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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)
renin angiotensin aldosterone map illustration
Renin-Angiotensin-Aldosterone System
ACE – Angiotensin converting enzyme
ADH – antidiuretic hormone

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.