The response to proportional assist ventilation (PAV) was tested in four normal subjects during heavy exercise and in five ventilator-dependent patients recovering from assorted medical disorders. The apparatus consisted of a rolling-seal piston coupled to a motor that generated pressure in proportion to inspired flow and inspired volume, with the gains adjusted such that the proportionality between airway pressure (Paw) and instantaneous patient-generated pressure (Pmus) was approximately 1:1 (i.e., machine-amplified patient effort by a factor of 2). Normal subjects responded to PAV by decreasing their own effort, as judged from esophageal pressure, such that the changes in ventilation and breathing pattern were rather small (VE: 64.8 +/- 3.6 during PAV versus 56.0 +/- 4.3, p less than 0.01; VT: 2.39 +/- 0.24 versus 2.02 +/- 0.17, p less than 0.05; f: 27.5 +/- 1.9 versus 28.0 +/- 2.2, NS). In patients, elastance ranged from 20 to 35 cm H2O cm/L, resistance ranged from 5 to 10 cm H2O/L/s, and maximal inspiratory pressure ranged from -16 to -65 cm H2O. After a period of observation during synchronized intermittent mechanical ventilation (SIMV) the patient was switched to PAV and maintained on it for 1 to 3 h. No patient had to be replaced on SIMV because of discomfort or deterioration in any of the monitored variables. During PAV peak airway pressure was less than half the value observed with the IMV breaths (16.6 +/- 2.4 versus 35.4 +/- 3.4 cm H2O, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

We wished to determine the independent effect of inspiratory flow rate (VI) on respiratory output in the awake state. Seven normal subjects were connected to a volume-cycled ventilator in the assist/control mode. While the tidal volume setting remained constant, inspiratory flow rate was increased in steps (3 to 4 min each) from 30 to 90 L/min and then back to 30 L/min. Flow pattern was square, and all breaths were subject-triggered. Spontaneous respiratory rate (f) increased in all subjects as VI increased. Mean (+/- SD) f at 30 and 90 L/min were 8.8 (+/- 1.7) and 14.1 (+/- 4.4) min-1, respectively (p less than 0.01). VE increased (10.1 +/- 1.9 at 30 L/min to 16.3 +/- 5.6 at 90 L/min p less than 0.01) and the percentage of end-tidal CO2 decreased (4.7 (+/- 0.5) at 30 L/min to 3.3 (+/- 0.7) at 90 L/min (p less than 0.01)). The response was graded and reversible. The change in f was nearly complete within the first two breaths after transition, and there was no systematic tendency for f to change beyond this early response. The rate of change in airway pressure prior to triggering (dp/dt) increased as VI increased (5.3 +/- 2.0 cm H2O/s at 30 L/min to 10.8 +/- 2.6 cm H2O/s at 90 L/min; p less than 0.01). We conclude that inspiratory flow rate exerts an excitatory effect on respiratory frequency and on the rate of rise of inspiratory activity in conscious humans. This may be relevant to the mechanism of ventilatory response to various respiratory stimuli and to the management of patients receiving mechanical ventilation.

Provide simple method for decreasing risk of thermal injury when removing casts.

The purpose of this study was to evaluate the extent of inhibition to respiratory rhythm associated with high volumes of ventilation during volume-cycled mechanical ventilation (neuromechanical inhibition). Two approaches were used. 1) In 18 normal awake subjects, ventilator tidal volume (VT) in the assist/control mode (A/C) was increased in steps from the minimum tolerable level up to 80% of the subject's inspiratory capacity or ventilator's maximum VT. We looked for appearance of intermittent apnea or a reduction in spontaneous rate (f). 2) Another 18 normal awake subjects were placed on controlled mechanical ventilation (CMV). When apnea was established, we abruptly terminated CMV and measured the time before the appearance of the next spontaneous effort. In the assist mode (protocol 1), we did not observe intermittent apnea because VT was increased from [from 944 +/- 198 to 1,867 +/- 277 (SD) ml], and there was only a modest reduction in f (14.1 +/- 3.9 to 12.4 +/- 4.0 breaths/min). End-tidal PCO2 (PETCO2) decreased precipitously as VT was increased. In protocol 2, we did not observe apnea after discontinuation of CMV in any subject. Total breath duration of the first breath after discontinuation did not differ significantly from total breath duration during A/C in the same subjects (4.84 +/- 2.2 vs. 5.2 +/- 2.0 s). This similarly applied regardless of route of breathing (nose vs. mouth) or PETCO2 level at time of discontinuation. We conclude that neuromechanical inhibition is quite weak and provides very little negative feedback that may help control PCO2 in the face of excessive VT and f demands of the subject.