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)

Results:

• 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.