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V.

Pathophysiology

ETIOLOGIC RISK FACTORS


AGENT Family history of hypertension ,
Idiopathic/ unknown diabetes, heart failure
Stress
High salt, high fat intake
Age

Stiffness of large arteries (such as Aorta) as


Part of aging process

Hypoperfusion of blood to organs


(such as kidneys) and tissues

RAAS Activation

Sensed by the Juxtaglomerular


Cells of the kidneys

Triggers the release of renin

It will go to the liver

ANGIOSTENSINOGEN
Converted to Angiotensin 1

It will go to the lungs


Angiotensin Converting Enzyme
Converts Angiotensin 1 to
Angiotensin 2

Stimulates the Adrenal cortex Vasoconstriction

Release of aldosterone

Na retention (increase circulatory decrease Preload increase Afterload


Blood volume)
Increase BP increase RR increase Peripheral Resistance

Increase BP increase chloride Left Ventricle wall stress

Oxygen consumption insufficient Left ventricle Hypertrophy Concentric LVH


Oxygen as shown in Xray
Anaerobic respiration
Pale decreased blood pumped coronary flow reserve Diastolic
By the heart Pressure
Lactic acid, pyruvic acid ATP produced Fibrosis
Production blood supply (vital organs) Diastolic filling
Weakness/ Systolic Heart
Irritation of nerve endings easy fatigability myocardial ischemia failure LVEDP

Chest pain myocardial infarction Pulmonary Atrial Fibrilation Diastolic


congestion Heart
Failure
Shortness of breath/ DOB

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