Page 321 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

312 ACID-BASE DISORDERS

and respiratory acidosis resulting from diaphragmatic dogs, mixed metabolic alkalosis and respiratory alkalosis
compression by the distended stomach. 37 are more common in patients with chronic respiratory
A recent study evaluated the acid-base balance of disease placed on diuretics. Severe alkalemia is only likely
neonatal dogs over the first hour following birth under to occur in dogs with long-standing respiratory acidosis

normal birthing conditions, following dystocia and fol- and a compensatory increase in [HCO 3 ] that are placed
lowing birthing assisted by oxytocin administration. It on a ventilator. This maneuver acutely lowers PCO 2 ,

was shown that independent of how the dogs were born, whereas [HCO 3 ] remains high for approximately 24
all had respiratory and metabolic acidosis 5 minutes fol- hours. 22 Severe alkalemia also was observed in dogs with
lowing birth. The ecbolic effect of oxytocin aggravated severe canine babesiosis caused by Babesia canis rossi. 30
the metabolic component of the acidosis compared with Because most patients with this mixed disorder have
the other two birthing groups. Regardless of the metabolic alkalosis superimposed on chronic respiratory
conditions of birth, the hypercapnia resolved within 1 alkalosis, therapy usually is directed at correcting the met-
hour, but the metabolic component (reflected in the base abolic alkalosis. In addition, compensation for simple
deficit) persisted. It was concluded that at birth a mixed chronic respiratory alkalosis is so effective that the pH
respiratory metabolic acidosis is present and that adverse is usually normal. Therefore correction of the metabolic
events during birthing aggravate acid-base balance. 32a alkalosis will be associated with normalization of pH even
Systemic pH is very low in patients with combined if the chronic respiratory alkalosis cannot be treated. The
metabolic and respiratory acidosis, and specific therapy goal of treatment in metabolic alkalosis is to replace the
6
must be initiated quickly. In those patients in which lac- chloride deficit while providing sufficient potassium
tic acidosis is the cause of metabolic acidosis, tissue hyp- and sodium to replace existing deficits. Dehydrated
oxia is the most likely underlying cause, and therapeutic patients should be rehydrated accordingly. Definitive
measures should be taken to augment oxygen delivery treatment of the underlying disease process prevents
to the tissues and to reestablish cardiac output. 33 Patients recurrence of the metabolic alkalosis.
should be artificially ventilated if necessary. This will
reduce PCO 2 and increase pH. Sodium bicarbonate is Hyperchloremic and High-AG
not indicated to treat patients with metabolic acidosis that Metabolic Acidoses
also have respiratory acidosis because they cannot excrete This mixed disorder usually is seen in patients with renal
the CO 2 generated by NaHCO 3 administration. The failure, in the resolving phase of ketoacidosis, or in
CO 2 will diffuse into the cells and further decrease intra- patients with high-AG acidosis that develop diarrhea or
cellular pH. Sodium bicarbonate may be considered in receive fluid therapy (see Box 12-7). The pH and

ventilated patients with [HCO 3 ] less than 5 mEq/L [HCO 3 ] are low, and the diagnosis is suggested by an
because at this concentration even a small decrease in increase in unmeasured anions and a chloride gap of less
serum bicarbonate is associated with a large decrease in than 4 mEq/L (see Table 12-4).
serum pH. 20 In this situation, small titrated doses of Human patients with chronic renal failure (serum cre-
NaHCO 3 are used as a temporizing measure to maintain atinine concentration of 2 to 4 mg/dL) initially develop

[HCO 3 ] greater than 5 mEq/L while attempts to hyperchloremic acidosis. With progression of the disease
improve oxygenation are continued. (See Chapter 10 (serum creatinine concentration of 4 to 14 mg/dL), met-
for further discussion of lactic acidosis.) abolic acidosis progresses, but the further decrease in
total CO 2 is associated with an increase in unmeasured
Respiratory Alkalosis and strong ions (e.g., sulfate, acetate) and hyperpho-
Metabolic Alkalosis sphatemia, whereas hyperchloremia remains

This mixed disorder is commonly present in human unchanged. 60 However, human patients with advanced
patients with hepatic failure or in those with congestive renal failure sometimes may have a simple acid-base disor-
47,56
heart failure and pulmonary edema who are treated with der, either hyperchloremic or high-AG acidosis.
diuretics. These patients have low PCO 2 , high [HCO 3 ], Patients with diabetes mellitus may have a mixed high-

and high pH, and their alkalemia may be severe. Similar AG and hyperchloremic acidosis because of development
clinical conditions also occur in small animal medicine of diarrhea or in the resolving phase of the ketoacidotic
(see Box 12-7), but severe alkalemia is not common. crisis. 47,56 Hyperchloremia in the recovery phase
Mixed respiratory and metabolic alkalosis was not develops for at least three reasons: (1) large volumes of
observed in a study of 20 dogs with alkalemia identified saline are administered; (2) KCl is infused in large doses;
from 962 dogs in which blood gas analysis was and (3) ketones are lost in the urine and NaCl is
performed. 48 In dogs with experimental metabolic alka- reabsorbed by the kidneys. 40 As discussed earlier, human
losis, superimposition of chronic respiratory alkalosis patients with chronic hepatic disease may have enhanced
causes a decrease in [HCO 3 ] sufficient not only to pre- proximal renal tubular sodium reabsorption that may

vent development of significant alkalemia but also to off- limit distal H þ secretion. 5 This may lead to
set entirely the effect of hypocapnia on plasma [H ]. 34 In hyperchloremic acidosis, decreased lactate metabolism,
þ