CARDIOVASCULAR DISEASE

Blood circulation inside the heart

Enters through superior and inferior vena cava

Right atrium

Passes through tricuspid valve

Enters right ventricle

Passes through pulmonary valve

Pulmonary arteries

Lungs

Pulmonary vein

Left atrium

Passes through the mitral valve

Left ventricle
Cycle: systole relaxation and filling of chambers
Diastole contraction and emptying of the chambers
Causes : risks factor
Non modifiable: gender, Age (women are affected after menopause), family history,
Modifiable: cigarette smoking, hyperlipidimea, DM, HPN, obesity, lack of exercises,
stress, oral contraceptives
ANGINA PECTORIS
Angina Pectoris is usually caused by atherosclerosis of the coronary vessels,
the incidence is high with persons with HPN, DM, aortic regurgitation caused by
rheumatic heart disease. Typically, this is triggered by cold, exercise, anything that
would increase the work load of the heart and myocardial O2 consumption.
Categories of Angina Pectoris
Unstable angina preinfarction angina, crescendo angina, intermittent coronary
syndrome. This is characterized by increase in severity frequency or duration of
symptoms without infarction spasm with or without atherosclerotic heart disease
Variant angina Prinzmetals angina is thought to develop coronary artery. Occurs
during normal exercises or stress

Pathophysiology
Angina pectoris or chest pain is a clinical syndrome due to insufficiency of blood flow


Imbalance between myocardial O2 supply and O2 demands create transient
myocardial ischemia

Underlying mechanism that causes pain is probably related to the change from
aerobic metabolism to anaerobic metabolism

Product of anaerobic metabolism, lactic acid, may initiate sensory receptors and
cause pain
MYOCARDIAL INFARCTION
Acute myocardial infarction means one or more regions of the heart muscle
experience a severe and prolonged decrease O2 supply because of insufficient
coronary blood flow.
Acute myocardial infarction is caused by sudden blockage of one of the
branches of the coronary artery. It maybe extensive enough to interfere with cardiac
function and cause immediate death, or may cause necrosis of a portion of the
myocardium with subsequent healing by scar formation or fibrosis.
Coronary occlusion term for blockage of the coronary artery
Blockage maybe due to: 1. Formation of thrombus in the coronary artery
2. Progression of atherosclerosis
3. Prolonged constriction of the arteries
Pathophysiology
Prolonged ischemia lasting more than 35 minutes produces irreversible damage and
necrosis

Severe coronary artery disease precipitates thrombus formation

Intramural hemorrhage into atheromatous plaques causes lesion to enlarge and

occlude the vessel

The plaque ruptures in to the vessel lumen, thrombus forms on top of the ulcerated
lesion with resultant vessel occlusion

The contractile properties of the cardiac muscle within the necrotic area becomes
permanently impaired

Final extent of the infarct depends on the ability of the surrounding ischemic tissues
to recruit collateral
circulation. The development of new vessels within the heart to compensate for the
damaged artery
CLINICAL MANIFESTATIONS
a. Chest pain
1. Severe, diffuse steady substernal pain of a crushing and squeezing nature
2. Not relieved by rest or sublingual vasodilator therapy, but requires narcotics
3. May radiate to the arms (commonly on left), shoulders, neck, back and jaw
4. Continuous for more than 15 minutes

b.
c.
d.
e.
f.
g.
h.

5. Produces anxiety, fear resulting in heart rate, blood pressure, respiratory

rate
Diaphoresis, cool clammy skin, facial pallor
Hypertension or hypotension
Bradycardia or tachycardia
Palpitations, dyspnea
Disorientation, confusion restlessness
Fainting, marked weakness
Nausea, vomiting, hiccups

MANAGEMENT
Therapy is aimed at the protection of the ischemic and injured heart tissue to
preserve muscle function, reduce the infarct size, and prevent death
Oxygen therapy
Improves oxygenation to ischemic heart muscle
Pain control
1. Opiate analgesic therapy
a. Morphine is used to relieve pain, to improve cardiac hemodynamics
by reducing preload and after load, and to provide anxiety relief
b. Meperidene (Demerol) useful for clients that are allergic to morphine
or sensitive to respiratory depression
2. Vasodilator therapy
a. Nitroglycerine (sublingual, IV) promotes venous (low-dose) and
arterial (high-dose) as well as relaxation of coronary blood vessel and
prevention of coronary spasms
b. Myocardial oxygen demand is reduced with subsequent pain relief
c. Persistent chest pain requires prompt action (IV nitroglycerin)
3. Anxiolytic therapy
a. Benzodiazepines are used with analgesics when anxiety complicates
chest pain and its relief
Pharmacologic Therapy
a. Anti-thrombosis: Activase, Streptase, Retavase
b. Aspirin: to prevent platelet activation
c. Anticoagulation therapy
d. Beta blockers: promote blood flow in small vessels of the heart
e. Anti-dysrhythmic therapy: Lidocaine reduces ventricular irritability
f. Calcium channel blockers: improve the balance of O2 supply and
demand

NURSING DIAGNOSES
Pain related to an imbalance in oxygen demand and supply
Decreased cardiac output related to decreased cardiac contractility and
dysrhythmias
Anxiety related to chest pain, fear of death, threatening environment, invasive
therapies and uncertain prognosis
NURSING INTERVENTIONS
Reducing pain
Alleviating anxiety
Maintaining hemodynamic stability
Increasing activity intolerance
Preventing bleeding

 Maintaining tissue perfusion

CONGESTIVE HEART FAILURE (CHF)
CHF is a clinical syndrome that results from the hearts inability to pump the
amount of oxygenated blood necessary to meet the metabolic requirements of the
body.
PATHOPHYSIOLOGY
Inadequate cardiac output triggers a number of compensatory responses that are
geared toward maintaining adequate perfusion to vital body organs

Initial response is stimulation of the sympathetic nervous system

Cardiac compensatory mechanisms (increases in heart rate, vasoconstriction, and

heart enlargement) occur to assist failing heart

Compensates for heart inability to pump effectively and maintain sufficient blood flow
to organs and tissues at rest

Increase rate & force of myocardial contraction

Vasoconstriction

Peripheral
(Shunts arterial blood away from
less
vital organs: skin &
kidney/ towards body organ:
brain. Constriction of the veins
increases venous return to the
heart w/c the cardiac volume
and dilates ventricle. The
stretch of myocardial muscle
fiber enhances contractility)

Physiologic stressors that increase the work load of the heart(exercise, infection) may
cause this mechanism to fail and precipitate the clinical syndrome associated with
failing heart (elevated ventricular/atrial pressures, sodium and water retention,
decreased cardiac output, circulatory and pulmonary congestion)

The compensatory mechanisms may hasten the onset of failure because they
increase afterload cardiac work

Due to disorder from the heart muscle resulting in decreased contractile properties of
the heart; coronary heart disease leading to MI; HPN; valvular heart disease;
congenital heart disease;

Left-sided heart failure/right-sided heart failure

LEFT-SIDED HEART FAILURE (FORWARD FAILURE)

1. Congestion occurs mainly in the lungs from backing up of blood into pulmonary
veins and capillaries
a. Shortness of breath, dyspnea on exertion, paroxysmal nocturnal dyspnea
( due to reabsorption of dependent edema that has developed during the
day) orthopnea, pulmonary edema
b. Cough may be dry, unproductive; often occurs at night
2. Fatigability from low cardiac output, nocturia, insomnia, dyspnea, catabolic
effect of chronic failure
3. Restlessness
4. Tachycardia
RIGHT-SIDED HEART FAILURE (BACKWARD FAILURE)
Signs and symptoms of elevated pressures and congestion in systemic veins and
capillaries:
1. Edema of ankles, unexplained weight gain (pitting edema is obvious after
retention of at least 4.5 kg or 10 lbs. of fluid)
2. Liver congestion may produce upper abdominal pain
3. Distended neck veins
4. Abnormal fluids in the body cavities (pleural space, abdominal cavity)
5. Anorexia and nausea from hepatic and visceral engorgement
6. Nocturia diuresis occurs at night with rest and improved cardiac output
7. Weakness
Cardiovascular findings in both types
1. Cardiomegaly detected by physical examination and chest x-ray
2. Ventricular gallop evident on auscultation; ECG
3. Rapid heart rate
4. Development of pulsus alterans(alteration in strength of the beat)
Diagnostic evaluation
1. ECG may show ventricular hypertrophy and strain
2. Echocardiography ventricular hypertrophy, dilation of chambers, and abnormal
wall motion
3. Chest x-ray may show cardiomegaly, pleural effusion, vascular congestion
4. ABG studies may show hypoxemia due to pulmonary vascular congestion
5. Liver function studies maybe altered because of hepatic congestion
Management
Treatment is directed at eliminating excessive accumulation of body water, increasing
the force and efficiency of myocardial contraction, reducing the workload of the heart.
This could be achieved through promoting rest and administering pharmacologic
agents.
a. Diuretics
1. Eliminates excess water and decrease ventricular pressures.
2. A low-sodium diet and fluid restriction complement the therapy
3. Some diuretics may have slight venodilator properties
b. Positive Inotropic Agents
1. Increases hearts ability to pump more effectively by improving contractile
force of the muscle
2. Digoxin (Lanoxin)may only be effective in severe cases of failure
3. Dopamine (Intropin) also improves renal blood flow in low dose range
4. Dobutamine (Dobutrex)
5. Milrinone (Primacor) and amrinone (Inocor) are potent vasodilators

c. Vasodilator therapy
1. By relaxing capacitant vessels (veins and venules), vasodilators reduces
ventricular filling pressure (preload) and volume
2. By relaxing resistance vessels (arterioles), vasodilators can reduce
impedance to the left ventricular ejection and improve stroke volume
3. Vasodilators used in CHF:
a. Nitrates such as nitroglycerin (Tridil), isosorbide dinitrate (Isordil),
nitroglycerin ointment predominantly dilates systemic veins
b. Hydralazine (Apresoline)) predominantly affects the arterioles;
affects the arteriolar tone
c. Prazosin (Minipress) balanced effect on both arterial and venous
circulation
d. Sodium nitroprusside (Nipride) predominantly affects arterioles
e. Morphine sulfate (Duramorph) decreases venous return, decreases
pain and anxiety and thus cardiac load
NURSING INTERVENTIONS
Provide oxygen 2 6 L/min as prescribed
Place patient on semi-fowlers position or HFP
Provide rest and activity
Reinforce the importance of energy conservation and planning for activities
that avoid fatigue
Encourage activity within prescribed restriction; monitor for tolerance to
activity (dyspnea, fatigue, increase pulse rate that does not stabilized)
Assist ADL: encourage independence within clients limitations
Provide diversionary activity
Monitor for fluid and potassium imbalance; record weight daily
Provide skin care particularly over edematous area
Assist in attaining an adequate nutrition intake
Monitor for constipation
Give prescribed medications: Digitalis, take apical pulse before administration;
diuretics, assess for hypokalemia, vasodilators
HEALTH TEACHINGS
Monitor for the following: weight gain of 1-1.5 kg. (2-3 lb) over a short period of
time (about days)
Loss of appetite, shortness of breath, orthopnea, swelling of ankle feet or
abdomen, persistent cough, frequent nighttime urination
Avoid salty foods and medications with sodium content (laxatives and antacids)
Eat several small meals everyday rather than 3 large meals a day
Report signs of hypotension (light-headedness, syncope, rapid pulse)

CARDIOGENIC SHOCK
Cardiogenic shock state of primary origin that occurs when the heart muscle loses its
contractile power, extensive damage of the left ventricle (40%) due to myocardial
infarction commonly initiates a perpetuating shock cycle.
Cardiac output
Cardiac function

Coronary artery perfusion

Cardiac ischemia

PATHOPHYSIOLOGY
Cardiac function is severely impaired and cardiac output is low

Shock progresses coronary artery perfusion decreases

cardiac output results in lack of blood and oxygen to the heart as well as other
organs of the body (brain and kidneys)

Cardiac muscle ishemia

Lack of blood and oxygen to the heart muscle furhter decline the contractile power,
and continued inability of the heart to provide blood and oxygen to vital organs

Further decrease action

May lead to cardiomyopathy, severe valvular dysfunction, and ventricular aneurysm

CLINICAL MANIFESTATIONS
1. Confusion, mental lethargy (due to poor perfusion of the brain)
2. Restlessness, low systolic pressures
3. Oliguria urine output less than 30mL/hr for at least 2 hours due to decrease
perfusion of the kidneys
4. Cold clamy skin (blood is shunted from mt pereripheral circulation to profuse
vital ogans)
5. Weak pulses, fatigue, hypotension due to inadequate cardiac output
6. Dyspnea, tachypnea, cyanosis (increased left ventricular pressures, result in
left atrial and pulmonary pressures causing pulmonary congestion)
7. Dysrhythmias (due to lack of oxygen to the heart muscle)
8. Chest pain due to lack of oxygen and blood to the heart muscle

COMPLICATIONS
1. Neurologic impairment
2. Acute respiratory distress syndrome
3. Renal failure
4. Multiorgan dysfunction syndrome
5. Death

NURSING DIAGNOSES
Decreased cardiac output related to impaired contractility due to extensive heart
muscle damage
Impaired gas exchange related to pulmonary congestion due to elevated left
ventrilcular pressures
Altered tissue perfusion (renal, cerebral,cardiopulmonary, GI and peripheral) related
to decreased blood flow
Anxiety related to intensive care environment and threat of death
NURSING INTERVENTIONS
Improving cardiac output
1. Establish continuous ECG monitoring to detect dysrhythmias , which
increase myocardial oxygen consumption
2. Monitor blood pressure and mean arterial pressure (MAP) with intra-arterial
line
3. Measure and record urine output every hour for indwelling catheter and
fluid intake
4. Obtain daily weight
5. Evaluate serum electrolytes for hyponatremia and hypokalemia
6. Be alert on incidence of chest pain (indicates myocardial ischemia and may
further extend heart damage
Improving oxygenation
1. Monitor rate and rhythym of respiration every hour
2. Auscultate lung fields for abnormal sounds (coarse crakles indicate severe
pulmonary congestion)
3. Administer O2
4. Elevate head of bed 20 30 degrees as tolerated (may worsen hypotension)
to facilitate lung expansion)
5. Observe for frothy pink-tinged sputum and cough (pulmonary edema)
Maintain tissue perfusion

PERICARDITIS
Pericarditis is an inflammatory process of the visceral or parietal pericardium or both.
It maybe acute or chronic, and infection may spread from or to myocardium.
Acute pericarditis is furhter classified as fibrinous or exudate. The exudate maybe
serous, purulent or hemorraghic. When fluid accumulates in the pericadial sac,
cardiac temponade (compression of heart from bood or fluid) causes decreased
venous return to the heart and decrease ventricular emptying.
Chronic pericarditis is referred to as chronic constrictive or adhesive pericarditis. It is
times 2 more prevalent in men than in women. It may result from fibrosing of the
perocardial sac secondary to trauma or neoplastic disease.
Signs and symptoms of Pericarditis
Acute:Severe precordial chest pain referred to neck, shoulder, left arm: intensified
when lying supine, coughing or breathing deeply or swallow breathing
Chronic: dyspnea, fatigue, congestive heart failure

MYOCARDITIS
Myocarditis is an inflammatory disease of the myocardium that causes an infiltration
in the myocardial interstitium and injury to adjacent myocardial cells that is atypical
of infarction. Myocarditis maybe primarilywith an unknown etiology, or secondarily,
from an identifiable cause such as drug hypersensitivity, toxicity, and infection.
Myocarditis is difficult to study in human beings, because if frequently remains
underdiagnosed until chronic cardiac dysfunction and congestive heart failure
becomes become clinically obvious
Patients with myocarditis are often treated with bed rest and digitalis to prevent heart
failure and cardiogenic shock. Immunosuppression may be beneficial in reducing
myocardial inflammation.
Signs and symptoms of Myocarditis
Maybe asymptomatic
Nonspecific complaints of dyspnea or exertion, palpitations, precordial chest
pain, fever tachycardia
ENDOCARDITIS
Endocarditis is the inflammation of the endocardium and most often of the heart
valves. The more recent method of classification of infective endocarditis is on the
basis of causative organism, for example, enterococcal endocarditis or streptococcal
endocarditis. It may occur in acute or subacute forms.
Acute endocarditis occur rapidly, often on normal heart valves, and if untreated may
cause death within days or weeks.
The subacute form develops more gradually, usually on previously damaged heart
valves and responds well to treatment.
The infecting organisms are carried by a turbulent blood flow and deposited on the
heart valves or elsewhere on the endocardium.

The turbulent blood flow occurs in the areas of myocardial anomalies

Mitral valve prolapse

ventricular septal
defects

The organisms bombard the heart valves, becomes embedded in the valve matrix

May result in vegetative growths that may scar and perforate the leaflets until it
breaks free of the valve
Vegetative emboli enters organs such as spleen or kidney, abscesses may form.
Signs and symptoms of
Endocarditis
Gradual onset: malaise, achiness, fever, splenomegaly, clubbing fingers,
Olsers nodes on fingers, petechiae in conjunctiva and mouth, cardiac murmur,
anemia

RHEUMATIC HEART FEVER (Rheumatic Endocarditis)

Rheumatic fever is an acute inflammatory reaction and may progress with mild
symptoms and go undiagnosed, or the disease maybe subclinical with no symptoms.
Damages are done to the heart particularly the valves resulting in valve leakage
(regurgitation) and/or obstruction (narrowing or stenosis). The patient develops
cardiac manifestations of years later. On careful history taking, a recollection of a
child illness confirming the likelihood of rheumatic fever is usually found
The pericardium, myocardium, and endocardium can be involved

The affected tissue develops area of necrosis (Aschoff bodies) leaving scar tissue

The leaflets of a valve may fuse during the healing process

The affected valve become fibrous and incompetent

Signs

and symptoms of Rheumatic fever/Rheumatic heart disease

Symptoms follow pharyngeal infection in 1 4 weeks
Recurrent join pain; warm swollen joints
Heart murmur, friction rub, cardiac arrhythmias, congestive heart failure
Symptoms of streptococcal pharyngitis
a. Sudden onset of sore throat; throat reddened with exudates
b. Swollen, tender lymph nodes at angle of the jaw
c. Headache and fever 38.9 C to 40. 0 C (101 to 104 F)
d. Abdominal pain

Nursing Assessment
1. Ask patient about symptoms of fever or throat or joint pain
2. Ask patient about chest pain, dyspnea, fatigue
3. Observe for skin lesion or rashes on trunk and extremities
4. Palpate for firm, nontender movable nodules near tendons and joints
Nursing Diagnoses
1. Hyperthermia related to disease process
2. Decreased cardiac output related to decreased cardiac contractility
3. Activity intolerance related to joint pain and easy fatigability
Nursing Interventions
Reducing fever
Maintaining adequate cardiac output
Maintaining activity