Transdiaphragmatic Pressure Time Product Research Articles

Patient-ventilator interaction during noninvasive pressure supported spontaneous respiration in patients with hypercapnic COPD

Noninvasive pressure support ventilation (NPSV) demands triggering with each breath. This study investigates the effects of NPSV via face mask on breathing pattern, ventilation and respiratory muscle loading in patients with hypercapnic stable COPD. 7 patients (age 66 +/- 9 years; FEV1 43 +/- 13% predicted; PaO2 52 +/- 19 mmHg; PaCO2 58 +/- 12 mmHg) were included. The physiologic variables were evaluated during spontaneous breathing and at the end of a 60 minutes period with NPSV. Inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP) were adjusted to 12-14 cm H2O and 3 cm H2O, respectively. Respiratory muscle activity was measured as esophageal and transdiaphragmatic pressure time product (PTPes and PTPdi). Non-triggering was observed only occasionally. Compared to unsupported spontaneous breathing NPSV improved ventilation: PaCO2 was reduced from 58 +/- 11 mmHg to 50 +/- 14 mmHg (p +/- 0.05). Respiratory muscles were unloaded by 30% (p +/- 0.05). Breathing frequency and breathing pattern did not change. In patients with hypercapnic stable COPD NPSV effectively recognizes and supports breathing efforts. As a result ventilation is improved and respiratory muscles are unloaded.

Nonchemical influence of inspiratory pressure support on inspiratory activity in humans.

To determine whether nonchemical inhibition of respiratory activity occurs during inspiratory pressure support (IPS) ventilation (IPSV), respiratory motor output (in 9 subjects), obtained by calculating transdiaphragmatic pressure-time products, and central respiratory output (in 5 subjects), obtained by integrating the electromyographic activity of the diaphragm (EMGdi) during mechanical inspiratory time, EMGdi per minute, and electrical inspiratory time, as determined from onset to peak EMGdi, were compared during spontaneous ventilation (control) and IPSV with (IPS+CO2) and without (IPS) correction of hypocapnia. Both IPS and IPS+CO2 induced significant decreases in transdiaphragmatic pressure-time products (46 +/- 31 and 53 +/- 23%, respectively), EMGdi during mechanical inspiratory time (49 +/- 12 and 57 +/- 14%, respectively), EMGdi per minute (65 +/- 22 and 69 +/- 15%, respectively), and electrical inspiratory time (73 +/- 8 and 65 +/- 6%, respectively). Because correction of hypocapnia failed to eliminate the marked inhibition of both respiratory and central motor output seen with IPS, we conclude that nonchemical inhibition of respiratory activity occurs during IPSV.

Effects of chest wall counterpressures on lung mechanics under high levels of CPAP in humans.

We assessed the respective effects of thoracic (TCP) and abdominal/lower limb (ACP) counterpressures on end-expiratory volume (EEV) and respiratory muscle activity in humans breathing at 40 cmH2O of continuous positive airway pressure (CPAP). Expiratory activity was evaluated on the basis of the inspiratory drop in gastric pressure (DeltaPga) from its maximal end-expiratory level, whereas inspiratory activity was evaluated on the basis of the transdiaphragmatic pressure-time product (PTPdi). CPAP induced hyperventilation (+320%) and only a 28% increase in EEV because of a high level of expiratory activity (DeltaPga = 24 +/- 5 cmH2O), contrasting with a reduction in PTPdi from 17 +/- 2 to 9 +/- 7 cmH2O . s-1 . cycle-1 during 0 and 40 cmH2O of CPAP, respectively. When ACP, TCP, or both were added, hyperventilation decreased and PTPdi increased (19 +/- 5, 21 +/- 5, and 35 +/- 7 cmH2O . s-1 . cycle-1, respectively), whereas DeltaPga decreased (19 +/- 6, 9 +/- 4, and 2 +/- 2 cmH2O, respectively). We concluded that during high-level CPAP, TCP and ACP limit lung hyperinflation and expiratory muscle activity and restore diaphragmatic activity.