Assisting ventilation in respiratory failure by negative pressure ventilation and by rocking bed.

The present study was undertaken to evaluate the effectiveness of acute ventilation by rocking bed (RB) and by negative-pressure ventilator (NPV) on arterial oxygenation and carbon dioxide tension in seven patients in whom respiratory failure (PaCO2 [+/- SD], 64 +/- 4 mm Hg; PaO2, 54 +/- 10 mm Hg) was consequent on nonobstructive ventilatory impairment. The increase in SaO2 (percent above baseline, 5 percent RB and 6 percent NPV) was similar for both methods, but a greater fall in PCO2 (percentage change in PCO2, 3 percent RB; 15 percent NPV; p less than 0.05) was observed during NPV. Diaphragmatic and accessory muscle electrical activity was markedly reduced during NPV but remained unchanged or increased on RB. Asynchronous breathing was frequently observed with RB but only rarely with NPV. These preliminary results suggest that effective mechanical ventilatory support could be achieved with either RB or NPV. However, their long-term effects as compared with those of positive-pressure ventilation remain to be explored.

Reversal of sleep-induced hypoventilation and chronic respiratory failure by nocturnal negative pressure ventilation in patients with restrictive ventilatory impairment.

The efficacy of negative pressure ventilation (NPV) in alleviating sleep-induced reductions in alveolar ventilation and in producing long-term clinical benefits was studied in 5 patients (54 +/- 8 yr of age; mean +/- SD) with chronic respiratory failure secondary to restrictive ventilatory impairment (VC, 40 +/- 14% predicted; TLC, 72 +/- 18% predicted; FEV1/FVC, 89 +/- 15%). In control sleep studies, arterial O2 saturation decreased from 81 +/- 6% during wakefulness to 79 +/- 1% during non-REM sleep and to 67 +/- 3% during REM sleep, and transcutaneous PCO2 increased from 80 +/- 16 mm Hg during wakefulness and non-REM sleep to 87 +/- 16 mm Hg during REM sleep. Nocturnal NPV in a cuirass ventilator improved baseline ventilation during wakefulness and prevented deterioration of alveolar ventilation during sleep. Upper airway obstruction during sleep induced by NPV was successfully managed with either a tricyclic medication or nasal CPAP. After 8 wk of nocturnal NPV, all patients felt considerably better. Daytime resting arterial PCO2 decreased from 56 +/- 2 to 46 +/- 3 mm Hg (p less than 0.05) and PO2 increased from 51 +/- 9 to 70 +/- 10 mm Hg (NS). Four patients have continued NPV at home on a regular basis and have returned to full-time employment. We conclude that nocturnal NPV is an effective method of preventing sleep-induced reductions in alveolar ventilation and a practical method of long-term management of patients with nonobstructive chronic respiratory failure.