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CLINICALLY SIGNIFICANT PHYSIOLOGIC CHANGES FROM RAPIDLY ADMINISTERED HYPERTONIC SOLUTIONS: ACUTE OSMOL POISONING
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1970
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Sodium ChlorideHypertensionRapid InjectionCerebral Vascular RegulationBlood FlowCerebrospinal FluidIntracranial PressureToxicologyBrain InjuryBlood Flow MeasurementClinical ToxicologyHealth SciencesCsf PressurePoisoningCerebral Blood FlowPharmacologyNeurophysiologyAcute Osmol PoisoningPhysiologyForensic ToxicologyAnesthesiaMedicinePharmacokineticsAnesthesiology
The rapid injection of hypertonic solutions, e.g., 0.9M sodium bicarbonate, creates a potential hazard from intracranial hemorrhage secondary to the shift of water from the CNS and the accompanying fall in cerebrospinal fluid (CSF) pressure. CSF pressure and other relevant variables were followed as 2.5M sodium chloride in a dosage of 10 mEq/kg given intravenously to cats over periods of 3 and 60 minutes. The fast infusion produced a sharp rise in CSF pressure followed by a precipitous fall. The rise parallelled the rise in venous pressure and fall in hemoglobin secondary to a transient increase in plasma volume. The slower infusion produced neither the sudden rise in CSF pressure nor the marked expansion of plasma volume, but did produce the same fall in CSF pressure. The rise in plasma volume and fall in hemoglobin concentration following a rapid hypertonic infusion may transiently improve the appearance of a cyanotic patient without necessarily improving his oxygenation. Since the osmolal load of these experiments is in the range of current clinical usage, when such osmolal loading is necessary, slow administration is suggested to avoid hemorrhage.