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Pathophysiology of STEMI Explained

This document discusses the progression of coronary artery disease from modifiable and non-modifiable risk factors to myocardial infarction. Risk factors like hypertension, smoking, and stress can lead to endothelial dysfunction and the buildup of plaque in coronary arteries over time due to chronic inflammation. Rupture of vulnerable plaque can cause thrombus formation, suddenly blocking blood flow and oxygen delivery to heart muscle, leading to ischemia, necrosis, and reduced cardiac output if not resolved. Left ventricular failure and associated symptoms may develop if the infarction is large.

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Mary Sutingco
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181 views2 pages

Pathophysiology of STEMI Explained

This document discusses the progression of coronary artery disease from modifiable and non-modifiable risk factors to myocardial infarction. Risk factors like hypertension, smoking, and stress can lead to endothelial dysfunction and the buildup of plaque in coronary arteries over time due to chronic inflammation. Rupture of vulnerable plaque can cause thrombus formation, suddenly blocking blood flow and oxygen delivery to heart muscle, leading to ischemia, necrosis, and reduced cardiac output if not resolved. Left ventricular failure and associated symptoms may develop if the infarction is large.

Uploaded by

Mary Sutingco
Copyright
© © All Rights Reserved
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

Modifiable Risk Factor:

Exposure to Non-modifiable risk


-Overweight
atherosclerotic risk factor:
-Physical inactivity
- history of hypertension factors Age
-stress Male
family history of MI
Endothelial dysfunction

Expression of adhesion molecules in


Arterial spasm
endothelium

Influx of lipids and macrophages in Reduced blood flow


intima-media space

Formation of atheromatous plaque under chronic Increased vascular resistance


inflammation

Increase in blood pressure


Progressive scarring and calcification of plaque due to
inflammation

Sudden reversible obstruction


Vulnerable plaque erosion

Thrombus formation in arteries with or without


embolisation

Total Occlusion in coronary artery

Decreased coronary perfusion

Angina Reduced oxygen demand

Unstable angina Thrombolysis

Permanent thrombus

Acute cardiac ischemia

ischemic necrosis
ischemic necrosis

Decreased cardiac output


Infarction of the myocardium
Sinus bradycardia

Release of lactic acid, Stimulation of


Reduced myocardial contractility
pyruvic acid and autonomic nerve
other metabolites peripheral system
Left-sided heart tfailure

nausea Pulmonary congestion


Excessive sweating

Shortness of breath, pulmonary


edema

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