Acute effects of external negative pressure ventilation in chronic obstructive pulmonary disease compared with normal subjects

Abstract

This study compares the acute physiological effects of external negative pressure ventilation (ENPV) in normal subjects and patients with chronic obstructive pulmonary disease (COPD). The equipment consisted of an airtight jacket (Pneumosuit) and vacuum pump. Minute ventilation (V̇E) was recorded using a ligh-emitting turbine transducer. Oxygen uptake (V̇O2) and carbon dioxide output (V̇CO2) were calculated every 30 s. Measurements were made at rest and during ENPV with pressures of -20 cmH2O and -40 cmH2O. The ventilator rate was fixed at 16·min-1. In 10 normal subjects, V̇E increased from 8.6 to 22.9 l·min-1 (p < 0.01) accompanied by an increase in V̇CO2 from 0.25 to 0.39 l·min-1 (p < 0.01). In 10 normocapnic COPD patients (arterial carbon dioxide tension (PaCO2) <6.0 kPa) V̇E increased from 11.5 to 17.1 l·min-1 (p < 0.01) whilst in 10 hypercapnic patients (PaCO2 >6.0 kPa) V̇E increased from 9.7 to 12.4 l·min-1 (p < 0.01). A change in V̇CO2 was not detected in the COPD patients, and V̇O2 did not change in any group. Arterial blood samples were obtained in eight hypercapnic patients. Baseline mean physiological deadspace ventilation (V̇D) was calculated to be 4.9 l·min-1 (56% of V̇E) whilst V̇E was 8.8 l·min-1 in this subgroup. During ENPV, arterial oxygen tension (PaO2) increased from 6.8 to 8.2 kPa (p < 0.01) whilst PaCO2 decreased from 6.8 to 5.8 kPa (p < 0.01) suggesting that despite the large physiological deadspace, a significant increase in alveolar ventilation had occurred. In advanced COPD, thoracic compliance falls and limits the ventilatory response to ENPV. Despite this, useful improvement of blood gases was obtained using modest external negative ventilatory pressures of -20 cmH2O. Maintenance of these changes over longer periods of ENPV has yet to be proven.