Angina Pectoris: Definition, Etiology, Clinical Manifestations and Pathophysiology

Definition of Angina Pectoris

1. Angina pectoris is chest pain caused by myocardial ischemia and temporary or reversible. (Fundamentals of nursing cardiothoracic, 1993)

2. Angina pectoris is a chronic syndrome in which the client had suffered the typical chest pain like pressure, or feel heavy in the chest that often radiating to the left arm that arise at the time of the activity and immediately lost when the activity stops. (Prof. Dr. H.M. Sjaifoellah Noer, 1996)

3. Angina pectoris is a term used to describe the type of discomfort that are usually located in areas retrosternum. (Practical Guidance Cardiovascular).

Etiology of Angina Pectoris
  • Arteriosclerosis
  • Coronary artery spasm
  • Severe anemia
  • Arthritis
  • Aortic insufficiency
Clinical Manifestations of of Angina Pectoris
  • Substernal or retrosternal chest pain radiating to the neck, throat area inter scapula or left arm.
  • Quality of pain, such as distressed heavy objects, such as pressing, hot, sometimes just a bad feeling in the chest (chest discomfort).
  • Duration of pain lasted 1 to 5 minutes, no more than 30 minutes.
  • Pain lost (decreases) when the rest-sleep or administration of nitroglycerin.
  • Accompanying symptoms: shortness of breath, feeling tired, sometimes appearing cold sweat, palpitations, dizzines.
  • EKG: ST segment depression, inverted T waves.
  • EKG: often normal at the time of the attack did not arise.
Pathophysiology of Angina Pectoris

The mechanism of the onset of angina pectoris is based on inadequate oxygen supplied to the cells caused by myocardial arterial rigidity and narrowing of the lumen of the coronary arteries (coronary arteriosclerosis). It is not known exactly what causes arteriosclerosis, it is clear that no single factor was responsible for the development of arteriosclerosis. Arteriosclerosis is a disease of the coronary arteries are most commonly found. When a tissue workload increases, the need for oxygen also increases. If demand increases in the healthy heart dilates the coronary artei and more blood flow and oxygen to the heart muscle. However, if the rigidity or coronary artery had narrowed by arteriosclerosis and can not dilate in response to increased demand for oxygen, then an ischemic (lack of blood supply) myocardium.

Presence of endothelial injury resulting in loss of production of No (nitric oxide), which serves to inhibit a variety of reactive substances. In the absence of this function can cause smooth muscles to contract and arises spasmus aggravate coronary lumen narrowing due to myocardial oxygen supply is reduced. Narrowing or block is not so apparent cause symptoms if not reached 75%. If the narrowing of more than 75% and is triggered by the excessive activity of the coronary blood supply is reduced. Myocardial cells using anaerobic glycogen to meet their energy needs. Metabolism produces lactic acid which lowers the pH of the myocardium and cause pain. When energy demand decreases cardiac cells, the oxygen supply becomes inadequate and back muscle cells oxidative phosphorylation to form energy. This process does not produce lactic acid. With the loss of lactic acid pain will subside.

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