This study was undertaken to define the effect of acute hypocapnia on intraoperatively recorded somatosensory evoked potentials (SSEPs). Median nerve SSEPs were studied in ten anesthetized neurologically normal adult patients undergoing elective nonneurologic surgery. End-tidal carbon dioxide tension (ETCO2) was allowed to stabilize for 15 min before SSEP recordings were obtained during normocapnia (N) (ETCO2 = 39.9 +/- 1.45 mm Hg), hypocapnia (H) (ETCO2 = 20.6 +/- 1.07 mm Hg), and after return to normocapnia (NR). Although a trend toward a reduction in the latencies of all SSEP components was evident, only the cervical (CII), and cortical (N1 and P1) latencies decreased significantly with H when compared to N. Mean latencies for CII, N1, and P1 (+/- SD) were, respectively, 14.80 +/- 1.14, 20.93 +/- 1.50, and 25.17 +/- 2.88 msec during N, and 14.50 +/- 1.13, 20.25 +/- 1.49, and 24.23 +/- 2.52 msec during H. On return to normocapnia, latencies were unchanged from N. Cortical latencies were affected to a greater extent than subcortical ones. Aside from a small but statistically significant increase in CII amplitude at H (2.05 +/- 0.55 microV vs 1.83 +/- 0.49 microV at N), SSEP amplitudes were unaffected by hypocapnia. The authors conclude that acute hypocapnia in neurologically normal patients results in a small reduction of SSEP latencies. The magnitude of the change is such that it is unlikely to interfere with recording or interpretation of intraoperative SSEPs.