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The movement of water and solutes out of the intravascular space and into the interstitial space is dependent on opposing osmotic and hydrostatic pressures. Hydrostatic pressure is caused by the pumping action of the heart and the diameter (resistance) of the vessels/capillaries forcing water and molecules that are small enough to pass through the membrane out of the vessel and into the interstitial fluid. Within the vascular system, only the capillaries have semi-permeable membranes so it is here this ‘filtration’ occurs. At the arteriole end of the capillary, the hydrostatic pressure exceeds the osmotic pressure, moving solutes out of the plasma and into the interstitial space. At the venous end, hydrostatic pressure is reduced and the osmotic pressure within the vessel (plasma) is higher so water is pulled back into the vessel and circulating volume (van Wissen and Breton 2004). The osmotic pressure is provided by plasma proteins that are too large to pass through the membrane even under pressure. Oedema can result if the membranes become permeable to protein; osmotic pressure is then reduced, resulting in excess of water moving into the interstitial space. Pulmonary oedema is caused by this mechanism at the site of the lungs. Sepsis or a systemic inflammatory response is an example of a condition where the capillary membranes become more permeable to protein.

Osmolarity and fluid balance

Sodium is the most influential electrolyte in fluid balance and is the primary cation (positively charged ion) of the ECF. The concentration of sodium in the ECF has the most profound effect on its osmolarity and therefore water balance. If ECF osmolarity increases (for example, with increased intake of sodium, reduced fluid intake, increased loss of fluid), osmoreceptors of the hypothalamus detect very slight changes (1–2% increase) in plasma osmolarity (Marieb and Hoehn 2010) and trigger the thirst response which in turn encourages oral fluid intake in an attempt to restore the balance (Figure 8.1).

Figure 8.1 Cellular membrane.

Hormonal mechanisms and the kidneys are highly influential in fluid and electrolyte balance and again are also triggered in response to changing osmolarity and/or plasma volumes. Antidiuretic hormone (ADH) is released from the posterior pituitary gland (in response to stimulus of the osmoreceptors in the hypothalamus) (van Wissen and Breton 2004) and acts on the tubules and collecting ducts of the kidneys, inhibiting water excretion and encouraging water reabsorption. If plasma osmolarity falls (indicating water excess), these mechanisms are suppressed by a negative feedback loop; the osmoreceptors are no longer stimulated. This in turn inhibits ADH release; renal tubules no long conserve water and thirst is reduced, leading to a reduction of oral intake and restoration of balance. ADH is also released in the renin-angiotensin response to a reduction in blood pressure (detected by baroreceptors in blood vessels); more detailed information on this mechanism can be found in Chapter 12.

Aldosterone is a mineralocorticoid and is secreted by the adrenal cortex in response to increased osmolarity and/or decreased blood pressure (part of the renin-angiotensin system). It acts on the renal tubules, initiating the active transport of sodium (and hence water) from the tubules and collecting ducts back into the plasma and circulating volume (Baumberger-Henry 2008).

These homoeostatic mechanisms are very effective in maintaining fluid and electrolyte balance in health and act to compensate for fluid imbalances to ensure effective cellular function. However, these compensatory mechanisms are not sustainable and will eventually fail if ill health or imbalance persists. For example, in continued haemorrhage, the body will compensate by conserving water and vasoconstricting vessels in an attempt to increase blood pressure and volume. Continued haemorrhage and failure to replace lost fluids will lead to cellular and organ dysfunction which in turn