Hyperkalaemia

Hyperkalaemia can occur due to the following causes listed in Table 1.

Table 1. Causes of hyperkalaemia

Hyperkalaemia makes the resting membrane potential less negative, reducing the threshold potential. This initially results in a more excitable cell; however, if the resting membrane potential is greater than threshold potential, depolarisation results but repolarisation cannot occur, and the cell becomes less excitable. This results in a bradyarrhythmia with ECG changes of tented T waves, short QT interval, prolonged PR interval, widening of QRS complex, decreased amplitude and widening of P waves.

Muscle weakness can also occur due to hyperkalaemia due the same mechanisms of cardiac arrhythmias, resulting in reduced cellular excitability.

Another complication of hyperkalaemia is acidaemia. As the serum potassium concentration increases, it causes intracellular movement of potassium in exchange for an extracellular movement of hydrogen ions. Therefore, part of the life-threatening condition associated with hyperkalaemia is also the acidaemia.

Treatment for hyperkalaemia should be considered with a potassium of >6.0 mmol/L. The severity of the ECG changes will depend on the chronicity of the disease, therefore some animals may display clinical signs, while some may not. Treatment options for hyperkalaemia are described in Table 2.

Table 2. Treatment options for hyperkalaemia

When considering the treatment options, consider the severity of hyperkalaemia and its clinical signs, how quickly you want to resolve it, and what the underlying condition is. If the hyperkalaemia is life-threatening, the first step is to administer calcium gluconate, as it will stabilise the resting membrane potential within 5–15 minutes. It does not treat the hyperkalaemia itself, but instead treats the life-threatening arrhythmia.

If the patient is in shock, the next step would be to treat the shock with a fluid bolus. When considering the type of fluids, Hartmann's is recommended over 0.9% NaCl, as 0.9% NaCl has a higher concentration of chloride contributing to acidosis. Hartmann's has a lower concentration of chloride; and in addition, lactate, which acts as a buffer which will help reverse any acidosis if present.

Insulin and glucose will cause intracellular movement of potassium, lowering the serum concentration. If the patient is only mildly hyperkalaemic or not showing clinical signs of hyperkalaemia, the author gives glucose without insulin, as insulin administration will cause hypoglycaemia. The glucose must be diluted 1:1 with Hartmann's or water for injection as the hyperosmolality can cause phlebitis. However, in more life-threatening hyperkalaemia, regular insulin (Actrapid®) is indicated with concurrent glucose bolus followed by 2.5–5% glucose in the intravenous fluids, with blood glucose monitoring. The type of insulin must be a short-acting insulin, which the most commonly available brand is Actrapid®.

Sodium bicarbonate is reserved for refractory hyperkalaemia (unresponsive to the above treatment) or in severe metabolic acidosis (pH<7.0). The bicarbonate will cause intracellular movement of potassium, lowering the serum concentration. The reason bicarbonate is resolved for severe cases is as sodium bicarbonate can have side effects.

Another option for refractory hyperkalaemia is intravenous terbutaline, which causes intracellular translocation of potassium via the Na⁺/K⁺-ATPase pump.

Once the patient is cardiovascularly stable, address the underlying cause. If there is a urethral obstruction, pass a urinary catheter; if there is uroperitoneum, place a urinary catheter and abdominal drain (the author’s preference is a Mila chest drain placed in the abdomen). Discontinue any drugs which will cause iatrogenic hyperkalaemia (e.g., spironolactone, IV potassium supplements). If the hyperkalaemia is due to acute kidney injury, consider a diuretic such as furosemide. If the hyperkalaemia is associated with acidaemia, treat the underlying acidosis.

If life-threatening hyperkalaemia persists despite the above therapeutics, peritoneal dialysis or haemodialysis is recommended.

Hypokalaemia

Hypokalaemia can occur due to causes listed in Table 3.

 Table 3. Causes of hypokalaemia

Clinical signs of hypokalaemia are uncommon, but can occur if potassium concentration is <2.5 mmol/L. Potassium is necessary for maintenance of normal resting membrane potential. Therefore, one of the most common clinical sign of hypokalaemia is neuromuscular weakness, including a plantigrade stance, ventral flection of the neck, wide based stance, stiff hind limbs and hypermetria of the fore limbs. Severe cases can result in respiratory arrest from neuromuscular weakness. Myocardial cells are also affected, due to a high intracellular/extracellular potassium concentration ratio inducing a state of electrical hyperpolarisation, leading to prolongation of the action potential. Thus, atrial and ventricular tachyarrhythmias, atrioventricular dissociation and ventricular fibrillation can occur. Classical ECG signs can include peaked P wave, prolonged PR interval, ST segment depression, decreased T wave amplitude and widening of QRS complex. Due to the change in action potential, hypokalaemia-associated arrhythmias can be resistant to type I antiarrhythmics (e.g., lidocaine). Metabolic consequences of hypokalaemia include glucose intolerance, where there is reduced release of insulin from the pancreas. Severe hypokalaemia can also inhibit normal renal tubular function. And, metabolic alkalosis can occur due to intra- extracellular exchange of hydrogen ions.

Treatment involves intravenous administration of potassium chloride (KCl) (or potassium phosphate if concurrent hypophosphataemia is also present). Intravenous KCl should not be administered at a rate greater than 0.5 mmol/kg/h, due to adverse cardiac effects. Table 4 lists the recommended potassium concentration to be added to a 1L bag of fluids, and the maximum rate it can be administered at. In the rare circumstance that the hypokalaemia is life threatening, potassium can be delivered at a faster rate with careful ECG monitoring. It's worth noting that when adding potassium to a bag of fluids, the potassium should be mixed well to prevent large concentrations of potassium at the bottom of the bag. In addition, all fluid bags should be labelled to prevent accidental blousing of potassium-containing fluids. Another important point is that potassium is very hyperosmolar and can cause thrombophlebitis, therefore should not be administered through a peripheral catheter at concentrations greater than 60 mmol/L. If higher concentrations are required, a long stay (e.g., jugular catheter) should be used; or another alternative is to have two IV catheters so each IV catheter is delivering half the concentration. If the patient can tolerate oral potassium supplementation, oral potassium supplementation can be given at 2–44 mmol per dog (depending on size) or 2–8 mEq per cat, divided over 24 hours.

Table 4. Potassium (K⁺) dosing for correction of hypokalaemia

References

References are available upon request.