Fluid, Electrolyte and Acid–Base Balance

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Fluid, Electrolyte and Acid–Base Balance

The realization that the enzyme systems and metabolic processes responsible for the maintenance of cellular function are dependent on an environment with stable electrolyte and hydrogen ion concentrations led Claude Bernard to describe the ‘milieu interieur’ over 100 years ago. Complex homeostatic mechanisms have evolved to maintain the constancy of this internal environment and thus prevent cellular dysfunction.

BASIC DEFINITIONS

Osmosis refers to the movement of solvent molecules across a membrane into a region in which there is a higher concentration of solute. This movement may be prevented by applying a pressure to the more concentrated solution – the effective osmotic pressure. This is a colligative property; the magnitude of effective osmotic pressure exerted by a solution depends on the number rather than the type of particles present.

The amounts of osmotically active particles present in solution are expressed in osmoles. One osmole of a substance is equal to its molecular weight in grams (1 mol) divided by the number of freely moving particles which each molecule liberates in solution. Thus, 180 g of glucose in 1 L of water represents a solution with a molar concentration of 1 mol L–1 and an osmolarity of 1 osmol L–1. Sodium chloride ionizes in solution and each ion represents an osmotically active particle. Assuming complete dissociation into Na+ and Cl–, 58.5 g of NaCl dissolved in 1 L of water has a molar concentration of 1 mol L–1 and an osmolarity of 2 osmol L–1. In body fluids, solute concentrations are much lower (mmol L–1) and dissociation is incomplete. Consequently, a solution of NaCl containing 1 mmol L–1 contributes slightly less than 2 mosmol L–1.

The term osmolality refers to the number of osmoles per unit of total weight of solvent, whereas osmolarity refers to the number of osmoles per litre of solvent. Osmolality (unlike osmolarity), is not affected by the volume of various solutes in solution. Confusion regarding the apparently interchangeable use of the terms osmolarity (measured in osmol L–1) and osmolality (measured in osmol kg–1) is caused by their numerical equivalence in body fluids; plasma osmolarity is 280–310 mosmol L–1 and plasma osmolality is 280–310 mosmol kg–1. This equivalence is explained by the almost negligible solute volume contained in biological fluids and the fact that most osmotically active particles are dissolved in water, which has a density of 1 (i.e. osmol L–1 = osmol kg–1). As the number of osmoles in plasma is estimated by measurement of the magnitude of freezing point depression, the more accurate term in clinical practice is osmolality.

Cations (principally Na+) and anions (Cl– and image) are the major osmotically active particles in plasma. Glucose and urea make a smaller contribution. Plasma osmolality (POSM) may be estimated from the formula:

image

Osmolality is a chemical term and may be confused with the physiological term, tonicity. This term is used to describe the effective osmotic pressure of a solution relative to that of plasma. The critical difference between osmolality and tonicity is that all solutes contribute to osmolality, but only solutes that do not cross the cell membrane contribute to tonicity. Thus, tonicity expresses the osmolal activity of solutes restricted to the extracellular compartment, i.e. those which exert an osmotic force affecting the distribution of water between intracellular fluid (ICF) and extracellular fluid (ECF). As urea diffuses freely across cell membranes, it does not alter the distribution of water between these two body fluid compartments and does not contribute to tonicity. Other solutes that contribute to plasma osmolality but not tonicity include ethanol and methanol, both of which distribute rapidly throughout the total body water. In contrast, mannitol and sorbitol are restricted to the ECF and contribute to both osmolality and tonicity. The tonicity of plasma may be estimated from the formula:

image

COMPARTMENTAL DISTRIBUTION OF TOTAL BODY WATER

The volume of total body water (TBW) may be measured using radioactive dilution techniques involving either deuterium or tritium, both of which cross all membranes freely and equilibrate rapidly with hydrogen atoms in body water. Such measurements show that approximately 60% of lean body mass (LBM) is water in the average 70 kg male adult. As fat contains little water, females have proportionately less TBW (55%) relative to LBM. TBW decreases with age, decreasing to 45–50% in later life.

The distribution of TBW between the main body compartments is illustrated in Figure 12.1. One-third of TBW is contained in the extracellular fluid volume (ECFV) and two-thirds in the intracellular fluid volume (ICFV). The ECFV is subdivided further into the interstitial and intravascular compartments. In addition to the absolute volumes of each compartment, Figure 12.1 shows the relative size of each compartment compared with body weight.

SOLUTE COMPOSITION OF BODY FLUID COMPARTMENTS

Intracellular Fluid

This differs from ECF in that the principal cation is potassium and the principal anion is phosphate. In addition, there is a high protein content. In contrast to the capillary endothelium, the cell membrane is permeable selectively to different ions and freely permeable to water. Thus, equalization of osmotic forces occurs continuously and is achieved by the movement of water across the cell membrane. The osmolalities of ICF and ECF at equilibrium must be equal. Water moves rapidly between ICF and ECF to eliminate any induced osmolal gradient. This principle is fundamental to an understanding of fluid and electrolyte physiology.

Figure 12.2 shows the solute composition of the main body fluid compartments. Although the total concentration of intracellular ions exceeds that of extracellular ions, the numbers of osmotically active particles (and thus the osmolalities) are the same on each side of the cell membrane (290 mosmol kg–1 of solution).

WATER HOMEOSTASIS

Normal day-to-day fluctuations in TBW are small (< 0.2%) because of a fine balance between input, controlled by the thirst mechanisms, and output, controlled mainly by the renal–ADH (antidiuretic hormone) system.

The principal sources of body water are ingested fluid, water present in solid food and water produced as an end-product of metabolism. Intravenous fluids are another common source in hospital patients. Actual and potential outlets for water are classified conventionally as sensible and insensible losses. Insensible losses emanate from the skin and lungs; sensible losses occur mainly from the kidneys and gastrointestinal tract. Figure 12.3 depicts the daily water balance in a 70 kg adult in whom input and output balance. It should be noted that sources of potential loss are not evident in this diagram. For example, over 5 L of fluid are secreted daily into the gut in the form of saliva, bile, gastric juices and succus entericus, yet only 100 mL of fluid is present in faeces. This illustrates the potential that exists for significant fluid loss in the presence of disease.

PRACTICAL FLUID BALANCE

Calculation of the daily prescription of fluid is an arithmetic exercise to balance the input and output of water and electrolytes.

Table 12.1 shows the electrolyte contents of five intravenous solutions used commonly in the United Kingdom. These solutions are adequate for most clinical situations. Two self-evident but important generalizations may be made regarding solutions for intravenous infusion.

Normal Maintenance Needs

Water. Regardless of the disease process, water and electrolyte losses occur in urine and as evaporative losses from skin and lungs. It is evident from Figure 12.3 that a normothermic 70 kg patient with a normal metabolic rate may lose 2500 mL of water per day. Allowing for a gain of 400 mL from water of metabolism, this hypothetical patient needs about 2000 mL day–1 of water. As a rule of thumb, a volume of 30–35 mL kg–1 day–1 of water is a useful estimate for daily maintenance needs.

Sodium. The normal requirement is 1 mmol kg–1 day–1 (50–80 mmol day–1) for adults.

Potassium. The normal requirement is 1 mmol kg–1 day–1 (50–80 mmol day–1) for adults.

Thus, a 70 kg patient requires daily provision of 2000–2500 mL of water and approximately 70 mmol each of Na+ and K+. This could be administered as one of the following:

Abnormal Losses

These are common in surgical patients. They may be sensible or insensible and either overt or covert.

Losses from the gut are common, e.g. nasogastric suction, diarrhoea and vomiting or sequestration of fluid within the gut lumen (e.g. intestinal obstruction). Although the composition of gastrointestinal secretions is variable, replacement should be with saline 0.9% with 13–26 mmol L–1 of potassium as KCl. If losses are considerable (> 1000 mL day–1), a sample of the appropriate fluid should be sent for biochemical analysis so that electrolyte replacement may be rationalized.

Increased insensible losses from the skin and lungs occur in the presence of fever or hyperventilation. The usual insensible loss of 0.5 mL kg–1 h–1 increases by 12% for each °Celsius rise in body temperature.

Sequestration of fluid at the site of operative trauma is a form of fluid loss which is common in surgical patients. Plasma-like fluid is sequestered in any area of tissue injury; its volume is proportional to the extent of trauma. This fluid is frequently referred to as ‘third-space’ loss because it ceases to take part in normal metabolic processes. However, it is not contained in an anatomically separate compartment; it represents an expansion of ECFV. Third-space losses are not measured easily. Sequestered fluid is reabsorbed after 48–72 h.

Existing Deficits

These occur preoperatively and arise primarily from the gut. The difficulty in correcting these deficits relates to an inability to quantify their magnitude accurately. Fluid and electrolyte deficits occur directly from the ECF. If the fluid lost is isotonic, only ECFV is reduced; however, if water alone or hypotonic fluid is lost, redistribution of the remaining TBW occurs from ICF to ECF to equalize osmotic forces.

Dehydration with accompanying salt loss is a common disorder in the acutely ill surgical patient.

Assessment of Dehydration

This is a clinical assessment based upon the following.

History. How long has the patient had abnormal loss of fluid? How much has occurred, e.g. volume and frequency of vomiting?

Examination. Specific features are thirst, dryness of mucous membranes, loss of skin turgor, orthostatic hypotension or tachycardia, reduced jugular venous pressure (JVP) or central venous pressure (CVP) and decreased urine output. In the presence of normal renal function, dehydration is associated usually with a urine output of less than 0.5 mL kg–1 h–1. The severity of dehydration may be described clinically as mild, moderate or severe and each category is associated with the following water loss relative to body weight:

Perioperative Fluid Therapy

In addition to normal maintenance requirements of water and electrolytes, patients may require fluid in the perioperative period to restore TBW after a period of fasting and to replace small blood losses, loss of ECF into the ‘third space’ and losses of water from the skin, gut and lungs.

Blood losses in excess of 15% of blood volume in the adult are usually replaced by infusion of stored blood. Smaller blood losses may be replaced by a crystalloid electrolyte solution such as compound sodium lactate; however, because these solutions are distributed throughout ECF, blood volume is maintained only if at least three times the volume of blood loss is infused. Alternatively, a colloid solution (human albumin solution or more usually a synthetic substitute) may be infused in a volume equal to that of the estimated loss.

Third-space losses are usually replaced as compound sodium lactate. In abdominal surgery (e.g. cholecystectomy), a volume of 5 mL kg–1 h–1 during operation, in addition to normal maintenance requirements (approximately 1.5 mL kg–1 h1) and blood loss replacement, is usually sufficient. Larger volumes may be required in more major procedures, but one should be guided by measurement of CVP or other measures of preload.

In the postoperative period, normal maintenance fluids should be administered (see above). Additional fluid (given as saline 0.9% or compound sodium lactate) may be required in the following circumstances:

Normally, potassium is not administered in the first 24 h after surgery as endogenous release of potassium from tissue trauma and catabolism warrants restriction. The postoperative patient differs from the ‘normal’ patient in that the stress reaction modifies homeostatic mechanisms; stress-induced release of ADH, aldosterone and cortisol causes retention of Na+ and water and increased renal excretion of potassium. However, restriction of fluid and sodium in the postoperative period is inappropriate because of increased losses by evaporation and into the ‘third space’.

This syndrome of inappropriate ADH secretion may persist for several days in elderly patients, who are at risk of symptomatic hyponatraemia if given hypotonic fluids in the postoperative period. Elderly, orthopaedic patients taking long-term thiazide diuretics are especially at risk if given 5% glucose postoperatively. Such patients may develop water intoxication and permanent brain damage as a result of relatively modest reductions in serum sodium concentration.

After major surgery, assessment of fluid and electrolyte requirements is achieved best by measurement of CVP and serum electrolyte concentrations. Fluid and electrolyte requirements in infants and small children differ from those in the adult (see Ch 36).

Patients with renal failure require fluid replacement for abnormal losses, although the total volume of fluid infused should be reduced to a degree determined by the urine output.

SODIUM AND POTASSIUM

Disorders of Sodium/Water Balance

Hypernatraemia

Hypernatraemia is defined as a plasma sodium concentration of more than 150 mmol L–1 and may result from pure water loss, hypotonic fluid loss or salt gain. In the first two conditions, ECFV is reduced, whereas salt gain is associated with an expanded ECFV. For this reason, the clinical assessment of volaemic status is important in the diagnosis and management of hypernatraemic states. The common causes of hypernatraemia are summarized in Table 12.3. The abnormality common to all hypernatraemic states is intracellular dehydration secondary to ECF hyperosmolality. Primary water loss resulting in hypernatraemia may occur during prolonged fever, hyperventilation or severe exercise in hot, dry climates. However, a more common cause is the renal water loss that occurs when there is a defect in either the production or release of ADH (cranial diabetes insipidus) or an abnormality in response to ADH (nephrogenic diabetes insipidus).

TABLE 12.3

Causes of Hypernatraemia

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