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Heart: pathophysiology of CHF

ISSN 2398-2950

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Physiology

  • 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 output 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 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  →  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 (supraoptic 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.
    The adverse effect of this is to create a high preload, resulting in volume overload, high venous pressures, and development of congestive heart failure.

Heart failure

  • As heart disease progresses the cardiovascular system is eventually unable to maintain adequate CO and/or normal venous pressures - this is called decompensated failure.
  • During heart failure, fluid is retained because of activation of the RAA system, thus increasing the volume of blood being returned to the heart and causing myocardial stretch.
  • Initially this is beneficial, however the ability of the ventricle to enlarge is limited.
  • The body's homeostatic priority is to maintain blood pressure at the expense of increased afterload and increased venous and capillary pressures.
  • This, combined with reduced venous capacitance  →  increased pressure within the ventricle during filling and increased pressure in the atrium.
  • Peripheral arteriolar constriction mediated by alpha 1 receptor stimulation, angiotensin II, vasopressin, etc increases peripheral vasculature resistance and maintains blood pressure.
  • However a high afterload increases myocardial wall stress, which can compromise CO further.
  • Increased filling pressures, increased venous pressures and reduced venous capacitance compromise the Starling forces of the capillary exchange, so capillary pressure increases.
  • Finally, the pressure in the vessels exceeds the forces acting to retain fluid within the vessel and fluid leaks into the interstitial space  →  edema (congestive heart failure).

Classification of heart failure

  • Heart failure can be classified according to the side of the heart predominantly affected (left or right) and to whether failure results in reduced CO or congestion.

Backward heart failure

  • The body's homeostatic priority is to maintain blood pressure at the expense of increased afterload and increased venous and capillary pressures.
  • Congestive left heart failure is characterized by an increase in pressure in the pulmonary veins  →  congestion of the pulmonary circulation making the lungs stiff and gas transfer inefficient.
  • Fluid extravasates in the interstitium and then the alveoli of the lung (pulmonary edema).
  • In cats, pleural effusion Pleural effusion can also be observed with left sided heart failure. 
  • In congestive right heart failure blood accumulates in the systemic veins resulting in the accumulation of fluid in body tissues and body cavities (ascites, pleural effusion).
  • Hepatomegaly may result from venous congestion.
  • Pleural effusion also results from right heart failure due to increased venous filling pressures and reduced pleural venous drainage to the systemic venous circulation.
    While a patient may present initially with signs of left or right failure this often progresses to biventricular failure.
  • Low volume pericardial effusion may also be identified.

Forward heart failure

  • This is much less common than backward failure since the compensatory mechanisms aim to maintain CO at the expense of all else. It occurs much less commonly in cats than dogs, as dilated cardiomyopathy is rare in cats. 
  • Poor circulation to the brain can result in syncopal episodes or generalized lethargy/ collapse.
  • Poor renal perfusion may lead to compromised renal function and pre-renal azotemia Uremia.

Chronic changes

  • Chronically increased ventricular end-diastolic pressures and/or increased afterload result in structural sarcomere changes in the myocardium. Increased end-diastolic volume and pressure  →  sarcomere replication in series (eccentric hypertrophy). Increased afterload (especially with a pressure overload condition), causes sarcomere replication in parallel (concentric hypertrophy).
  • Fast heart rates and increased afterload increase myocardial work load and oxygen consumption, while compromising diastolic coronary perfusion. Myocardial hypoxia occurs which may be responsible for the development of dysrhythmias Heart: dysrhythmia.

Further Reading

Publications

Refereed papers