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Patho MI

Myocardial infarction is caused by a blockage in the coronary arteries that reduces blood flow and oxygen to the heart muscle. Risk factors include age, smoking, obesity, high blood pressure, diabetes, and diet. When oxygen demand exceeds supply, the heart cells switch to anaerobic metabolism which builds up lactic acid and damages cell membranes, altering heart muscle contraction and decreasing cardiac output. This triggers baroreceptors and sympathetic receptors to increase heart rate and contractility further worsening the ischemia.

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2K views

Patho MI

Myocardial infarction is caused by a blockage in the coronary arteries that reduces blood flow and oxygen to the heart muscle. Risk factors include age, smoking, obesity, high blood pressure, diabetes, and diet. When oxygen demand exceeds supply, the heart cells switch to anaerobic metabolism which builds up lactic acid and damages cell membranes, altering heart muscle contraction and decreasing cardiac output. This triggers baroreceptors and sympathetic receptors to increase heart rate and contractility further worsening the ischemia.

Uploaded by

banyenye25
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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PATHOPHYSIOLOGY OF MYOCARDIAL INFARCTION ETIOLOGY: FACTORS

Coronary atherosclerotic heart disease Coronary thrombosis/Embolism Decrease blood flow with shock & or hemorrhage Direct trauma -

RISK
age smoking obesity HPN diabetes diet

Imbalance of blood supply and demand Myocardial ischemia

Occlusion of coronary artery Cellular processes compromised Decrease of oxygen Cell switch to anaerobic metabolism Lactic acid builds up in the cell Cell membrane permeability Specific enzyme release Stimulation of nerve fibers Pain impulses to the CNS
Increased peripheral vasoconstriction

Decrease of myocardial oxygen supply Increased cellular hypoxia Altered cell membrane Int. Decrease of myocardial contractility Decreased cardiac output Decreased arterial pressure Stimulation of baroreceptors Stimulation of sympathetic receptors

Increased myocardial contractility Increased HR Decreased diastolic filling Decreased myocardial tissue perfusion

Increased after load

Increased myocardial oxygen demand

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