Distribution of Body Water

Water in the body is distributed throughout the various body fluid compartments. The simplest subdivision is into an intracellular and an extracellular compartment, with the two compartments separated by the cell membrane (Figure 35-1). On average, a 70-kg adult has 42 L of water, of which two thirds (28 L) is intracellular and one third (14 L) is extracellular. The extracellular fluid is made up of the interstitial fluid (11 L), which bathes the cells and includes the lymph, the plasma (3 L), and the cavity or transcellular fluids, of which the largest volume is secretory fluids in the lumen of the gastrointestinal tract.

The distribution of water in the various compartments determines the size of the compartments and is governed by solute particles and physical forces that maintain equilibrium across membranes separating these compartments. Osmotic forces and hydrostatic pressures are the prime determinants of water distribution in the body.

Osmotic forces across a semipermeable membrane (impermeable to solutes but permeable to water) separating two compartments govern the distribution and direction of water movement between these compartments. This concept is explained simply in Figure 35-2. The two compartments, A and B, which contain the same volume of fluid but different numbers of solute particles are separated by a semipermeable membrane. Water diffuses across the membrane in both directions, but more water molecules diffuse from compartment A, a region of higher water concentration (lower solute concentration), to compartment B, which is a region of lower water concentration (higher solute concentration). This process of net movement of water caused by a concentration difference of water or solutes is called osmosis. Osmosis of water results in the expansion of compartment B at the expense of compartment A. No further net diffusion of water occurs when the solute concentrations in both compartments are equal, that is, when osmotic equilibrium is established. To reach this state of equilibrium, the volume of compartment B has increased at the expense of compartment A. This situation can occur only when the two compartments are flexible volumetrically so that the net flow of water from one compartment to another does not create a pressure difference across the membrane. However, if the walls of compartment B do not expand, the increase in hydrostatic pressure in compartment B due to influx of water will oppose further inflow of water. The amount of pressure to be applied in order to prevent the inflow of water through the membrane into compartment B is called osmotic pressure (Rose and Post, 2001). The osmotic pressure of a solution therefore reflects the concentration of osmotically active particles in that solution.

The process of osmosis also explains the movement of water across cell membranes. Most cell membranes are semipermeable, that is, relatively impermeable to most solutes but highly permeable to water. Although water is a polar molecule, it is able to penetrate the nonpolar lipid region of membranes through a group of transmembrane channel proteins called aquaporins (AQPs), which form channels through which water can readily diffuse. The number of AQPs, also known as water channels, differs in membranes of different tissues. In some cells, the number of AQPs, and thus the permeability to water, can be altered in response to hormones. In the steady state, the volume of water that diffuses across the membrane in either direction is balanced precisely so that no net diffusion of water occurs and the volume of the cell remains unchanged. However, under certain conditions, when a concentration difference for water develops across the cell membrane by active transport of solutes, osmotic forces will develop across the cell membrane and water will move rapidly between these two compartments until an osmotic equilibrium is achieved. When this happens, net influx of water causes the cell to expand, whereas net efflux of water causes the cell to contract. Therefore at equilibrium the osmolar concentration (osmolarity) of the intracellular and interstitial fluid compartments remain similar, at approximately 290 mOsm/L.

Iso-osmotic, Hypo-osmotic, and Hyperosmotic Solutions

The terms iso-osmotic, hypo-osmotic, and hyperosmotic are used to describe the relation of osmolar concentrations between different solutions. When two solutions are of equal osmolarity, they are iso-osmotic. A solution is hypo-osmotic when its osmolarity is lower than that of the reference solution and hyperosmotic when its osmolarity is higher. When cells are suspended in a hypo-osmotic solution, water enters the cells, causing them to expand. Conversely, when cells are suspended in a hyperosmotic solution, water diffuses out of the cells, causing them to contract. One would expect that, when cells are suspended in an iso-osmotic solution, no net flux of water would occur and cell size would remain the same. This is true only if cells are suspended in an iso-osmotic solution in which no net movement of solutes occurs across cell membranes. If cells are suspended in an iso-osmotic solution containing a highly permeant solute, such as urea, it diffuses into cells along its concentration gradient, causing an osmotic flow of water into cells, and the cells expand (Figure 35-3). Thus another term, tonicity, is used to describe the physiological osmolar concentration of a solution.

Fluid Distribution Between Plasma and Interstitial Fluid Compartments

Plasma circulates throughout the body and provides a medium for transporting water, solutes, and gases from one part of the body to another. As the blood flows through the capillaries, interstitial fluid is delivered continuously to tissues by ultrafiltration near the arterial ends and returned to the circulation near the venous ends by forces across the capillary endothelium. In this way, the absorbed solutes and water from the gastrointestinal tract and dissolved oxygen from the lungs are carried to the tissues by plasma and by interstitial fluid. Similarly, metabolic waste products, including dissolved carbon dioxide from tissues, are carried by the same route but in the opposite direction, to the kidneys, liver, and lungs to be eliminated. Therefore, as first described by Claude Bernard (1813–1879) as the milieu intérieur, the interstitial fluid constitutes the immediate environment of the body cells.

The interstitial fluid protects the cells in the body from direct contact with the external environment and acts as a buffer for the cells from sudden changes in solute and water content caused by ingestion or loss from the body. The body possesses various physiological control systems that regulate the elimination of solutes and water from the body, so that the composition and volume of the plasma and, indirectly, the composition and volume of the interstitial and intracellular fluids are maintained relatively constant.

A small fraction of interstitial fluid is continuously drained away through lymphatic channels. This fluid, called lymph, drains into the thoracic duct and returns to the circulation via the right subclavian vein. The total volume of lymph is small, about 1 to 2 L. Transcellular, or cavity, fluids are generally considered to be specialized secretory fluids produced by active transport processes occurring across epithelial cells. These fluids differ from interstitial fluid in that they are not simple ultrafiltrates of plasma; their compositions differ markedly from that of plasma and are adapted specifically to the function of a particular organ. Examples of transcellular fluids are fluids in the lumen of the gastrointestinal tract, the cerebrospinal fluid, and fluids in the intraocular, pleural, peritoneal, and synovial spaces. Of these, intraluminal gastrointestinal fluid constitutes the largest fraction. The total volume occupied by these fluids is small, about 1 to 2 L.

Movement of Fluid Across Capillary Endothelium

The fenestrations (20- to 100-nm diameter pores) of the capillary endothelium are highly permeable to almost all solutes in the plasma except proteins, so that interstitial fluid and plasma have a similar composition except for the higher concentration of proteins in the plasma. Except in the brain, diffusion and bulk flow of protein-free plasma constitute the most important means by which net movement of nutrients, gases, metabolic end products, and fluid occur across the capillary walls. Two factors, the Gibbs–Donnan equilibrium and the Starling forces, affect the distribution of solutes and flow of protein-free plasma through these fenestrations.

Gibbs–Donnan Equilibrium

On average, the concentration of proteins in the interstitial fluid is less than 10 g/L, compared with 73 g/L in the plasma. The differential concentration of protein affects the distribution of diffusible ions and osmotic pressures across the capillary endothelium. When two fluid compartments, A and B, are separated by a semipermeable membrane, the concentrations of any diffusible cation or anion are equal across the membrane so that no differences in concentration exist for any of the ions. On the basis of thermodynamic principles, Gibbs and Donnan showed that at equilibrium, the product of the concentrations of diffusible cations and anions in the two compartments are equal and electrical neutrality is maintained:

[Cation]A×[Anion]A=[Cation]B×[Anion]B

When a nondiffusible cation or anion is added to one of the compartments, the diffusible ions will redistribute themselves so that the concentration of each ion will no longer be equal across the cell membrane.

At normal plasma pH of 7.4, the majority of plasma proteins behave as negatively charged particles. Because proteins are confined to the vascular compartment, electrical neutrality in the plasma can be maintained only by an unequal distribution of the smaller diffusible ions, resulting in lower concentrations of each of the diffusible anions and higher concentrations of each of the diffusible cations in the plasma than in the interstitial fluid. At a normal concentration of plasma protein (73 g/L) this effect is small, with the concentration of monovalent anions (for example, chloride) about 5% lower and that of monovalent cations (for example, sodium and potassium) approximately 5% higher in the plasma than in the interstitial fluid. For all practical purposes, the concentrations of ions in the plasma and interstitial fluid can be considered to be about equal.

Starling’s Law

The concentration difference of proteins across capillary endothelium not only affects the distribution of diffusible ions, but also causes an osmotic gradient across the capillary endothelium. This osmotic gradient exerts a pressure that is called the colloid osmotic pressure or oncotic pressure. Colloid osmotic pressure together with hydrostatic pressure are of physiological importance in determining net water movement across the capillary endothelium.

Starling first proposed the concept that the two opposing forces governing water movement across the capillary endothelium are created by the difference in hydrostatic pressure and the difference in colloid osmotic pressure across the capillary wall (Taylor, 1981). Therefore four variables determine the movement of fluid: hydrostatic pressures and protein concentrations in the plasma and the interstitial fluid. The following equations describe the forces responsible for net water movement across an idealized capillary endothelium:

Netdrivingpressure=(Pc−Pif)−(πc−πif)

Netvolumeofwaterflow=Kf[(Pc−Pif)−(πc−πif)]

where K_f is the permeability coefficient (product of water permeability and filtration surface area) of the capillary endothelium, P_c is the capillary hydrostatic pressure, P_if is the interstitial fluid hydrostatic pressure, π_c is the capillary colloid osmotic pressure, and π_if is the interstitial fluid colloid osmotic pressure.

As blood flows along the capillary, the balance of these forces is a net pressure gradient favoring the movement of a small amount of fluid from the arterial end of the capillary into the interstitium. This causes hydrostatic pressure to decrease along the length of the capillary so that much of the fluid reenters the capillary at the venous end (Figure 35-4). The small amount of fluid that remains in the interstitium is returned to the circulation by the lymphatic vessels, which empty into the subclavian vein via the thoracic duct (Taylor, 1981).

Under normal circumstances, the difference in hydrostatic pressure between capillary blood and interstitial fluid favors filtration out of the capillary, and the difference in colloid osmotic pressure favors absorption of interstitial fluid into the capillary. An imbalance in any of these forces affects net movement of water across the capillary endothelium and ultimately will affect distribution of fluid between the plasma and interstitial compartments. For example, a decrease in plasma protein concentration in disease states, such as liver and kidney diseases, results in an accumulation of fluid in the interstitial spaces, causing edema.

Other factors that may affect the distribution of fluid across capillary endothelium include the integrity of the endothelium and the lymphatic drainage system. An increase in capillary permeability allows plasma albumin to enter the interstitium to an abnormal extent, thereby reducing the difference in colloid osmotic pressure (i.e., πc−πif in Starling’s equation). This increase in permeability occurs in sepsis, venom shock, drug overdose, and anaphylactic reactions, and it can cause large volumes of fluid to leak from the vascular to the interstitial space. The lymphatic system can reduce the volume of edema fluid by returning it to the intravascular system via the thoracic duct. Blockage of lymphatic drainage causes accumulation of fluid in the interstitial fluid compartment.

Loss of Water

Water is lost from the body by essentially four different routes: respiratory tract, skin, gastrointestinal tract, and kidneys. Of these four, water loss from the kidneys is the most important and is regulated by various neuroendocrine pathways to maintain a constant osmolarity of the body fluids.

Water Loss through Respiratory Tract and Skin

Insensible Water Loss

Water is lost continuously from the body by two passive evaporative routes: from the upper respiratory tract during respiration and from the skin. These passive evaporative losses are termed “insensible losses” or “insensible perspiration” because they occur continuously and without our awareness. The amount of evaporative water loss from the respiratory tract depends on the ventilatory volume and water pressure gradient. A water pressure gradient occurs because expired air is saturated with moisture to a vapor pressure of about 47 mm Hg, whereas the vapor pressure of inspired air is usually less than 47 mm Hg. An individual loses an average of between 0.14 and 0.47 L daily by this route; the amount of the loss depends on body size, the degree of physical activity, and ambient temperature and humidity. It is to be expected that evaporative water loss from the lungs is increased in physical activity and when the atmospheric vapor pressure decreases (i.e., in cold, dry climates). Insensible water loss from the skin, which occurs independent of sweating, averages between 0.3 and 0.5 L daily for an individual living in a temperate environment and doing minimal physical activity (Geigy Scientific Tables, 1981).

On average, an individual will lose a total of 0.4 to 0.9 L of water daily from insensible loss through both the respiratory tract and skin. When body temperature rises higher than 39° C, evaporative loss from the respiratory tract increases because of a significant increase in the respiratory minute volume (Reithner, 1981). The increase in water loss by the respiratory route can be as much as an additional 0.1 L daily at elevated body temperatures. Dermal losses can increase much more due to sweating.

Sweat

Dermal losses due to sweating at high body temperatures can be substantial. Cutaneous water loss due mainly to sweating can increase by as much as 6 to 8 times the basal level when rectal temperature is above 39.5° C (Lamke et al., 1980).

The volume of water lost as sweat is highly variable, depending on the environment and the physical activity of the individual. In hot weather and during strenuous activity, evaporation of sweat from the skin is an effective means of dissipating the excess heat from the skin thus cooling the body and defending the core temperature of the body. For every gram of water that evaporates from the skin, 0.58 kcal of heat is lost from the body. Daily water losses as sweat are determined by the body’s need for evaporative heat loss and are influenced by the environment and the metabolic rate. Water loss as sweat is substantially less in an environment of moderate temperature and humidity than in a warm, humid environment where loss through perspiration can be considerable.

Normally the volume of sweat in a 65-kg adult doing light work at an ambient temperature of 29° C (84.2° F) amounts to about 2 to 3 L daily, but it can increase to a maximum of about 2 to 4 L per hour for a short time in an unacclimatized individual who is performing heavy physical activity in a hot and humid environment. This levels off to about 0.5 L per hour over a 24-hour period as the duration of perspiration increases (Geigy Scientific Tables, 1981). Even at maximal sweating, the rate of heat loss may not be rapid enough to dissipate the heat from the body. When the body temperature rises to a critical level, higher than 40.5° C (105° F), the individual is likely to develop heatstroke. However, after acclimatization to hot weather for a few weeks, an individual will have greater tolerance of the hot and humid environment and can as much as double his or her sweating rate. Evaporation of this large volume of sweat effectively removes the excess heat from the body. Acclimatization also involves a decrease in the concentration of sodium chloride in the sweat, allowing for better conservation of sodium chloride (Takamata et al., 2001). The loss of several liters of sweat a day in a hot climate results in serious losses of both sodium chloride and water, which need to be replaced.

Water Loss by the Gastrointestinal Tract

The volume of water loss in feces is small, about 0.1 L a day, and does not cause problems with water balance unless excessive loss occurs during diarrhea. The volume of fluid ingested varies among individuals but averages about 1.7 L daily. Added to this ingested volume, the small intestine receives an additional 7 L of secretory fluids, which are made up of salivary, gastric, biliary, pancreatic, and intestinal secretions. Normally approximately 90% to 95% of these fluids is absorbed by the small intestine, and the remainder by the colon, leaving only approximately 0.1 L of water to be excreted in the feces. Absorption of water in the intestine is passive, along an osmotic gradient created by the absorption of nutrients from the lumen of the intestine into the plasma. In diseases of the gastrointestinal tract, large volumes of water can be lost in the feces, causing diarrhea. This occurs in gastroenteritis due to bacterial or viral infection or in any situation in which absorption of nutrients is compromised. Certain bacterial toxins, such as cholera toxin, can increase the secretion of sodium chloride from the crypt cells of the small intestinal mucosa into the lumen of the small intestine. The lumen becomes hyperosmotic, and water diffuses from the plasma into the lumen, causing diarrhea. Several liters of fluid, up to 10 to 20 L, can be lost, resulting in dehydration (Hall, 2011b).

Water Loss by the Kidneys

Renal water loss varies depending on solutes and water load. However, there is a minimal volume of water that has to be excreted because of the limit on how much the kidneys can concentrate urine. For a 65-kg reference man, the minimal urine volume that an adult must produce, assuming consumption of an average North American diet and normal

CLINICAL CORRELATION

Heat Acclimatization

Humans have relatively efficient heat dissipation mechanisms, but the thermoregulatory mechanism may be overwhelmed in a number of conditions, resulting in the development of hyperthermia. The risk of hyperthermia occurs when individuals move from a cool temperate climate to a tropical climate and perform physical exertion, or when athletes perform in tropical conditions without prior conditioning to the hot, and particularly hot and humid, ambient conditions. The inability to adequately dissipate body heat leads to a steady rise in body core temperature with the consequence of heat-related illness, which ranges from heat cramps to heatstroke. Prompt transfer to a cooler environment with adequate ventilation to accelerate body heat dissipation, adequate fluid replacement, and cessation of physical activity is essential for treatment of an individual with heat-related illness.

Conditioning the body to the hot environment by repeated bouts of exercise will improve the physiological responses of a healthy individual. This improvement of the individual’s thermoregulatory responses to heat stress is known as heat acclimatization. The adaptation process is obtained several days after exposure and is usually fully achieved after 14 days, although it has been found that, in well-trained athletes, the heat-induced impairment of physiological responses and performances is still evident after 14 days (Voltaire et al., 2002). During acclimatization, a number of physiological adaptations to improve the individual’s thermoregulatory ability occur. Typical physiological changes include heightened sweating response, reduced sodium concentration in the sweat, expanded plasma volume, and greater stability in cardiovascular function during exercise in the heat. Not only is sweating more profuse, it begins sooner and at a lower body temperature to improve dissipation of body heat. Water evaporation from the sweat provides the primary avenue of heat loss in order to defend the body’s core temperature. Evaporation of 1 g of water from sweat at 30° C dissipates 0.58 kcal (2.43 kJ) of heat from the body (Geigy Scientific Tables, 1981). In addition, after adaptation, the greatly reduced sodium concentration in the sweat due to increased secretion of aldosterone is important, because it helps to conserve body sodium by minimizing sodium loss from the body. The resulting higher plasma osmolarity at a given sweat output will improve the thermoregulatory responses to heat stress (Takamata et al., 2001).

Heat stress, especially in competitive athletes, causes a spectrum of symptoms ranging from heat cramps to heatstroke (Squire, 1990). Heat cramps are an acute disorder of skeletal muscle characterized by brief, intermittent, and excruciating muscle cramps. Heat cramps often occur in people who are acclimatized to perform in hot climates and who consume a large amount of water to replace water losses without accompanying salt replacement. Although acclimatization is associated with diminished sodium concentration in the sweat, the loss of sodium in sweat can be considerable as the rate of sweat secretion increases. This condition can be prevented by adequate salt intake together with water replacement.

Heat exhaustion is caused by profuse sweating in a hot environment when the volume of water lost is not replaced by voluntary drinking and the plasma volume becomes depleted. There is dilation of blood vessels in the skin in an attempt to dissipate body heat. The resultant decrease in peripheral resistance together with depletion of plasma volume causes weakness and fainting. Body temperature in this individual is only moderately raised. The weakness and fainting is a safety mechanism, which, by the cessation of physical exertion in a hot and humid environment, prevents further rise in body temperature, thereby ensuring that the heat loss mechanism is not overextended. Treatment by external cooling and adequate hydration should be instituted in heat exhaustion. Prolonged untreated heat exhaustion can lead to heatstroke, in which body temperature increases steadily because of a complete breakdown in heat regulation. When this happens, the individual fails to sweat even in the face of a rapidly rising body temperature. When the elevated body temperature reaches a critical level, collapse, delirium, seizures, or coma occurs.

Thinking Critically

Exercise in the heat places the athlete at risk for heat illness. Children are at even greater risk for heat illness because their thermoregulatory mechanism is less efficient. Therefore it is important for the sports medicine team to be familiar with preventing and treating heat-related illness, especially in children and adolescents.

1. How does one prevent heat illness in athletes?

2. How does one treat heat illness when it occurs during sports competition?

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