Initially help maintain CO but ultimate worsen heart function.
Enlargement of chambers of heart—pressure in heart is elevated over time (LV)—increase CO, adaptive mechanism to cope with increasing blood volume, becomes inadequate because the elastic elements of muscle fibers are overstretched and overstrained.
An increase in muscle mass and cardiac wall thickness in response to overwork and strain, slowly occurs, increase in CO and maintenance of tissue perfusion, has poor contractility.
First mechanism triggered in low CO states, least effective compensatory mechanism, happens because of inadequate SV and low CO, thus a release of epi and norepi which increases HR, myocardial contractility, and peripheral vasoconstriction. Increases myocardium’s need for O2 and workload of an already failing heart Increases SVR and afterload. Diastolic failure intolerant of increased HR.
CO decreases blood flow to kidney decreases causing decrease in glomerular blood flow—juxtaglomerular apparatus release renin, increase in peripheral vasoconstriction- release of aldosterone causing sodium retention. Increases Preload and afterload. Hypothalamus senses and causes posterior pituitary to secrete ADH causes water retention.
Compensatory mechanism cause ventricle to remodel becomes less effective pump.