a reduction in the
volume of blood returning to the ventricles. Diuresis, venodilating
agents, excessive loss of blood, or dehydration reduce preload. Preload
is increased by increasing the return of circulating blood volume to the
ventricles. Controlling the loss of blood or body fluids and replacing
fluids (blood transfusions and intravenous fluid administration) are
examples of ways to increase preload.
 Afterload, or resistance to ejection of blood from the ventricle, is the
second determinant of stroke volume.
 Contractility refers to the force generated by the contracting
myocardium.
 Blood Pressure- Systemic arterial BP is the pressure exerted on the
walls of the arteries during ventricular systole and diastole. It is
affected by factors such as cardiac output; distention of the arteries;
and the volume, velocity, and viscosity of the blood. A normal BP in
adults is considered a systolic BP less than 120 mm Hg over a diastolic
BP less than 80 mm Hg. High BP, called hypertension, is defined by
having a systolic BP that is consistently greater than 140 mm Hg or a
diastolic BP greater than 90 mm Hg.Blood Pressure Systemic arterial
BP is the pressure exerted on the walls of the arteries during
ventricular systole and diastole. It is affected by factors such as cardiac
output; distention of the arteries; and the volume, velocity, and
viscosity of the blood. A normal BP in adults is considered a systolic
BP less than 120 mm Hg over a diastolic BP less than 80 mm Hg.
High BP, called hypertension, is defined by having a systolic BP that
is consistently greater than 140 mm Hg or a diastolic BP greater than
90 mm Hg
 The difference between the systolic and the diastolic pressures is
called the pulse pressure
 Postural (orthostatic) hypotension is a sustained decrease of at least
20 mm Hg in systolic BP or 10 mm Hg in diastolic BP within 3
minutes of moving from a lying or sitting to a standing position. It is
usually accompanied by dizziness, lightheadedness, or syncope
 Tricuspid and mitral valve closure creates the first heart sound (S1).
 Closure of the pulmonic and aortic valves produces the second heart
sound (S2), commonly referred to as the “dub” sound. The aortic
component of S2 is heard the loudest over the aortic and pulmonic
areas
 An S3 (“DUB”) is heard early in diastole during the period of rapid
ventricular filling as blood flows from the atrium into a noncompliant
ventricle. It is heard immediately after S2. “Lub-dub-DUB” is used to
imitate the abnormal sound of a beating heart when an S3 is present.
 S4 heard just before S1 is generated during atrial contraction as blood
forcefully enters a noncompliant ventricle.
 Murmurs are created by turbulent flow of blood in the heart. The
causes of the turbulence may be a critically narrowed valve, a
malfunctioning valve that allows regurgitant blood flow
 A harsh, grating sound that can be heard in both systole and diastole is
called a friction rub. It is caused by abrasion of the inflamed
pericardial surfaces from pericarditis. Because a friction rub may be
confused with a murmur
 The electrical stimulation is called depolarization, and the mechanical
contraction is called systole. Electrical relaxation is called
repolarization, and mechanical relaxation is called diastole.
 The P wave represents the electrical impulse starting in the SA node
and spreading through the atria. Therefore, the P wave represents atrial
depolarization.
 The QRS complex represents ventricular depolarization. Not all QRS
complexes have all three waveforms.
 The T wave represents ventricular repolarization
 The U wave is thought to represent repolarization of the Purkinje
fibers; although this wave is rare, it sometimes appears in patients with
hypokalemia (low potassium levels), hypertension, or heart disease.
 The PR interval is measured from the beginning of the P wave to the
beginning of the QRS complex and represents the time needed for
sinus node stimulation, atrial depolarization, and conduction through
the AV node before ventricular depolarization
 The ST segment, which represents early ventricular repolarization,
lasts from the end of the QRS complex to the beginning of the T wave.
 The QT interval, which represents the total time for ventricular
depolarization and repolarization, is measured from the beginning of
the QRS complex to the end of the T wave.
DISORDERS OF THE CARDIOVASCULAR SYSTEM:
1. RHEUMATIC ENDOCARDITIS:
 Acute rheumatic fever, which occurs most often in school-age
children, may develop after an episode of group. A beta-hemolytic
streptococcal pharyngitis. Patients with rheumatic fever may develop
rheumatic heart disease as evidenced by a new heart murmur,
cardiomegaly, pericarditis, and heart failure. Prompt and effective
treatment of “strep” throat with antibiotics can prevent development of
rheumatic fever. Streptococcus is spread by direct contact with oral or
respiratory secretions. Although bacteria are the causative agents,
malnutrition, overcrowding, poor hygiene, and lower socioeconomic
status may predispose individuals to rheumatic fever.
2. INFECTIVE ENDOCARDITIS:
 Infective endocarditis is a microbial infection of the endothelial
surface of the heart. It usually develops in people with prosthetic heart
valves, cardiac devices (pacemaker), or structural cardiac defects.
 Invasive procedures, particularly those involving mucosal surfaces can
cause a bacteremia, which rarely lasts more than 15 minutes. However,
if a patient has any anatomic cardiac defects or implanted cardiac
devices, bacteremia can cause bacterial endocarditis. Bacteremia also
may be caused by IV drug abuse, body piercing.
 A deformity or injury of the endocardium leads to accumulation of
fibrin and platelets (clot formation) on the endocardium. Infectious
organisms, usually staphylococci or streptococci, invade the clot and
endocardial lesion. Other causative microorganisms include
fungi.Infection most frequently results in platelets, fibrin, blood cells,
and microorganisms that cluster as vegetations on the endocardium.
Vegetations may embolize to other tissues throughout the body. As the
clot on the endocardium continues to expand, the infecting organism is
covered by new clot and concealed from the body’s normal defenses.
Infection may erode through the endocardium into underlying
structures (e.g., valve leaflets), causing tears or other deformities of
valve leaflets, dehiscence of prosthetic valves, deformity of chordae
tendineae, or mural abscesses
 Primary presenting symptoms of infective endocarditis are fever and a
heart murmur.Fever may be intermittent or absent, especially in
patients who are receiving antibiotics or corticosteroids, in older
adults, and in those who have heart failure or kidney injury. A heart
murmur may be absent initially but develops in almost all patients.
Murmurs that worsen over time indicate progressive damage from
vegetations or perforation of a valve or rupture of chordae
tendineae.Small, painful nodules may be present in Small, painful
nodules may be present in
 Antibiotic therapy usually is given for 2 to 6 weeks every 4 hours or
continuously by IV infusion. Parenteral therapy is given in doses that
produce a high serum concentration for a significant period to ensure
eradication of the dormant bacteria within dense vegetations.
 The nurse monitors the patient’s temperature. The patient may have a
fever for weeks. The nurse administers antibiotic, antifungal, or
antiviral medication as prescribed or educates the patient to take them
as prescribed. Patients need enough fluids to keep their urine light
yellow. Good infection control and prevention practices include
appropriate hand hygiene by both patients and caregivers. Heart
sounds are assessed. A new or worsening murmur may indicate
dehiscence of a prosthetic valve, rupture of an abscess, or injury to
valve leaflets or chordae tendineae. Patients with infective endocarditis
are at high risk for another episode of infectious endocarditis.
3. MYOCARDITIS:
 Myocarditis, an inflammatory process involving the myocardium, can
cause heart dilation, thrombi on the heart wall (mural thrombi),
infiltration of circulating blood cells around the coronary vessels and
between the muscle fibers, and degeneration of the muscle fibers
themselves.
 Myocarditis usually results from viral bacterial, rickettsial, fungal,
parasitic, metazoal, protozoal, or spirochetal infection. It also may be
immune related, occurring after acute systemic infections such as
rheumatic fever. It may begin in one small area of the myocardium and
then spread throughout the myocardium. The degree of myocardial
inflammation and necrosis determines the degree of interstitial
collagen and elastin destruction. The greater the destruction, the
greater is the hemodynamic effect and resulting signs and symptoms.
 Patients may be asymptomatic, with an infection that resolves on its
own. However, they may develop mild-to-moderate symptoms and
seek medical attention, often reporting fatigue and dyspnea, syncope,
palpitations, and occasional discomfort in the chest and upper
abdomen. The most common symptoms are flulike.Patients may also
sustain sudden cardiac death or quickly develop severe congestive
heart failure.
 Bed rest also helps decrease myocardial damage and the complications
of myocarditis. Physical activity is increased slowly, and the patient is
instructed to report any symptoms that occur with increasing activity,
such as a rapidly beating heart. The nurse assesses for resolution of
tachycardia, fever, and any other clinical manifestations. The
cardiovascular assessment focuses on signs and symptoms of heart
failure and dysrhythmias. Patients with dysrhythmias should have
continuous cardiac monitoring with personnel and equipment readily
available to treat life-threatening dysrhythmias. Anti-embolism
stockings and passive and active exercises should be used because
embolization from venous thrombosis and mural thrombi can occur,
especially in patients on bed rest
4. PERICARDITIS:
 Pericarditis refers to an inflammation of the pericardium, which is the
membranous sac enveloping the heart.
 The inflammatory process of pericarditis may lead to an accumulation
of fluid in the pericardial sac (pericardial effusion) and increased
pressure on the heart, leading to cardiac tamponade. Frequent or
prolonged episodes of pericarditis also may lead to thickening and
decreased elasticity of the pericardium, or scarring may fuse the
visceral and parietal pericardium. These conditions restrict the heart’s
ability to fill with blood (constrictive pericarditis). The pericardium
may become calcified, further restricting ventricular expansion during
ventricular filling (diastole). With less filling, the ventricles pump less
blood, leading to decreased cardiac output and signs and symptoms of
heart failure. Restricted diastolic filling may result in increased
systemic venous pressure, causing peripheral edema and hepatic
failure.
 The most characteristic symptom of pericarditis is chest pain, although
pain also may be located beneath the clavicle, in the neck, or in the left
trapezius (scapula) region. Pain or discomfort usually remains fairly
constant, but it may worsen with deep inspiration and when lying
down or turning.The most characteristic clinical manifestation of
pericarditis is a creaky or scratchy friction rub heard most clearly at
the left lower sternal border. Other signs may include a mild fever,
increased WBC count, anemia, and an elevated ESR or Creactive
protein level. Patients may have a nonproductive cough or hiccup.
Dyspnea, as well as respiratory splinting because of pain upon
inspiration, and other signs and symptoms of heart failure may occur
as a result of pericardial compression due to constrictive pericarditis or
cardiac tamponade.The heart rate may increase to maintain cardiac
output.
 Analgesic medications and NSAIDs such as aspirin or ibuprofen may
be prescribed for pain relief during the acute phase. Patients with chest
pain often benefit from education and reassurance that the pain is not
 due to a heart attack. Pain may be relieved with a forward-leaning or
sitting position. To minimize complications, the nurse helps the patient
with activity restrictions until pain and fever subside., the nurse
encourages gradual increases of activity. However, if pain, fever, or
friction rub recurs, activity restrictions must be resumed. The nurse
educates the patient and family about a healthy lifestyle to enhance the
patient’s immune system. The nurse monitors the patient for heart
failure. Patients with hemodynamic instability or pulmonary
congestion are treated as if they had heart failure.
5. HEART FAILURE/CONGESTIVE HEART FAILURE:
 clinical syndrome resulting from structural or functional cardiac
disorders that impair the ability of the ventricles to fill or eject blood
 HF is recognized as a clinical syndrome characterized by signs and
symptoms of fluid overload or inadequate tissue perfusion. Fluid
overload and decreased tissue perfusion result when the heart cannot
generate cardiac output (CO) sufficient to meet the body’s demands
for oxygen and nutrients. The term heart failure indicates myocardial
disease in which impaired contraction of the heart (systolic
dysfunction) or filling of the heart (diastolic dysfunction) may cause
pulmonary or systemic congestion.
 The most common type is an alteration in ventricular contraction
called systolic heart failure, which is characterized by a weakened
heart muscle. A second type is diastolic heart failure, which is
characterized by a stiff and noncompliant heart muscle, making it
difficult for the ventricle to fill.
 As HF develops, the body activates neurohormonal compensatory
mechanisms. These mechanisms represent the body’s attempt to cope
with the HF and are responsible for the signs and symptoms that
develop. Systolic HF results in decreased blood ejected from the
ventricle. The decreased blood flow is sensed by baroreceptors in the
aortic and carotid bodies. The sympathetic nervous system is then
stimulated to release epinephrine and norepinephrine. The purpose of
this initial response is to increase heart rate and contractility and
support the failing myocardium, but the continued response has
multiple negative effects.As the heart’s workload increases,
contractility of the myocardial muscle fibers decreases. Decreased
contractility results in an increase in end-diastolic blood volume in the
ventricle, stretching the myocardia.muscle fibers and increasing the
size of the ventricle (ventricular dilation). One way the heart
compensates for the increased workload is to increase the thickness of
the heart muscle (ventricular hypertrophy).
LEFT SIDED HEART FAILURE:
 Pulmonary congestion occurs when the left ventricle cannot effectively
pump blood out of the ventricle into the aorta and the systemic
circulation. The increased left ventricular end-diastolic blood volume
increases the left ventricular end-diastolic pressure, which decreases
blood flow from the left atrium into the left ventricle during diastole.
The blood volume and pressure build up in the left atrium, decreasing
flow through the pulmonary veins into the left atrium. Pulmonary
venous blood volume and pressure increase in the lungs, forcing fluid
from the pulmonary capillaries into the pulmonary tissues and alveoli,
causing pulmonary interstitial edema and impaired gas exchange.
 The clinical manifestations of pulmonary congestion include dyspnea,
cough, pulmonary crackles, and low oxygen saturation levels. An extra
heart sound, the S3, or “ventricular gallop,” may be detected on
auscultation. It is caused by abnormal ventricular filling
 The patient may report orthopnea, difficulty breathing when lying flat.
Patients with orthopnea may use pillows to prop themselves up in bed,
or they may sit in a chair and even sleep sitting up. Some patients have
sudden attacks of dyspnea at night, a condition known as paroxysmal
nocturnal dyspnea (PND).
RIGHT SIDED HEART FAILURE:
 When the right ventricle fails, congestion in the peripheral tissues and
the viscera predominates. This occurs because the right side of the
heart cannot eject blood effectively and cannot accommodate all of the
blood that normally returns to it from the venous circulation. Increased
venous pressure leads to jugular venous distention (JVD) and
increased capillary hydrostatic pressure throughout the venous system.
 Systemic clinical manifestations include edema of the lower
extremities, hepatomegaly, ascites, and weight gain due to retention of
fluid. Hepatomegaly and tenderness in the right upper quadrant of the
abdomen result from venous engorgement of the liver. The increased
pressure may interfere with the liver’s ability to function.
ASSESSMENT AND DIAGNOSTIC FINDINGS:
 Assessment of ventricular function is an essential part of the initial
diagnostic workup. An echocardiogram is usually performed to
determine the EF, identify anatomic features such as structural
abnormalities and valve malfunction, and confirm the diagnosis of HF.
 A chest x-ray and a 12-lead electrocardiogram (ECG) are obtained to
assist in the diagnosis. Laboratory studies usually performed during
the initial workup include serum electrolytes, blood urea nitrogen
(BUN), creatinine, liver function tests, thyroid-stimulating hormone,
complete blood count (CBC), BNP, and routine urinalysis. The BNP
level is a key diagnostic indicator of HF; high levels are a sign of high
cardiac filling pressure and can aid in both the diagnosis and
management of HF
MEDICAL MANAGEMENT:
 Oral and intravenous (IV) medications, major lifestyle changes,
supplemental oxygen, and surgical interventions including
implantation of cardiac devices and cardiac transplantation.
 Providing comprehensive education and counseling to the patient and
family. Lifestyle recommendations include restriction of dietary
sodium; avoidance of smoking, including passive smoke; avoidance of
excessive fluid and alcohol intake; weight reduction when indicated;
and regular exercise.
 Angiotensin-Converting Enzyme Inhibitors ACE inhibitors play a
pivotal role in the management of systolic HF. Available as oral and
IV medications, ACE inhibitors promote vasodilation and diuresis,
ultimately decreasing afterload and preload. Vasodilation reduces
resistance to left ventricular ejection of blood, diminishing the heart’s
workload and improving ventricular emptying.
 Angiotensin Receptor Blockers-ARBs block the vasoconstricting
effects of angiotensin II at the angiotensin II receptors
 Hydralazine and Isosorbide Dinitrate-Nitrates cause venous
dilation, which reduces the amount of blood return to the heart and
lowers preload. Hydralazine lowers systemic vascular resistance and
left ventricular afterload.
 Beta-Blockers Beta-blockers are also considered first-line therapy and
are routinely prescribed in addition to ACE inhibitors.They relax blood
vessels, lower blood pressure, decrease afterload, and decrease cardiac
workload. Betablockers, such as carvedilol and sustainedrelease
metoprolol (Toprol XL), have been found to improve functional status
and reduce mortality and morbidity in patients with HF.
 Diuretics are prescribed to remove excess extracellular fluid by
increasing the rate of urine produced in patients with signs and
symptoms of fluid overload. Loop diuretics, such as furosemide
(Lasix), inhibit sodium and chloride reabsorption mainly in the
ascending loop of Henle. HF patients with severe volume overload are
generally treated with a loop diuretic first.
6. MYOCARDIAL INFARCTION
 In unstable angina, there is reduced blood flow in a coronary artery,
often due to rupture of an atherosclerotic plaque. A clot begins to form
on top of the coronary lesion, but the artery is not completely
occluded.
 In an MI, plaque rupture and subsequent thrombus formation result in
complete occlusion of the artery, leading to ischemia and necrosis of
the myocardium supplied by that artery. Vasospasm (sudden
constriction or narrowing) of a coronary artery, decreased oxygen
supply, and increased demand for oxygen are other causes of MI. In
each case, a profound imbalance exists between myocardial oxygen
supply and demand.The area of infarction develops over minutes to
hours. As the cells are deprived of oxygen, ischemia develops, cellular
injury occurs, and the lack of oxygen results in infarction, or the death
of cells.
 Chest pain that occurs suddenly and continues despite rest and
medication is the presenting symptom in most patients with
ACS.Patients may present with a combination of symptoms, including
chest pain, shortness of breath, indigestion, nausea, and anxiety. They
may have cool, pale, and moist skin. Their heart rate and respiratory
rate may be faster than normal.
MANAGEMENT:
 receive supplemental oxygen, aspirin, nitroglycerin, and morphine.
Morphine is the drug of choice to reduce pain and anxiety. It also
reduces preload and afterload,decreasing the work of the heart.