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1. Frank-Starling Mechanism: Heart failure causes a downward shift in the Frank Starling curve, which causes a decrease in SV. (See figure below and Fig 9.3 on page 215) Decrease in SV causes increase in preload, which subsequently increases SV. Helps to empty LV and preserve CO. However, if patient is in the flat part of the curve, an increase in preload does not have much impact on cardiac output. But, increased preload (or increased end-diastolic volume) does cause an increase in end-diastolic pressure, which is transmitted to the pulmonary vasculature and causes congestion (or edema if right heart failure.)
2. Neurohormonal Alterations: In response to ↓ CO, these mechanisms maintain BP by increasing total peripheral resistance and increasing intravascular (increases SV.) BP = CO x TPR These mechanisms are helpful initially, but chronic activation contributes to heart failure.
A. Adrenergic Nervous System: ↓ COÆ ↓ BPÆ ↓ baroreceptor firingÆ ↑ sympathetic outflow and ↓ parasympathetic outflow. Causes an ↑ HR, ↑ CTY (β1), and vasoconstriction (α1).
Increased HR and CTY causes increase in CO
Vasoconstriction increases venous return to the heart, which increases preload and therefore increases SV, but only IF the ventricle is operating on the ascending portion of the curve (see figure above.)
Vasoconstriction also increases TPR and helps maintain BP
Renin-Angiotensin-Aldosterone System: release of renin stimulated by:
decreased renal artery perfusion
decreased salt delivery to kidneys
direct stimulation of β2 receptors by adrenergic NS