Page 418 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

408 FLUID THERAPY

Hypoproteinemia also may affect the balance between concentration of inhalants, and a higher dose may be
hydrostatic and colloid osmotic pressure, leading to required to maintain anesthesia. 180
increased loss of fluid from the capillaries. This effect is
of particular concern to the anesthetist because it may HYPOKALEMIA
increase the likelihood of pulmonary edema formation. Hypokalemia can lead to muscle weakness, cardiac
Total plasma protein and colloid osmotic pressure typi- arrhythmias, hypotension, and renal insufficiency with
cally decrease during anesthesia in dogs whether or not associated metabolic acidosis in dogs and cats. In patients
fluids are administered. 52,198 Clinically, this effect is of with mild hypokalemia but no clinical signs and no identi-
limited importance unless there is a strong possibility that fiable underlying cause, it probably is unnecessary to treat
left atrial pressure is increased (e.g., low oncotic pressure the animal. The patient with hypokalemia that is likely to
in an animal with mitral regurgitation). have a whole-body deficit of potassium should be treated
to correct this deficit if possible. The usual recommenda-
HYPERPROTEINEMIA tion is to correct the deficit at a maximal rate of 0.5 mEq/
Increased plasma protein concentration is of concern only kg/hr, although higher rates can be used if a severe deficit
as a sign of hypovolemia. In normally hydrated dogs and of total body potassium is suspected (up to 1.0 mEq/kg/
cats with hyperproteinemia, it is the globulins that are hr). If the hypokalemic patient must be anesthetized, it is
increased, and this fraction has less impact on protein important to monitor for cardiac arrhythmias and to rec-
binding of drugs and oncotic pressure than does albumin. ognize that the heart will be refractory to class I antiar-
However, hyperproteinemia may be a cause of pseudohy- rhythmic drugs (e.g., quinidine, procainamide,
ponatremia if the total protein concentration exceeds lidocaine) and more sensitive to the toxic effects of digi-
10 g/dL. talis glycosides. Hypotension may occur because there is a
decrease in systemic vascular resistance possibly related to
HYPONATREMIA decreased sensitivity to angiotensin II. 66 The pressor
Rapid correction of hyponatremia may be necessary to response to norepinephrine is normal. If muscle relaxants
treat cerebral edema (usually only when serum sodium are to be used, it is prudent to start with a dose that is 30%
is <130 mEq/L). With acute hyponatremia, rapid cor- to 50% lower than the normal dose and titrate the final
rection may not cause any complications in the brain, dose to effect. Care should be taken administering glu-
but with chronic hyponatremia, a rapid change in serum cose, sodium bicarbonate, or b 2 -agonists because they
sodium concentration can lead to an osmotic demyelin- tend to decrease serum potassium concentration. If a
ation syndrome or myelinolysis occurring one to several potassium-supplemented solution is to be used during
days after therapy. 111,131 In both acute and chronic anesthesia to correct the deficit, it should be used in con-
situations, the rate of change should be approximately junction with a solution containing a normal concentra-
0.5 to 1 mEq/hr unless the patient is manifesting signs tion of potassium (4 to 5 mEq/L), and the two solutions
of cerebral edema, in which case initial therapy with 3% should be clearly labeled. If the animal requires a bolus of
saline may be used to increase serum sodium concentra- fluid during anesthesia, the solution with normal potas-
tion by 5 to 6 mEq/L over 2 to 3 hours. Ideally, sium concentration should be used, thus reducing the risk
hyponatremia should be corrected before surgery; how- of iatrogenic hyperkalemia. Solutions containing more
ever, given the required time frame, this is not always pos- than 60 mEq/L of potassium should be given via a cen-
sible. Therefore the anesthetist must be prepared to tral vein.
monitor changes in serum sodium concentration care-
fully to prevent myelinolysis. It may be necessary to HYPERKALEMIA
administer a diuretic to facilitate excretion of free water Hyperkalemia also is associated with muscle weakness and
(see Chapter 3). cardiac arrhythmias. If these signs are present, it is crucial
to reduce the effects of hyperkalemia even though it is not
HYPERNATREMIA possible to reduce total body potassium content without
Rapid correction of hypernatremia can lead to acute cere- treating the primary condition (e.g., oliguric renal failure,
bral edema. If the patient is severely hypovolemic, it is urethral obstruction). Animals with moderate
important to correct that deficit using a solution with a hyperkalemia (6 to 7 mEq/L) are more likely to develop
sodium concentration similar to that of the patient. arrhythmias during anesthesia even if they have not
If the animal is not severely dehydrated and the serum demonstrated electrocardiographic abnormalities earlier.
sodium exceeds 165 mEq/L, correction should proceed Therapy for hyperkalemia includes administration of cal-
slowly to achieve a rate of change of 0.5 to 1 mEq/hr cium to alter the threshold potential of cells, sodium
using 0.45% NaCl or 5% dextrose. In dogs, administra- bicarbonate to alter the flux of potassium across the cell
tion of 5% dextrose at 3.7 mL/kg/hr should decrease membrane, and glucose to facilitate movement of potas-
the serum sodium concentration by 1 mEq/hr. sium into cells. Insulin may be used with glucose to pre-
Hypernatremia may increase the minimum alveolar vent hyperglycemia, but the blood glucose concentration