alkalemia

Clinical manifestations of secondary brain injury are Hypoxemia (Pa[O.sub.2] <60mm Hg; [O.sub.2] Saturation <90%), Acid-base disorders (Acidemia: pH <7.35; alkalemia: pH >7.45), Hypercapnia (PaC[O.sub.2] >45mm Hg), Hypocapnia (PaC[O.sub.2] <35mm Hg), Hypotension (SBP <90mm Hg), Hypertension (SBP >160mm Hg, or mean arterial pressure >110mm Hg), Hyponatremia (serum sodium <142mEq/L), Hyperglycemia, Hypoglycemia, Fever, Hypothermia, Anemia (Hemoglobin (Hb <10g/dl) and Infections.

Incidence of metabolic alkalemia in hospitalized patients.

The basic method involves classifying the arterial pH as Normal, Acidemia or Alkalemia and then assessing the PaC[O.sub.2] and HC[O.sub.3]-to see which one is causing the pH to be abnormal.

This section also now states that "serum alkalinization with intravenous sodium bicarbonate and hyperventilation [as needed] should be instituted in patients manifesting significant toxicity such as QRS widening," and that "dysrhythmias despite adequate alkalemia may respond to overdrive pacing, beta-agonist infusions, and magnesium therapy"

Marked hyperlactatemia associated with severe alkalemia in a patient with thrombotic thrombocytopenic purpura.

The cation shifts are reversed in alkalemia, and the plasma [K.sup.+] concentration tends to fall and the intracellular [K.sup.+] content increases.

The negative outcomes associated with bicarbonate therapy include hypokalemia, paradoxical cerebral acidosis, prolonged ketoanion production, and late alkalemia. Additionally, bicarbonate therapy decreases cerebral and peripheral oxygen delivery secondary to a shift to the left of the oxyhemoglobin dissociation curve thus increasing the affinity of the hemoglobin molecule for oxygen.