An estimated 12% of blocked cats present with hyperkalemia, which can range from clinically insignificant ([K+] 5 to 6 mEq/L)
to fatal ([K+] ≥ 9 mEq/L).1 Potassium increases secondary to decreased GFR, which causes ineffective excretion of potassium from the kidneys in the
distal tubules as well as an inability of the kidneys to excrete the potassium in the urine.3 Because this is a potentially deadly problem, measure serum potassium concentrations in every patient with urethral obstruction.
Figure 1. The normal cardiac cell action potential (black line). The normal resting cell membrane potential is approximately
-70 mV. The normal threshold cell membrane potential is approximately -50 mV. All cells at rest have high intracellular potassium
concentrations and high extracellular sodium concentrations. All channels allow for movement of ions from an area of high
concentration to an area of low concentration. The green line indicates alterations that occur when the body is hyperkalemic.
As potassium concentration rises, the body reacts by moving potassium intracellularly through the effects of insulin, epinephrine,
and the increased potassium concentration in the extracellular fluid.3 Additionally, the body increases renal excretion of potassium through the effects of aldosterone.3-5 Increases in the intracellular concentration of potassium cause the resting membrane potential to become less negative (i.e. greater than the standard resting membrane potential of -70 mV) (Figure 1). The increased resting membrane potential inactivates both fast sodium channels (making it more difficult for the cell to
depolarize) and sodium/potassium ATPase pumps, which typically work to maintain the normal gradient of sodium and potassium
on either side of the cell membrane.5 When the cells of the atria are affected, they become unable to control automaticity of the heart and arrhythmias can result
(Table 1), culminating in sinus arrest, a ventricular escape rhythm, and death.
In clinical cases, the classic arrhythmias are often not seen at all or are seen at unexpected potassium concentrations. This
is because other metabolic abnormalities—such as hypocalcemia, acidosis, and hypermagnesemia—can interact with potassium or
can directly affect ECG results. Hypocalcemia prolongs the plateau phase of the action potential, resulting in prolongation
of the S-T and Q-T intervals.3,5 In one study, 34% of obstructed cats were hypocalcemic.2 Acidosis, which occurs in about 40% of obstructed cats, occurs because of the acidifying effects of the uremic acids coupled
with an inability to excrete hydrogen ions.2 The body reacts to acidosis by moving hydrogen ions into cells in exchange for moving potassium ions out of cells, thus
increasing serum potassium concentrations and potentially altering the ECG. Acidosis also causes release of calcium into the
bloodstream, which alters ECG findings.5 Finally, some obstructed animals have increased serum magnesium concentrations, which also can alter the ECG results.5
Table 1 ECG Abnormalities Noted Experimentally at Differing Serum Potassium Concentrations*
Treating hyperkalemia. The definitive treatment for hyperkalemia is to reestablish urine flow and GFR either by passing a urinary catheter or otherwise
diverting or removing the urine. Other treatments for hyperkalemia involve intravenous fluid therapy alone or in addition
to drugs. Drug options for hyperkalemia include dextrose or insulin and dextrose (to reduce the serum potassium concentrations),
sodium bicarbonate (to reduce the serum potassium concentrations), or calcium gluconate (to reduce the effects of hyperkalemia
on the heart). See Table 2 for dosing recommendations.
Table 2 Drug Dosages for Treating Hyperkalemia
Intravenous fluids dilute the potassium and lower its serum concentration. In addition, fluids increase excretion through
the kidneys by increasing GFR. In cases in which the obstruction was easily removed and the cat seems metabolically stable
(no cardiac effects; cat is not obtunded), fluids may be the only treatment required to reduce the potassium.
Administration of dextrose (which stimulates endogenous insulin production by pancreatic beta cells) or insulin with dextrose
leads to insulin binding to its receptor. This in turn activates the sodium/potassium ATPase pump, which moves potassium into
the cell, transiently reducing hyperkalemia and reestablishing the extracellular to intracellular potassium gradient so that
cells can repolarize and therefore depolarize again.4
Sodium bicarbonate is given to reduce the pH in the extracellular space. This stimulates the exchange of intracellular hydrogen
ions for extracellular potassium ions to reduce the pH in the extracellular space.4 The exact mechanism for this exchange is unknown, but the net effect is to move potassium into the cell, again reestablishing
the extracellular to intracellular potassium gradient.4
Calcium gluconate works differently—it increases the cell's threshold membrane potential and, thus, reestablishes the cell's
ability to normally depolarize despite its increased resting membrane potential.3 Calcium gluconate does not directly alter the serum potassium concentrations.
While all these treatments will work to protect against the ill effects of excessive potassium, sodium bicarbonate has the
highest risk of creating iatrogenic complications and should be avoided in all but severely acidotic patients (i.e. pH < 7.1).