, Research Paper
“Symptoms and Causes of Heart Attacks”
A heart attack (myocardial infarction) is the death of heart muscle due to the loss of blood supply. Usually, the loss of blood supply is caused by a complete blockage of a coronary artery by a blood clot. A coronary artery is an artery that supplies blood to the heart muscle. Death of the heart muscle causes chest pain and electrical instability of the heart muscle tissue. Electrical instability of the heart causes ventricular fibrillation (chaotic electrical disturbance). Orderly transmission of electrical signals in the heart is important for the regular beating (pumping) of the heart. A heart undergoing ventricular fibrillation quivers, and can not pump or deliver oxygenated blood to the brain. Permanent brain damage and death can occur unless oxygenated blood flow is restored within five minutes.
Approximately one million Americans suffer a heart attack annually. Four hundred thousand of these victims die as a result. Many of the heart attack deaths are due to ventricular fibrillation of the heart that occurs before the victim can reach any medical assistance or the emergency room. These electrical disturbances of the heart can be treated with medications once the patient reaches the hospital. Therefore, 90% to 95% of heart attack victims who make it to the hospital survive. The 5% to 10% who later die are those who have suffered major heart muscle damage.
Early heart attack deaths can be avoided if a bystander starts CPR (cardiopulmonary resuscitation) within five minutes of the onset of ventricular fibrillation.
CPR involves breathing for the victim and applying external chest compression to make the heart pump. When paramedics arrive, medications and/or electrical shock (cardioversion) to the heart can be administered to convert ventricular fibrillation to a normal heart rhythm. Therefore, prompt CPR and rapid paramedic response can improve the survival chances from a heart attack.
A heart attack is caused by the formation of a blood clot on a cholesterol plaque located on the inner wall of an artery to the heart (coronary artery). Cholesterol is a fatty chemical that is part of the outer lining of cells in the body. Cholesterol plaque is the formation of a hard, thick substance on the artery walls which is caused by deposits of cholesterol on the artery walls; a process that begins in the late teens. Over time, the accumulation of cholesterol plaque causes thickening of the artery walls and narrowing of the arteries; a process called atherosclerosis. Plaque accumulation can be accelerated by smoking, high blood pressure, elevated cholesterol, and diabetes. Ultimately, atherosclerosis causes significant narrowing of the coronary arteries. During exercise or excitement, the narrowed coronary arteries cannot increase the blood supply to meet the increased oxygen demand of the heart muscle.
Heart muscle that is starved of blood oxygen, a condition called ischemia causes chest pain (angina). Chest pain that occurs with exercise is called exertional angina. Exertional angina is reversible, and subsides with rest. Occasionally, for unknown reasons, the surface of the cholesterol plaque can become sticky, causing blood clotting. When a
blood clot forms on top of this plaque, the artery becomes completely blocked, causing death of the heart muscle (heart attack).
Heart attack patients are monitored in the hospital for 3 to 6 days prior to discharge home. Rhythm disturbances, shortness of breath due to heart failure, or recurrent pains are indications for further therapy such as balloon angioplasty, medications, or bypass surgery. Patients gradually increase their activity under observation. Before discharge, low level stress tests are useful for detecting significant residual narrowing in the coronary arteries, rhythm changes, and heart muscle failure. They also guide the physicians in prescribing activity regimens after discharge.
Before resuming full activity or work, several weeks are needed for the area of the heart attack to heal. After a small heart attack, which is measured by the size of heart muscle damage, patients can resume normal activities after two weeks. These activities include returning to work as well as normal sexual activity. A moderate heart attack requires limited, gradually increasing activity for four weeks, while a large heart attack results in a six week recovery period. These time frames are necessary for the dead heart muscle to substantially complete the scarring process. During this healing period, patients
should avoid vigorous exertion and heavy lifting (over 20 pounds) or any activity that causes shortness of breath or sweating.
Sternlieb, Jack, M.D. Eight Steps To A Healthy Heart. Warner Books Inc: New York,
Norman, John C. Cardiac Surgery. Appleton-Century-Crofts: New York, 1972
Lindsey, Mary. Human Body. Dorling Kindersley Inc: New York, 1991