ADDED WORK OF BREATHING, VENTILATORY PATT ERN AND RECOGNIZABILITY OF READINESS FOR EXTUBATION DURING INSPIRATORY PRESSURE SUPPORT AND AUTOMATIC TUBE COMPENSATION

We measured the ventilatory pattern and additional work of breathing ( WOBadd) at three different levels of inspiratory pressure support [IFS 5, 10, 15 mbar above positive end-expiratory pressure (PEEP)] and in a new ventilatory mode, automatic tube compensation (ATC), in nine ope rative patients without lung injury nine patients ventilated for sever al following acute respiratory insufficiency (ARI). In ATC, endotrache aI tube resistance is compensated automatically by means of closed-loo p control of the calculated tracheal pressure. Pressure support in thi s mode, i.e. airway pressure above PEEP, is equal to the actual flow-d ependent pressure drop across the endotracheal tube (ETT). Airway pres sure rises at the beginning of inspiration and falls towards the end. As the tube resistance of ETT seriously hinders expiration and can cau se desynchronization between ventilator and patient, airway pressure i s reduced below PEEP during expiration in the same way as it is increa sed during inspiration. The result is a near-constant tracheal pressur e at PEEP both during inspiration and during expiration. This mode cou ld be best termed as ''electronic extubation''. The most striking diff erence between the postoperative patients and the ARI patients was the ir minute ventilation (17.8+/-1.85 1/min in ARI patients vs 7.3+/-3.1 1/min in the postoperative patients). In the postoperative patients au gmentation of IPS from 5 to 15 mbar induced a steady increase in tidal volume (V-T) and a consecutive decrease in respiratory rate (rr) comp ared with ATC (V-TATC,V-postop=463+/-78 ml; rr(ATC,postop)=16+/-4 min( -1); V-TIPS5,V-postop=505+/-79 ml; rr(IPS5,postop)=15+/-4 min(-1); V-T IPS 10,V-postop=562+/-86 ml; rr(IPS 15,postop) =14+/-4 min(-1): V-TIPS 15,V-postop=660+/-151 ml; rr(TPS 15, postop)=12+/-4 min(-1)), whereas the augmentation of IFS of 5 and 10 mbar in the ARI patients could no t compensate for the increase in rr and the decrease in V-T, after swi tching from ATC to LPS (V-TATC,V-ARI 724+/-308 ml, rr(ATC,ARI)=24+/-6 min(-1); V-TIPS 5,V- ARI=649+/-315 ml; rr(IPS 5,ARI)=27+/-8 min(-1); V -TIPS 10,V-ARI=653+/-353 ml; rr(IPS 10,ARI)=25+/-8 min(-1): Even IPS 1 5 was not able to reestablish V-T at the values observed during ATC (V -TIPS 15,V-ARI =680+/-312 ml). During ATC WOBadd was small in both pos toperative and ARI patients (WOBadd,ATC,postop =93+/-36 mJ/I, WOBadd,A TC,ARI=116 +/-72 mJ/l). In the postoperative patients, an inspiratory pressure support of 5 mbar was not sufficient to compensate WOBadd com pared with ATC. However, IFS 10 and 15 mbar were able to compensate fo r WOBadd (WOB (add.ATC 5,postop) WOBadd,IPS 5,postop =189+/-77 mJ/l; W OBadd,IPS 10,postop=55+/-30 mJ/l; WOBadd,IPS 15,postop=21+/-11 mJ/l). In the ARI patients an IPS 5, 10 or 15 mbar was not sufficient to comp ensate for WOBadd (WOBadd,IPS (5,ARI)=1126+/-262 mJ/l; WOBadd,IPS (10, ARI)863+/-253 mJ/l; WOBadd,IPS 15,ARI 763+/-298 mJ/l). Under ATC, WOBa dd was only 15% of WOBadd under IFS of 15 mbar. All but two patients w ere successfully extubated after the investigation. These two patients were not extubated because they were dependent on an FIO2 >0.5. Our r esults strongly indicate that ventilatory dependence in ARI patients m ay be caused by the ETT rather than by mechanical dysfunction of the l ung. ATC is a very helpful mode to use in distinguishing between venti latory failure caused by ETT and real ventilatory dependence.