Fluid Balance

8.2.1 Acid-Base Balance

Sustaining acid-base balance is one of the most crucial parts of maintaining homeostasis. The negative logarithm of hydrogen ions (H⁺) determines the pH of a solution.

In mammals, the pH varies from 7.0 to 7.8. A mild alteration in pH threatens various physiological functions, impairs cellular functions, and affects the structure and functions of macromolecules. Acids are constantly generated in the body. The formation of bases balances the acids produced. Hence, the acid-base balance is maintained. An acid is any substance that donates a proton (releases H⁺ in a solution). Among acids, some are strong acids, and some are weak. Strong acids freely ionise by giving up most of their hydrogen ions; thus, they reduce pH substantially. Weak acids have a minor effect on pH because they ionise only slightly, maintaining most of the H⁺ in chemically bound form. Any substance that can take proton is referred to as a base (accept an H⁺ ion). Bases can be strong or weak bases. A strong base affects the pH markedly by raising the pH as it has a stronger tendency to bind with hydrogen ions. Because it binds with fewer hydrogen ions, a weak base has little effect on pH.

Arterial blood has a pH of 7.36-7.44 (7.4), while interstitial fluid and venous blood have 7.35. The pH of the intracellular fluid lies between 6.0 and 7.4. (7.0). The body can maintain pH balance when the pH ranges from 7.0 to 7.8. The body tries to bring back the pH to a normal physiological level through various compensatory mechanisms whenever there is an alteration in pH beyond the normal range. Three basic systems regulate the concentration of hydrogen ions in body fluid:

1. Chemical buffer system: Mixes with acid or base right away to prevent excessive hydrogen ion concentration shifts.

2. Respiratory system: Controls carbon dioxide removal from extracellular fluid.

3. Kidney: Excretes acid or alkali, bringing the hydrogen ion concentration in the extracellular fluid back to normal.

Within a fraction of a second, the chemical buffer system (first line of defence) reacts to reduce the change in hydrogen ion concentration. The respiratory system (second line of defence) will intervene within minutes to keep hydrogen ion concentrations from fluctuating too much. Both the first and second lines of defence do neither remove nor add hydrogen ions to the body; instead, they bind them until a balance can be restored. Kidneys, the body’s third line of defence, react slowly and remove excess acid or base. Kidneys are the most potent acid-base balance mechanism, and they are responsible for the final correction of acid-base balance.

8.2.1.1 ChemicalBufferSystem

A buffer prevents pH fluctuations by converting a strong acid or base to a weak one. A chemical buffer system is made up of a weak acid and the conjugate base of that acid. Bicarbonate phosphate, protein, and haemoglobin are all essential chemical buffer systems in the body.

8.2.1.1.1 Bicarbonate Buffer System

It is a mixture of carbonic acid (a weak acid) and bicarbonate ions in a protonated state (an unprotonated substance—a weak base). In extracellular fluid, it is the most significant buffer system. Carbonic acid is formed when carbon dioxide is hydrated in the presence of carbonic anhydrase, which dissociates into HCO₃- and H⁺:

Carbonic acid behaves as a weak acid as the reaction progresses to the right, releasing H⁺ and reducing pH. When the reaction moves to the left, HCO3- functions as a weak base, binds H⁺, and raises the pH. When the pH drops, the reaction shifts to the left to raise the pH and restores it to normal. When the pH rises, the reaction will move to the right to lower the pH and return it to normal.

The pK of the bicarbonate system (6.1) and the pH of the extracellular fluid are very different (7.4).

As a result, the bicarbonate system is less effective than other chemical buffers. Compared to other chemical buffer systems, it plays a critical role in maintaining the pH of bodily fluids. The kidney and respiratory systems regulate this buffer system’s bicarbonate and carbon dioxide components separately. These two regulating systems operate continuously and simultaneously, resulting in a more productive and efficient bicarbonate buffer system.

8.2.1.1.2 PhosphateBufferSystem

It is the combination of hydrogen phosphate, HPO₄²- (weak base—unprotonated substance), and dihydrogen phosphate, H₂PO₄^- (weak acid—protonated substance). It works the same as the bicarbonate system:

When the reaction goes to the right, H⁺ is liberated and pH is lowered, and when the reaction goes to the left, H⁺ is bound and pH is raised. The optimal pK for this system is 6.8, which is close to the pH of body fluids. Hence, phosphate buffer has a more substantial buffering effect than an equal HCO3^- buffer. But phosphates are less in extracellular fluid than bicarbonates, and they are important in renal tubules and intracellular fluid.

8.2.1.1.3 ProteinBufferSystem

Proteins are more concentrated in intracellular fluid than bicarbonates and phosphates. Intracellular proteins are responsible for 60-70% of chemical buffering within cells. The capacity to buffer is attributed to the side groups of their amino acid residues. Some have a carboxyl (-COOH) side group that releases H⁺ as pH rises, lowering pH:

Others have amino (-NH₂) side groups, which bind H⁺ when pH drops too low, thus raising pH towards normal. The most important buffering amino acid is histidine:

The protein buffer system is more powerful in the plasma since their pK value is very near to 7.2 due to their high concentration in plasma.

8.2.1.1.4 Haemoglobin BufferSystem

It is the most effective protein buffer and the second most essential blood buffer. Because haemoglobin has a higher concentration than plasma proteins, it has a sixfold better buffering capacity. Haemoglobin in the form of reduced haemoglobin (Hb^-) and their weak acid (HHb) form buffer. It works the same as the bicarbonate system:

The chemical buffer system as a whole works together. Whenever the concentration of H⁺ in extracellular fluid changes, the equilibrium of the buffer system changes as well, and the isohydric principle describes this phenomenon.

8.2.1.2 RespiratoryRegulation

The bicarbonate buffer system equation demonstrates that adding carbon dioxide to bodily fluid boosts H⁺ concentration and reduces pH, while removing carbon dioxide has the opposite effect. It is the foundation for the respiratory system’s high buffering capacity. This technology neutralises 2-3 times the amount of acid that a chemical buffer system can balance:

Pneumatic ventilation is stimulated by an increase in partial pressure of carbon dioxide (PCO₂) and a decrease in pH. As a result, excess carbon dioxide is ejected. The reaction shifts to the left. As a result, the concentration of H⁺ is reduced, and free H⁺ becomes a member of the water molecule. When H⁺ levels decline, pH rises and inhibits pulmonary ventilation. Carbon dioxide builds up as a result of this process. As the reaction progresses to the right, the pH decreases. Chemoreceptors are responsible for this impact. Based on their location, chemoreceptors are divided into central chemoreceptors and peripheral chemoreceptors.

Central chemoreceptors are chemosensitive areas on the ventral surface of the medulla.

They stimulate the respiratory centres, generating a rise in tidal volume and breathing rate. These receptors are sensitive to variations in the concentration of H⁺ ions in the brain’s interstitial fluid and cerebrospinal fluid (CSF). Because H⁺ ions have a difficult time crossing the blood-brain barrier (BBB), changes in H⁺ ion concentration in the blood have a much smaller effect on stimulating the chemosensitive area. Carbon dioxide passes through BBB easily.

Carbon dioxide may easily cross the BBB; hence, increased blood PCO2 raises the PCO2 of interstitial fluid and cerebrospinal fluid. CO₂ is quickly hydrated in the interstitial fluid and CSF, forming carbonic acid. Carbonic acid breaks down into H⁺ and HCO₃^-. Chemoreceptors detect a rise in hydrogen ion concentration, which causes the respiratory centres to be stimulated. Increased alveolar ventilation is caused by an increase in breathing rate and depth.

Aortic and carotid bodies are peripheral receptors. The aortic arch contains a cluster of chemoreceptors known as aortic bodies. The vagus nerve provides a signal to the dorsal respiratory group in the medulla oblongata. Carotid bodies are oval nodules found in the left and right common carotid arteries’ walls. The glossopharyngeal nerve provides an impulse to the dorsal respiratory group. The aortic and carotid bodies will be stimulated by an increase in PCO₂ and hydrogen ions in the blood. They then activate the brain’s respiratory regions, resulting in enhanced breathing.

8.2.1.3 Renal Regulation

The kidneys neutralise more acid and base than the respiratory system or chemical buffers. The kidneys remove hydrogen ions from the body, and the other buffer systems can lower their concentration by attaching it to other molecules. Three primary mechanisms regulate the extracellular fluid hydrogen ion concentration: (1) hydrogen ion secretion,

(2) reabsorption of filtered bicarbonate ions, and (3) bicarbonate ion generation.

The rate of H⁺ secretion by renal tubules is primarily determined by the intracellular pH of renal tubular cells. An increase in pH lowers H⁺ secretion by the kidney, and lowering of pH increases hydrogen ion secretion. Intracellular pH of cells of renal tubule changes as blood pH or PCO₂ changes. Therefore, acidaemia and hypercapnia increase hydrogen ion secretion. In contrast, alkalaemia and hypocapnia reduce hydrogen ion secretion.

The proximal convoluted tubule secretes 85% of hydrogen ions. In contrast, the intercalated cells of the second half of the distal convoluted tubule, collecting tubule, and collecting duct secrete the remaining 15%.

Secondary active transport secretes hydrogen ions in the proximal convoluted tubule (sodium-hydrogen counter-transport). Carbon dioxide is either diffused into tubular cells or produced by cell metabolism. In the presence of carbonic anhydrase, it will mix with water to generate carbonic acid, which will then dissociate into HCO₃- and H⁺. Sodiumhydrogen counter-transport transports hydrogen ions into the tubular lumen. Carbon dioxide and water will result from the reaction of H⁺ with filtered bicarbonate. Carbon dioxide penetrates tubular cells and becomes carbonic acid when it reacts with water.

Primary active transport secretes hydrogen ions in intercalated cells (second half of distal convoluted tubule, collecting tubule, and collecting duct). Carbonic acid is formed when dissolved carbon dioxide in the cell reacts with water to create bicarbonate ions (which are reabsorbed in the blood) and hydrogen ions, released into tubules by the hydrogen ATPase process.

As a result, whenever hydrogen ions are secreted into the renal tubules, the same amount of filtered HCO₃- is reabsorbed. Only a small percentage of surplus H⁺ in ionic form can be eliminated in the urine when more hydrogen ions are produced than HCO₃- filtered into the tubular fluid. Urine can only be acidified to roughly a pH of 4.5, and it means that most of the hydrogen ions expelled must be bound by bases rather than being free in solution.

When hydrogen ions are titrated with bicarbonate ions in the tubular fluid, a bicarbonate ion is reabsorbed for each hydrogen ion released. In the tubular fluid, excess hydrogen ions will mix with buffers other than bicarbonates, such as ammonia buffer and phosphate buffer, resulting in new bicarbonate, which enters the blood. When extracellular fluid includes surplus hydrogen ions, kidneys reabsorb filtered bicarbonate from the tubular fluid and generate new bicarbonate ions. Although urea and citrate buffer systems exist, they are of minor consequence.

8.2.1.3.1 PhosphateBuffer

As the tubular fluid is acidified with hydrogen ion secretion, hydrogen phosphate (HPO₄²^-) takes up and binds hydrogen ions to form dihydrogen phosphate, H₂PO₄²^-, predominantly. Part of the cation (Na) that electrically balances H₂PO₄²^- in the glomerular filtrate is exchanged with a secreted hydrogen ion and thus is returned to the blood.

8.2.1.3.2 AmmoniaBuffer

Tubular epithelial cells produce ammonia, which diffuses into the tubules. In the renal tubular fluid, ammonia interacts with hydrogen ions to generate ammonium ions and then combines with chloride ions to form ammonium chloride. Each time an ammonia molecule combines to generate ammonium, the concentration of ammonia in tubular fluid decreases, which causes more ammonia to diffuse from epithelial cells. Chloride ions make up the majority of anions in the tubular fluid. The tubular fluid will fall below 4.5 if all hydrogen ions are carried with chloride ions. Still, ammonia mixes with hydrogen ions and chloride ions to generate ammonium chloride, a weak acid.

Glutamine produced in the liver is transferred to the proximal convoluted tubule, thick ascending limb of the loop of Henle, and distal convoluted tubule epithelial cells. A single glutamine molecule is digested inside the cell to produce two ammonium ions and two bicarbonate ions. The sodiumammonium counter-transport mechanism secretes ammonium ions into the tubular lumen. This method reabsorbs two bicarbonate ions into the bloodstream for every glutamine molecule digested. As the level of acidity rises, the amount of glutamine digested by collecting duct tubular cells increases.

Urine pH is used to determine the amount of hydrogen ions present in the urine. It reflects the acid-base state of an animal. The ability of the kidneys to regulate hydrogen ion and bicarbonate concentrations in the blood determines the pH of urine. The pH of a dog’s or cat’s urine is between 6.0 and 7.5. Dairy cows have an average urine pH of 8.10, with a range of 7.27-8.71, and the mean urine pH of beef cows is 7.73, with a range of 7.42-8.12. The pH of an animal’s urine fluctuates based on its diet. Urine produced by high-protein diets, such as those consumed by carnivores, is neutral to acidic. The urine of herbivores is more alkaline than that of carnivores. Forages having high K-salt concentrations cause a high dietary cation-anion difference resulting in alkaline urine. Further, with the buffering that happens in reaction to gastric acids, any animal can produce alkaline urine shortly after eating.

8.2.2 Acid-Base Balance Disturbances

The rate of the conjugate base to their weak acids determines the pH of the ECF. Buffer base refers to the overall amount of buffer base in whole blood, including bicarbonate, haemoglobin, and other minor bases (BB). These bases are called metabolic components, and they play a role in setting blood pH. Acid-base disruption occurs when the ECF gains or loses strong acid or base (Cl^- or HCO₃^-). At a pH of 7.4, the ratio of bicarbonate to carbonic acid in the extracellular fluid is 20:1. When carbonic acid levels rise, the ratio changes, resulting in a lower pH. Acidosis occurs when the pH goes below 7.5 due to a lack of bicarbonate or an increase in carbon dioxide partial pressure in the blood. In contrast, alkalosis happens when the pH rises above 7.4 due to an excess of bicarbonate or a decrease in carbon dioxide partial pressure in the blood.

Hydrogen ions diffuse into the cells to maintain electrical neutrality in acidosis, while potassium flows out of the cell. Intracellular proteins buffer hydrogen ions that enter the cell. As a result of the exchange between hydrogen and potassium, the cell loses a net amount of cation. Hyperpolarisation occurs when a cation is lost from a cell. The formation of the action potential in muscle cells and neurons is hindered. Acidosis reduces the activity of both the central nervous system and the muscles. Severe acidosis can result in unconsciousness and death. In alkalosis, hydrogen ions diffuse out of the cell, and potassium enters the cell. The membrane potential becomes more positive with the net gain of cations in the cell. As a result, neural tissue hyperexcitability and muscular overstimulation occur, resulting in tetany, convulsions, or respiratory paralysis.

Respiratory disturbances are acid-base imbalances caused by changes in the partial pressure of carbon dioxide in the blood. Acid-base imbalances due to alterations in bicarbonate levels are called metabolic disturbances. Metabolic acidosis, metabolic alkalosis, pulmonary acidosis, and respiratory alkalosis are acid-base abnormalities.

8.2.2.1 Metabolic Acidosis

Metabolic acidosis is defined as a gain of strong acid or a loss of base from the ECF. In metabolic acidosis, acidaemia will be present. It happens in ketosis, diabetes mellitus, and renal acidosis, where bicarbonate is lost in the urine due to tubular reabsorption failure. It also occurs in diarrhoea, where bicarbonate is lost. Due to a decrease in bicarbonate ions, the pH drops.

As a result, all blood buffer bases drop. In most cases, the partial pressure of carbon dioxide in the plasma does not vary. A drop in pH causes increased alveolar ventilation and reduced carbon dioxide partial pressure. Reduced carbon dioxide partial pressure will restore the natural ratio of conjugate base to weak acid. However, the total bases will be lower than usual, necessitating renal correction, i.e. H⁺ ion excretion and plasma HCO₃^- restoration.

8.2.2.2 Metabolic Alkalosis

ECF results in the acquisition of base (OH^- or HCO₃^-) or the loss of strong acid. The symptoms of metabolic alkalosis are chronic vomiting (loss of stomach acid), potassium deficit (due to excessive renal excretion of hydrogen ions), and oxidation of organic acids. The parenteral introduction of bicarbonate solutions also causes metabolic alkalosis.

There is an increase in HCO₃^- in ECF, increasing the base content in all of these situations. The body’s reaction is the polar opposite of that seen in metabolic acidosis. Alkalaemia causes a rise in pH, reducing lung ventilation and raising carbon dioxide partial pressure. Respiratory compensation brings the pH back to normal. Kidneys correct the condition by decreasing the secretion of H⁺ ions and increasing the excretion of HCO₃^-.

8.2.2.3 Respiratory Acidosis

When the rate of CO₂ clearance by the lungs falls below the rate of CO₂ creation in the body, respiratory acidosis develops. It raises the partial pressure of carbon dioxide in the blood (hypercapnia). The inability of the lungs to exhale CO₂ at a regular pace is the primary cause of respiratory acidosis. It can occur by a lack of ability to enlarge the thorax due to a defect in the chest wall or respiratory muscles or any obstruction in the respiratory system that limits normal gas movement in the lungs.

A rise in PCO₂ causes an increase in H₂CO₃, and buffer reaction prevents the fall of pH caused by the increase in H₂CO₃. Renal compensation then follows. With a surge in plasma HCO₃^-, low pH enhances H⁺ secretion into the urine.

8.2.2.4 Respiratory Alkalosis

In alveolar hyperventilation, the rate of removal of CO₂ exceeds the rate of creation in the body developing respiratory alkalosis. Low plasma PCO₂ (hypocapnia) and alkalaemia will be present. Increased alveolar ventilation is induced by aberrant activation of respiratory centres in the brain, either directly (as in ammonia poisoning) or indirectly (through peripheral chemoreceptors) through lower partial pressure of oxygen. Even when the partial pressure of carbon dioxide falls, there will be no change in the plasma concentration of bicarbonates at first. Non-bicarbonate buffers cause an immediate reaction. Thus, HCO₃ falls, and haemoglobin proteinate ions increase. Alkalaemia depresses H⁺ ion secretion by renal tubules and increases the outflow of filtered HCO₃^- within a few hours, causing renal compensation. These result in further lowering of plasma HCO₃^-, and the ratio of HCO₃^- to H₂CO₃ moves back to normal.

8.2.3 Dehydration and Clinical Management

Clinical conditions affecting the hydration, acid-base, and electrolyte status are common in veterinary practice. As these conditions may result in harmful, often life-threatening consequences, recognition and management are vital.

8.2.3.1 Dehydration and Its Management

In small animal practice, dehydration is frequently linked to gastro-enteric diseases such as vomiting and diarrhoea that change electrolyte and acid-base status. Neonatal calf diarrhoea is a severe illness that causes severe dehydration in newborns. Dehydration status is assessed by physical examination and laboratory tests. Skin elasticity (skin turgor) is a valuable guide for evaluating dehydration. It can be carried out in the forehead in dogs and the neck region in cattle. With dehydration of about 5-6%, the loss of skin elasticity is mild, whereas in 10% dehydration, the skin often remains ‘tented’. With higher percentages of dehydration, the animal becomes moribund. If the dehydration level is less than 5%, it cannot be reliably assessed by clinical findings. The relatively higher percent of body water in neonates and the variation in skin elasticity in older animals make the skin turgor test a less reliable tool in these age groups. Obesity can also affect skin tenting. Tacky mucous membrane on examination is suggestive of early stages of dehydration. With dry mucous membranes, the dehydration will be more than 6%. Eyeballs sunken in orbit are also noticed as dehydration increases. Rapid and weak pulses, coldness of extremities, animal appearing depressed, and prolonged capillary time indicate severe dehydration; shock may manifest. These clinical findings are noticed with more than 12% dehydration and have a grave prognosis. Eyeball recession (mm) and skin tent duration (seconds) are good indicators of calves’ percentage dehydration and fluid replacement requirement. Dehydration is measured in the lab using packed cell volume (PCV) and total solids. Dehydration causes a rise in PCV and total solids. An increase in urine specific gravity can also detect dehydration. The aetiology of the existing disease should also be considered when interpreting laboratory findings, as disorders such as anaemia and hyperproteinaemia can cause variances. Fluid therapy for the management of dehydration has a quantitative aspect that is based on the correction of existing deficiencies, ongoing losses, and maintenance requirements.

The existing deficit is calculated as:

Deficit (hydration) in litres

= %of dehydration (in decimals) ? body weight in kg

Based on the formula used, a 300 kg cow with 8% dehydration would require about 24 L to correct the existing deficit. For ongoing losses, general thumb rules dictate the volume of fluid that needs to be replaced and may vary based on age and species. To meet daily needs, a volume of 50 mL/ kg is required in dogs. Owing to the higher percent of extracellular fluid in young animals, their maintenance requirements are greater. A rate of 5 mL/kg/h or 120 mL/ kg/day is required in calves, almost double the adult maintenance needs. The guidelines of the American Animal Hospital Association-American Association of Feline Practitioners suggest 2-6 mL/kg/h as maintenance rate in dogs; the formula suggested for 24 h is 132 ? body weight in kg^0.75. Correction of ongoing losses depends on the type of loss (e.g. vomiting) and the number of episodes. The primary aim is to correct ongoing losses in 2-3 h. In 24 h, the patient’s hydration status should be restored based on the total volume needed. Careful monitoring of the patient is essential during fluid therapy for signs of fluid overload. In such a case, reassess the status and adjust the rate of fluid administration. Tachypnoea crackles on auscultation, and watery nasal discharge suggests fluid overload. The volume requirement and rate of administration would be considerably different in animals with diseases affecting the organs like kidney and heart and in shock states.

Common routes of administration include intravenous, subcutaneous, and oral routes. Severe dehydration warrants intravenous fluid therapy. In patients with minimal dehydration, subcutaneous fluid administration can be considered. Isotonic fluids (normal saline and Ringer’s lactate) are utilised for subcutaneous delivery. If vomiting is not present, the oral route may be used. Oral rehydration treatments are useful in preventing dehydration and electrolyte loss in calves. It is best to keep the amount of fluid given to calves to roughly 1-1.5 L at a time. Because of the practical challenges in intravenous fluid delivery in terms of the volume that needs to be provided, oral rehydration salts are now frequently suggested in adult cattle to overcome dehydration. However, if the animal is recumbent, the volume that can be administered orally will be reduced. An oral rehydration mix for cattle is sodium chloride 7 g, potassium chloride 1.25 g, and calcium chloride 0.5 g added to 1 L of water. This preparation is not an alkalinising solution, like other oral rehydration therapy preparations in calves. Calves with diarrhoea develop metabolic diseases in many instances due to hypovolaemia or specific diseases. Oral rehydration formulas for calves primarily have sodium and potassium, glucose, and chloride. Sodium bicarbonate, magnesium, acetate, and propionate are also included in some preparations for calves. Acetate and propionate act as metabolisable bases, which are converted to bicarbonate in the liver. These bases are considered superior to direct administration of sodium bicarbonate.

Moreover, they can act as an energy source and support sodium and water transport out of the small intestine. Fluid is administered intraosseously in paediatric patients and small dogs and cats when access to the intravenous route is difficult. The intraperitoneal route is also considered in such patients, provided that conditions like ascites and peritonitis are absent.

8.2.3.2 Types of Parenteral Fluids

The fluids utilised in clinical practice are divided into crystalloids and colloids. In veterinary medicine, crystalloid fluids are often used to treat dehydration. Fluids are classed as isotonic, hypertonic, or hypotonic based on their osmolality. Fluids having an osmolality similar to that of extracellular fluids (about 270-310 mOsmol/L) can be regarded as isotonic for all practical purposes. Normal saline (0.9% NaCl) and lactated Ringer’s solution are two common examples. These fluids ‘seep’ into other body compartments and are redistributed within extracellular compartments. Only less than one-third of the total volume of fluids administered intravenously will be present in circulation after 1 h of administration. When administered, hypertonic fluids are useful to draw large quantities of fluid into circulation and are preferred in conditions like gastric dilatation and volvulus in dogs. Hypertonic fluids should not be used in cases of dehydration. Dextrose 50% is a hypertonic crystalloid used to manage ketosis in bovines. Sodium bicarbonate as a 5% solution is employed to treat carbohydrate engorgement of ruminants. Hypertonic saline (3% or 7% NaCl) is used in veterinary practice to manage intracranial pressure in head trauma conditions. Hypertonic saline is also used in hypovolaemic shock management, as the volume required for resuscitation is relatively less than isotonic fluids. Hypertonic saline should not be used in dehydrated patients. Preparations like 0.45% NaCl and dextrose 5% are hypotonic fluids. Crystalloid fluids can further be classified, based on usage, as replacement fluids and maintenance fluids. Replacement fluids (e.g. normal saline) have higher sodium concentration and lower potassium levels than maintenance fluids and are indicated in cases of ongoing fluid and electrolyte losses, as in vomiting. A combination of half-strength dextrose (2.5%) and NaCl (0.45%) is also isotonic and is used as a maintenance fluid along with potassium chloride supplementation. It can be used after the ongoing electrolyte imbalances, and dehydration is corrected. The pH of the fluids may also vary. Normal saline has a pH of 5.5 and that of lactated Ringer’s is 6.5.

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Dehydration Management in Birds

Panting during periods of increased ambient temperature can lead to respiratory alkalosis in birds as excessive carbon dioxide losses occur. Dietary electrolyte (Na⁺ + K⁺-Cl^-) balance and electrolyte [(K⁺ + Cl^-)/Na⁺] ratio in the feed need to be monitored to alleviate the physiological and metabolic changes of heat stress. These electrolytes are considered important in managing acid-base balance and osmotic pressure of body fluids. In heatstroke, cooling the bird is an emergency measure that owners can try before veterinary aid is available. It involves the use of tap water or tepid water, and cold water should not be used for the purpose. The birds can also be misleading with water making sure that the water has good contact with skin. Moistening the feet and beak is also required.

Colloids can be broadly classified into natural colloids and synthetic colloids. Blood and blood products (albumin) are examples of natural colloids. Hydroxyethyl starch and dextran are synthetic colloids. Due to their higher molecular weight, these intravenous preparations remain in circulation for more extended periods (‘crystalloids seep fast’). A veterinary product of hydroxyethyl starch available in India has a molecular weight of 130 kDa. Indications for the use of synthetic colloids are in the management of acute hypovolaemia and maintenance of plasma oncotic pressure. The volume required for fluid resuscitation when plasma expanders are used would be considerably less than that of crystalloids. A clinician needs to be aware of the potential signs of hypersensitivity and organ injury when natural and synthetic colloids are used (Table 8.7).

8.2.3.3 Acid-Base Imbalances and Electrolyte Abnormalities

Acid-base imbalances and electrolyte abnormalities often have life-threatening effects on animals. The disorders vary from carbohydrate engorgement in ruminants to hypokalaemia associated with diabetic ketoacidosis in dogs. The use of blood gas and electrolyte analysers would be beneficial in detecting these variations and monitoring treatment.

Carbohydrate engorgement of cattle (lactic acidosis) results in metabolic acidosis and dehydration, requiring intravenous sodium bicarbonate therapy to manage the acidosis and intravenous fluids to correct the dehydration. Base deficit measurement is the ideal method for deciding on the bicarbonate quantity to be administered. In a severe case of metabolic acidosis, sodium bicarbonate required (in mmol) is base deficit (from blood analysis) ? 0.5 (or 0.3) ? body weight in kg. Half the calculated dosage needs to be administered for 3-4 h, and the patient values need to be reassessed before administering sodium bicarbonate further. In dogs with chronic renal disease, bicarbonate medication may be required to keep the bicarbonate level between 18 and 24 mmol/L. Thumb guidelines are also employed in ruminant practice to determine the amount of sodium bicarbonate to deliver in cases of lactic acidosis, depending on the clinical severity, because direct access to the laboratory may not be possible in many farms. In urea toxicosis of ruminants, dilute

Table 8.7 Types of dehydration and fluids administered
Type of dehydration	Fluids preferred^a
Isotonic dehydration (normal serum sodium levels)	Isotonic fluids like normal saline and Ringer’s lactate
Hypertonic dehydration (elevated serum sodium)	Fluids with ‘free water’ (dextrose 5%)
Hypotonic dehydration (Low serum sodium—Not commonly encountered in clinical practice)	Normal saline

^aFluid administration also depends on the severity of the condition, primary aetiology, metabolic status, and electrolyte imbalances. Oral rehydration can be tried in less severe cases, especially when vomiting is absent

acetic acid (vinegar) is administered orally to manage ruminal alkalosis. Hypercapnia can result from airway obstruction and pulmonary disease; respiratory acidosis manifests. In dogs, tracheal collapse, brachycephalic syndrome, and chronic bronchial diseases can result in respiratory acidosis. Two or more separate acid-base abnormalities characterise mixed acid-base disorders. Interpretation of the results is essential in deciding the treatment options in such cases.

Diseases, conditions like vomiting, and drugs can contribute to electrolyte imbalances. Renal failure and hypoadrenocorticism can result in hyperkalaemia in dogs. Hypochloraemia and hyponatraemia were reported in hypoadrenocorticism. Hypokalaemia and hyponatraemia can be associated with diabetic ketoacidosis. In ruminants, hypochloraemic, hypokalaemic alkalosis occurs in left abomasal displacement. Administration of furosemide, a loop diuretic, can cause hyponatraemia. Hypokalaemia, hypocalcaemia, and hypomagnesaemia can also result in this drug’s administration. Hyperphosphataemia that arises in many cases of chronic kidney disease may warrant dietary phosphate restriction and the use of phosphate binders. Loss or excess of electrolyte management is challenging in many clinical settings. Intravenous potassium chloride administration is carried out after dilution in normal saline and needs to be monitored carefully due to the cardio-toxic effects of potassium. Fluid and electrolyte therapy will have to be tailored based on the primary disease and the body system involved.

Learning Outcomes

• The water in the body is divided into intracellular and extracellular fluid compartments (plasma, lymph, and interstitial and transcellular fluids). The plasma and interstitial fluid in vertebrates are similar in composition, but the ECF and ICF in all animals are significantly different, with NaCl prevailing in the ECF and potassium and organic molecules dominating in the ICF.

• ECF volume and osmolarity are both regulated in mammals to maintain fluid balance. Controlling ECF osmolarity prevents hyper- or hypotonicity from causing variations in ICF volume. The baroreceptor reflex and plasma-interstitial fluid shifts regulate ECF volume in the short term, which is critical in the long-term regulation of blood pressure. Water and salt balances are used to regulate osmolarity and volume.

• In acid-base balance, the management of free hydrogen ions in physiological fluids is critical to survival. Free hydrogen ions are liberated by acids, whereas bases accept free hydrogen ions. The hydrogen ion concentration is expressed using the pH scale. Hydrogen ion fluctuations affect neuron, enzyme, and potassium ion activity. From metabolic activities, hydrogen ions are constantly added to bodily fluids.

• The major ECF buffer is the bicarbonate buffer system. Intracellularly, the peptide and protein buffer system, which includes haemoglobin in erythrocytes, is crucial. Buffers are only a temporary solution because they do not remove excess hydrogen ions; thus, the second and third lines of defence are required. The second line of defence is the respiratory system, which regulates hydrogen ions by adjusting ventilation. Carbon dioxide is removed when breathing occurs more deeply, but it is retained when breathing happens less deeply. Excretory systems control both bicarbonate and hydrogen ions in the ECF and constitute the third line of defence that aid in acid-base homeostasis. Cells in kidneys can release hydrogen ions and reabsorb bicarbonate, while other cells can do the opposite. Some cells release ammonia trap hydrogen ions as ammonium in acidosis.

• Hypoventilation causes respiratory acidosis, caused by an increase in carbon dioxide. Hyperventilation causes respiratory alkalosis, caused by a reduction in carbon dioxide. A decrease in plasma bicarbonate is linked to metabolic acidosis induced by acute diarrhoea, diabetes, intense exertion, or uraemia. Hyperventilation causes respiratory alkalosis caused by a reduction in carbon dioxide. Vomiting can cause metabolic alkalosis, marked by an increase in bicarbonate.

(continued)

• Body fluid, electrolyte, and acid-base homeostasis must be maintained and regulated to the sustained body’s functions. The body has several compensating processes to keep fluid, electrolytes, and acidbase balance; if its compensating systems fail to maintain homeostasis, it can have profound, even life-threatening implications. Fluid treatment can help with these problems.

Exercises

Objective Questions

Q1. Which is the most effective buffer system in the intracellular fluid?

Q2. Which is the major cation of the extracellular fluid?

Q3. Which is the first line of defence in acid-base regulation?

Q4. What does the isohydric principle state?

Q5. How many bicarbonate ions are returned to the blood for each glutamine metabolised within tubular epithelial cells?

Q6. What are the only means by which water output can be significantly controlled?

Q7. Which hormone is released from the heart when there is an increase in sodium level and blood volume?

Q8. What amount of fluid is required to correct 8% dehydration in a 300 kg cow?

Q9. Which fluid compartment has the major part of the body’s water?

Q10. Which electrolyte is the chief determinant of cellular volume and intracellular osmolarity?

Q11. Where does the reabsorption of cerebrospinal fluid occur explicitly?

Q12. Which are the major electrolytes involved in the total osmolarity of the interstitial fluid and plasma?

Q13. Which condition is indicated when there is increased excretion of ammonium chloride in urine?

Q14. What amount of water forms when one gram of fat is oxidised?

Q15. Which type of acid-base imbalance is observed in the carbohydrate engorgement of cattle?

Subjective Questions

Q1. Explain in detail body water compartments.

Q2. Which are the methods for measuring body water?

Q3. What is cerebrospinal fluid? Explain the formation, absorption, and functions of cerebrospinal fluid.

Q4. How is acid-base regulated in the body?

Q5. Which are the acid-base imbalances?

Q6. What is dehydration, and how is it managed?

Q7. Which are the common electrolyte abnormalities?

Q8. Which are the important electrolytes in the body fluids?

Q9. How is water intake and water output regulated?

Q10. Which are the different types of parenteral fluids?

Answer to Objective Questions

A1. Protein

A2. Sodium

A3. Chemical buffering

A4. The buffers of the blood and body fluids do not act independent of each other, but rather react in unison

A5. Two

A6. Through regulation of urine volume

A7. Atrial natriuretic factor

A8. 24 L

A9. Intracellular fluid

A10. Potassium

A11. Arachnoid villi

A12. Sodium and chloride ions

A13. Acidosis

A14. 1.1 mL of water

A15. Metabolic acidosis

Keywords for Answer to Subjective Questions

A1. Intracellular fluid, extracellular fluid, transcellular fluid

A2. Indicator dilution technique, haematocrit

A3. Choroid plexus, arachnoid villi, buoyancy

A4. Chemical buffers, respiratory system, kidney

A5. Metabolic acidosis, metabolic alkalosis, respiratory alkalosis, respiratory acidosis

A6. Diarrhoea, skin turgor test, Ringer’s lactate

A7. Hyperchloraemia, hyperkalaemia, hypernatraemia, hypocalcaemia, hypochloraemia, hypokalaemia

A8. Sodium, potassium, phosphate, chloride, hydrogen, bicarbonate, calcium

A9. Antidiuretic hormone, thirst, urine, atrial natriuretic factor

A10. Crystalloids, colloids, isotonic, hypertonic, isotonic

Fluid Balance

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