ANGINA PECTORIS

Definition
Angina pectoris is a clinical syndrome usually characterized by episodes or
paroxysms of pain or pressure in the anterior chest. It is a pain of cardiac origin which
radiates to the shoulders , jaw and arms of left side of body. The cause is usually insufficient
coronary blood flow. The insufficient flow results in a decreased oxygen supply to meet an
increased myocardial demand for oxygen in response to physical exertion or emotional stress.

CANADIAN CARDIOVASCULAR SOCIETY CLASSIFICATION OF ANGINA

CLASS ACTIVITY EVOKING ANGINA

I Prolonged exertion
II Walking >2 blocks
III Walking <2 blocks
IV Minimal or rest

TYPES OF ANGINA

1) Stable angina: predictable and consistent pain that occurs on exertion and is relieved
by rest
2) Unstable angina (also called preinfarction angina or crescendo angina): symptoms
occur more frequently and last longer than stable angina. The threshold for pain is
lower, and pain may occur at rest.
3) Intractable or refractory angina: severe incapacitating chest pain
4) Variant angina (also called Prinzmetal’s angina): pain at rest with reversible ST-
segment elevation; thought to be caused by coronary artery vasospasm.

PATHOPHYSIOLOGY
Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima of the arterial
wall. The continued development of atherosclerosis involves an inflammatory response.T
lymphocytes and monocytes infiltrate the area to ingest the lipids and then die; this
causes smooth muscle cells within the vessel to proliferate and form a fibrous cap over
the dead fatty core. These deposits, called atheromas or plaques, protrude into the lumen of
the vessel, narrowing it and obstructing blood flow. If the cap is thin, the lipid core may
grow, causing it to rupture and hemorrhage into the plaque, allowing a thrombus to
develop. The thrombus may obstruct blood flow, leading to angina and sudden cardiac
death or an acute myocardial infarction (MI), which is the death of heart tissue.

Etiology

Angina is usually caused by atherosclerotic disease. Several factors are associated with
typical anginal pain:

• Physical exertion, which can precipitate an attack by increasing myocardial oxygen demand
• Exposure to cold, which can cause vasoconstriction and an elevated blood pressure, with
increased oxygen demand
• Eating a heavy meal, which increases the blood flow to the mesenteric area for digestion,
thereby reducing the blood supply available to the heart muscle
• Stress or any emotion-provoking situation, causing the release of adrenaline and increasing
blood pressure, which may accelerate the heart rate and increase the myocardial workload

Clinical Manifestations
Ischemia of the heart muscle may produce pain or other symptoms,
 a feeling of indigestion
 a feeling of choking
 heavy sensation in the upper chest
 chestdiscomfort
 agonizing pain accompanied by severe apprehension and a feeling of impending
death.
 The pain is often felt deep in the chest behind the upper or middle third of the sternum
(retrosternal area). Typically, the pain or discomfort is poorly localized and may
radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, usually the
left arm.
 The patient with diabetes mellitus may not have severe pain with angina because the
neuropathy that, dulling the patient’s perception of pain.
 A feeling of weakness or numbness in the arms, wrists, and hands may accompany the
pain,
 shortness of breath, pallor, diaphoresis, dizziness or light-headedness, and nausea and
vomiting.

ASSESSMENT AND DIAGNOSTIC FINDINGS

The diagnosis of angina is often made by evaluating the clinical manifestations of ischemia
and the patient’s history.
 A 12-lead ECG and blood laboratory values help in making the diagnosis. The patient
may undergo an exercise or pharmacologic stress test in which the heart is monitored
by ECG, echocardiogram, nuclear scan, or invasive procedures (cardiac
catheterization and coronary artery angiography).
 C-reactive protein (CRP) is a marker for inflammation of vascular endothelium. An
elevated blood level of homocysteine, an amino acid, has also been proposed as an
independent risk factor for cardiovascular disease.

MEDICAL MANAGEMENT

The objectives of the medical management of angina are to decrease the oxygen demand of
the myocardium and to increase the oxygen supply. These objectives are met through
pharmacologic therapy and control of risk factors.

PHARMACOLOGIC THERAPY

1) NITROGLYCERIN. Nitrates, nitroglycerin (Nitrostat, Nitrol, Nitrobid IV)

Action: Help to reduce myocardial oxygen consumption, which decreases ischemia
and relieves pain. Nitroglycerin dilates primarily the veins and, in higher doses, also
dilates the arteries. It helps to increase coronary blood flow by preventing vasospasm
 and increasing perfusion through the collateral vessels. Dilation of the veins causes
venous pooling of blood throughout the body. As a result, less blood returns to the
heart, and filling pressure (preload) is reduced. Nitrates in higher doses also relax the
systemic arteriolar bed and lower blood pressure (decreased afterload). Nitrates may
increase blood flow to diseased coronary arteries and through collateral coronary
arteries. Nitroglycerin may be given by several routes: sublingual tablet or spray,
topical agent, and intravenous administration.

2) BETA-ADRENERGIC BLOCKING AGENTS. Beta-blockers such as

propranolol, metoprolol (Losar), and atenolol.

Action :They will reduce myocardial oxygen consumption by blocking the beta-
adrenergic sympathetic stimulation to the heart. The result is a reduction in heart rate,
slowed conduction of an impulse through the heart, decreased blood pressure, and
reduced myocardial contractility (force of contraction) that establishes a more
favorable balance between myocardial oxygen needs (demands) and the amount of
oxygen available (supply). This helps to control chest pain and delays the onset of
ischemia during work or exercise. Beta-blockers reduce the incidence of recurrent
angina, infarction, and cardiac mortality.
Cardiac side effects and possible contraindications include hypotension,
bradycardia, atrioventricular heart block, and heart failure, depression, fatigue.

3) CALCIUM CHANNEL BLOCKING AGENTS. Eg: verapamil, nifidipine,

amilodipine
Action :Some decrease sinoatrial node automaticity and atrioventricular node
conduction, resulting in a slower heart rate and a decrease in the strength of the heart
muscle contraction (negative inotropic effect). These effects decrease the workload of
the heart. Calcium channel blockers also relax the blood vessels, causing a decrease in
blood pressure and an increase in coronary artery perfusion. Calcium channel blockers
increase myocardial oxygen supply by dilating the smooth muscle wall of the
coronary arterioles; they decrease myocardial oxygen demand by reducing systemic
arterial pressure and the workload of the left ventricle. They may be used by patients
who cannot take beta-blockers, who develop significant side effects from beta
blockers or nitrates, or who still have pain despite beta blocker and nitroglycerin
therapy.
Side effects: Hypotension atrioventricular blocks, bradycardia, constipation, and
gastric distress.

4) ANTIPLATELET AND ANTICOAGULANT MEDICATIONS. Antiplatelet

medications are administered to prevent platelet aggregation, which impedes blood
flow.
a) Aspirin. Aspirin prevents platelet activation and reduces the incidence of MI and
death in patients with CAD.
b) Clopidogrel and Ticlopidine. Clopidogrel is given to patients who are allergic to
aspirin or given in addition to aspirin in patients at high risk for MI.
c) Heparin. Unfractionated heparin prevents the formation of new blood clots.

5) OXYGEN ADMINISTRATION. Oxygen therapy is usually initiated at the onset of

chest pain in an attempt to increase the amount of oxygen delivered to the
 myocardium and to decrease pain. Oxygen inhaled directly increases the amount of
oxygen in the blood.

SURGICAL MANAGEMENT

Revascularization procedures to restore the blood supply to the myocardium include

percutaneous coronary interventional (PCI) procedures (eg, percutaneous transluminal
coronary angioplasty [PTCA], intracoronary stents, and atherectomy), CABG, and
percutaneous transluminal myocardial revascularization (PTMR).

NURSING DIAGNOSES

Ineffective myocardial tissue perfusion secondary to CAD, as evidenced by chest pain or

equivalent symptoms
• Anxiety related to fear of death
• Deficient knowledge about the underlying disease and methods for avoiding complications
• Noncompliance, ineffective management of therapeutic regimen related to failure to accept
necessary lifestyle changes.

COLLABORATIVE PROBLEMS/ POTENTIAL COMPLICATIONS

Potential complications that may develop include the following,
which are discussed in the chapters indicated:
• Acute pulmonary edema
• Congestive heart failure
• Cardiogenic shock
• Dysrhythmias and cardiac arrest
• MI
• Myocardial rupture
• Pericardial effusion and cardiac tamponade