Recent experimental and clinical observations suggest a neuroprotective role of hypercarbia following hypoxia-ischemia, and conversely an unfavorable neuro outcome with hypocarbia. Our study objective was to determine the relationship between initial arterial PCO2 and early neuro outcome following PA. We studied three groups of inborn infants admitted (adm) to the NICU between Jan 93 - June 94. Group I (n=48) non-asphyxiated infants, i.e., cord arterial pH >7.00, adm with suspected sepsis, tachypnea, or IDM without respiratory support (RS) and with negative (neg) neuro exam. Group II(n=18) severe fetal acidemia (FA), i.e., cord pH ≤7.00, base deficit (BD)>-12 mEq/L, no RS, neg neuro exam. Group III (n=7) FA, intubated, normal chest radiograph, abnormal neuro exam with seizures. Cord pH, pCO2, and BD were compared with arterial values obtained within one hour of admission(mean±SD). No differences in initial heart rate or mean blood pressure were noted between groups. Profound, rapid ↓ in pCO2 (mean change for II 65±22 mmHg, III 96±41 mmHg) restored pH to near normal in II but not III infants. Group III infants exhibited ↑ pCO2 despite intubation and ↑ BD -18±6 vs -12±6 (II) and -6±3 (I).Conclusions: 1) Following PA, spontaneous hypocarbia in response to profound acidosis may be a marker for intact neuro function and does not convey an adverse early neuro outcome. 2) Relative hypercarbia, despite RS with clear lungs, suggests ↓ pulmonary perfusion, and coupled with persistent acidosis, points to a more severe in utero insult. 3) The relationship of hypo/hypercarbia and neuro outcome is complex and requires further study. P<0.05, *I vs II, ** II vs III.Table
