Congestive Heart Failure

Cardiac heart failure: (CHF) is the pathophysiologic state resulting from impaired cardiac function that renders the heart unable to maintain an output sufficient for the metabolic requirements of the tissues and organs of the body.

CHF is characterized by either or both:

• Diminished cardiac output (forward failure) ---> decreased perfusion of tissues

• Back pressure -> venous congestion and oedema (backward failure or congestive failure)

Before the heart fails there is adaptation ( work) by the myocardium to overcome the problem; first by Increased contractility, neurohormonal mechanisms and then by muscular hypertrophy. If stimulus persists (beyond adaptive mechanisms) then heart may fail.

Left-sided heart failure: major causes include ischaemic heart disease, hypertension, aortic & mitral valve disease and myocardial disease.

Manifestations:

• Pulmonary congestion and oedema secondary to impairment of lung vascular outflow (most common)

• Renal perfusion decreases leading to:

  • Further salt and water retention (renin-angiotensin system)

  • Ischaemic acute tubular necrosis

  • Impairment of waste excretion, causing prerenal azotemia (uraemia)

• CNS perfusion decreases, often resulting in hypoxic encephalopathy (with symptoms ranging from irritability to coma)

Right-sided heart failure: typically consequence of left-sided failure.

One-sided failure cannot exist in isolation for long (exemplified in this case) and heart failure usually become generalised fairly soon. Pure right-sided heart failure may be caused by intrinsic disease of the lungs or pulmonary vasculature causing functional right ventricular outflow obstruction (cor pulmonale) or tricuspid or pulmonary valvular disease.

The changes that occur are minimal in the lung and are mainly due to backwards failure with widespread congestion and oedema, affecting:

Venous system:

• Raised jugular venous pressure

• Portal, systemic and dependent peripheral (e.g. feet, ankles, sacrum) congestion and oedema & effusions (pleural and peritoneal [ascites])

Liver:

• Hepatomegaly with centrilobular congestion and atrophy of central hepatocytes, producing a ‘nutmeg’ appearance (chronic passive congestion)

• In severe hypoxia, centrilobular necrosis can occur; if chronic, healing with fibrosis create cardiac sclerosis (not true cirrhosis) of the liver
  

Kidney:

• Congestive splenomegaly with sinusoidal dilation, focal haemorrhages and later hemosiderin deposits and fibrosis

• Renal congestion, hypoxic injury and acute tubular necrosis, more marked in right sided than in left sided CHF
  

Subcutaneous tissues: shows generalised oedema with protein-poor fluid in gravitational distribution (ankles if ambulant, sacral if bedfast)

Congestion of other organs such as brain or bowel may also give rise to symptoms which are generally less striking

Category: Pathology Notes