Background:Adequacy of ventilation must be continually evaluated during anesthesia, and quantitative monitoring of carbon dioxide or volume of expired gas is strongly encour¬aged. But, it is not reliable to determine the adequacy of ventilation during deliberate hypotension because of the changes in the arterial to end tidal carbon dioxide gradient which occur in these conditions. The aim of the present study was to assess the following during hypotensive anesthesia for middle ear surgery: 1.) The magnitude of changes in P (a-ET) CO2 gradient. 2.) Changes in the lung compliance as well as in the ratio of physiological dead space to tidal volume (Vdphys/VT). 3.) To correlate between (ETCO2) and mean arterial blood pressure (MAP) at steady state of ventilation. 4.) To evaluate whether or not the ventilatory requirements remain unaltered during this procedure.Material and Methods: 100 patients aged 20-50 years, ASA I and II undergoing middle ear surgery under general anesthesia and controlled hypotension. A standard anesthetic technique was followed for all cases using, propofol, vecuronium, fentanyl and 100 % O2 supplemented with halothane. MAP was reduced to 60±5 mmHg in all patients using nitroglycerine infusion. The ETCO2, PaCO2, MAP, peak airway pressure plateau pressure and expiratory minute volume were recorded at two times: Time 1 (T1) measurements were taken after a steady state of ETCO2 of 35-40 mmHg for 10 min and before induction of hypotension. Time (T2) measurements were taken after steady state of MAP of 60±5 mmHg for 10 min.Results: (1) There is no evidence of correlation between MAP and either ETCO2, P(a-ET)CO2 gradient or Vd/Vt ratio during anesthesia with normal MAP or with controlled hypotension. (2) ETCO2 does not provide a stable reflection of PaCO2. (3) There was no statistically significant change in lung compliance between time 1and time 2. Conclusion: During anesthesia, once normocapnia is achieved with normal arterial blood pressures, there is hardly any need to decrease ventilation after induction of controlled hypotension. That means that ETCO2 does not reflect changes in PaCO2 because as P (a-ET) CO2 gradient is increased, PaCO2 remains in the clinically acceptable range the larger decrease in ETCO2 during controlled hypotension is mainly due to the increase in the Vd phys/Vt and V/Q ratios.