Potassium, phosphorus, and calcium treatment of severe abnormalities (Proceedings)
Potassium concentration is very commonly abnormal in critically ill patients. Most of the potassium in the body is located in the intracellular fluid compartment (140 mEq/L; 55 mEq/kg) while very little of it is located in the extracellular fluid compartment (4 mEq/L; 1 mEq/kg). Repolarization of electrically excitable cells is largely attributed to the rapid efflux of potassium. Resting membrane potential is determined by the equilibrium between potassium moving out of the cell in response to the intracellular-to-extracellular potassium gradient, and potassium moving back into to the cell in response to the extracellular-to-intracellular electronegativity.
HyperkalemiaHyperkalemia is primarily caused by oliguric/anuric renal disease, hypo-adrenocorticism, and iatrogenic causes. It may also be caused by rhabdomyolysis, metabolic (inorganic)/respiratory acidosis, periodic familial hyperkalemia. It may also be falsely elevated if the blood sample is not analyzed for a period of time due to hemolysis (only in the Akita dog) or from platelet or white cell degradation (only in severe thrombocytosis or leucocytosis).
Causes of hyperkalemia
Hyperkalemia causes membrane hypopolarization which may result in extrasystoles/fibrillation if the resting membrane potential is slightly more negative than threshold potential or asystole when resting membrane potential is slightly less negative. Hyperkalemia also increases potassium permeability which augments the repolarization phases of the electrocardiograph (tall, tented, narrow T-wave) and diminishes the depolarization phases (small P waves; prolonged P-R intervals; bradycardia, and widened QRS complexes). Hyperkalemia may also be associated with peripheral muscle weakness, decreased contractility, and weak pulse quality. Finally there is a blending of the QRS and T waves (a sinusoidal pattern), hypotension, and either ventricular asystole or fibrillation.
The plasma potassium measurement defines the plasma potassium concentration (normal, hyperkalemia, hypokalemia). The ECG changes define whether or not the animal is having any electrical problems from the potassium imbalance. There is considerable individual variation is this association. Severe hyperkalemia, for instance, that is associated with a fairly normal ECG complexes and at least "fair" pulse quality suggest that the animal's condition is not life-threatening and that therapy can be conservative. Moderate hyperkalemia associated with severe ECG changes suggests a life-threatening emergency requiring immediate and effective therapy.
Life-threatening hyperkalemia, defined by severe electrocardiographic disturbances, should be treated specifically. Calcium (0.2 ml of 10% calcium chloride or 0.6 ml or 10% calcium gluconate per kilogram of body weight , administered intravenously), by virtue of its effect on membrane threshold potential, antagonizes the effect of hyperkalemia and immediately returns the electrical performance toward normal. The effects of calcium are, however, short-lived, lasting only until the calcium is redistributed. Insulin and glucose (0.1 to 0.25 units of regular insulin/kg, administered as an intravenous bolus and 0.5 to 1.5 G of glucose/kg, respectively, administered as an intravenous infusion over two hours) is the common treatment for hyperkalemia. Patients should be monitored to make sure that they do not get excessively hypoglycemic. Bicarbonate will also cause the intracellular redistribution of potassium if it is going to be administered for acidosis. It is not a common choice for the treatment of hyperkalemia because animals commonly do not need to be alkalinized. Sympathomimetic drugs with beta2-agonist activity will also cause the intracellular redistribution of potassium but their therapeutic margin is narrow. Specific beta2 drugs (terbutaline) are associated with tachycardia and hypotension; while general beta1&2 drugs (epinephrine, dopamine) are associated with tachycardia, arrhythmias, and hypertension.