Chapter 5 Water, Electrolyte and acid-Base Balance

 

 

 

                      

 5.1 REQUIRED READING ASSIGNMENT:

Veterinary Clinical Pathology - Coles

• 1. Water, Electrolytes, and Acid-Base Balance -- pp 203-216. 

5.2 objectives and/or study questions:

Students should be answer the following questions at the completion of this unit.

5.3 Introduction: 

A knowledge of the normal state is essential for formulation of a logical and accurate plan of therapy for the patient with abnormalities in water, electrolyte and/or acid-base balance. This fundamental knowledge coupled with an understanding of the basic compensatory mechanisms utilized by the body to correct these alterations is the basis for effective fluid therapy. The goal of this fluid therapy is to re-establish and/or maintain in the body certain basic conditions which favor normal cellular metabolism. These basic conditions are not those required for normal functioning of one biochemical reaction, or one body organ, but are basic conditions required for all biochemical processes and all organs if normal function is to be restored. Specifically, the goals of this kind of fluid therapy are to insure that normal conditions prevail with respect to body water, tonicity of body fluids, specific body electrolytes and acid-base status.

5.4 GENERAL INFORMATION

5.4.1 Body Water (Body Fluid)

• 1. The proportion of water in an animal's body ranges from 45 to 70% of the total body weight and is inversely proportional to the body fat content.
• 2. Body Fluid is divided into two compartments which vary in their electrolyte make-up.
  • a. Intracellular fluid (ICF)
    • 1) 65 to 75% of the total body water
  • b. Extracellular fluid (ECF)
    • 1) Approximately 25% of the total body water
    • 2) Found in three locations:
      • a) Intravascularly (plasma)
      • b) Interstitially (including lymph)
      • c) Transcellularly (CSF, Joint fluid, Intestinal contents)
    • 3) Interstitial fluid is essentially an ultrafiltrate of plasma and water and electrolytes move freely within this compartment and between it and the intravascular fluid.
    • 4) Intravascular fluid has almost the same composition as interstitial fluid except for its higher protein level.
• 3. Sources of Water
  • a. Preformed water - water taken into the body as liquids and contained in solid foods.
  • b. Water of oxidation - water derived from oxidation of foods to carbon dioxide and water
    • 1) Continues to be formed from endogenous sources even though no exogenous water might be available.
    • 2) Produces about 12 ml of water from the metabolism of each 100 calories.
• 4. Water Loss
  • a. Normal water loss is through the kidneys, lungs, skin (perspiration) and gastrointestinal tract.
    • 1) urine accounts for slightly more than half the total fluid output of the body.
    • 2) Water loss through the kidney is controlled by antidiuretic hormone (ADH) in response to plasma osmotic pressure and by aldosterone, which controls renal sodium excretion.
    • 3) A decrease in body water, plasma sodium, or both is compensated for by an equivalent decrease in water, sodium excretion, or both.
  • b. Dehydration occurs when loss of body water exceeds intake.
    • 1) This may result from excessive water loss without compensatory increased intake or from decreased intake with normal water loss.
    • 2) Excessive loss of body fluid may occur in:
      • a) diarrhea
      • b) prolonged vomiting
      • c) sequestration of fluids in the digestive tract
      • d) prolonged fever
      • e) sweating
      • f) exudating burns or open wounds
      • g) excessive blood loss
      • h) uncontrolled polyuria without adequate compensatory water intake

5.4.2 Electrolytes

Substances that become ionized when placed in water

• 1. Electrolyte composition of body fluids
  • a. As previously stated, the body fluid compartments differ in their electrolyte concentrations. Table V.1 indicates the typical electrolyte concentrations in the various body fluid compartments.

TABLE V.1

REPRESENTATIVE ELECTROLYTE CONCENTRATIONS

IN THE BODY FLUID COMPARTMENTS

(mEg/L)

Electrolytes	Intracellular Fluid	Extracellular Fluid	Interstitial	ntravascular
Cations	-	-	-	-
Sodium	15	147	142	-
Potassium	155	4	5	5
Calcium	2	2.5	-	-
Magnesium	27	1	2	-
Anions	-	-	-	-
Bicarbonate	10	30	27	-
Chloride	1	114	103	-
Phosphate	100	2	2	-
Sulfate	20	1	1	-
Organic acids	1	7.5	-	5
Protein	62	0	16	-

• b. The total concentration of cations always equals that of the anions in all body fluids.

• 2. The unit of measurement for electrolytes is milli-equivalents per liter of fluid (mEq/L).
  • a. Milliequivalent values are measures of combining power and replace older methods of measuring electrolyte concentrations by weight (e.g., mg/dl and mg%) and volume (e.g., vol%).
  • b. A milliequivalent is the number of grams of solute contained in 1cc of a normal solution, and thus can combine equally with a similar portion of another normal solution.
  • c. Values expressed as mg%, mg/100 ml, or mg/dl can be converted to mEq/L by using the formula:

    ---

    mg/100 ml x 100

    atomic weight x valence = mEq/L

    ---

• 3. Specific Electrolytes
  • a. Sodium
    • 1) Approximately 1/2 of the total body concentration of sodium is found in ECF.
    • 2) The quantity of sodium in the body is controlled by dietary intake and loss.
    • 3) The most important route for sodium excretion is through the kidney. Most sodium presented to renal tubules is reabsorbed in a process controlled by aldosterone.
      • a) Renal reabsorption of sodium requires an equivalent passage of hydrogen or potassium ions in the opposite direction.
    • 4) Sodium is also lost in sweat and in digestive tract secretions.
      • a) In carnivores and most herbivores, sodium is reabsorbed in the lower intestinal tract.
      • b) In herbivores with large quantities of fluid in the feces, such as the cow and the horse, there may be considerable fecal loss of sodium.
    • 5) A decrease in plasma sodium concentration (hyponatremia) occurs most frequently because of excessive sodium loss.
      • a) from the gastrointestinal tract through diarrhea or vomition
      • b) in renal disease in which the sodium conservation mechanism is operating deficiently because of tubular damage
      • c) Hyponatremia may occur with hyperglycemia due to increased sodium excretion to prevent hyperosmolarity.
    • 6) An increase in plasma sodium concentration (hypernatremia) is rare and can occur when there is restricted water intake with excessive sodium intake, in advanced chronic renal failure with a low glomerular filtration rate, and with primary hyperaldosteronism.
  • b. Potassium
    • 1) Potassium concentration is low in ECF and high in most cells of the body.
    • 2) Most potassium is excreted by the kidneys through glomerular filtration and tubular secretion.
    • 3) Aldosterone facilitates excretion of potassium since it causes increased sodium reabsorption by promoting the exchange of sodium in tubular fluid for potassium in the tubular cell.
    • 4) Potassium excretion by the kidneys is also controlled by competition between potassium and hydrogen ions for reabsorption.
    • 5) Alterations in serum potassium levels occur when there is a disturbance in the equilibrium between potassium in the ICF and potassium in the ECF.
      • a) In alkalosis, potassium moves into the cell in exchange for hydrogen ions and may cause hypokalemia.
      • b) In acidosis, potassium moves out of the cell in exchange for hydrogen ions and may cause hyperkalemia.
    • 6) Plasma potassium increases about 0.6 mEq/L for each 0.1 unit decrease in blood pH. Therefore, if an acidotic animal has a normal plasma potassium level, it should be considered hypokalemic and corrective therapy should be initiated.
    • 7) In addition to its role in maintaining the tonicity of the ICF, potassium is of great importance in the mechanism of neuromuscular transmission.
      • a) Low concentrations of K+ in the ECF result in profound muscular weakness and ECG abnormalities.
      • b) High concentration of K+ in the ECF (10-12 mEq/L) result in severe myocardial disturbances and death due to cardiac arrest.
  • c. Chloride
    • 1) Chloride concentration is low in ICF and high in ECF.
    • 2) Excretion, absorption and distribution of chloride are passive processes in association with active sodium transport.
    • 3) Unusual reduction in chloride concentration in the absence of comparable change in sodium, usually reflects sequestration of gastric juice in the stomach or vomiting.
  • d. Bicarbonate
    • 1) Bicarbonate is mostly of endogenous origin in that it comes from the hydration of carbon dioxide to carbonic acid which then dissociates to bicarbonate and hydrogen ions.
    • 2) Bicarbonate is lost through secretions to the digestive tract and in the urine.
    • 3) Bicarbonate levels are regulated by respiratory and metabolic (kidney) processes.

5.4.3 Distribution of fluid among the two body fluid compartments

• 1. The distribution of fluid among the body fluid spaces is determined by osmotic pressures.
  • a. The homeostatic mechanisms of the body which maintain this function are designed to maintain the osmotic pressure of the extracellular fluid.
  • b. If ECF osmotic pressure can be maintained, it will also serve to maintain intracellular osmolarity.
  • c. If the osmotic pressure of the ECF is increased, water is removed from cells (ICF), producing cellular dehydration and a new state of equilibrium between ECF and ICF at a new and different osmolarity.
• 2. The plasma proteins are confined to the vascular space and, in that location, exert an osmotic force that holds fluid in the vessels in opposition to the tendency of the blood pressure to force fluid out of the vessels.
• 3. The tonicity (osmotic pressure) of the ICF and ECF is determined by the total number of particles (electrolyte ions) dissolved in each of these fluids.
  • a. The clinical unit of measurement for osmolality is milliosmoles (mOsm) per kilogram of water.
  • b. The normal osmolality of plasma in domestic animals is about 300 mOsm/kg of plasma water.
  • c. Since sodium is the most abundant ion in the ECF, the osmotic pressure of the ECF is largely determined by the sodium concentration.
  • d. Potassium is the most abundant ion in the ICF and has a comparable role in maintaining normal intracellular hydration.
• 4. Normal hydration of the body depends, therefore, not only on optimum water in the body, but on optimum protein, sodium, and potassium in the appropriate fluid compartments to hold the proper amount of water in each compartment.

5.5 ACID-BASE REGULATION IN THE BODY FLUIDS

Normal metabolic processes in an animal body result in the production of relatively large quantities of acids. These acids are transported to the excretory organs, i.e., the lungs and the kidneys, without causing marked alterations in blood pH. This sensitive control of blood pH in the normal range of 7.3 to 7.5 is accomplished by the combined effects of the blood buffer system, the respiratory system, and the renal system. The body responds quickly to alterations in blood pH. Correction in these alterations occurs in steps, with buffer systems providing the immediate response to any pH alteration, followed quickly by the respiratory response. Later, the kidney mechanism is initiated and sustains the corrective activity for a longer time span.

A buffer is a mixture of a weakly dissociated acid and a salt of that acid. The blood buffers that play a role in control of blood pH are:

• 1. Bicarbonate/carbonic acid system
• 2. Oxyhemoglobin:reduced hemoglobin system
• 3. Monopotassium phosphate:dipotassium phosphate system
• 4. Plasma protein system
• 5. Monosodium phosphate:disodium phosphate system 

The bicarbonate/carbonic acid buffer system is the single most important buffer system in the body fluids and our discussion will be restricted to this system.

5.5.1 The Bicarbonate/Carbonic Acid Buffer System

• 1. The Henderson-Hasselbalch equation is useful in understanding pH control of body fluids. This formula is as follows:

  pH = pK + log salt

  acid

The equation for the bicarbonate/carbonic system is:

pH = 6.1 + log [bicarbonate]

[carbonic acid]

Therefore, the pH of plasma is dependent upon the ratio of HCO3- to H2CO3. As can be seen in Figure V.1, the normal ratio between these substances is 20:1. when one changes without a comparable change in the other, the pH becomes abnormal.

• 2. Carbonic acid is formed when hydrogen from cell metabolism combines with bicarbonate or when carbon dioxide produced by cell metabolism is combined with water inside the erythrocyte to form carbonic acid under the influence of cellular carbonic anhydrase. Blood carbonic acid is in equilibrium with dissolved

Figure V.1

The Biocarbonate/Carbonic Acid Buffer system

 

 CO2 which is in turn controlled by ventilation. Abnormalities in carbonic acid or carbon dioxide, therefore, always result from abnormalities in ventilation.

• a. When ventilation is decreased, carbon dioxide accumulates, carbonic acid is increased, and the condition is called respiratory acidosis (seen in pneumonia, pulmonary edema, etc.)
• b. When hyperventilation occurs, carbon dioxide is reduced, carbonic acid is decreased below normal and the condition is respiratory alkalosis.

• 3. Bicarbonate concentration is influenced by non-respiratory mechanisms such as renal function, digestive tract function, and tissue metabolism.
  • a. Increased bicarbonate or a decrease in acid (HCl) would reflect metabolic alkalosis (seen in vomiting).
  • b. Decreased bicarbonate results in metabolic acidosis and is very common in cases of diarrhea.
• 4. The above acid-base disturbances are summarized in Table V.2.

TABLE V.2

LABORATORY FINDINGS IN CLASSI UNCOMPENSATED ACID-BASE IMBALANCES(ACUTE)   

 * BE = Base excess

N = Normal

5.5.2 Respiratory Control of Acid-Base Balance

• 1. The respiratory center found in the medulla oblongata is sensitive to blood levels of pCO2 and pH.
  • a. When blood pCO2 increases above the normal value, the respiratory rate increases.
  • b. When blood pH drops, the respiratory rate increases.
  • c. When blood pCO2 is low, respiratory rate decreases.
  • d. When blood pH is high, respiratory rate decreases.
• 2. This regulation of the rate of pulmonary ventilation in response to changes in pCO2 and pH serves as the basis for pulmonary compensation in alkalosis and acidosis.

5.5.3 Renal Control of Acid-Base Balance

• 1. Accumulation of nonvolatile acids and the subsequent depleting effect on bicarbonate ion content can be offset only by the renal ability to exchange sodium ions for hydrogen ions and the production of an acid urine.
  • a. As nonvolatile acid anions are filtered through the glomerulus, they are accompanied by an equivalent number of cations (e.g., Na+ ) in order to maintain electrical neutrality.
  • b. Through the activity of carbonic anhydrase, renal tubule cells combine carbon dioxide from their own metabolic activities with water to make carbonic acid which dissociates to hydrogen and bicarbonate ions.
  • c. The hydrogen ions pass into the tubule and an equivalent amount of sodium is returned accompanied by an equivalent amount of bicarbonate; thus, bicarbonate ions are replaced, hydrogen ions and nonvolatile acid anions are excreted and acid urine is produced.
  • d. The overall effect is restoration of the blood bicarbonate ion:carbonic acid ratio with a resultant correction of pH.

NOTE: In compensated acidosis or alkalosis, absolute concentrations of bicarbonate ions and carbonic acid may be changed, but as long as the ratio remains in the range of approximately 20:1, the pH may be in the normal range.

5.6 ACID-BASE DISTURBANCES

5.6.1 Respiratory Acidosis - carbonic acid excess (hypoventi-lation)

1. Causes

• a. Pneumonia
• b. Emphysema
• c. Pulmonary edema
• d. Pneumothorax
• e. Paralysis of respiratory muscles
• f. Morphine poisoning
• g. Barbiturate poisoning
• h. Occlusion of breathing passages
• i. In closed gas anesthesia when oxygen is adequate, but carbon dioxide removal is insufficient.

2. Clinical Signs

• a. Respiratory embarrassment
• b. Depression of central nervous system (disorientation, coma)

3. Laboratory findings

• a. Uncompensated
  • 1) Urine pH - more acid
  • 2) Blood pH - below 7.35
  • 3) Plasma bicarbonate - normal
  • 4) Elevated pCO2
• b. Partially Compensated
  • 1) Elevated pCO2
  • 2) Plasma bicarbonate - increased
  • 3) Plasma chloride - low; increased excretion of chloride by kidney to make more sodium available for bicarbonate.
  • 4) Blood pH - decreased, but higher than uncompensated
  • 5) Urine pH - acid 

4. Pathogenesis

• a. Normal balance 

 

•  b. Respiratory acidosis - carbonic acid excess due to hypoventilation 

 

• c. Body compensatory action
  • 1) If the primary cause is not in the respiratory center (e.g., CNS problem), the center will cause an increased pulmonary rate with a resultant decrease in pCO2.
  • 2) The renal compensatory mechanism will conserve bicarbonate ions and excrete hydrogen ions and nonbicarbonate anions to produce more acid urine. There is also increased reabsorption of bicarbonate. 
   

Partial Compensation 

 

Complete Compensation 

5.6.2 Respiratory Alkalosis - carbonic acid deficit (hyperventilation)

1. Causes - increased rate and depth of breathing

• a. Fever
• b. Oxygen lack
• c. Respiratory center stimulation (encephalitis, drugs such as salicylates)
• d. Hysteria and anxiety

2. Clinical signs

• a. Deep, rapid breathing
• b. Tetany, progressing to convulsions

3. Laboratory Findings

• a. Uncompensated
  • 1) Urine pH - more alkaline
  • 2) Blood pH - over 7.45
  • 3) Plasma bicarbonate - normal
  • 4) Decreased pCO2
• b. Partially Compensated
  • 1) Decreased pCO2
  • 2) Plasma bicarbonate - decreased
  • 3) Plasma chloride - normal to high
  • 4) Blood pH - increased, but lower than uncompensated.
  • 5) Urine pH - alkaline

4. Pathogenesis

• a. Normal balance 

   

b. Respiratory alkalosis - carbonic acid deficit due to hyperactive breathing which results in an increased loss of carbon dioxide from the lungs.

 

 c. Body compensatory action

1) The compensatory mechanisms are principally renal. Renal control is manifested by a decrease in ammonia formation, a decrease in bicarbonate reabsorption, retention of hydrogen ions (exchanged for sodium) and an increase in excretion of bicarbonate instead of chloride.

    

5.6.3 Metabolic (Nonrespiratory) Acidosis - bicarbonate deficit

1. Causes

• a. Extreme diarrhea - the digestive juices in the small intestine contain large amounts of sodium bicarbonate, and when these are lost in the feces as a result of diarrhea, the body is depleted of sodium ion.
• b. Renal insufficiency - causes retention of organic acid ions, inability to reabsorb bicarbonate and excrete hydrogen ions.
• c. Ketosis in which large amounts of ketonic acids are produced and accumulate in the tissues (diabetes mellitus, starvation).
• d. Lactic acid accumulation - heat stroke, excessive muscular activity, conditions of cellular hypoxia.
• e. Sequestration of intestinal contents.
• f. Excessive loss of saliva.

2. Clinical Signs

• a. Hyperpnea - rapid rate and increased depth of respiration
• b. Depression of central nervous system (disorientation, stupor, coma)

3. Laboratory Findings

• a. Uncompensated
  • 1) Urine pH - more acid
  • 2) Blood pH - below 7.35
  • 3) Plasma bicarbonate - decreased
  • 4) Normal pCO2
• b. Partially Compensated
  • 1) Decreased pCO2
  • 2) Plasma bicarbonate - decreased
  • 3) Blood pH - decreased, but higher than uncompensated
  • 4) Urine pH - acid

4. Pathogenesis

a. Normal balance

    

 b. Metabolic acidosis - ketone and/or excess chloride ions replace bicarbonate ions.

      

 c. Body compensatory action

• 1) The respiratory compensatory mechanism decreases pCO2 by increased respiratory rate.
• 2) The renal compensatory mechanism will conserve bicarbonate ions and excrete hydrogen ions and nonbicarbonate anions to produce more acid urine. There is also increased reabsorption of bicarbonate. 

       

 5.6.4 Metabolic Alkalosis - bicarbonate excess

1. Causes

Accumulation of bicarbonate in extracellular fluid as a result of excessive acid loss.

• a. Vomition - loss of chloride causes a compensatory increase in bicarbonate to maintain electrical neutrality
• b. Sequestration of abomasal juices in ruminants with high GI tract obstructions
• c. Potassium depletion with resultant movement of hydrogen ions into the intracellular fluid to replace lost potassium
• d. Hyperadrenocorticism
• e. Alkaline therapy

2. Clinical signs

• a. Depressed breathing - slow and shallow
• b. Tetany, progressing to convulsions

3. Laboratory Findings

• a. Uncompensated
  • 1) Urine pH - more alkaline
  • 2) Blood pH - over 7.45
  • 3) Plasma bicarbonate - increased
  • 4) Normal pCO2
  • 5) Plasma chloride - low
  • 6) Plasma potassium - may be low
• b. Partially Compensated
  • 1) Increased pCO2
  • 2) Plasma bicarbonate - increased
  • 3) Plasma chloride - low
  • 4) Plasma potassium - may be low
  • 5) Blood pH - increased, but lower than uncompensated
  • 6) Urine pH - alkaline (Paradoxical aciduria can occur)

4. Pathogenesis

a. Normal balance 

        

 b. Metabolic alkalosis - bicarbonate ion increased due to loss of chloride ion or to excess ingestion of bicarbonate.

         

 c. Body compensatory action

• 1) The respiratory response is a decrease in respiration in order to increase pCO2.
• 2) The compensatory renal mechanism is decreased sodium-hydrogen exchange, decreased ammonia formation, and increased excretion of bicarbonate.

   

5.7 EVALUATION OF CLINICAL PATIENTS

5.7.1 Some basic questions to be answered.

• 1. Is dehydration present?
• 2. Is the extracellular fluid hypertonic or hypotonic?
• 3. Is there an acid-base abnormality?
• 4. Is there an abnormality in the concentration of any specific important electrolytes?

5.7.2 Patient evaluation without laboratory tests.

1. The Clinical Examination

• a. Clinical signs of dehydration.
  • 1) Loss of skin turgor.
  • 2) Dryness of mucous membranes.
  • 3) Sunken eyes.
  • 4) Listlessness or depression.
• b. Clinical signs of acid-base abnormality.
  • 1) Abnormal respirations.
• c. Clinical signs of potassium disturbances.
  • 1) Muscular weakness.
  • 2) The electrocardiogram.
• d. Clinical signs of sodium disturbances - no specific signs.
• e. The value of the history and physical examination.
  • 1) Is dehydration the result of being off feed and not drinking?
  • 2) Has there been diarrhea?
  • 3) Could there be sequestration of fluid in the digestive tract?
  • 4) Has there been any other peculiar fluid loss?

2. The shortcomings of patient evaluation without laboratory tests.

• a. There are no objective facts.
• b. The guesses could be wrong.
• c. The patient may be unusual.
• d. There is no objective means of monitoring response to treatment.

3. More objective evaluation of the patient is indicated when:

• a. The patient is especially valuable.
• b. The clinical signs of a fluid balance disorder are unusually severe.
• c. Large quantities of fluid have been given which may have induced an electrolyte disorder.

4. Patient Therapy

When patient needs are poorly defined, therapy must be general and conservative. When patient needs are well defined, therapy can be more specific, more radical and more successful.

5.7.3 Patient evaluation by laboratory tests.

• 1. The only way to determine objectively what, if any, specific derangements are present in the patient.
• 2. Some areas of importance include dehydration per se, ECF tonicity, acid base disorders, and derangements of specific important electrolytes.
• 3. Evaluating the severity of dehydration.
  • a. Clinical signs can be misleading.
  • b. PCV or hemoglobin is very helpful as an indicator of hemoconcentration.
    • 1) Can be misled by preexisting anemia.
    • 2) Can be misled by normal horse contracting spleen and elevating values in blood.
  • c. Total serum or plasma protein is a useful double check for hemoconcentration.
    • 1) Easily done with a refractometer.
    • 2) Not subject to change with splenic contraction.
    • 3) May be misleading with preexisting protein abnormalities or concurrent protein losses.
  • d. Urea nitrogen
    • 1) Severe dehydration results in diminished renal function.
    • 2) High BUN is most often an indication of severe dehydration or shock.
  • e. The consensus of several of these determinations provides a much more reliable estimate of the presence and severity of dehydration than any one alone.
  • f. The effectiveness of treatment can be monitored objectively by one or more of these laboratory determinations.
• 4. Evaluating abnormal tonicity of the extracellular fluid.
  • a. No clinical signs indicate hypertonicity or hypotonicity.
  • b. ECF tonicity is related to the concentration of sodium since its related anions represent more than 90% of the electrolytes in the ECF.
  • c. High sodium indicates hypertonic ECF; low sodium indicates hypotonic ECF.
• 5. Evaluating acid-base balance in the patient.
  • a. Clinical signs of abnormal respiration may suggest an acid-base problem but it is difficult to determine if primary respiratory disorders exist or if disturbances seen are normal compensatory reactions to a metabolic disorder.
  • b. Respiratory disorders can only be identified accurately by estimation of carbonic acid in the blood. This is called pCO2. It is a measure of the partial pressure of dissolved gaseous CO2 in the blood. The pCO2 is elevated due to hypoventilation (respiratory acidosis) and is abnormally low due to hyperventilation (respiratory alkalosis).
  • c. Metabolic disorders are reflected in the plasma bicarbonate concentration. Low values indicate acidosis; high values indicate alkalosis.
  • d. The blood pH indicates the severity of the actual derangement in the body. Since it can be disturbed in respiratory disorders as well as in metabolic disorders, it is necessary to know the pCO2 and the bicarbonate to understand how an acid-base disorder developed and how it should be corrected.
  • e. When primary disorders of ventilation can be ruled out with confidence, the plasma bicarbonate value alone is a reliable indication of the presence, severity and character of metabolic acid-base disturbances.
  • f. Most commercial laboratories do a test called "CO2" or "total CO2." This is essentially a measure of bicarbonate, the metabolic factor, and is not, as the term implies, a measure of pCO2, the respiratory component.
• 6. Evaluating potassium status of the patient.
  • a. There are no clinical signs which are a reliable reflection of potassium abnormalities in the patient.
  • b. The electrocardiogram may be helpful but is is not often readily available.
  • c. Even accurate determinations of plasma potassium concentration are sometimes misleading because the vast majority of body potassium is in the ICF, not the ECF, and the ICF cannot be sampled.
  • d. Low serum or plasma potassium usually indicates serious depletion of body potassium.
  • e. Elevated potassium values are usually the result of severe acidosis causing intracellular K+ to more into the ECF. 
• 7. A battery of tests is necessary to answer the four important questions regarding fluid balance in a clinical patient.
  • a. A complete evaluation can be obtained best by a battery of nine tests:
    • 1) PCV, Total Protein, BUN, Na+, K+, Cl+, pH, pCO2, HCO3-.
    • 2) This can be done with a single 5 ml blood sample if it is anticoagulated with heparin. But, it must be drawn anaerobically and the tests must be done promptly. 
  • b. An abbreviated battery of tests is usually more practical:
    • 1) Total Protein, Na+, K+, HCO3- (or "total CO2")
    • 2) This battery can be run on serum or heparinized plasma. The sample need not be anaerobic and the tests need not be run promptly if the serum or plasma is removed from the cells soon after collection.
    • 3) The elimination of pH and pCO2 from this battery presupposes that no primary respiratory disorder is present. 

5.8 FLUID THERAPY PRODUCTS

A. General

• 1. We must know the composition of each product we use in order to use it correctly.
• 2. Composition must be in terms that are comparable with plasma values, i.e., milliequivalents per liter.
• 3. One can predict, from the composition of the fluid, what effect it will have on the patient.

B.Common Fluids

Common fluids can be "spiked" with additional quantities of electrolytes especially needed, e.g., potassium or bicarbonate.

• 1.Sterile, concentrated solutions of potassium chloride and sodium bicarbonate are commercially available for this purpose.
  • a.The concentrates contain approximately 1 mEq/ml.
  • b.Use of these products permits maintenance of sterile conditions.
• 2.Pure potassium chloride and sodium bicarbonate can be obtained and appropriate quantities added to other fluids when additional amounts are needed.
  • a.1 gram of sodium bicarbonate provides 12 mEq. of bicarbonate.
  • b.1 gram of potassium chloride provides 14 mEq. of potassium.
  • c.Sodium bicarbonate cannot be autoclaved. When bicarbonate powder has been added to a sterile solution it must be used without further sterilization. This represents a possible break in sterility.
• 3.When one is "spiking" fluids in this way, the fluid solution is usually quite abnormal in its composition; therefore, it is essential that the final composition of the fluid be known precisely if the administration of dangerous solutions is to be avoided.

C. Increase of Bicarbonate

C.Since bicarbonate cannot be autoclaved, most solutions do not contain this substance. Instead, they contain lactate or acetate ions which can be metabolized by the body. When this happens, endogenous bicarbonate replaces the acetate or lactate given. In this way, stable sterile solutions are available which, indirectly, make it possible to increase the bicarbonate in the body.

5.9 SELECTION AND USE OF FLUIDS AND ELECTROLYTES

5.9.1 Estimating the quantity of fluid required.

• 1.Slight dehydration represents a body fluid deficit of 6-8% body weight.
• 2.Severe dehydration represents a fluid deficit of 10-12% body weight.
• 3.Calculations are simplified if body weight is expressed in kilograms since a kilogram of fluid is one liter.

a.Example of severe dehydration:

500 kg horse with a fluid deficit of 10% body weight = 10% x 500 kg = 50 kg (50 liters) of fluid needed.

b.Example of slight dehydration:

500 kg horse with a fluid deficit of 6% body weight = 6% x 500 kg = 30 kg (30 liters) of fluid needed.

• 4.When unusual losses are continuing, e.g., diarrhea, the deficit is increasing even while replacement has been initiated.
• 5.The estimated requirement for fluid replacement need not be given in a short period of time. Except in critical cases, the calculated requirements can be replaced over a 24 to 36 hour period.

5.9.2 The kind of fluid to give.

• 1.The most conservative fluid therapy consists of using a "balanced" electrolyte solution, i.e., one having the same concentrations of the major electrolytes as normal plasma.
  • a.Such a fluid should not induce abnormalities in the patient.
  • b.It can be given by any route since it is isotonic.
  • c.Since it contains no toxic concentrations of any electrolyte, there is no danger in rapid administration except the danger of volume overload of the vascular system.
  • d.Such a fluid is lactated Ringer's solution.
• 2.This conservative therapy is indicated when there are no peculiar electrolyte disturbances or when there is no way to determine what, if any, electrolyte problems exist. It is not an effective means of correcting severe acidosis, hyponatremia, or hypokalemia.
• 3.When metabolic acidosis is likely, as in severe diarrhea, shock, and intestinal obstruction, and especially when it has been shown by laboratory tests to be a serious problem:
  • a.An unphysiologically high concentration of bicarbonate must be given to raise the low value in the patient to normal.
  • b.When additional sodium is also needed, as indicated by a low sodium value or as is predictable in diarrhea, a very useful solution is obtained by adding 3-5 grams of sodium bicarbonate to each liter of lactated Ringer's solution. The result is a high sodium-high bicarbonate solution ideally suited to the animal's condition.
  • c.If the sodium value is not low the fluid given should be high in bicarbonate but not abnormally high in sodium. such a solution is isotonic sodium bicarbonate or isotonic sodium lactate.
  • e.Correction of acidosis can be accomplished by the administration of very hypertonic solutions of sodium bicarbonate (5% NaHCO3 in saline) in relatively small quantities (2-3 L/500 kg). This must be accompanied by the administration of large quantities of balanced solutions such as lactated Ringer's.
  • f.When it is desirable to estimate the needs of the patient for bicarbonate, the following formula is useful:
• 1)HCO3- deficit/L x ECF (liters) = mEq. needed.
• 2)HCO3- deficit/L = Normal HCO3- - Patient HCO3- (This value is approximately 15 mEq/L in severe acidosis)
• 3)ECF = Body weight (kg) x 0.3. (The factor 0.3 is somewhat greater than the actual figure for ECF to insure adequate replacement).
• 4)Example: A 450 kg horse is severely dehydrated and severely acidotic. What are its fluid needs?
  • a)fluid volume requirement = 10% body weight = 10% X 450 kg = 40 - 50 liters of fluid.
  • b)Severe acidosis requires treatment with bicarbonate - how much is needed?

Patient HCO3- = 12 mEq/L

Normal HCO3- = 24 mEq/L

HCO3- deficit = 12 mEq/L

ECF est. - 0.3 x 450 kg = 135 L

HCO3- needed = 12 mEq/L x 135 L = 1620 mEq.

• c)Patient needs are estimated as 40-50 liters of fluid and 1500-2000 mEq of bicarbonate.
• d)Treatment Method #1: 3 liters of 5% NaHCO3 (1800 mEq) + 37 liters of balanced electrolyte solution.
• e)Treatment Method #2: 40 liters of balanced electrolyte solution supplemented with 3-4 grams of NaHCO3/L = 1500-2000 mEq NaHCO3.

• 4.Severe hypokalemia, potassium values less than 2.0 mEq/L, may require treatment with high potassium solutions.
  • a.Specific treatment is indicated if marked weakness or depression is seen.
  • b.It is probably not necessary if the animal has begun to eat since hay is high in potassium.
  • c.High concentrations of potassium should be administered with caution since the heart is so sensitive to slight elevations in serum potassium levels.
  • d.Supplementation of lactated Ringer's solution with 10 to 50 mEq/L of potassium chloride (1-3 grams/L) may be useful. The solutions containing 20-50 mEq/L should be given very slowly.
  • e.Potassium supplementation can also be done, with much greater safety, by oral administration of potassium chloride. Thirty grams in 8 liters of water, 2-3 times per day has been recommended.
  • f.Hyperkalemia is usually associated with acidosis and prompt correction of the acidosis usually corrects the hyperkalemia without the administration of potassium supplements.
• 5.When peculiar electrolyte derangements have developed, peculiar fluids must be used to correct the problem promptly.
• a.Such fluids are very unphysiological; while especially suited for their intended purpose, they are apt to induce severe abnormalities when used carelessly.
• b.The more unusual a fluid is, the more essential it is to be certain it is indicated.
• c.When objective patient evaluation by laboratory tests is not available, a more conservative (possibly less effective) fluid must be chosen.

5.9.3 The route for fluid administration

• 1.In severe dehydration, a major proportion of the fluid should be given intravenously.
• 2.Additional large quantities can be provided per os. This fluid is usually beneficial except in patients with intestinal obstruction.
• 3.Subcutaneous and intraperitoneal injections of fluid are not widely used in the horse but can be beneficial in smaller animals.

5.9.4 Miscellaneous Topics

• 1.An average daily intake of hay contains more potassium than 100 liters of lactated Ringer's solutions. Consumption of normal feed is the best way to replace potassium deficits. This also shows why potassium depletion is frequent in animals that are not eating.
• 2.Natural feeds contain very little sodium. Supplemental salt must always be available to herbivores. This is especially true when increased needs are present.
• 3.Water should always be available to dehydrated animals. Sometimes they will consume far more fluid voluntarily than can be given by any other means.
• 4.Electrolytes can be added to water for voluntary consumption, or administered by stomach tube. Do not make hypertonic solutions for oral use. Do not fail to provide pure water at all times as an alternative to electrolyte-containing water. It would be harmful to reduce water intake by the addition of repelling substances to the water.

5.9.5 Summary

• 1. Evaluate the patient objectively if possible.
• 2.Estimate the quantity of fluid that should be given.
• 3.Use balanced electrolyte solutions routinely.
• 4.When special problems can be anticipated, use special solutions.
• 5.Metabolic acidosis usually requires special attention.