CONGESTIVE HEART FAILURE Austin Community 充血性心脏衰竭奥斯丁社区.ppt

CONGESTIVE HEART FAILURE Austin Community 充血性心脏衰竭奥斯丁社区.ppt

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Renin-angiotensin-aldosterone system ? Neurohormonal responses (Low CO dec. in cerebral perfusion pressure-compensatory mechanisms- maintain CO) Antidiuretic hormone (ADH) secreted inc. water reabsorption in renal tubules water retention and inc. blood volume Endothelin- stimulated by ADH, catecholamines, and angiotensin II arterial vasoconstriction, inc. in cardiac contractility, cardiac hypertrophy Neurohormonal responses release proinflammatory cytokines (e.g., tumor necrosis factor) by cardiac myocytes in response to cardiac injury; depress cardiac function cardiac hypertrophy, contractile dysfunction, and myocyte cell death Neurohormonal responses: *overtime systemic inflammatory response cardiac wasting, muscle myopathy, fatigue *Consequences of compensatory mechanisms Ventricular dilation: Enlargement of heart chambers-elevated left ventricular pressure; initially effective adaptive mechanism; then mechanism inadequate, CO dec. * Frank-Starling law- inc. ventricular filling and myocardial stretch eventually results in ineffective contraction (typical inc. venous return inc. force of contraction) Hypertrophy: inc. in muscle mass and cardiac wall thickness in response to chronic dilation; heart muscle-poor contractility, inc. oxygen needs, poor coronary artery circulation, prone to ventricular dysrhythmias (sudden cardiac death) Counter-regulatory mechanisms (counteract negative effects) *Natriuretic peptides: atrial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP) (*hormones secreted by heart muscle) *Prolonged HF- depletes these factors. *(*BNP-note measure in CHF-secreted by ventricles due to fluid volume overload) (Lewis p. 752. Tab. 32-7) Released in response to inc. in atrial volume and ventricular pressure Promote venous and arterial vasodilation (reduce preload and afterload) –diuresis Natriuretic peptides- endothelin and aldosterone antagonists; Enhance dieresis, block effects of RAAS; inhibit development cardiac hypertrophy, po

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