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Common Congenital Heart Lesions - page 86 / 126





86 / 126

86 of 126

How renin works:

    • renin results in formation of angiotensin II, a potent vasoconstrictor, which increases TPR (renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II via ACE)

    • AII stimulates thirst, increases water intake ( intravascular volume)

    • AII causes adrenal cortex to release aldosterone, which causes sodium and water to be absorbed from the distal tubule ( intravascular volume)

    • Increase in TPR and intravascular volume causes increased CO

  • C.

    Anti-diuretic hormone (ADH, vasopressin)

    • Release stimulated by AII and baroreceptors

    • Promotes water reabsorption from the collecting duct, increasing intravascular volume

Negative Effects of Neurohormonal Compensatory Mechanisms

  • A.

    Increased Volume in the heart without substantial increases in SV exacerbates pulmonary congestion

  • B.

    Increased TPR increases afterload and impairs SV and CO

  • C.

    Increased HR causes increased metabolic demand, which reduces heart function (because heart can’t increase CO to meet demand)

  • D.

    Increased Sympathetic drive causes downregulation of beta receptors, resulting in decreased CTY

  • E.

    AII and Aldosterone stimulate fibrosis and heart remodeling via activation of cytokines

**Treatments for heart failure decrease compensatory mechanisms**

Role of ANP and BNP: atrial and B-type natriuretic peptides: beneficial hormones, released in response to cardiac stress and counteract compensatory mechanisms

  • 3.

    Ventricular Hypertrophy and Remodeling

    • In heart failure, wall stress is increased from either volume or pressure overload. σ= P r/ 2 h Chronically increased wall stress stimulates ventricular hypertrophy. Helps maintain contractile force and decreases wall stress, but hypertrophy causes an increased diastolic pressure.

    • Volume overload: LV is dilated due to increased volume in the heart. Results in eccentric hypertrophy, characterized by elongation of myocytes (series)

    • Pressure overload: increased afterload causes in higher systolic pressure. Results in concentric hypertrophy, characterized by increase in wall thickness without chamber dilation (parallel)

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