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.