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Patho of MI

This document outlines the pathophysiology of a myocardial infarction (MI). It lists precipitating factors like diabetes, diet, hyperlipidemia, and others that can lead to atherosclerosis. Atherosclerotic plaque can rupture, forming a thrombus that occludes a coronary artery. This cuts off blood supply to heart muscle, causing ischemia and ultimately cell death or MI if prolonged. The body responds by increasing heart rate, constricting vessels, and stressing the heart, but these compensations are insufficient to overcome the reduced blood flow caused by the blocked artery.

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Inchan Montesines
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603 views2 pages

Patho of MI

This document outlines the pathophysiology of a myocardial infarction (MI). It lists precipitating factors like diabetes, diet, hyperlipidemia, and others that can lead to atherosclerosis. Atherosclerotic plaque can rupture, forming a thrombus that occludes a coronary artery. This cuts off blood supply to heart muscle, causing ischemia and ultimately cell death or MI if prolonged. The body responds by increasing heart rate, constricting vessels, and stressing the heart, but these compensations are insufficient to overcome the reduced blood flow caused by the blocked artery.

Uploaded by

Inchan Montesines
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 DOC, PDF, TXT or read online on Scribd
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Precipitating

Factors: Predisposing
- Diabetes Mellitus Factors:
- Diet (high fat and - Age
high - Gender (male)
carbohydrates) - Family history of
- Hyperlipoproteine heart disease
mia
- Hypertension
- Obesity
- Sedentary

Thrombus formation due to ruptured or


cracked atherosclerotic plaque

Thrombus fully
Occlusion of the
occludes the
right coronary
vessels and
artery with right
involves the full
ventricular
thickness of the
infarction (Inferior
ventricular wall
wall MI)
for a prolonged
time (STEMI)

Imbalanced in myocardial oxygen supply and


demand

Ischemia

Increased Cellular Hypoxia

Altered Cell Membrane Int.

Decreased Myocardial
Contractivity

Decreased Cardiac
Output
Decreased Arterial
Pressure
Stimulation of
Baroreceptors

Stimulation of
Sympathetic Receptors

Increased Peripheral Increased


Vasoconstriction Myocardial Activity
Increased After Increased Heart
Load Rate

Decreased
Diastolic Filling

Decreased
Myocardial Tissue
Perfusion

Myocardial
Infarction

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