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    Final patho-HCVD

    Uploaded by

    Alvin Ramirez
    This document outlines the pathophysiology of hypertension. It describes how stiffening of the arteries due to aging causes hypoperfusion of organs and tissues, activating the renin-angiotensin-aldosterone system (RAAS). This leads to vasoconstriction, sodium retention, and increased blood pressure and cardiac workload. Over time, this causes left ventricular hypertrophy, reduced coronary flow, and can progress to heart failure if left untreated.

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    Attribution Non-Commercial (BY-NC)
    Download as DOCX, PDF, TXT or read online from Scribd

    Final patho-HCVD

    Uploaded by

    Alvin Ramirez
    786 views2 pages
    This document outlines the pathophysiology of hypertension. It describes how stiffening of the arteries due to aging causes hypoperfusion of organs and tissues, activating the renin-angiotensin-aldosterone system (RAAS). This leads to vasoconstriction, sodium retention, and increased blood pressure and cardiac workload. Over time, this causes left ventricular hypertrophy, reduced coronary flow, and can progress to heart failure if left untreated.

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    final patho-HCVD

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    This document outlines the pathophysiology of hypertension. It describes how stiffening of the arteries due to aging causes hypoperfusion of organs and tissues, activating the renin-angiotensin-aldosterone system (RAAS). This leads to vasoconstriction, sodium retention, and increased blood pressure and cardiac workload. Over time, this causes left ventricular hypertrophy, reduced coronary flow, and can progress to heart failure if left untreated.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    786 views2 pages

    Final patho-HCVD

    Uploaded by

    Alvin Ramirez
    This document outlines the pathophysiology of hypertension. It describes how stiffening of the arteries due to aging causes hypoperfusion of organs and tissues, activating the renin-angiotensin-aldosterone system (RAAS). This leads to vasoconstriction, sodium retention, and increased blood pressure and cardiac workload. Over time, this causes left ventricular hypertrophy, reduced coronary flow, and can progress to heart failure if left untreated.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    of 2

    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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