Page 564 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

552 FLUID THERAPY

QRS complex; and a small, wide, or absent P wave effect within 20 to 30 minutes. Dextrose (1 to 2 g/unit
(Figure 22-1). Severe hyperkalemia can lead to a of insulin as an IV bolus, then 1 to 2 g/unit of insulin in
sinoventricular rhythm, ventricular fibrillation, or stand- intravenous fluids administered over the next 4 to 6
still. Muscle weakness may be present with a serum potas- hours) is necessary to prevent hypoglycemia when insulin
sium concentration above 8 mEq/L. 18 Characteristic is used. Dextrose induces endogenous insulin release in
EKG changes may require emergency therapy before nondiabetic patients and can be used to control mild to
results of serum potassium concentration are available. moderate hyperkalemia without concurrent insulin
Pseudohyperkalemia may occur ex vivo if the red cell administration at a dose of 0.25 to 0.5 g/kg IV.
potassium content is high, as in Akita dogs. Metabolic acidosis from mineral acids causes an extra-
þ
Calcium gluconate 10% (0.5 to 1.0 mL/kg IV to cellular shift of K as H increases intracellularly. Correc-
þ
effect, given slowly) can be used in critical situations to tion of metabolic acidosis with bicarbonate allows an
restore cardiac membrane excitability, but it does not intracellular shift of K þ as the H þ is combined with

decrease potassium concentration. During infusion the HCO 3 and removed. The dose of sodium bicarbonate
ECG must be monitored, and the infusion slowed or used to treat hyperkalemia is based on the base deficit,
stopped if the arrhythmia worsens. The cardiac effects or 1 to 2 mEq/kg IV over 10 to 20 minutes. Sodium
should be apparent within minutes. Despite a rapid onset bicarbonate is contraindicated if partial pressure of car-
of action, the duration of its effect is less than 1 hour. 15 bon dioxide (PCO 2 ) is elevated or metabolic alkalosis is
Calcium administration increases the risk of soft tissue present, and it may cause hypernatremia or paradoxical
mineralization if hyperphosphatemia is present. CNS acidosis. If the ionized calcium concentration is
Several methods can be used to translocate potassium low, dextrose is preferred to bicarbonate because
10
intracellularly. Regular insulin (0.5 units/kg IV) has an alkalemia exacerbates hypocalcemia.

HYPERKALEMIA
5.5 to 6.5 mEq/L 6.5 to 8.0 mEq/L 8.0 to 10.0 mEq/L > 10.0 mEq/L
Potassium
EKG Normal Peaked T wave Absence of P wave Sinoventricular rhythm
Prolonged PR interval
Tall, peaked T wave Atrial standstill Biphasic QRS complex
Findings Prolonged P wave
with narrow base Intraventricular block Ventricular flutter
Appearance of Decreased amplitude Ventricular fibrillation
specific EKG of P wave Fascicular blocks Ventricular asystole
abnormalities is Widened QRS complex Bundle branch blocks
highly variable Depressed R wave QRS axis shift
and is not likely amplitude Progressive widening
precisely to K+ Depressed ST segment of QRS complex
concentration Q-T interval shortening Sinoventricular rhythm
listed (sine-wave pattern)
Conduction Increased myocyte
changes excitability
Shortened myocyte Prolonged membrane
action potential depolarization
Increased slope of Slowed myocardial
action potential conduction Shortened repolarization

EKG
examples
Mechanism
Treatments IV Fluids (no K + ) Dilution, removes k +
Onset
Furosemide 1-4 mg/kg IV Removes K +
15-30 min Sodium bicarbonate 1-2 mEq/kg IV slowly over 15 minutes Translocation
< 1 hr Dextrose 1 g/kg IV Translocation
30 min Regular insulin 0.5 u/kg IV + 2 g dextrose per unit insulin IV Translocation
20-40 min B-agonist – terbutaline 0.01 mg/kg IV slowly Translocation
3-5 min 10% Calcium gluconate 0.5-1.5 mL/kg IV slowly Membrane stabilization
Hours to days Polystyrene 2 g/kg in 3-4 divided doses PO Removes K +
15 min Dialysis (hemo or peritoneal) Removes K +
Figure 22-1 Clinical features of hyperkalemia and recommended treatment.