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HACVD Patho

The document summarizes the pathophysiology of heart and cardiovascular disease. It describes how LDL and triglycerides damage endothelial cells, leading platelets and monocytes to adhere and abnormal proliferation of smooth muscles. This causes inflammation and narrowing of blood vessels from atherosclerotic plaque formation. Over time, plaque rupture can decrease blood flow and increase vascular resistance, raising afterload and preload on the heart. As a compensatory mechanism, the heart undergoes hypertrophy but eventually fails in oxygen compensation, leading to tissue ischemia, injury, and infarction which decreases cardiac output and causes systemic hypoxia and multiorgan failure and death.

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Angel Filoteo
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51 views

HACVD Patho

The document summarizes the pathophysiology of heart and cardiovascular disease. It describes how LDL and triglycerides damage endothelial cells, leading platelets and monocytes to adhere and abnormal proliferation of smooth muscles. This causes inflammation and narrowing of blood vessels from atherosclerotic plaque formation. Over time, plaque rupture can decrease blood flow and increase vascular resistance, raising afterload and preload on the heart. As a compensatory mechanism, the heart undergoes hypertrophy but eventually fails in oxygen compensation, leading to tissue ischemia, injury, and infarction which decreases cardiac output and causes systemic hypoxia and multiorgan failure and death.

Uploaded by

Angel Filoteo
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
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Pathophysiology HACVD LDL and Tryglycerides

Damage to intimal endothelial cells

Platelets and Monocytes adhere to injured site

Abnormal proliferation of smooth muscles and connective tissue

Inflammation of blood vessels

Migration of monocytes beneath the endothelium and become macrophage

Permeability of endothelium

Formation of Atherosclerotic plaque (CXR: Atherosclerosis of thoracic aorta)

Narrowing of the blood vessel lumen

Blood flow Plaque hemmorrhage/rupture Vascular resistance

Afterload

Preload

Compensatory Mechanism: Myocardial Hypertrophy

Cardiomegaly

Increased O2 demands

Failure of O2 compensation

Cardiac Tissue Ischema

Cardiac Tissue Injury

Cardiac tissue Infarction

Decreased functioning contractile tissue

Cardiac output

Perfusion/Hypoperfusion

Systemic Hypoxia

Multiorgan Failure

Death

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