CORRECTION OF BLOOD-PH ATTENUATES CHANGES IN HEMODYNAMICS AND ORGAN BLOOD-FLOW DURING PERMISSIVE HYPERCAPNIA

Objectives: To determine whether changes in cardiac output, regional b lood flow, and intracranial pressure during permissive hypercapnia are blood pH dependent and can be attenuated by correction of intravascul ar acidemia. Design: Prospective, controlled study. Setting: Research laboratory. Subjects: Female Marine ewes. Interventions: Animals were instrumented with a pulmonary artery catheter, femoral arterial and ve nous catheters, a catheter in the third cerebral ventricle, and ultras onic flow probes on the left carotid, superior mesenteric, and left re nal arteries 1 wk before experimentation. At initiation of the protoco l, ewes underwent endotracheal intubation and mechanical ventilation u nder general anesthesia. Minute ventilation was reduced to induce hype rcapnia with a target Pace, of 80 torr (10.7 kPa). In the pH uncorrect ed group (n = 6), arterial blood pH was allowed to decreased without t reatment. In the pH corrected group (n = 5), 14.4 mEq/kg of sodium bic arbonate was given intravenously as a bolus to correct arterial blood pH toward a target arterial pH of 7.40 (dose calculated by the Henders on Hasselbalch equation). Measurements and Main Results: Arterial bloo d pH, Pco(2), cardiac output, intracranial pressure, and carotid, supe rior mesenteric, and renal artery blood flow rates were measured at no rmocapnic baseline and at every hour during hypercapnia for 6 hrs. In the pH-uncorrected group, arterial blood pH decreased from 7.41 +/- 0. 03 at normocapnia to 7.14 +/- 0.01 (p < .01 vs. normocapnia) as blood Pco(2) increased to 81.2 +/- 1.8 torr (10.8 +/- 0.2 kPa). In the pH co rrected group, arterial blood pH was 7.42 +/- 0.02 at normocapnia and was maintained at 7.37 +/- 0.01 while Paco(2) was increased to 80.3 +/ - 0.9 torr (10.7 +/- 0.1 kPa). Significant increases in cardiac output occurred with the initiation of hypercapnia for both groups (pH-uncor rected group: 4.3 +/- 0.6 L/min at normocapnia vs. 6.8 +/- 1.0 L/min a t 1 hr [p < .05]; pH-corrected group: 4.1 +/- 0.4 at normocapnia vs. 5 .7 +/- 0.4 L/min at 1 hr [p < .05]). However, this increase was sustai ned only in the uncorrected group. Changes in carotid and mesenteric a rtery blood flow rates, as a percent of baseline values, showed sustai ned significant increases in the pH-uncorrected groups (p < .05) and o nly transient (carotid at 1 hr) or no (superior mesenteric) significan t change in the pH-corrected groups. Conversely, significant increases in renal artery blood flow were seen only in the pH uncorrected group during the last 2 hrs of the experiment (p < .05). Organ blood flow, as a percent of cardiac output, did not change significantly in either group. Intracranial pressure increased significantly in the pH uncorr ected group (9.0 +/- 1.5 mm Hg at normocapnia vs. 26.8 +/- 5.1 at 1 hr , p < .05), and remained increased, while showing no significant chang e in the pH-corrected group (8.5 +/- 1.6 mm Hg at normocapnia to 7.7 /- 4.2 at 1 hr). Conclusions: Acute hypercapnia, induced within 1 hr, is associated with significant increases in cardiac output, organ bloo d flow, and intracranial pressure. These changes can be significantly attenuated by correction of blood pH with the administration of sodium bicarbonate, without adverse effects on hemodynamics.