Circulatory Compensation in Heart Failure
What are the compensatory measures that occur in heart failure?
The compensatory measures that occur in response to a fall in cardiac output include:
a) Increase in sympathetic tone – resulting in:
- increase in heart rate
- to maintain cardiac output
- increase in arterial vasomotor tone (increasing peripheral arterial resistance or afterload)
- to maintain blood pressure
- increase in venomotor tone
- to increase venous return which increases preload
- release renin from kidney
- elaborates angiotensin II and aldosterone which increase vasomotor tone (increasing afterload) and increase venous vasomotor tone (increasing preload) and increase Na and water retention (also increases preload)
- increase contractility
- promote arrhythmias
- increase MVO2 (myocardial oxygen demand)
b) Redistribute cardiac output to coronary and cerebral vascular beds and away from:
- cutaneous vascular beds causing
- pale mucus membranes
- slow capillary refill time
- cool extremities
- splanchnic vascular beds causing
- impaired intestinal absorption
- ischemic bowel with ulceration and hemorrhage
- renal vascular beds causing
- reduced GFR
- sodium retention and water retention
c) Increased thirst – causing fluid overload (increasing preload).
d) Increased arginine vasopressin (ADH) resulting in:
- increase arterial vasomotor tone (increasing afterload)
- increase fluid retention – fluid overload (increasing preload)
- Increased afterload –> reduces stroke volume; increases MVO2.
- Increased preload –> increases stroke volume; increases MVO2; pulmonary edema.
- Reduced renal perfusion.
- Increase HR –> increase MVO2; + increase cardiac output.
- Maintain blood pressure for coronary and cerebral perfusion
- Increase contractility –> increased MVO2; increase stroke volume.
- Promote dysrhythmias –> decrease cardiac output.
Comments: The net effect of these compensatory measures usually has deleterious effects on cardiac performance chronically.