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Angina Pectoris- definition, etiology, types, sign and symptoms, diagnosis, medical management, pharmacotherapy

ANGINA PECTORIS

DEFINITION

The word ‘angina’ has been derived from Latin word meaning “to choke”.

Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest.

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. In other words, the need for oxygen exceeds the supply.

ETIOLOGY

• 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

TYPES OF ANGINA

  • Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest
  • 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.
  • Intractable or refractory angina: severe incapacitating chest pain
  • Variant angina (also called Prinzmetal’s angina): pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm
  • Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient reports no symptoms

CLINICAL MANIFESTATIONS

  • Feeling of indigestion
  • Choking heavy sensation in the upper chest that ranges from discomfort to agonizing pain
  • Pain is felt deep in the chest behind the upper or middle third of the sternum (retrosternal area) and radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, usually the left arm.
  • Weakness or numbness in the arms, wrists, and hands
  • Shortness of breath
  • Pallor
  • Diaphoresis
  • Dizziness
  • Nausea and vomiting
  • Apprehension
  • Feeling of impending death.

ASSESSMENT AND DIAGNOSTIC FINDINGS

  • Patient’s history
  • 12-lead ECG
  • Blood laboratory values
  • Exercise or pharmacologic stress test
  • Echocardiogram
  • Nuclear scan
  • Cardiac catheterization
  • Coronary artery angiography
  • C-reactive protein (CRP) marker for inflammation of vascular endothelium
  • An elevated blood level of homocysteine (an amino acid)

 

MEDICAL MANAGEMENT

The objectives is to decrease oxygen demand of the myocardium and to increase the oxygen supply. This is met through

  • Pharmacologic therapy and control of risk factors.
  • Revascularization procedures to restore the blood supply to the myocardium include percutaneous coronary interventional(PCI) procedures (eg, percutaneous transluminal coronaryangioplasty [PTCA], intracoronary stents, and atherectomy), CABG, and percutaneous transluminal myocardial revascularization (PTMR).

 

PHARMACOLOGIC THERAPY

Nitroglycerin

Vasoactive agent to reduce myocardial oxygen consumption decreases ischemia and relieves pain. It dilates veins and in higher doses, dilates arteries. Dilation of veins causes venous pooling of blood throughout the body. As a result, less blood returns to the heart and filling pressure (preload) is reduced.

Nitroglycerin is given by several routes: sublingual tablet or spray, topical agent and intravenous administration. Sublingual nitroglycerin alleviates the pain of ischemia within 3 minutes.

 

Beta-Adrenergic Blocking Agents

Beta-blockers such as propranolol (Inderal), metoprolol (Lopressor) and atenolol (Tenormin) reduce myocardial oxygen consumption by blocking the beta-adrenergic sympathetic stimulation to the heart. The result is reduction in heart rate, slow conduction of an impulse through the heart, decreased blood pressure, and reduced myocardial contractility.

Cardiac side effects include hypotension, bradycardia, advanced atrioventricular block, and decompensated heart failure.

Patients taking beta-blockers are cautioned not to stop taking them abruptly, because angina may worsen and MI may develop. Beta-blocker therapy needs to be decreased gradually over several days before discontinuing it.

 

Calcium Channel Blocking Agents

Calcium channel blockers decreasesinoatrial node automaticity and atrioventricular node conduction,resulting in a slower heart rate and decrease in strengthof heart muscle contraction (negative inotropic effect). Theseeffects decrease the workload of the heart.

The calcium channel blockers most commonly used are amlodipine (Norvasc), verapamil (Calan) and diltiazem (Cardizem).

Side effects include hypotension, atrioventricular blocks, bradycardia, constipation and gastric distress.

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