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Objectives: Proportional assist ventilation is devised to increase airway pressure in proportion to inspiratory effort. A systematic study of the performance of this new mode of ventilation has not been presented. We tested in the laboratory the capability of proportional assist ventilation to unload the work of breathing in proportion to ventilatory drive, under a variety of mechanical loads., Design: During variations of "ventilatory drive" (i.e., tidal volume), unloading of the work of breathing by proportional assist ventilation was contrasted with unloading by pressure-support ventilation., Setting: The respiratory laboratory of a university-affiliated teaching hospital., Subject: A bellows-in-a-box lung model, powered by a sine wave air flow generator., Interventions: Proportional assist and pressure-support ventilation were preset to provide comparable support at a baseline "ventilatory drive" of 0.7-L tidal volume. The set levels of proportional assist and pressure-support ventilation were subsequently applied to five tidal volumes, from 0.2 to 1.2 L. Three levels of inspiratory support and three settings of mechanical load were evaluated., Measurements and Main Results: Proportional assist ventilation significantly (p < .05) reduced the work of breathing of the lung model at all but the lowest tidal volume (0.2 L). The preset proportion of ventilatory support (30%, 50%, and 70%) unloaded the work of breathing uniformly as ventilatory drive was varied at tidal volumes of > or = 0.5 L, but not always at tidal volumes of < or = 0.4 L. In contrast, pressure-support ventilation overassisted low tidal volumes and underassisted high tidal volumes (p < .05)., Conclusions: In a lung model, a prototype system delivering proportional assist ventilation provided uniform unloading of the work of breathing as the ventilatory drive was varied within a tidal volume range of 0.5 to 1.2 L. These findings confirm the theoretical modeling of proportional assist ventilation. This system, however, failed to properly unload low tidal volumes of 0.2 to 0.4 L.

Background: Prolonged inhibition of diaphragmatic function occurs after thoracic and upper abdominal surgery. It was hypothesized that thoracic epidural anesthesia on the day after a thoracotomy could block inhibitory neural pathways and increase the shortening of costal and crural diaphragmatic segments., Methods: Pairs of sonomicrometer crystals were implanted into the costal and crural regions of the diaphragm through a right lateral thoracotomy in 14 30-kg, 4-5-month-old lambs. One day after surgery, a thoracic epidural catheter was placed at the T8-T9 level. Regional diaphragmatic shortening normalized to end-expiratory length (%LFRC), was measured by sonomicrometry in these awake lambs. Changes in gastric (delta Pgas), esophageal (delta Pes), and transdiaphragmatic (delta Pdi) pressures were measured with transnasal balloon catheters. End-tidal carbon dioxide (FETCO2), costal and crural electromyogram (Edi), and tidal volume (VT) were measured. Inductance plethysmography was used in four lambs to assess relative contributions of the rib cage and abdomen to VT. Control values were obtained during quiet breathing and while rebreathing at up to 10% FETCO2. To block thoracic dermatomes, 1% or 2% lidocaine was injected through the epidural catheter. Measurements were repeated after each lidocaine injection., Results: There was no change of resting length with 1% lidocaine; costal resting length increased by 22% with 2% lidocaine. After 2% lidocaine, costal %LFRC increased from control both during quiet breathing (8.7 +/- 0.7 to 18.1 +/- 1, mean +/- SEM%) and at FETCO2 10% (22.1 +/- 2 to 33.7 +/- 3%). VT during quiet breathing was unchanged after 1% lidocaine but increased from 235 +/- 16 to 283 +/- 28 ml after 2% lidocaine. At 10% FETCO2, delta Pdi was unchanged after 1% lidocaine and decreased from 36.5 +/- 4.3 to 26.3 +/- 4.9 cmH2O after 2% lidocaine. Regional delta Edi was unchanged with both 1% and 2% lidocaine at rest and during carbon dioxide rebreathing. Plethysmography in three lambs showed a reduction in rib cage contribution to tidal volume with 2% lidocaine during quiet breathing., Conclusions: Improved postoperative tidal volume and diaphragmatic shortening after thoracic epidural blockade may be due to changes of chest wall conformation and resting length and a shift of the workload of breathing from the rib cage to the diaphragm caused by intercostal muscle paralysis.

Background: Diaphragmatic function is believed to be inhibited after thoracic surgery and may be improved by thoracic epidural anesthesia., Methods: Diaphragmatic function after a thoracotomy was monitored by implanting one pair of sonomicrometry crystals and two electromyogram (EMG) electrodes on the costal diaphragm of six patients undergoing an elective pulmonary resection. Crystals and EMG electrodes remained in place for 12-24 h., Results: During mechanical ventilation, costal diaphragmatic length (as a percent of rest length; %LFRC) decreased passively as tidal volume (VT) increased (%LFRC = 2.81 + 1.12 x 10(-2) VT (ml), r = 0.99). During spontaneous ventilation, the costal shortening (2.1 +/- 2.3 %LFRC) was less than during mechanical ventilation (7.9 +/- 3.0 %LFRC, P < 0.05) at the same VT. Comparing spontaneous ventilation before and 30 min after thoracic epidural anesthesia, there were increases of VT (390 +/- 78 to 555 +/- 75 ml), vital capacity (1.37 +/- 0.16 to 1.68 +/- 0.21 l), and esophageal (-8.5 +/- 1.5 to -10.6 +/- 1.7 cmH2O), gastric (-0.7 +/- 0.8 to +0.8 +/- 0.8 cmH2O), and transdiaphragmatic (7.7 +/- 1.5 to 11.5 +/- 1.9 cmH2O) pressures, but diaphragmatic EMG and shortening fraction remained constant. In three of six patients, epidural anesthesia produced paradoxical segment lengthening upon inspiration., Conclusions: Thoracotomy and pulmonary resection produce a marked reduction of active diaphragmatic shortening, which is not reversed by thoracic epidural anesthesia despite improvement of other indices of respiratory function.

Aminophylline has been reported to augment diaphragmatic contraction, although this remains a controversial finding. We studied the effect of aminophylline on regional diaphragmatic shortening, changes in transdiaphragmatic pressure (delta Pdi), and integrated regional electromyographic (EMG) activity of the diaphragm (Edi) after a right thoracotomy in nine lambs using sonomicrometry, esophageal and gastric balloons, and EMG. Sonomicrometer crystals and EMG leads were implanted into the costal and crural regions of the diaphragm through a right thoracotomy, and a tracheostomy was performed. The animals were studied while awake within 4 days after surgery. Fractional costal and crural diaphragmatic shortening was measured using the sonomicrometer; delta Pdi was calculated from esophageal and gastric pressures. Respiratory variables were measured through the tracheostomy. Data were collected during quiet breathing and during CO2 rebreathing. After control measurements, aminophylline (10 mg/kg) was administered intravenously, producing a serum concentration of 17.7 +/- 1.5 micrograms/ml. Aminophylline did not augment shortening, increase delta Pdi, or overcome postoperative diaphragmatic inhibition acutely in the awake sheep after a right lateral thoracotomy. A small decrease of end-tidal CO2, from 5.2% to 4.9%, was measured at rest during aminophylline infusion, but Edi was unchanged. Although during CO2 rebreathing diaphragmatic shortening increased, the addition of aminophylline did not further augment shortening. Our data in awake lambs suggest that aminophylline does not improve diaphragmatic contraction in the acute postoperative period.