ISSN 2398-2950      

Heart: pathophysiology of CHF


Mark Oyama


  • Feline heart disease is characterized by cardiac dysfunction (often diastolic dysfunction), activation of compensatory mechanisms, progressive cardiac injury due to maladaptive compensatory mechanisms, congestive heart failure Heart: congestive heart failure, and arrythmias Heart: dysrhythmia Heart: pathophysiology of heart failure .
  • In cats with hypertrophic Heart: hypertrophic cardiomyopathy or restrictive cardiomyopathy Heart: restrictive cardiomyopathy, the heart has poor diastolic function, that is, relaxation and diastolic filling of the ventricles is impaired. Poor cardiac filling leads to decreases in cardiac ouptut and activation of compensatory mechanisms that are designed to increase heart rate, increase blood volume, and maintain arterial blood pressure.
  • Diastolic heart failure does not typically require specific drugs to increase contractility, rather, the treatment of diastolic failure is to reduce preload (diuretics), slow heart rate (beta-blockers, calcium channel blockers) and improve relaxation.

Compensatory mechanisms

  • In response to the initial cardiac injury, the sympathetic nervous system and the renin-angiotensin-aldosterone (RAA) system respond 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   →   decreased vagal tone 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   →   maintenence of blood pressure   →   increased afterload on a failing heart.
    • On central nervous system (CNS), effects   →   increased sympathetic outflow.
    • On CNS (supraoptic nucleus of hypothalamus)   →   increased synthesis and release of vasopressin (antidiuretic hormone) by the neurohypophysis (posterior pituitary).
  • Chronically elevated angiotensin II 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.
    The adverse affect of this is to create a high preload, resulting in volume overload, high venous pressures, and development of congestive heart failure.

Heart failure

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Classification of heart failure

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Further Reading


Refereed papers

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