ISSN 2398-2942      

Heart: pathophysiology of CHF


Mark Oyama

Liz Bode


  • Canine heart disease is characterized by cardiac dysfunction (often systolic or valvular dysfunction), activation of compensatory mechanisms, progressive cardiac injury due to maladaptive compensatory mechanisms, congestive heart failure Heart: congestive heart failure , and arrythmias Heart: dysrhythmia.
  • In dogs with dilated cardiomyopathy Heart: dilated cardiomyopathy (DCM) , the heart has poor systolic function, ie contractility of the ventricles is impaired. Poor cardiac contraction leads to decreases in cardiac output and activation of compensatory mechanisms that are designed to increase heart rate, increase blood volume, and maintain arterial blood pressure.
  • In dogs with mitral valve disease Heart: mitral valve degenerative disease , the heart suffers from volume overload. The forward cardiac output is decreased by loss of stroke volume through the defect in the mitral valve. Poor cardiac output leads to activation of compensatory mechanisms.
  • In dogs with heart failure, typically used treatments attempt to reduce blood volume (diuretics), reduce activation of compensatory mechanisms (ACE-inhibitors ACE inhibitor: overview, spironolactone Spironolactone ) and improve contractility (pimobendan Pimobendan ).

Compensatory mechanisms

  • As cardiac injury occurs, the sympathetic nervous system and the renin-angiotensin-aldosterone (RAA) system responds to increase cardiac output (CO).
  • These systems are also activated when cardiac output falls due to falling blood pressure (BP) or cardiac disease. Deactivation of baroreceptors in the aortic arch and carotid sinus → parasympathetic withdrawal and increased sympathetic drive (circulating adrenaline and noradrenaline as well as sympathetic nervous system).
  • This increases heart rate (if possible), increases contractility (if possible), by beta receptor stimulation. Vasoconstriction occurs due to alpha 1 receptor activation. These mechanisms increase cardiac output (cardiac output = stroke volume x heart rate: CO = SV x HR) and blood pressure (blood pressure = cardiac output x total peripheral vascular resistance: BP=CO x TPR).
  • Reduced renal perfusion pressure and sympathetic stimulation increases renin release from the juxtaglomerular apparatus in the kidneys → angiotensinogen conversion to angiotensin I and angiotensin II (via the action of angiotensin converting enzyme (ACE)).
  • Angiotensin II acts:
    • On zona glomerulosa of adrenal cortex releasing aldosterone → acts on distal convoluted tubule of nephron ’ kidney retains chloride, sodium and water.
    • As a potent vasoconstrictor → increase in total peripheral vascular resistance → maintenance of blood pressure → increased afterload on a failing heart.
    • On central nervous system (CNS), effects → increased sympathetic outflow.
    • On CNS (supra-optic nucleus of hypothalamus) → increased synthesis and release of vasopressin (antidiuretic hormone) by the neurohypophysis (posterior pituitary).
  • Chronically elevated angiotensin II/ aldosterone stimulates myocardial remodeling and vascular smooth muscle cell remodeling (peripheral vasculature changes).
  • Vasopressin release is also mediated by a fall in cerebral perfusion pressure.
    The adverse effect of this is to create a high afterload, resulting in increased myocardial wall stress, which can compromise cardiac output further.
  • Sodium and water retention and venular constriction increases venous volume and venous pressure. This aims to increase preload to utilize the Frank-Starling mechanism → increased stroke volume.

Heart failure

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Classification of heart failure

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Further Reading


Refereed papers

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