Disorder of

Cardiovascular
System
 At the end of the session you will be able to :
1. Discuss the function of cardiovascular systems
2. Identify Risk factors for cardiovasculardisease
3. describe causes, pathophysiology, diagnostic tests, and
treatments for several common cardiovascular disorders.
4. Identify the sign and symptoms of selected cardiac
disease

OBJECTIVES 5.Explain the diagnostic management and treatment

modalities of cardiovascular disorder .

4. Discuss the pathophysiology and nursing care of

each
Understanding the cardiovascular system

 The cardiovascular system begins its activity when

the fetus is barely 1 month old, and it’s the last
system to cease activity at the end of life.
The heart, arteries, and veins make up the cardiovascular system.

These structures transport life- supporting oxygen and nutrients to

cells, remove metabolic waste products, and carry hormones from one

part of the body to another.

 FUNCTION

• Transport life-supporting oxygen and nutrients to cells.

• Remove metabolic waste products.

• Carry hormones from one part of the body to another.

• Circulation requires normal heart function, which propels blood

through the system by continuous rhythmic contractions.



Circulation requires normal heart

function, which propels blood through
the system by continuous rhythmic
contractions.
 Oxygen Balancing Act

A critical balance exists between myocardial oxygen supply

and demand.

 A decrease in oxygen supply or an increase in

oxygen demand can disturb this balance and
threaten myocardial function.
 Risk Factors

  Modifiable factors & Some risk factors

can be avoided or altered, potentially slowing the disease process or even
reversing it. risk factors of cardiac disease include:
Elevated serum lipid levels
Hypertension
Cigarette smoking
Diabetes mellitus
Sedentary lifestyle
Stress
Obesity
Excessive intake of saturated fats, carbohydrates, and salt.
 Cont…..
 Nonmodifiable risk factors
 Four nonmodifiable factors increase a person’s risk
of cardiovascular disease:

Age

Male gender

Family history

Race.
 Age

 Susceptibility to cardiovascular disease increases with age;

disease before age 40 is unusual. However, the age-disease
correlation may simply reflect the longer duration of exposure to
other risk factors.
 Women are less susceptible than men to heart disease until
after menopause; then they become as susceptible as men.
One theory proposes that estrogen has a protective effect.
A positive family history also increases a person’s chances of

developing premature cardiovascular disease.

Although it affects all races, blacks are most susceptible

to cardiovascular disease.
 Cardiovascular Disorders

Cardiogenic shock

MI

Heart failure

Hypertension

• Rheumatic fever and rheumatic heart disease.

01 Cardiogenic Shock
Cardiogenic shock

 Sometimes called pump failure, cardiogenic shock is a condition of diminished cardiac

output that severely impairs tissue perfusion as well as oxygen delivery to
the tissues.
 It reflects severe left-sided heart failure and occurs as a serious complication in some
patients hospitalized with acute MI.
 Cardiogenic shock typically affects patients whose area of infarction exceeds 40% of the
heart’s muscle mass. In these patients, mortality may exceed 85%.
 Most patients with cardiogenic shock die within 24 hours of onset.
 The prognosis for those who survive is extremely poor.
 How it happens
Regardless of the underlying cause, left ventricular dysfunction triggers a series of
compensatory mechanisms that attempt to increase cardiac output and, in turn, maintain
vital organ function.
As cardiac output falls, baroreceptors in the aorta and carotid arteries initiate responses in
the sympathetic nervous system.
These responses, in turn, increase heart rate, left ventricular filling pressure, and peripheral
resistance to flow to enhance venous return to the heart.
These compensatory responses initially stabilize the patient but later cause the patient to
deteriorate as the oxygen demands of the already compromised heart rise.
These events comprise a vicious cycle of low cardiac output, sympathetic compensation,
 Cardiogenic shock produces signs
of poor tissue perfusion
• Cold, Pale, Clammy Skin
• Drop In Systolic Blood Pressure To 30 Mm Hg Below
Baseline
• Weak Peripheral Pulses
• Tachycardia
• Rapid, Shallow Respirations
• Oliguria (Urine Output Less Than 20 Ml/Hour)
• Restlessness, Confusion
• Narrowing Pulse Pressure
• Cyanosis
 DIAGNOSTIC TESTS

1. Pulmonary artery pressure (PAP) monitoring shows increased PAP

2. Invasive arterial pressure monitoring shows hypotension.

3. Arterial blood gas analysis reveals metabolic acidosis and hypoxia.

4. ECG may reveal evidence of an acute MI, myocardial ischemia.

5. Cardiac enzymes and troponin levels are elevated. • Echocardiography

shows left ventricular dysfunction, valvular disease

 TREATMENT
The aim of treatment is to enhance cardiovascular status by increasing cardiac output,
improving myocardialperfusion, and decreasing cardiac workload. Treatment combines
variouscardiovascular drugs and mechanical assist techniques.

Drug therapy may include:

 I.V. dopamine, a vasopressor that increases

 blood pressure and blood flow to the kidneys, and I.V. dobutamine, agents that increase
myocardial contractility and cardiac output. I.V. nitroprusside, a vasodilator, may be used

 with a vasopressor to further improve cardiac output by decreasing afterload and

reducing preload.
 Mechanical- Assist Techniques

The intra-aortic balloon pump (IABP) is a mechanical-assist device

that attempts to improv e coronary artery perfusion and decrease
cardiac workload.
02 Myocardial
infarction MI
 Myocardial infarction MI

 an acute coronary syndrome, results from reduced blood flow

through one of the coronary arteries. This causes myocardial
ischemia, injury, and necrosis.

 In North America and Western Europe, MI is one of the leading

causes of death. Death usually results from cardiac damage or
complications. Mortality is about 25% in men and 38% in women
within 1 year of experiencing an MI.
 How it happens

 MI results from occlusion of

one or more of the coronary
arteries.

 Occlusion can stem from

atherosclerosis, thrombosis,
platelet aggregation, or
coronary artery stenosis or
spasm.
 Predisposing factors

 Aging
 Diabetes mellitus
 Elevated serum triglyceride,
 Hypertension& Obesity
 Positive family history of CAD
 Sedentary lifestyle
 Smoking & stress
 Use of amphetamines or cocaine.
 Excessive intake of saturated fats, carbohydrates, or salt
Susceptibility increases with age
 Elderly patients are more prone to complications
and death.
The most common complications after an acute MI include:
 arrhythmias • cardiogenic shock • heart failure
causing pulmonary edema • pericarditis.
 Other complications include: • rupture of the atrial
or ventricular septum, ventricular wall, or valves
 MI results from prolonged ischemia to the myocardium with irreversible cell
damage and muscle death. Functionally, MI causes:
 Reduced contractility with abnormal wall motion
 Altered left ventricular compliance
 Reduced ejection fraction
 Elevated left ventricular end-diastolic pressure
 All mis have a central area of necrosis or infarction surrounded by an area of
injury. The area of injury is surrounded by a ring of ischemia. Tissue
regeneration doesn’t occur after an MI because the affected myocardial
muscle is dead.
 Scar tissue that forms on the necrotic area may
inhibit contractility. When this occurs, the
compensatory mechanisms (vascular constriction,
increased heart rate, and renal retention of sodium
and water) kick in to try to maintain cardiac output.
 Ventricular dilation also may occur. If a lot of scar tissue
forms, contractility may be greatly reduced. The patient
may develop heart failure or cardiogenic shock.
 The cardinal symptom of MI is persistent,
crushing substernal pain that may radiate to the left
arm, jaw, neck, or shoulder blades.
 The pain is commonly described as heavy,
squeezing, or crushing and may persist for 12 hours
or more.
 However, in some patients particularly elderly or
diabetic patients pain may not occur at all. In others,
it may be mild and confused with indigestion
  Other clinical effects include:

 A Feeling Of Impending Doom

 Fatigue
 Nausea
 Vomiting
 Shortness Of Breath
 Cool Extremities
 Diaphoresis
 Anxiety
 Restlessness.
  These tests help diagnose MI:

 Serial 12-lead ECG Abnormalities include serial ST segment

depression and ST- segment elevation and Q waves, representing scarring
and necrosis.
 Serum creatine kinase (CK) levels are elevated, especially the CK-MB
isoenzyme,
 Troponin I, a structural protein found in cardiac muscle, is elevated.
 Myoglobin is released with cardiac muscle damage and elevated levels
may be detected as soon as 2 hours after an MI.
03 Heart failure
 Heart failure

When the myocardium can’t pump effectively

enough to meet the body’s metabolic needs,

heart failure occurs. Pump failure usually occurs

in a damaged left ventricle, but it may also

happen in the right ventricle. Usually, left- sided

heart failure develops first.

Heart failure Classification
 Pathophysiology
Heart failure may result from a primary abnormality of the heart muscle
 For example, an infarction that impairs ventricular function and prevents the heart from
pumping enough blood.

Heart failure may also be caused by problems unrelated to MI:

• Mechanical disturbances in ventricular filling during diastole, due to blood volume that’s
too low for the ventricle to pump, occur in mitral stenosis secondary to rheumatic heart
disease or constrictive pericarditis and in atrial fibrillation.
 Pathophysiology

Systolic hemodynamic disturbances—such as excessive cardiac

workload caused by volume overload or pressure overload limit the
heart’s pumping ability.This problem can result from mitral or aortic
insufficiency, which leads to volume overload. It can also result from
aortic stenosis or systemic hypertension, which causes increased
resistance to ventricular emptying and decreased cardiac output.
 Factors favorable to failure

• Arrhythmias, such as tachyarrhythmias, which can reduce ventricular filling

time.

• Pregnancy and thyrotoxicosis, which increase cardiac output

• Pulmonary embolism, which elevates PAP, causing right-sided heart failure

• Infections, which increase metabolic demands and further burden the heart

• Anemia, which leads to increased cardiac output to meet the oxygen needs of
the tissues
• Increased physical activity, increased salt or water intake, emotional stress, or
failure to comply with the prescribed treatment regimen for the underlying
heart disease.
 Cont…Factors favorable to failure

• Getting complicated
Eventually, sodium and water may enter the lungs, causing pulmonary
edema, a life- threatening condition. Decreased perfusion to the brain, kidneys,
and other major organs can cause them to fail. MI can occur because the oxygen
demands of the overworked heart can’t be met.
 Signs and Symptoms of Heart Failure

The early signs and symptoms of heart failure

include:

• Fatigue

• Hepatomegaly.

• Neck vein engorgement

• Exertional, paroxysmal, and nocturnal dyspnea

 Signs and Symptoms of Heart Failure

Later signs and symptoms include: Cont…

• Tachypnea • Pallor
• Palpitations • Oliguria
• Dependent edema • Gallop rhythm
• Unexplained, steady weight gain • Inspiratory crackles on auscultation
• Nausea • Dullness over the lung bases
• Chest tightness • Hemoptysis
• Slowed mental response • Cyanosis
• Anorexia • Marked hepatomegaly
• Hypotension • diaphoresis • narrow pulse • Pitting ankle enema
pressure • Sacral edema in bedridden patients
 DIAGNOSTIC TESTS

These tests help diagnose heart failure:

ECG reveals ischemia, tachycardia, and extrasystole.

Echocardiogram identifies the underlying cause as well as the type and severity of the
heart failure.

Chest X-ray shows increased pulmonary vascular markings, interstitial edema, or

pleural effusion and cardiomegaly.

PAP monitoring shows elevated PAP, PAWP, and left ventricular end-diastolic pressure
in left-sided heart failure
Heart Failure Treatment
 Rheumatic Fever and
04 Rheumatic Heart
Disease
 Rheumatic Fever and Rheumatic Heart
Disease
Rheumatic fever develops commonly in childhood after infection of the upper
respiratory tract with group A beta hemolytic streptococci.
Rheumatic heart disease refers to the cardiac manifestations of rheumatic fever
and includes pancarditis (myocarditis, pericarditis, and endocarditis).
Highest in children between ages 5 and 15.
Cardiac involvement develops in up to 50% of patients.
CAUSE

Group A beta hemolytic streptococci.

 PATHOPHYSIOLOGY

a hypersensitivity reaction to group A beta-

hemolytic streptococcal infection.

The antigens of group A streptococci bind to

receptors in the heart, muscle, brain, and
synovial joints, causing an autoimmune
response.

Carditis may affect the endocardium,

myocardium, or pericardium
Later, the heart valves may be damaged, causing chronic
valvular disease.(valvular stenosis,reugitation and damage to
heart muscle)
 CLINICAL MANIFESTATION

• Polyarthritis or migratory joint pain

• Erythema marginatum
• Subcutaneous nodules
• Chorea — rapid jerky movements
• Temperature of at least 100.4 f
• New mitral or aortic heart murmur.
• Pericardial friction rub
• Chest pain
• Dyspnea, tachypnea, non productive cough, bibasilar crackles, and edema
due to heart failure in severe rheumatic carditis.
 DIAGNOSTIC TESTS
• Jones criteria revealing either two major criteria, or one major
criterion and two minor criteria, plus evidence of a previous
group A streptococcal infection are necessary for diagnosis.
 DIAGNOSTIC TESTS

• Antistreptolysin-O titer may be elevated

• Throat cultures

• ESR, or CRP and elevated WBC for inflammation.

• Echocardiography and Cardiac catheterization provides information on valvular

damage
and left ventricular function.
 TREATMENT
 Prompt treatment of all group A beta-hemolytic streptococcal pharyngitis
with oral
 penicillin V or I.M.

 Salicylates to relieve fever and pain and minimize joint swelling.

 Corticosteroids if the patient has carditis or if salicylates fail.

 Strict bed rest to reduce cardiac demands.

Surgery:
• Corrective surgery, such as commissurotomy, valvuloplasty, or valve valvuloplasty
replacement. commissurotomy

• Prophylactic antibiotics for dental work and other invasive or surgical

procedures to prevent endocarditis.
05 Cardiomyopathy
 CARDIOMYOPATHY

Cardiomyopathy generally applies to disease of the heart muscle fibers, and it occurs in
three main forms:
1. Dilated Cardiomyopathy
2. Hypertrophic Cardiomyopathy (2 TYPES)
• common form is caused by aortic valve stenosis.
• hypertrophic obstructive cardiomyopathy (HOCM), is due to a genetic
abnormality.

3. Restrictive Cardiomyopathy (extremely rare).

 ETIOLOGY

Dilated cardiomyopathy usually due to idiopathic, or primary, disease,

Sometimes secondary to identifiable causes.

HOCM usually inherited as a non sex-linked autosomal dominant trait.

 PATHOPHYSIOLOGY
Dilated cardiomyopathy results from extensively damaged myocardial muscle fibers and is
characterized by a grossly dilated, hypodynamic ventricle that contracts poorly and, to a
lesser degree, by myocardial hypertrophy.
dilated cardiomyopathy which affects systolic function, hypetrophic cardiomyopathy
primarily affects diastolic function.
Restrictive cardiomyopathy is characterized by stiffness of the ventricle caused by left
ventricular hypertrophy and endocardial fibrosis and thickening, thus reducing the ability
of the ventricle to relax and fill during diastole. Moreover, the rigid myocardium fails to
contract completely during systole. As a result, cardiac output falls.
 CLINICAL MANIFESTATION
DILATED CARDIOMYOPATHY
• shortness of breath (orthopnea, exertional dyspnea, or paroxysmal nocturnal dyspnea)
• fatigue
• irritating dry cough at night
• edema
• liver engorgement
• jugular vein distention
• peripheral cyanosis
• sinus tachycardia
• atrial fibrillation
• diffuse apical impulses
• pansystolic murmur (mitral and tricuspid insufficiency secondary to cardiomegaly and weak
papillary muscles)
• S3 and S4 gallop rhythms.
 CLINICAL MANIFESTATION

HYPERTROPHIC CARDIOMYOPATHY

 Dyspnea
 Fatigue,
 Angina
 Irregular pulse
 Peripheral pulse with a characteristic double impulse (pulsus biferiens)
 CLINICAL MANIFESTATION
HOCM RESTRICTIVE CARDIOMYOPATHY

• Fatigue
• Systolic ejection murmur
• dyspnea
• Angina • Orthopnea
• Syncope • Chestpain
• Activity intolerance • Edema
• Abrupt arterial pulse secondary to vigorous • liver engorgement
left ventricular contractions • peripheral cyanosis
• Pallor
• Irregular pulse
• S3 or S4 gallop rhythms due to heart failure
• Systolic murmurs
 DIAGNOSTIC TESTS

• Echocardiography confirms dilated cardiomyopathy.

• ECG and angiography rule out ischemic heart disease. ECG may also show biventricular
hypertrophy, sinus tachycardia, atrial enlargement, and, in 20% of patients, atrial
fibrillation.

• Chest X-ray may reveal cardiomegaly associated with any of the cardiomyopathies.

• Cardiac catheterization with possible heart biopsy can be definitive with HOCM.

• Diagnosis requires elimination of other possible causes of heart failure and arrhythmias.
 TREATMENTS
DILATED CARDIOMYOPATHY
Treatment seeks to correct the underlying causes and to improve the heart’s pumping ability.

Angiotensin-converting enzyme (ACE) inhibitors reduce afterload through vasodilation, thereby

reducing heart failure.

Diuretics are commonly given with an ACE inhibitor to reduce fluid retention.

Antiarrhythmics, cardioversion, and pacemakers may control arrhythmias.

Treatment may also include oxygen, a sodium-restricted diet, and bed rest.

Surgical interventions : may include revascularization, such as CABG, if dilated cardiomyopathy

results from ischemia.
 TREATMENTS
HYPERTROPHIC CARDIOMYOPATHY

Optimal control of hypertension

Aortic valve replacement if valve I stenotic

Verapamil or diltiazem to reduce ventricular stiffness and elevated diastolic pressures

Cardioversion to treat atrial fibrillation

Anticoagulation to reduce the risk of systemic embolism with atrial fibrillation.

 TREATMENTS
HOCM

● Beta-adrenergic blockers to slow the heart rate

● Antiarrhythmic drugs, Anticoagulates.
● Cardioversion to treat atrial fibrillation
● Verapamil or diltiazem
● Ablation of the atrioventricular node and implantation of a dual-chamber pacemaker
(controversial), in the patient with HOCM and ventricular tachycardia, to reduce the
outflow gradient by altering the pattern of ventricular contractions

ICD to treat ventricular arrhythmias

 Treatments
SURGERY
Ventricular myotomy or myectomy

Mitral valve replacement to treat mitral insufficiency

(controversial)

Heart transplantation for in tractable symptoms

valve replacement
Ventricular myotomy
 TREATMENTS
RESTRICTIVE CARDIOMYOPATHY

• Treatment of the underlying cause.

• Although no therapy exists for restricted ventricular filling, digoxin (Lanoxin),

diuretics, and a restricted sodium diet to ease the symptoms of heart failure.
06 HYPERTENSION
 HYPERTENSION

Hypertension, an elevation in diastolic or systolic blood pressure, occurs as two major

types:

1. Essential (primary)hypertension, the most common and

2. Secondary hypertension, which results from renal disease or another

identifiable cause.
 ETIOLOGY
1. Primary Hypertension Secondary hypertension
Advancing age . Brain tumor, quadriplegia, and head injury
Diabetes mellitus . Coarctation of the aorta
excess renin Excessive alcohol consumption
Excessive alcohol consumption Family history. Gestational hypertension
High intake of saturated fat . Hormonal contraceptives,
High intake of sodium Mineral deficiencies Cocaine
(calcium, potassium, and magnesium) Antinflammatory drugs.
Obesity Pheochromocytoma, cushing’s syndrome,
Sedentary lifestyle Sleep apnea Hyperaldosteronism, andthyroid, pituitary,
Stress Tobacco use Or parathyroid dysfunction.
Race (most common in blacks) Renal artery stenosis and parenchymal disease
 PATHOPHYSIOLOGY
• Several theories help to explain the development of hypertension. It’s thought to arise
: Changes in the arteriolar bed that cause increased
resistance

abnormally increased tone in the sensory nervous system that originates in the
vasomotor system centers, causing increased peripheral vascular resistance .

Increased Blood Volume Resulting From Renal Or

Hormonal Dysfunction

Increased Arteriolar Thickening Caused By Genetic Factors,

Leading To Increased Peripheral Vascular Resistance

abnormal renin release, resulting in the formation of angiotensin II,

which constricts the arterioles and increases blood volume.
PATHOPHYSIOLOGY
• The pathophysiology of secondary hypertension is related to the underlying disease.

• In chronic renal disease. Insult to the kidney from chronic glomerulonephritis or renal
artery stenosis interferes with sodium excretion, the renin-angiotensin-aldosterone system
, or renal perfusion, causing blood pressure to increase.
 Clinical Manifestation
hypertension usually produces no
symptoms, (SILENT KILLER):
Signs and symptoms may include:
Blood pressure
Throbbing occipital headaches upon
waking
Drowsiness
Confusion
Vision problems(blurry vision as a
result of retinal damage)
Nausea.
secondary hypertension to have clinical
manifestations of the primary disease.
(Other clinical effects don’t appear until
complications develop as a result of vascular
changes in target organs. These effects include) :
Left Ventricular Hypertrophy
Angina
MI
Heart Failure
Stroke
Transient Ischemic Attack
Nephropathy
Peripheral Arterial Disease
Retinopathy
 DIAGNOSTIC TESTS
Serial blood pressure measurements may be useful.
• In urinalysis, protein, red blood cell (RBC), and WBC levels may indicate
glomerulonephritis.
• Elevated blood glucose levels may indicate diabetes.
• Complete blood count may reveal anemia (causes a high-output state resulting in
hypertension) or polycythemia (increases the risk of hypertension and stroke).
• Lipid profile reveals elevated total cholesterol and low-density lipoprotein levels.
Serum potassium levels are less than 3.5 mEq/L, indicating adrenal dysfunction
(primary hyperaldosteronism).
ECG may show left ventricular hypertrophy or ischemia.
• Chest X-ray may show cardiomegaly.
 TREATMENT
Lifestyle modification including :
 Weight reduction, use of a dietary approaches to stop hypertension (DASH) diet.
 Learning relaxation techniques,
 Exercising regularly,
 Quitting smoking, and
 Limiting alcohol use.
Medication
 Drug therapy for uncomplicated hypertension usually begins with :
 a thiazide diuretic,
 an ACE inhibitor, or
 a beta adrenergic blocker.
 Other antihypertensive drugs include:
 angiotensin II receptor blockers,
 alpha-receptor blockers,
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