Which two factors regulate movement of fluid from one compartment to another?

Sodium

Sodium concentration is an expression of the relative numbers of sodium molecules to water molecules in the extracellular fluid (ECF). Sodium concentration is important to transcellular fluid flux. Abnormalities in sodium concentration (hyponatremia <140 mEq/L dog, <149 mEq/L cat; and hypernatremia >150 mEq/L dog, >162 mEq/L cat) may occur in any combination with abnormalities in ECF sodium and water content (dehydration, edema). Abnormalities in sodium concentration usually can be attributed to changes in free water. Free water must be added to reduce a sodium concentration (hypernatremia = free water deficit) and taken away to increase it (hyponatremia = free water excess). Free water may be gained by drinking water, may be administered in the form of 5% dextrose in water, or may occur secondary to high levels of antidiuretic hormone. Free water may be lost via evaporation (lungs and skin) or losing fluids, which are low in sodium compared with normal ECF (diarrhea, vomitus, urine). Abrupt changes of sodium concentrations of more than about 15 to 17 mEq/L (in either direction) should be avoided because they may be associated with untoward transcellular water shifts and unfavorable neurologic consequences.

The combination of hypernatremia and hypervolemia can be caused by impermeant solute gain (excessive sodium intake or administration) or hyperadrenocorticism. The combination of hypernatremia and normovolemia can be caused by diabetes insipidus (central or nephrogenic), reset osmostat, fever, or high environmental temperatures, or may be iatrogenic (inadequate access to water). The combination of hypernatremia and hypovolemia (dehydration) can be caused by water loss in excess of sodium through extrarenal routes (vomiting, diarrhea, third space, burns) or via renal routes (osmotic or chemical diuresis, chronic renal failure, postobstructive diuresis). Hypernatremia causes ECF hyperosmolality and intracellular dehydration. The cells first manifesting signs of dehydration are those of the CNS (depressed mentation, restlessness, irritability, muscle twitching/tremors, hyperreflexivity, muscle rigidity/spasticity, ataxia, myoclonus, tonic spasms, coma). Tissue shrinkage can cause intracranial hemorrhage. Acute hypernatremia (<6 hours) should be treated by the rapid administration of free water (in the form of 5% dextrose in water). In acute hypernatremia, the plasma sodium level may be corrected more quickly. In time the intracellular compartment increases its intracellular osmoles to offset the effects of the extracellular sodium aberration and restore intracellular water volume toward normal. Chronic hypernatremia (>24 hours) must be treated with caution to lower the sodium no faster than 1 mEq per hour to avoid water intoxication. The clinical signs of water intoxication are acute obtundation. Rapid volume replacement in the hypernatremic patient initially should be treated with a solution with a sodium concentration that is close to that of the patient (within 6 mEq of the patient’s plasma sodium level). The sodium concentration is then slowly decreased by administering 5% dextrose in water at the rate of about 3.7 mL of water/kg body weight per hour.

The combination of hyponatremia and normal plasma osmolality is referred to as pseudohyponatremia and is most often associated with hyperlipidemia or hyperproteinemia. Hyponatremia with high plasma osmolality is usually the result of hyperglycemia or mannitol infusion. Patients with hyponatremia and low plasma osmolality are further divided based on volume status. Causes of hyponatremia, low plasma osmolality and hypervolemia include congestive heart disease, severe liver disease, nephrotic syndrome, or advanced renal failure. If the patient is normovolemic (with hyponatremia and low plasma osmolality) antidiuretic drugs, myxedema coma of hypothyroidism, or hypotonic fluid therapy should be considered as possible etiologies. Hypovolemic patients (with hyponatremia and low plasma osmolality) may have renal (hypoadrenocorticism, diuretic administration) or extrarenal causes (vomiting, diarrhea, third space, cerebral salt wasting, syndrome of inappropriate antidiuretic hormone secretion).

Hyponatremia causes intracellular edema and has been associated with obtundation, anorexia, muscle weakness and wasting, and GI signs. Common coexisting electrolyte problems include hypochloremia, hyperkalemia, and hyperphosphatemia. Mild hyponatremia requires no special consideration beyond therapy directed to the underlying disease process and volume restoration with any ECF replacement solution. Acute severe hyponatremia (<6 hours) should be treated by the rapid administration of saline. In time the intracellular compartment decreases its intracellular osmoles to offset the effects of the extracellular sodium aberration and restore intracellular water volume toward normal. Chronic hyponatremia (>24 hours) must be treated with caution so as to raise the sodium no faster than 0.5 mEq per hour to avoid myelinolysis. Initially, volume problems should be treated with a solution having a sodium concentration that is close to that of the patient. The sodium concentration is then slowly increased by administering a hypertonic saline solution at a rate of about 0.3 mEq of sodium/kg per hour. The clinical signs of myelinolysis occur 2 to 7 days after inappropriate correction of severe hyponatremia and include spastic quadriparesis, facial palsy, dysphagia, vocal dysfunction, and mental confusion to coma.

Distribution of Fluids

Fluids in the body are distributed in two compartments: the intracellular fluid (ICF) volume and the extracellular fluid (ECF) volume. The ECF is composed of interstitial fluid, plasma, lymph, and transcellular fluids such as synovial, pleural, abdominal, and cerebrospinal fluids. The transcellular fluids do not normally contribute to signficant fluid losses, but in disease states such as pleuropneumonia or peritonitis, they can contribute significantly to volume deficits. For example, it is not unusual to drain 10 to 20 L of fluid from the pleural cavity of horses with severe pleuropneumonia. Additionally, the volume of gastrointestinal secretions in horses plays an important role in fluid distribution. The normal volume of gastrointestinal secretion in horses is approximately equivalent to the extracellular fluid volume, representing about 100 L every 24 hours in a 500-kg horse.1 Therefore significant fluid sequestration and loss can occur with intestinal obstruction or colitis. The volume of total body water (TBW) represents 60% of body weight in adults and up to 80% in neonates. The ECF volume represents

Body solutes are not distributed equally through TBW. In plasma, sodium is the main cation, and bicarbonate and chloride are the main anions. Proteins contribute to the negative charges, and they also provide oncotic pressure. Albumin or molecules of similar size are the main contributors to oncotic pressure. The interstitial fluid accounts for about 75% of the ECF, and it is composed mainly of sodium, bicarbonate, and chloride, but the concentration of protein there is lower than in plasma. The slightly increased concentration of anions and decreased concentration of cations in interstitial fluids occurs because of the greater concentration of protein in plasma (according to the Gibbs-Donnan equilibrium). In clinical practice, this difference is small, so that the measured concentration of solutes in plasma is thought to reflect the concentration of solutes throughout the ECF. Table 3-1 lists normal plasma concentrations of electrolytes in adult horses. The composition of the intracellular fluid compartment is different: the important cations are potassium and magnesium, and the important anions are phosphates and proteins (Figure 3-1).

Transfer of fluid between compartments is an important consideration when planning fluid administration. Some important concepts govern these mechanisms. Osmolality is defined as the concentration of osmotically active particles in solution per kilogram of solvent (mOsm/kg), whereas osmolarity is the number of particles of solute per liter of solvent (mOsm/L). In biologic fluids, the difference between the two concentrations is negligible, and the two terms are often used interchangeably. Normal plasma osmolality in adult horses ranges from 275 to 312 mOsm/kg, and it varies slightly between breeds. Lower values are reported for normal foals.7,8 The effective osmolality, or tonicity, is the osmotic pressure generated by the difference in osmolality between two compartments. Colloid oncotic pressure is the osmotic pressure generated by proteins, mainly albumin, and is measured using a colloid osmometer (Wescor, Logan, UT). Normal values of 15.0 to 22.6 mm Hg for foals and 19.2 to 31.3 mm Hg for adult horses have been reported.9,10 Water and ionic solute exchange between the vascular and interstitial compartments occurs at the capillary level and is rapid; equilibrium is reached within 30 to 60 minutes. The rate of exchange or net filtration that occurs between these compartments is controlled by a balance between the forces that favor filtration (capillary hydrostatic pressure and tissue oncotic pressure) and the forces that tend to retain fluid within the vascular space (plasma oncotic pressure and tissue hydrostatic pressure). These relationships are described by Starling's law:

Net filtration=Kf[(Pcap−Pint)−σ(πp−πint)]

where Kf is the filtration coefficient, which varies depending on the surface available for filtration and the permeability of the capillary wall; Pcap and Pint represent the hydrostatic pressures in the capillary or in the interstitium; πp and πint are the oncotic pressures in the plasma or interstitial fluid; and σ is the reflection coefficient of proteins across the capillary wall.

Exchanges between the interstitial and the intracellular compartment are governed by the number of osmotically active particles within each space. Sodium is the most abundant cation in the ECF. Consequently, sodium accounts for most of the osmotically active particles in the ECF. Other osmotically active compounds that make a significant contribution to ECF osmolarity are glucose and urea. The most commonly used formula for estimation of serum osmolarity is as follows11:

ECF osmolality=2[Na+]+glucose18+urea2.8

Cell membranes are permeable to urea and K+. Therefore the effective osmolarity is calculated as follows:

ECF osmolality=2[Na+]+glucose18

The osmolar gap is the difference between measured osmolarity and calculated osmolarity; an increased osmolar gap can exist when unmeasured solutes, such as mannitol, are present.12

Exchanges between the extracellular and intracellular compartments are comparatively slow, taking up to 24 hours to reach equilibrium.

BODY WATER BALANCE

Total body water represents approximately 60–70% of body weight in adult horses and is comprised of the extracellular and intracellular spaces (Table 23.2). The extracellular compartment includes the intravascular (plasma), interstitial and transcellular fluid (gastrointestinal tract water and lymph). The distribution of water between plasma and interstitial fluid is maintained by differences in colloidal osmotic and hydrostatic pressure, and also depends on the integrity of the endothelium.

Water balance is the difference between input and output. This is determined by the intake of water and fluid contained in food, and by the generation of water due to protein, fat and carbohydrate metabolism, versus water loss through urine and feces, respiratory tract and skin. The normal water intake for a 450 kg adult horse is approximately 20–30 L/day, although this can vary depending on the water content of the diet, ambient temperature and activity level. The largest component of water loss is through the urine.

Dehydration is defined as a reduction in total body water. In the critical care setting, this usually refers to losses in the interstitial fluid compartment. Dehydration occurs with water deprivation, either through lack of access to water or through the inability to swallow. It also follows excessive fluid loss, most commonly from the gastrointestinal tract, but also sweating or urinary losses. As opposed to hydration status, circulating volume refers to the intravascular fluid compartment. In dehydration, circulating volume may be decreased, but if the onset of dehydration is insidious, it may be maintained despite a reduction in total body water. The effective circulating volume is also reduced when fluid is sequestered in abnormal quantities within one part of the body (third-space accumulation), in hemorrhage and in hypovolemic shock.

B Extracellular Fluid Volume

The ECF should be viewed as a physiological rather than a strictly definable anatomical space (Carlson et al., 1979a). The ECF volume of adult animals ranges from 0.15 to 0.30 l/kg body weight (Carlson et al., 1979a; English, 1966b; Evans, 1971; Hankes et al., 1973; Hix et al., 1953; Kohn, 1979; Spurlock et al., 1985; Thornton and English, 1977; Zweens et al., 1975), depending on the species and the volume dilution procedure used. Regulation of ECF volume is a complex process in which a variety of factors interact. The ECF consists of all the fluids located outside the cells and includes the plasma (0.05 l/kg), interstitial fluid and lymph (0.15 l/kg), and the transcellular fluids (Edelman and Leibman, 1959; Rose, 1984; Saxton and Seldin, 1986). The transcellular fluids, which include the fluid content of the gastrointestinal tract, are generally considered a subcomponent of the ECF. In small animal species, the fluid content of the gastrointestinal tract is relatively small (Strombeck, 1979). In the large animal herbivore species, a substantial volume of fluid is normally present within the gastrointestinal tract. In the horse, this may amount to 30 to 45 l (Carlson, 1979a), and in cattle, the forestomach may contain as much as 30 to 60 l of fluid (Phillipson, 1977). During periods of water restriction and certain other forms of dehydration, this gastrointestinal fluid reservoir can be called on to help maintain effective circulating volume (McDougall et al., 1974). All of the fluids of the ECF contain sodium in approximate concentrations of 130 to 150 mEq/l H2O. Sodium provides the osmotic skeleton for the ECF, and the sodium content is the single most important determinant of ECF volume (Rose, 1984). Sodium deficits result in decreases in ECF volume, whereas sodium excess is most often associated with water retention and results in edema (McKeown, 1986; Rose, 1984).

Body fluid compartments

Total body water accounts for 61–72% of the body weight (BW) of mature horses (Table 4-1: Julian et al 1956, Deavers et al 1973, Carlson et al 1979, Judson & Mooney 1983, Carlson 1987, Sneddon et al 1993, Forro et al 2000, Fielding et al 2004, 2007, 2008, Lindinger et al 2004, Waller & Lindinger 2005, Forro & Lindinger 2006) and has been estimated at 66–84% BW of foals varying with foal age or dilution method used (Oftedal et al 1983, Doreau et al 1986, Geerken et al 1988).

Total body water (TBW) is distributed within cells (intracellular) or outside of cells (extracellular). The intracellular fluid compartment (ICF) is estimated at 38–53% of body weight (BW) (Table 4-1). The extracellular fluid compartment (ECF) comprises fluid in blood, interstitial fluid (ISF), bone, connective tissue, and transcellular fluid. The ECF compartment has been estimated at 22–26% BW (Table 4-1; Andrews et al 1997, Fielding et al 2003, 2004, 2007, 2008, Waller et al 2008). Transcellular fluids are contained within epithelial-lined compartments such as the gut and urinary bladder. Depending on diet, the fluid sequestered by the horse's gastrointestinal content can account from 9 to 21% of equid weight (Robb et al 1972, Coenen & Meyer 1987, Gee et al 2003, Sneddon et al 2006) and has been speculated to be a fluid reservoir for the horse during physical activity and other brief periods when water is inaccessible (Sneddon & Argenzio 1998). The fluid holding capacity of the diet influences the water content in the equine gastrointestinal tract. Hay-fed horses had a total intestinal fluid capacity of 188 ml/kg BW which was 84% greater than horses fed a complete feed (102 ml/kg BW) (Coenen & Meyer 1987). Moreover, 77% of gut water in hay-fed horses was in the large bowel compared to 65% in horses fed complete feed. The large reservoir of gut fluid may explain why horses drink intermittently rather than sip continuously.

Total body water decreases linearly with age in horses and foals (Agrabriel et al 1984, Doreau et al 1986). The ECF of newborn foals is about 40% of BW but declines to 25% of body weight in adult horses (Table 4-1; Spensley et al 1987). Likewise, plasma volume in newborns is higher (9.6% BW) (Table 4-1) than in mature horses (4.7% BW) (Spensley et al 1987). These differences underscore why the approaches for fluid therapy in the foal must differ to that used for the mature horse.

Management of sodium deficiency

The essential steps in treating sodium deficiency and ECF volume depletion are to attempt to treat the causes of sodium and water loss and to adequately replace the fluid already lost. The amount of fluid replacement must be balanced against measured or estimated losses, both intra- and extracorporeal. The measurement of body weight is a useful adjunct to monitoring; an increase in weight may indicate accumulation of interstitial or transcellular fluid. Accurate fluid balance charts (see Table 4.4) should indicate a positive or negative balance, but even the most assiduously prepared charts (many are not) provide only an approximate estimate of balance, especially when confounding problems such as pyrexia (increasing insensible losses) or hypermetabolic states (increasing metabolic water) intervene. Vital signs: pulse, blood pressure and central venous pressure (if measured), all provide additional useful information to improve the practice of the art.

The type of replacement will be dependent on cause and severity. Mild forms of sodium deficit, such as caused by overtreatment with diuretics or chronic salt-losing nephropathy, may be adequately treated with oral sodium and water supplementation. For more severe forms of sodium deficit, intravenous infusion is required; the types of fluids available are shown in Table 4.5. All of them are iso- or hypoosmolal to normal plasma. Hyperosmolal fluids, such as 1.8% or 5% sodium chloride or 2.74% or 8.4% sodium bicarbonate, are not appropriate treatments for sodium depletion with clinical evidence of reduced ECF volume, even in the presence of hyponatraemia, as infusions of such fluids will increase ECF volume in part by shifting fluid from the ICF volume.

Hypoosmolal fluids may be used when sodium deficit is associated with a greater degree of water deficit, that is, sodium deficit in association with hypernatraemia.

Protection and Lubrication

There are some smaller collections of fluid that are not inside cells and yet cannot exchange freely with the main mass of ECF by diffusion across highly permeable capillary membranes. Examples are the vitreous and aqueous humors in the chambers of the eye, the cerebrospinal fluid that surrounds the brain and the spinal cord, and the synovial fluid in the capsules of joints. These are by no means ICFs, but they are secreted by layers of specialized cells (e.g., in the ciliary body, choroid plexus, or synovial membranes) which surround them and separate them from the main body of ECF. They may be called transcellular fluids, because the only approach to them by diffusion from the continuous ECF is across cellular membranes with their specialized and restricted permeability. These specialized fluids serve to maintain the size and shape of the eyeball, to protect the brain from trauma due to sudden movements by reducing its effective weight by flotation, and to lubricate the joints.

The cells are tiny aquatic organisms, and the ECF is the pond in which the live. It has been aptly called a middleman fluid because it accommodates exchanges of matter and energy between cells and other cells in remote parts of the body as well as between cells inside the body and the external environment from which they eventually derive their nutrients and the oxygen they need to utilize these. The famous French physiologist, Claude Bernard, died in 1878 correcting the proofs of the book in which he characterized the ECF as an internal environment within which the cells live a sheltered life, protected from the vicissitudes of an external world that is variable and often hostile. Bernard enunciated the principle that the constant properties of this internal environment are a necessary condition for the free, independent life of higher organisms. Indeed, a substantial part of the subject matter of physiology is concerned with homeostatic mechanisms that operate to stabilize the chemical and physical properties of the internal environment.

What two factors regulate movement of fluid between compartments?

What 2 components determine the body's fluid distribution?

What are the two 2 main components of the extracellular fluid compartment?

What are the two major factors that regulate the movement of water and electrolytes from one fluid compartment to the next quizlet?