Fluid management during mechanical ventilation is complicated by both the influence of positive-airway pressure on normal homeostatic control of bodily fluids, and the interaction of mechanical ventilation with fluid status. Hypovolemia may lead to hemodynamic intolerance of positive-airway pressure, and fluid overload may result in both impaired gas exchange and respiratory mechanics and deleterious systemic effects. In patients with acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS), positive fluid balance has been associated with both fewer ventilator-free days, and longer intensive care unit (ICU) stay, and with mortality in prospective randomized1 and observational2 studies, respectively.
In the normal adult male, total body water accounts for approximately 60% of body weight. In turn, approximately 40% of body weight is intracellular water and approximately 20% is distributed into the extracellular fluid volume, made up of interstitial fluid (approximately 16%), plasma volume (approximately 4%), and usually negligible volumes of lymph and transcellular fluid (cerebrospinal fluid and pericardial, intrapleural, and peritoneal fluid). Tissues such as brain, kidney, liver, and muscle have high water contents (70% to 80%) but adipose tissue has low water content (approximately 10%). Consequently, women, who tend to have more adipose tissue, have a lower total body water (approximately 50% of body weight). Total body water decreases in the elderly because of a loss of muscle mass.
The extracellular volume is distributed in interstitial fluid and plasma volume, and consists of two compartments. Seventy percent of the volume is rapidly equilibrating (approximately 20 minutes), and the remainder slowly equilibrates (approximately 24 hours) in dense connective tissue and bone. Sodium balance regulates the extracellular volume, whereas water balance regulates the intracellular volume.
Water balance is primarily determined by thirst and the renal action of arginine vasopressin, also termed antidiuretic hormone, which is secreted from the posterior pituitary following synthesis in the hypothalamus, in response to a wide variety of stimuli, particularly plasma osmolality. Vasopressin activates V2 receptors on the basolateral surface of the distal renal tubule and collecting duct, leading to an increase in water permeability, and reabsorption of filtrate, through fusion of aquaporin-2 with the luminal membrane. Vasopressin also reduces water clearance by decreasing renal medullary blood flow, and independently increases the renal medullary concentration gradient by stimulating a urea transporter.4
Under normal circumstances, a plasma osmolality of 280 mOsm/kg suppresses vasopressin secretion allowing maximal urinary dilution. As osmolality progressively rises to 295 mOsm/kg, so does the secretion of vasopressin, with an associated reduction in free water clearance. The kidney can normally concentrate filtrate up to 1200 mOsm/kg under the influence of vasopressin, although this tends to deteriorate with age and renal dysfunction. Table 65-1 lists other stimuli that influence vasopressin secretion. High-pressure stretch receptors in the aortic arch and carotid sinus sense a significant (>10%) fall in blood pressure ...