Electrolyte and acid-base disturbances are relatively common in different clinical situations and require accurate evaluation, treatment and monitoring.

A thorough understanding of the interactions between the acid-base balance, electrolytes and homeostasis of body fluids, as well as the possible consequences of the different treatments is required. The lack of this knowledge can transform a successful diagnosis in a therapeutic failure with serious consequences for the patient. However, there are some basic rules that can simplify an issue that sometimes seems intricate.

Bases of Interpretation of Blood Gases

Normal pH values vary with the species and the laboratory, so you should know the reference values for your conditions. In general the following values are supported:

The interpretive approach must be done in orderly steps: Build a table of 3 rows and 3 columns and label the columns from left to right as acidosis, normal and alkalosis.

Evaluate the pH, acid (<7.35), normal (7.35–7.45) or alkaline (>7.45) and place these data in the corresponding column in the second row. Evaluate the respiratory component or PCO₂. According to the equation for calculating the systemic pH

pH = pK + log [HCO₃^-]/PCO₂

The pH will vary inversely to the PCO₂; hypocapnia is accompanied by alkalosis and hypercapnia with acidosis. Then place the PCO₂ component in the 3rd row below the corresponding column. Finally, we evaluate the metabolic component; HCO₃ varies in direct proportion to the pH. If HCO₃<18 mEq/L, the patient has metabolic acidosis and metabolic alkalosis when the HCO₃>24 mEq/L, and place this component in the corresponding column.

For example:

pH=7.26
PCO₂=40 mm Hg
HCO₃^-=15 mEq/L

The interpretation is metabolic acidosis without respiratory compensation. When we evaluate blood gases at this time we proceed to assess the degree of hypoxemia or PaO₂ and tissue hypoxia or anaerobic metabolism but we are not going to include this part of the patient evaluation in this summary.

Metabolic Acid-Base Imbalance

The most common causes of metabolic acidosis include lactic acidosis (shock), diabetic ketoacidosis, azotemia and uremia, toxins such as salicylates, methanol and ethylene glycol and hyperchloremic acidosis caused from the loss of bicarbonate-rich fluids secondary to severe diarrhea and pyelonephritis. Metabolic alkalosis usually presents in association with hypochloremia. It can either be non chlorine respondent like in the cases of hyperaldosteronism or primary hypoadrenocorticism and chlorine respondent which usually are secondary to gastric vomits, diuretic therapy and post-hypercapnia.

Treatment

The priority is to restore the cardiovascular stability and to correct the water deficit; this reduces acidosis by promoting aerobic metabolism, hepatic metabolism of lactic acid, increasing glomerular filtration rate and renal excretion of H⁺. For this purpose we perform what is known as end-goal directed therapy (EGDT) by fluid volume load. We administer a 10 to 15 ml/kg Ringer lactate bolus in 6 minutes for previously healthy adult dogs or in 10 minutes for puppies, cats and patients with congestive heart failure. Then, we control our target parameters or 100 mm Hg, Presión arterial media PAM >60–80 mm Hg, rellene yugular <2 segundos, reducción de la diferencia entre la temperatura central y periférica DT">goals after 5 minutes (FC 100–110, FR 20–40), systolic blood pressure >100 mm Hg, mean arterial pressure MAP >60–80 mm Hg, jugular refilling time <2 seconds, delta temperature TD<4 (the gap between the central and peripheral temperature), improving the level of conscience and lactate clearance).These boluses will be repeated until we achieve normal venous pressure, which we evaluate by the jugular refilling time which must be less than 2 seconds. If the venous pressure is corrected but not the MAP or tissue perfusion values, we should evaluate cardiac inotropism, the presence of arrhythmias and peripheral vascular resistance. In diabetic patients with ketoacidosis, fluid load reduces glycemia by 30–50% and the concentration of proglycemic hormones thus increasing the cellular response to insulin and the metabolization of ketoacids. In chronic cases (clinical signs of decompensation >48 hours), it is very important to consider plasma osmolality in order to adjust the therapeutic measures. Plasma osmolarity is calculated by the following formula:

Osmolarity = 2 (Na + K) + glucose/18 + BUN/2.8

Normal plasma osmolarity is 290 to 310 mOsm/L in dogs and 308 to 335 mOsm/L in cats. Hyperglycemia with hyperosmolarity causes hyponatremia. When hyperglycemia is chronic, cells accumulate idiogenic (amino acids) osmoles, so that the osmotic pressure between the intracellular and extracellular components is balanced. In these patients rapid correction of osmolarity produces acute cellular edema which can result in permanent neurological damage.

Therefore it is very important in chronic ketoacidosis patients to slowly correct the plasma osmolality in at least 24 hours. Fluid therapy starts with the EGDT, as soon as the primary goals are achieved we should calculate the amount of fluid needed to correct dehydration and sensitive and insensitive losses which should correct within 24 hours. The correction of tissue perfusion allows hepatic metabolization of ketoacids and renal partial excretion of glucose excess, thus decreasing proglycemic hormones such as cortisol and adrenaline production. Fluid therapy also allows partial restoration of sodium deficit, which along with the metabolic elimination of idiogenic osmoles reduces osmolar shock.

Insulin treatment is incorporated then after 4 hours of initiation of fluid therapy and only when potassium is in the high normal range. The goal is to maintain blood glucose above 250 mg/dl during the first 4 to 6 hours in order to allow the replacement of sodium and full glucose correction within 24 to 36 hours.

[Base deficit x body weight (kg)]/4 = mEq of bicarbonate deficit

There is another more conservative formula for calculating the dose of bicarbonate
0.4 x body weight (kg) x (12 - HCO₃^- measured) = replacement dose in mEq

However as a result of the possible adverse effect of bicarbonate:

 Iatrogenic alkalosis

 Tissue hypoxia because it increases the hemoglobin oxygen affinity

 Hypocalcemic tetany: rapid correction of acidosis decreases ionized calcium

 Hyperosmolarity: 8.5% solution = 1500 mOsm

 Paradoxical cerebral acidosis, dissociated CO₂ diffuses the hematoencephalic membrane much faster than the HCO₃.

The following guidelines are followed to administer sodium bicarbonate

1.  Do not routinely treat minor bases deficit <10 mEq/l.

2.  Do not treat arterial pH greater than 7.20 unless there is cardiovascular instability and only after correcting tissue perfusion.

3.  When the administration is considered necessary, calculate the deficit and administer only a quarter to a half of the total calculated dose and repeat blood gases in 5 to 10 minutes.

The most common treatment for metabolic alkalosis is correcting the underlying electrolyte imbalance (potassium or chloride); generally, this is sufficient to achieve adequate correction of acid-base status. When this is not enough, ammonium chloride can be administered using the same formula described for bicarbonate and sometimes we can also infuse diluted hydrochloric acid solutions.

References

1.  Shapiro BA, Harrison RA, Cane RD, Templin R. Clinical Application of Blood Gases. 4th edition. St. Louis: Year Book Medical Publishers Inc. 1989. Médica Panamericana Editorial.

2.  Harold D. Arterial and venous blood gases. In: Wingfield WE, Raffe MR, eds. The Veterinary ICU Book. Jackson, WY: Teton NewMedia; 2002.

3.  DiBartola SP. Fluid, Electrolyte and Acid-Base Disorders in Small Animal Practice. 3rd edition. Philadelphia, PA: Saunders; 2005. Veterinary Editions Multimédica.