Urinary Alkalinization

Urinary alkalinization will promote the excretion of long-acting barbiturates only, as explained earlier. The reasons for this singular application are pharmacologically based. Long-acting barbiturates tend to be weaker acids (lower p Ka values), less lipid soluble, less protein bound, and are appreciably excreted in the urine compared with shorter-acting barbiturates. In basic solutions, long-acting barbiturates (weak acids) are relatively more ionized. Since only nonionized drug forms can cross cell membranes, these barbiturates will be trapped in the tubular fluid and excreted if the urinary pH favors the ionized form. Alkalinizing the urine is not effective for shorter-acting barbiturates because these drugs have higher p Ka values (stronger acids), are more protein bound, and are metabolized primarily by the liver. The 5- to 10-fold increase in basal excretion rate is best accomplished by giving a 1 to 2 meq/kg sodium bicarbonate intravenous bolus, followed by 50 to 100 meq in 500 mL of 5% D/W. Drip rate is sufficient if it maintains an arterial pH of 7.45 to 7.50, urinary pH of 8.0, and urinary output of 2 mL/kg/h. Serum potassium must remain at least 4 meq/L to achieve continuous urinary alkalinization. Adequacy of therapy should be monitored every 2 to 4 h. 35

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