There was a significant difference in the degree of relaxation of the adductor pollicis muscle and the vocalis muscle. The laryngeal muscles exhibited a shorter response time than the adductor pollicis and recovered more quickly. These results confirm the feasibility of intra-operative neuromonitoring of the recurrent laryngeal nerve during neuromuscular blockade.

Pulmonary structure was analysed by means of computed tomography (CT) in 20 lung-healthy patients, relating tissue density to the attenuation value (AV) of a picture element. Regional density of pulmonary tissue (rlung) was determined using mean lung density in five regions of interest (ROI1-5) (sector method). Vertical and horizontal distributions of x-ray attenuation were analysed by density profiles, relating AV values to evenly distributed and normalised length scales. In group I (n = 12), CT-densitometry was obtained in awake, supine patients and after induction of general anaesthesia. In group II (n = 8), the effect of mechanical ventilation with positive end-expiratory pressure (PEEP, 1.0 kPa [10 cmH2O]) was studied. In the awake state, a vertical tissue density difference between the top and bottom of the lung was found in all patients, accounting for a mean of 0.235 g.cm-3 (right lung) and 0.199 g.cm-3 (left lung). Only minor changes were seen in the horizontal lung density profiles. After induction of anaesthesia, x-ray attenuation of ROI1-4 showed no significant differences when compared with the awake state. The basal lung areas (ROI5) revealed a significantly increased tissue density (P < or = 0.01), reaching mean values of 0.94 g.cm-3 (right lung) and 0.814 g.cm-3 (left lung). Similarly, vertical density profiles showed a markedly enhanced rlung of the bottom of the lung in all patients, interpreted as atelectasis. The amount of atelectasis accounted for 4.8 +/- 2.6% (right lung) and 4.7 +/- 2.1% (left lung) of the intrapulmonary area.(ABSTRACT TRUNCATED AT 250 WORDS)

TEA has no effect on VA/Q distribution, gas exchange and intrathoracic blood volume in the awake state and does not influence development of Qs/QT and VA/Q inequality after induction of general anaesthesia.

Single breath nitrogen washout tests were analyzed in dogs (n = 8) with healthy lungs and after development of emphysema. The animals were in the supine position and studied during anaesthesia and mechanical ventilation (FiO2 = 0.4, FiN2 = 0.6). During controlled expiration with constant flow (VE = 0.15 l/s) onset of phase IV of the alveolar plateau was related to airway closure of dependent lung regions (closing volume CV). In the control state, CV accounted for 6.2 +/- 1.5% VC, and closing capacity (CC) was lower than functional residual capacity (FRC). Likewise, gas exchange was normal in all animals (PaO2 = 24.7 +/- 3.32 kPa, PaCO2 = 5.18 +/- 0.53 kPa, PA-aO2 = 2.6 +/- 0.3 kPa). Panlobular emphysema (PLE) was induced by inhalation of papain (100 mg/kg). After three weeks development of PLE was documented by measurements of lung volumes (functional residual capacity (FRC), expired vital capacity (EVC), total lung capacity (TLC), residual volume (RV], pulmonary mechanics (dynamic and static compliance (Cdyn, Cstat), mean airway resistance (Raw], gas exchange (PaO2, PaCO2, PA-aO2), and by radiomorphological analysis. In the PLE-group, FRC and RV (p less than or equal to 0.05), and Cstat (p less than or equal to 0.01) were significantly elevated. CV increased to 16.2 +/- 2.7% VC (p less than or equal to 0.01) and CC exceeded FRC by 80 ml, indicating that tidal volume breathing took place within the range of closing volume. Oxygenation was significantly impaired (PaO2 = 18.6 +/- 3.72 kPa, PA-aO2 = 6.5 +/- 1.1 kPa, p less than or equal to 0.05), but not CO2-elimination. Pathological analysis by radiomorphological means showed dissiminate parenchymal lesions compatible with emphysema of grade II severity located predominantly in subpleural areas. In dogs with papain-induced PLE, premature closure of dependent airways is enhanced, which is due to structural changes and a loss of elastic recoil in the lungs.

A case of severe unilateral chest trauma with bronchopleural fistula is presented. Ventilatory therapy consisted of asynchronous independent lung ventilation (AILV). The injured lung was ventilated with intermittent positive pressure ventilation (IPPV) [tidal volume (TV) = 200 ml, f = 25/min, I:E = 0.5, minute volume (MV) = 5.0 l/min, FiO2 = 0.4], and the unaffected lung was ventilated with continuous positive pressure ventilation (CPPV) (TV = 600 ml, f = 12/min, I:E = 0.5, MV = 7.2 l/min, PEEP = 0.5 kPa, FiO2 = 0.4). Adequate gas exchange was obtained (PaO2 = 14.5 +/- 2.3 kPa, PaCO2 = 5.5 +/- 0.7 kPa), but high air leakage volumes persisted. Thus, differential low-flow CPAP (V = 5.0-7.5 l/min, PEEP = 0.5 kPa, FiO2 = 0.4) of the injured lung and CPPV (TV = 600 ml, f = 12/min, MV = 7.2 l/min, I:E = 0.5, PEEP = 0.5 kPa, FiO2 = 0.4) of the unaffected lung was applied for 36 hours. Further deterioration of pulmonary function was prevented, and the bronchopleural fistula closed after several hours. After another period of AILV the patient was treated with conventional mechanical ventilation, and finally weaned with high-flow CPAP.