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Pathophysiology CHF Mine

This document outlines the pathophysiology of heart failure. It describes how non-modifiable risk factors like family history and age, along with modifiable risk factors like an unhealthy diet, smoking, and alcohol can lead to the buildup of cholesterol in artery walls and the development of atherosclerosis. Over time, this narrowing of blood vessels reduces blood flow to the heart and body, causing the heart to work harder and become less efficient. This increased workload stresses the heart and can eventually lead to congestive heart failure if left untreated.

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Calimlim Kim
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344 views2 pages

Pathophysiology CHF Mine

This document outlines the pathophysiology of heart failure. It describes how non-modifiable risk factors like family history and age, along with modifiable risk factors like an unhealthy diet, smoking, and alcohol can lead to the buildup of cholesterol in artery walls and the development of atherosclerosis. Over time, this narrowing of blood vessels reduces blood flow to the heart and body, causing the heart to work harder and become less efficient. This increased workload stresses the heart and can eventually lead to congestive heart failure if left untreated.

Uploaded by

Calimlim Kim
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

Modifiable Non-modifiable
*Diet *Family history of hpn,
-high fat, high sodium heart problems
*alcohol
*smoking *Age:76 yrs. old

Bad cholesterol (LDL) congest into the wall of


arteries

Activation of specialized cells

Theyll become enlarge cholesterol and rich cell


(film cells)

Invasion to the vessel wall

Atherosclerosis

Increase size of the plaque

Narrowing of the vessels

vasoconstriction
Decrease oxygenated blood flowing into the heart
Hypertension muscle

Decrease heart contraction

Decrease blood flow Reduces efficiency of myocardium through


all over the body damage and overloading

Activation of RAAS
Decrease oxygen supply Increase systemic vascular
and demand resistance
The kidney will
release Renin
Chest pain Stimulation of adrenergic
system
Angiotensinogen
Increase force of left
ventricle contraction
Angiotensin I
Increase left ventricle
workload
Angiotensin II (ACE)

Aldosterone Increase left ventricle


oxygen demand
Increase sodium
Left ventricle hypoxia
Water retention
Pulmonary edema

Bipedal Edema Pulmonary vascular


resistance
Right ventricular failure

Activity Intolerance Weakness and Decrease cardiac output


Easy fatigability
Ventricular remodelling

Progressive loss of
cardiac output

Myocardial hypertrophy

Loss of myocytes

Congestive heart failure

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