What confirms the presence of a myocardial infarction?
a. a full description of the pain
b. the presence of elevated serum cholesterol and triglycerides
c. all your own patterns for serum isoenzymes and the ECG
d. leukocytosis and elevated C-reactive protein
Answer: C:-).
definitely C.
You can do blood try-out for lactate dehydrogenase,creatine kinase and CKMB as all this will elevate for cardiac arrest (MI) c--- just very soon the ekg has specific changes. cpk mb is elevated but I don't know how long up to that time it returns to normal..
C C.
Characteristic patterns for serum isoenzymes and the ECG
Acute myocardial infarction (MI) is defined as loss or necrosis of myocardial cells. It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes. Myocardial infarction occur when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms that are designed to maintain usual operating function and hemostasis. Ischemia at this critical threshold level for an extended time period results surrounded by irreversible myocardial cell damage or death.1-3
Critical myocardial ischemia may turn out as a result of increased myocardial metabolic demand and/or decreased transference of oxygen and nutrients to the myocardium via the coronary circulation. An interruption in the supply of myocardial oxygen and nutrients occurs when a thrombus is superimposed on an ulcerated or unstable atherosclerotic plaque and results surrounded by coronary occlusion. A high-grade (> 75%) fixed coronary artery stenosis due to atherosclerosis or a dynamic stenosis associated with coronary vasospasm can also limit the supply of oxygen and nutrients and precipitate an MI. Conditions associated next to increased myocardial metabolic demand include extremes of physical exertion, severe hypertension (including forms of hypertrophic obstructive cardiomyopathy), and severe aortic valve stenosis. Other cardiac valvular pathologies and low cardiac output states associated near a decreased aortic diastolic pressure, which is the prime component of coronary perfusion pressure, can also precipitate MI.1-3
Myocardial infarction can be subcategorized on the basis of anatomic, morphologic, and diagnostic clinical information. From an anatomic or morphologic standpoint, the two types of MI are transmural and nontransmural. A transmural MI is characterized by ischemic necrosis of the full concreteness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium. A nontransmural MI is defined as an area of ischemic necrosis that does not extend through the full mass of myocardial wall segment(s). In a nontransmural MI, the area of ischemic necrosis is limited to any the endocardium or the endocardium and myocardium. It is the endocardial and subendocardial zones of the myocardial wall segment that are the least perfused regions of the heart and are most adjectives to conditions of ischemia. An older subclassification of MI, based on clinical diagnostic criteria, is determined by the presence or non-attendance of Q waves on an electrocardiogram (ECG). However, the presence or absence of Q top does not distinguish a transmural from a non-transmural MI as determined by pathology.4
A more common clinical diagnostic classification scheme is also base on ECG findings as a means of distinguishing between two types of MI—one that is distinct by ST elevation and one that is not. The distinction between an ST-elevation MI and a non-ST-elevation MI also does not distinguish a transmural from a non-transmural MI. The presence of Q waves or ST segment elevation is associated next to higher early mortality and morbidity; however, the fantasy of these two findings does not confer better long-term mortality and morbidity.4
The most common etiology of MI is a thrombus superimposed on a ruptured or unstable atherosclerotic plaque.5
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