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Although interest in diseases which cause malfunction to the heart and the body at large has increased in recent years, a great deal of literature pertains to pathopysiology of heart myocardial infarction. The heart is the fundamental part of the body to which living things solely depends on to exist. Research has it that ultimate attention has been given to this area and as such deaths from heart attacks as often referred to has drastically decreased. Doctors allover the world have made researches and resolved that the risk of a persistent myocardial infarction decreases with strict blood pressure management and lifestyle changes, predominantly smoking cessation, regular exercise, a sagacious diet for patients with heart disease, and limitation of alcohol intake. Further studies have initiated various ways of beating down heart myocardial infarction. There are current studies that show that another form of cell death called apoptosis also partakes or acts a part in the course of tissue damage following myocardial infarction. There is also a view stating palpably that complications may occur immediately in the acute face, but may be time dependent to grow as a result of chronic problem after a myocardial infarction or heart attack has occurred. There is also a mechanism known as the cardiac defibrillator designed for the purpose of bringing to an end or terminating fatal arrhythmias. The result of this study will help you understand the pathophysiology of heart myocardial infarction and its complications.

1.0 Introduction

It is essential to start by knowing what pathophysiology is. Pathophysiology is derived from two Greek words Pathos-meaning “suffering or disease” and Physiologia- combining physis meaning “nature” plus logos meaning “study”.Unlike anatomy which is the study of normal structure physiology is the study of normal, healthy bodily function. Pathophysiology comes in when something interrupts normal physiological progression. Pathology is the "study of the nature and cause of disease or the outcome of disease in the body. Consequently, Pathophysiology looks at the precise malfunctioning that comes from or - alternately - causes disease”.

1.2 Pathophysiology of heart myocardial infarction

Narrowing our view, a myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, totally occluding the artery and preventing blood flow downstream. Non-ST-elevated myocardial infarction and ST-elevated myocardial infarction are the two subtypes of acute coronary syndrome acute myocardial infarction refer to. They are most often but not always a symptom of coronary artery disease. The majority of generally triggering occurrence is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which consequently pilots to a clotting cascade, every so often ensuing in whole occlusion of the artery. The steady buildup of cholesterol and fibrous tissue in plaques in the wall of arteries, the coronary arteries in this case, typically over decades is what is known as Atherosclerosis. The reflection of artery lumen tapering   being the result of decades of progressive atherosclerosis is done by Blood stream column irregularities perceptible on angiography. There is a propensity that cholesterol and fibrous tissue in tablet form or plaques can become unbalanced, rupture or fracture, and furthermore enhance a thrombus (blood clot) that occludes the artery; this process can take place in minutes. What leads to myocardial infarction (necrosis of downstream myocardium) is when a massive plague rupture takes place in the coronary vasculature.

Provided damaged or impaired blood flows to the heart and stays long enough, it prompts a process called the ischemic cascade; the heart cells in the area of the occluded coronary artery die (primarily via necrosis) and consequently do not re-grow. In place of the dead heart cells in the area a collagen scar forms. There are current studies that show that another form of cell death called apoptosis also partakes or acts a part in the course of tissue damage next to myocardial infarction. The patient's heart will be permanently damaged as result of this. And the patient is put to risk for potentially life threatening arrhythmias because of this scarring myocardial, and may lead to the formation of a ventricular aneurysm that can rupture with catastrophic effects.

It is also notice that injured tissue of the heart is liable conduct electrical impulses more slowly than normal heart tissue. The disparity in conduction velocity between injured and uninjured tissue can prompt re-entry or a response loop that is thought to be the cause of numerous lethal arrhythmias. The ventricular fibrillation (V-Fib/VF) is the most serious of these arrhythmias; it is an exceedingly quick and disordered heart rhythm that is the foremost cause of sudden cardiac death. Another life threatening arrhythmia is ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. Conversely, ventricular tachycardia more often than not results in brisk heart rates that tend to avoid the heart from efficiently pump blood. Blood pressure and Cardiac output and blood are likely to go down to ghastly points, which consequently can lead to additional coronary ischemia and extension of the infarct. This is very bad for steady operation of the heart.

There is a gadget that has been designed specifically to end the existences of these deadly arrhythmias. The cardiac defibrillator is a device that was exclusively designed to bring to an end these potentially lethal arrhythmias. The mechanism works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "restarting" the heart. This mechanism or the treatment depends on time and the probability of successful defibrillation turn down fast after the commencement of cardiopulmonary arrest. This is development that has assisted so much in heart myocardial treatment

 1.3 Complications

After the heart attack complications may occur immediately in the acute face. May be time dependent to grow .this might be as a result of chronic problem. Subsequent to an infarction, a dire complication is a reoccurrence of another infarction, which possibly will occur in the same region if there are any live cells left in the in infarction or in the realm of another atherosclerotic coronary artery

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