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Common Congenital Heart Lesions - page 94 / 126

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94 / 126

94 of 126

PATHOPHYS

  • it starts from myocyte injury Æ decr contractility Æ decr SV

  • hallmark = ventricular dilation (volume overload) w/ decr contractile fxn …

  • as SV and CO impaired, 2 compensatory effects:

    • o

      Frank-Starling mech where elevated EDV increases stretch on myofibers and thus incr subsequent SV

      • o

        Neurohormonal activation

        • primarily sympathetic NS Æ incr HR and CTLY

        • kidneys spit out renin b/c of decline in renal blood flow Æ activation of renin-angiotensin-aldosterone axis Æ incr TPR and intravascular volume

  • b/c of compensation, pt may be asymptomatic in early stages… but …

  • compensation can actually be harmful in long run

      • o

        constant arteriolar vasoconstriction and incr systemic resistance make afterload bigger and so harder for LV to eject blood forward… and rise in intravascular volume further burdens ventricles Æ end result is pulmonary and systemic congestion

      • o

        chronically elevated ang II and aldosterone contributes to myocardial/vascular remodeling with fibrosis

  • as ventricles enlarge over time, the mitral and tricuspid valves may fail to close together properly in systole Æ valvular regurg…

  • 3 detrimental conseq of valvular regurg:

      • o

        excessive volume and pressure loads on atria Æ atria dilate Æ atrial fibrillation

      • o

        regurg into LA further decr forward SV into aorta

      • o

        when regurg volume returns to LV during diastole, it adds to the volume overload

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