Right heart failure pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Right ventricular hypertrophy or RVH is the predominant change in chronic cor pulmonale although in acute cases dilation dominates. Both hypertrophy and dilation are the result of increased right ventricular pressure.
Acute Dilation
Dilation is essentially a stretching of the ventricle, the immediate result of increasing the pressure in an elastic container.
Chronic Right Ventricular Hypertrophy
Ventricular hypertrophy is an adaptive response to a long-term increase in pressure. Additional muscle grows to allow for the increased contractile force required to move the blood against greater resistance.
Pathophysiology of cor pulmonale
To be classified as cor pulmonale, the cause must originate in the pulmonary circulation system. Two major causes are vascular changes as a result of tissue damage (e.g. disease, hypoxic injury, chemical agents etc.), and chronic hypoxic pulmonary vasoconstriction. RVH due to a systemic defect is not classified as cor pulmonale.
There are several pathophysiologic mechanisms leading to pulmonary arterial hypertension and cor pulmonale:
- Pulmonary vasoconstriction
- Compression of the pulmonary vasculature by lymph nodes or tumors
- Anatomic changes in vascularization of the lung
- Increased blood viscosity (e.g. polycythemia vera[1])
- Idiopathic or primary pulmonary hypertension
- Increased volume overload of the right ventricle (e.g. Atrial septal defect)
- Chronic hypoventialtion of the lung due to mechanical defects (e.g. diaphragmatic paralysis)
Nutmeg Liver
As a result of right ventricular failure, blood backups up into the system venous system, including the hepatic vein. Chronic congestion in the centrilobular region of the liver leads to hypoxia and fatty changes of more peripheral hepatocytes, leading to what's known as nutmeg liver.