If all the determinations realized in the same individual are not in- dependant as clearly shown, the bias is not affected and the standard deviation of the bias is underestimated. Yours faithfully, E Bizouarn References l. Altman DG, Bland JM (1983) Measurement in medicine: the analy- sis of method comparison studies. The Statistician 32:307-317 2. Bland JM, Altman DG (1986) Statistical methods for assessing agreement between two methods of clinical measurement. Lancet I:307-310 3. Bizouarn P, Soulard D, Blanloeil Y, Guillet A, Goarin Y (1992) Oxy- gen consumption after cardiac surgery - a comparison between cal- culation by Fick's principle and measurement by indirect calorimetry. Intensive Care Med 18:206-209 P. Bizouarn, MD, D~partement d'Anesth&ie*R6animation, H6pital G. et R. La~nnec, F-44035 Nantes Cedex 01, France 305 PIP (cm H20 ) 100 80 60 40 Propofol bolus dose / 2o r Propofol infusion I I I I I i I I I I 0 1 2 3 4 5 6 7 8 9 10 1t 12 13 14 h Fig. 1. Modifications of peak inspiratory pressure with unmodified tid- al volume in the first 14 h of treatment Propofol induces bronchodilation in a patient mechanically ventilated for status asthmaticus Dear Sir, Severe status asthmaticus (SA) is commonly observed in ICU and is treated with B2 mimetic drug, aminophylline, steroids with associated mechanical ventilatory support. In the past, a large incidence of barotrauma has been reported in SA patients receiving mechanical ven- tilation; therefore SA patients are generally anesthetized, paralyzed and ventilated with low respiratory frequencies and low tidal volumes [I]. Heavy sedation is prescribed to obtain machine adaptation and respira- tory drive reduction; however, the presence of intrinsic bronchodilation properties has never been reported for the sedatives of common clinical use. Propofol is currently used in ICU for long term sedation of me- chanically ventilated adult patients [2]; it has been shown recently that propofol prevents fentanyl induced bronchoconstriction and induces bronchodilation, in patients with chronic hyperreactive disease and chronic obstructive pulmonary disease [3-5]. We report a patient with status asthmaticus, mechanically ventilated after heavy sedation, in wich the administration of propofol produced an important bron- chodilaton. A 23-year-old man was transferred to our ICU from the emergency room where he had been intubated and ventilated after a cardiac arrest due to status asthmaticus, unresponsive to conventional treatment (aminophylline 480 mg i.v., adrenaline 0.5 mg s.c. and methylpredniso- lone 2 g i.v.). On ICU admission he was manually ventilated, as mechan- ical ventilation was impossible (peak inspiratory pressure 100 cmH20), despite heavy sedation with flunitrazepam (5 mg i.v.) and paralysis with pancuronium bromide (8 mg i.v.). After 20 rain of manual ventilation with oxygen 100%, he had a respiratory acidosis (pH 7.21, PaO 2 107, PaCO; 71, BE -5); connected to a Servo 900 C (Siemens) with the fol- lowing settings: RR 8/rain ~; Vt 10 ml Kg - 1, I: E i : 2, square wave, no PEEP, FIO 2 0.5, he showed high peak inspiratory pressure (90 cmHaO ) and high values of intrinsic PEEP, (20 cmH20 ) evaluated with a pro- longed tele-expiratory airway occlusion. Continuous infusion of salbutamol was started (0.6 mg Kg-1) and sedation with flunitrazepam i.v. infusion was continued (0.1 mg/Kg/h); at this dose the patient was areflexic. After 2 h bronchospasm persisted despite salbutamol dose in- crease to 1.2 mg/Kg and a bolus dose of prednisolone (400 mg i.v.). Se- dation with propofol was attempted: after a bolus dose of 70 mg was administered, peak inspiratory pressure decreased to 70 cmH20. The effect lasted for }0min, and a subsequent slow increase to the preceeding values of peak impiratory pressure was observed. A second dose of 70 mg was administered, producing again a dramatic decrease in peak inspiratory pressure from 90-63 cmH20. Also PEEPi and to- tal resistances of the respiratory system showed a decrease, from 14-10.5H20 and from 25.5-15.5cmH2Ol-ls -2, respectively. In view of this good result, sedation with propofol was continued for 10 h, observing a constant decrease of peak inspiratory pressure and autoPEEP values. The following day the patient was rapidly weaned and extubated and, after 5 days, he was discharged in good clinical con- dition. In this case report propofol induced bronchodilation has been proved not only by measuring peak inspiratory pressure and autoPEEP values but also with the direct measurement of the total resistances of the respiratory system. Non-specific bronchodilation effect has been observed in status asthmaticus with sedation; however we administered propofol in an al- ready anesthetized patient, and the relationship between injection and bronchodilatation was observed several times (Fig. 1). The use of pro- pofol as a sedative agent could be an interesting alternative in view of the rapid metabolism and of the intrinsic bronchodilation activity. Pro- spective controlled trials are needed to confirm this aspect. Yours faithfully G. Conti, A. Ferretti, G. Tellan, M. Rocco and A. Lappa References i. Darioli R, Perret C (1984) Mechanical controlled hipoventilation in status asthmaticus. Am Rev Respir Dis 129:385-387 2. Aitkenhead AR, Willats SM, Park GR, Collins CH, Ledingham MCA, Pepperman ML, Coates PD, Bodenham AR, Smith MB, Wal- lace PGM (1989) Comparison of propofol and midazolam for seda- tion in critically ill patients. Lancet 704-709 3. Cigarini I, Bonnet F, Lorino AM, Harf A, Desmonts JM (1990) Comparison of the effect of fentanyl on respiratory mechanics under propofol or thiopental anaesthesia. Acta Anaesth Scand 34:253 -256 4. Pedersen CH (1992) The effect of sedation with propofol on postop- erative bronchoconstriction in a patients with hiperreactive airways disease. Intensive Care Med 18:45-46 5. Conti G, Dell'Utri 13, Vilardi V, de Blasi RA, Pelaia P, Antonelli M, Buff M, Rosa G, Gasparetto A (1993) Propofol induces bronchodila- tion in mechanically ventilated chronic obstructive pulmonary dis- ease (COPD) patients. Acta Anaesth Scand 37:105-109 Dr. G. Conti, Universit/t degli Studi di Roma "La Sapienza", Istituto di Anestesiologia e Rianimazione Poticlinico Umberto I, 1-00161 Rome, Italy