The Connection in Angina with Myocardial Infarction


Emergency Medical


MLA Formation


11 May 2004


It was just another day at work. There I was taking a patient back to his room after his physical therapy. He had complained of feeling “a little full” after his lunch. I helped him get back into bed and I left the room. I went back to the department to ambulate another patient. Ten minutes later an overhead page: “code blue in wing two” “code blue in wing two” My heart started racing, I could almost feel the adrenaline pumping. A cardiac arrest. I rushed to see if I could help. To my surprise it was Mr. Smith. There he was lifeless: a nurse rushed to get the CPR board, another one had a BVM mask they began performing cardiopulmonary resuscitation. At the same time the ambulance had transported a patient from dialysis. The two men came to the rescue.


Like Mr. Smith, there are many people that live knowing they have a cardiovascular disease, but others are unaware of how close they are to experience the main cause of death here in the United States. It is estimated that ½ of Americans will eventually die from a Heart Disease. The American Heart Association predicts than in 2004 more than 1 million Americans will suffer a heart attack (Heart Attack). Fortunately, this can easily be avoided by living a healthier lifestyle. However, the average person is not aware of the signs and symptoms or how to assist a person in the event of a cardiac arrest. Heart Disease is the leading cause of death, by recognizing the relationship between angina pectoris and myocardial infarction death could be postponed.


Angina pectoris and myocardial infarction are very dangerous conditions that require prompt attention. The American Heart Association describes angina as the medical term for chest pain or discomfort caused by coronary heart disease. The Merck Manual of Diagnosis and Therapy classifies angina pectoris as a “clinical syndrome due to myocardial ischemia characterized by precordial discomfort or pressure, typically precipitated by exertion and relieved by rest or sublingual nitroglycerin” (sec.16). Furthermore, Acute myocardial infarction, commonly known as a heart attack, is defined as death of heart muscle following obstruction of blood flow (Browner et al., 351-352) from one or more of the coronary arteries initiated myocardial ischemia and necrosis (“Atlas” 58-59). At times it is difficult to separate angina from a myocardial infarction since both have similar etiologies:


Angina is usually cause by atherosclerosis in a coronary artery and rarely does a spasm or embolism can cause it (Browner et al. 351-352). However, other diseases and emotional and/or physical stress can cause angina either by directly increasing cardiac work or in combination with a preexisting coronary artery disease. This includes but is not limited to aortic regurgitation, hypertrophic subaortic stenosis and calcific aortic stenosis (“Angina”). In addition, a large meal, sudden fear, strong emotions or extreme temperature change my cause an attack (Browner 351-352). Angina pectoris occurs when the cardiac work and oxygen need exceeds the ability of the coronary arteries to deliver oxygen rich blood. The major determinants of cardiac oxygen demand are the heart rate, systolic tension or arterial pressure and contractility, therefore an increase on anyone of these factors in a person with an already diminish coronary blood flow could induce angina.



Fig. 1. Angina


In myocardial infarction a reduced blood flow through one or more of the coronary arteries will initiate cardiac ischemic and necrosis usually caused by a blood clot. These blood clots do not usually form in normal arteries. However, a clot may form if the artery has some atheroma on its inside lining. Atheroma is like fatty patches or \'plaques\' which develop on the inside lining of arteries. The Merck manual, a pharmaceutical research company reports that in more than 90% of patients with acute myocardial infarction (AMI), a previously atherosclerotic plaque causes an acute thrombosis obstructing the artery that supplies the damage area. In addition, the endothelial change in the plaque induces an altered platelet function contributing to thrombotic occlusion (sec. 16). Similar to angina, an arterial embolism rarely causes an MI, but unlike angina an MI can develop by a coronary spasm due to cocaine used or idiopathic. Some risk factors for MI include family history,