Prior

By F. Prior, V. Morecroft, R. Fergusson, T. Gourlay, K. Taylor. 2020

Several theories have been put forward to describe the development of oedema. The forward theory (1-5) suggests that a failing heart reduces the arterial pressure to an extent where normal renal function is compromised. Renal, nervous and endocrine mechanisms are stimulated which result in retention of fluid and water. The backward theory (6,7) suggests that a failing heart is unable to pump sufficiently to prevent the pooling of blood on the venous side of the circulatory system increasing venous pressure and decreasing renal perfusion. The subsequent water and sodium retention results in expansion of the extracellular space. The third, and currently most popular hypothesis, suggests that oedema results from a decreased effective extracellular volume (8) when normal feedback mechanisms respond inappropriately to increased plasma renin, aldosterone and ADH levels (9) . Fluid leaks into the interstitium either as a result of decreased oncotic pressure or increased hydrostatic pressure in the capillaries (10). Oedema is characterised by accumulation of water and salt, stimulation of the sympathetic nervous system (11), activation of the renin/angiotensin/aldosterone cascade 9 and clinical evidence of increased extracellular volume expansion. All of these theories are based to a greater or lesser extent on the Starling Hypothesis of fluid exchange (12) published 100 years ago. Starling was the first to suggest that fluid balance and fluid exchange are governed by the balance of the hydrostatic and osmotic pressures within the capillaries (12,13). The hydrostatic pressure was known to reduce from about 40 mmHg at the arterial end of the capillary to about 10 mmHg at the venous end. The osmotic pressure difference between the plasma and the interstitial fluid (osmotic gradient) was assumed to remain constant down the length of the capillary. The hydrostatic pressure was assumed to exceed the osmotic gradient at the arterial end and fall to less than the osmotic gradient at the venous end of the capillary. In this way fluid was forced out at the arterial end and drawn back at the venous end of the capillary (Fig. 1). Fluid balance was achieved when the volume of fluid forced Artificial Kidney and Dialysis The International Journal of Artificial Organs / Vol. 22 / no. 3, 1999 / pp. 138-144