Background: Diaphragm dysfunction is a primary cause of ventilatory im
pairment after upper abdominal surgery. Laparoscopic procedures may re
sult in less dysfunction. To test this, diaphragmatic function was stu
died in ten healthy adult patients undergoing elective laparoscopic ch
olecystectomy and in five undergoing laparoscopic hernia repair. Metho
ds. Respiratory gas exchange, ventilation, and breathing pattern were
measured before and 3 h after surgery. Respiratory drive was evaluated
from the relationship of P0.1 to end-tidal carbon dioxide (PET(CO2))
during tidal breathing. Diaphragm contractile function was assessed fr
om maximal transdiaphragmatic pressure (Pdi(max)), and Pdi during a ma
ximal sniff maneuver (Pdi(sniff)). Results: Oxygen consumption and car
bon dioxide production did not change after surgery. Pdi(max) decrease
d by more than 50% in the laparoscopic cholecystectomy group, but Pdi(
sniff) did not change. Tidal volume and the ratio of inspiratory time
over total cycle time decreased by 30% and 13%, respectively, PET(CO2)
increased by 9%, and minute ventilation did not change. In contrast,
there was no variation in ventilatory function in patients undergoing
laparoscopic hernia repair. In both groups, P0.1 did not change, which
excludes depressed respiratory drive as an explanation for the decrea
sed Pdi(max) in laparoscopic cholecystectomy. Contractile failure of t
he diaphragm was discounted as well, because Pdi(sniff) did not change
, even in the laparoscopic cholecystectomy group. Conclusions: Althoug
h laparoscopic cholecystectomy does not increase metabolic demands in
the early postoperative period, it impairs diaphragm function. The int
ernal site of surgical intervention appears to be the critical variabl
e determining diaphragmatic inhibition after laparoscopic abdominal su
rgery.