Blood gas changes and hypophosphatemia in lactate-induced panic.
Alkalosis is prominent among the many physiologic and biochemical effects of sodium lactate infusion. Though this is partially due to the conversion of lactate to bicarbonate, the metabolic component, it may also be secondary to hyperventilation before and during the infusion, the respiratory component. We analyzed pH, carbon dioxide pressure, bicarbonate, and inorganic phosphate from patients with panic disorder and agoraphobia with panic attacks and from normal controls both before and during lactate infusion. Our findings extend earlier work demonstrating that many such patients are chronic hyperventilators. Both metabolic and respiratory alkalosis develop in all subjects during lactate infusion, but only hyperventilation-induced hypocapnia differentiates patients at the point of lactate-induced panic from nonpanicking patients and normal controls. Finally, low inorganic phosphate levels at baseline appear associated with patients who will panic during the subsequent lactate infusion. This last unexpected finding may reflect hyperventilation or an abnormality in intracellular glycolysis.
D000328:Adult; D000471:Alkalosis / Q000209:etiology*; D000472:Alkalosis, Respiratory / Q000209:etiology; D001008:Anxiety Disorders / Q000097:blood / Q000139:chemically induced*; D002245:Carbon Dioxide / Q000097:blood; D005239:Fear; D005260:Female; D006801:Humans; D006985:Hyperventilation / Q000150:complications; D007773:Lactates / Q000008:administration & dosage / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D010200:Panic; D010710:Phosphates / Q000097:blood*
D007773:Lactates; D010710:Phosphates; D002245:Carbon Dioxide; D019344:Lactic Acid; D010100:Oxygen