The risk factors of heart attacks include age as men who are above 45 years and women above 55 years are at a higher risk of getting heart attacks. Tobacco is a leading factor through direct smoking and exposure to second-hand smoke ( Heusch & Gersh, 2016) . Having high blood pressure also puts one at risk of getting a heart attack. A high cholesterol level is the other risk factor for the condition. People with obesity are also at high risk of getting heart attacks. People with stress and those who have a family history of heart attacks are also at a higher risk of facing the condition. Research also shows that people with illicit drug use also have a higher risk of getting the condition.
The cell injury that Mr. Smith had undergone was Necrosis. This occurs as the hypoxic cells transition from aerobic metabolism to anaerobic metabolism to maintain the levels for cell survival. Necrosis plays a role in the death of cardiomyocytes as mitochondrial rupture usually releases cellular contents increasing cell necrosis ( Reed, Rossi, & Cannon, 2017) . During the heart attack, Mr. Smith had a reduced flow of blood to the heart signifying to the cells of the heart not getting enough oxygen. If the reduction of blood lasts long, the cells of the heart could die because of cellular necrosis.
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Reversible cell injury can be stopped through removing or destroying the stimulus causing the injury. However, the irreversible cell injury has usually gone past the level where the cells can go back to their normal functioning capacity. During reversible cell injury, fat accumulation and protrusions of the cell membrane occur. Irreversible cell injury usually results in acidosis of the cellular environment and the destruction of organelles ( Carrick et al., 2016) . Irreversible cell injury usually leads to necrosis and cell death irreversible cell injury is usually characterized by factors such as mitochondrial swelling, damage to the plasma membrane, and increased acidosis. In reversible cell injury, the cell can return to the steady state through the process of altering the cellular conditions while the irreversible cell injury is severe and results in the death of cells.
The pathophysiology of acute myocardial infarction has been found to be complex due to the many functions involved. When loss of myocardium occurs, there is the impairment of the global cardiac function. It causes reduced cardiac output as well as a cardiogenic shock ( Carrick et al., 2016) . Pulmonary congestion and edema can occur if the left ventricular function is impaired. The pain and anxiety that occurs because of the myocardial infarction usually activate the sympathetic nervous system resulting in systemic vasoconstriction as well as cardiac stimulation. The process of sympathetic activation helps in maintaining arterial pressure but can also lead to an increase in myocardial oxygen demand increasing the risk of myocardial hypoxia, which further impairs the cardiac function.
Mr. Smith has some risk factors such as advanced age, being of the male gender, a history of CAD, as well as unstable angina. Mr. Smith's atherosclerosis also causes the CAD. The narrowing of his lumen has increased the likelihood of him having an MI ( Heusch & Gersh, 2016) . After lifting heavy furniture, Mr. Smith comes to the ER having pain in his left chest, sweating, and having shortness of breath. It is after EKG that coronary artery occlusion is established to be in the left anterior artery. The most common finding is that he had a clot and necrosis had already started occurring leading to a section of his heart muscles having dead cells.
References
Carrick, D., Haig, C., Ahmed, N., Rauhalammi, S., Clerfond, G., Carberry, J... & Hood, S. (2016). Temporal evolution of myocardial hemorrhage and edema in patients after acute ST‐segment elevation myocardial infarction: pathophysiological insights and clinical implications. Journal of the American Heart Association , 5 (2), e002834.
Heusch, G., & Gersh, B. J. (2016). The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: a continual challenge. European heart journal , 38 (11), 774-784.
Reed, G. W., Rossi, J. E., & Cannon, C. P. (2017). Acute myocardial infarction. The Lancet , 389 (10065), 197-210.
