TABLE 238 Etiology of Hyperkalemia

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Clinical manifestations of hyperkalemia usually result from derangement in membrane polarization. Cardiac manifestations are the most serious. They include ECG

changes ranging from

6.5 to 7.5 meq/L :tall peaked T waves, short QT interval, and prolonged PR interval

7.5 to 8.0 meq/L :QRS widening, and flattening of the P wave

10 to 12 meq/L :the QRS complex may degrade into a "sine wave" pattern

Ventricular fibrillation, complete heart block, and asystole may occur. Death from hyperkalemia is usually the result of diastolic arrest or ventricular fibrillation. Neuromuscular manifestations include weakness, paresthesias, areflexia, and ascending paralysis. The gastrointestinal symptoms include nausea, vomiting, intermittent intestinal colic, and diarrhea. Patients with slowly developing hyperkalemia often tolerate serum [K +] of 7 to 8 meq/L, whereas, with acute elevations, significant problems, including cardiac arrest, can occur at most lower levels.

TREATMENT If there are no cardiac derangements, the initial step in the treatment of hyperkalemia is to confirm the presence of "true" hyperkalemia. Immediate cessation of further K+ administration as well as clinical determination of severity will drive management. Asymptomatic patients with relatively small elevation of K + (5.0 to 6.0 meq/L) require determination and treatment of the underlying cause. As patients become symptomatic, management must become more aggressive. It is divided into three phases:

1. Membrane stabilization (especially cardiac tissue)

2. Shift K+ from ECF to ICF

3. Removal of K+ from the body

Membrane stabilization can be achieved with calcium gluconate or calcium chloride. This is usually indicated in any patient with evidence of cardiac irritability or acutely elevated levels of greater than 7.5 meq/L. It acts to antagonize the effect of K + on the cardiac conduction system. It is administered in a dose of 10 to 20 mL of 10% calcium gluconate (4.6 meq/10 mL) or as 5 mL of 10% calcium chloride (13.6 meq/10 mL) intravenously over 2 to 5 min. The effect of calcium occurs within 1 to 3 min of administration and remains pharmacologically active for up to 1 h.

If calcium is to be given to a patient on digitalis, great caution must be exercised, as hypercalcemia potentiates the toxic cardiac effects of digitalis. If it is to be given in this setting, it is best added to 100 mL of D5W and infused slowly over at least 20 to 30 min, allowing a more even distribution throughout the extracellular space.

Patients without evidence of cardiac irritability or instability may be approached more slowly. The shifting of K + to the ICF can be achieved in various ways. The administration of 50 g of glucose with 5 to 10 units of regular insulin intravenously will help to redistribute K +. Onset of action is approximately 30 min, with duration of action from 4 to 6 h. Some authorities believe that in patients with normal pancreatic function, glucose administration alone suffices, as the patient's own physiologic mechanism will result in insulin secretion. After the initial glucose has been administered, 1 L of 20% glucose with 20 to 40 units of regular insulin may be infused over the next 2 to 4 h, if necessary. Sodium bicarbonate acts through both antagonism and redistribution. It should be administered as 50 to 100 meq (1 to 2 ampules) intravenously over 2 min. Its onset of action is 5 to 10 min, with duration of 1 to 2 h. Lastly, b agonists help to redistribute K + into cells. The most practical route of administration is nebulized albuterol.

The removal of K+ from the body can be achieved in three ways: via the urine, via stool, or through dialysis. Diuretics block the reabsorption of K +, leading to increased excretion. Furosemide is the drug of choice, administered at 40 mg intravenously. Other diuretic options include ethacrynic acid or other loop diuretics. For obvious reasons, avoid K+-sparing diuretics. Cation-exchange resins such as sodium polystyrene (Kayexalate) can be taken either orally or rectally. Each gram of sodium resin exchanges and thus eliminates about 1 meq of K+. Orally, 15 to 50 g of sodium polystyrene is given with 50 mL of a 20% sorbitol solution every 4 to 6 h. The sorbitol helps overcome the constipating effect of the resin and speeds bowel transit. Rectal administration is 20 g in 200 mL of a 20% sorbitol solution every 4 h, with the enema retained for at least 30 min. Care must be taken in patients with fluid overload or those sensitive to Na +. Congestive heart failure may be precipitated. Dialysis is reserved for severely ill patients or those already on dialysis. Peritoneal dialysis or hemodialysis may be instituted depending on the situation.

If a dangerous tachyarrhythmia develops, all of the foregoing steps may have to be undertaken nearly simultaneously ( T.a.ble 2.3.-9.). In patients with oliguric renal failure, hemodialysis (or peritoneal dialysis) stat consultation for dialysis should also be undertaken.

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