2.2.5 Oedema formation
2.2.5 Oedema formation

CHF may result in clinical signs as a result of a failure to maintain cardiac output, or because of the development of congestive signs. Oedema formation results in a dilutional hypoproteinaemia in the interstitium, reducing the oncotic pressure. After some time, an equilibrium develops and oedema formation becomes self-limiting. However, the position of the equilibrium may be changed if excessive water retention results in a fall in the oncotic pressure of the blood. Other factors may also affect the development of oedema. The left atrium (LA) plays an important role in limiting the effects of mitral regurgitation (MR) which can lead to CHF. With severe MR, end-diastolic pressure rises in the LV resulting in an increase in LA pressure. This in turn increases pressure in the pulmonary veins, resulting in pulmonary oedema. However, the thin-walled atrium can expand to dampen the effects of the increased pressure from the pulmonary circulation. This takes some time (days), but will decrease the tendency for pulmonary oedema formation as a result of MR. For this reason, signs of pulmonary oedema are often most severe when MR develops acutely, for example as a result of ruptured chordae tendineae.