Background: Prolonged controlled mechanical ventilation depresses diaphragmatic efficiency. Assisted modes of ventilation should improve it. We assessed the impact of pressure support ventilation versus neurally adjusted ventilator assist on diaphragmatic efficiency. Method: Patients previously ventilated with controlled mechanical ventilation for 72 hours or more were randomized to be ventilated for 48 hours with pressure support ventilation (n =12) or neurally adjusted ventilatory assist (n = 13). Neuro-ventilatory efficiency (tidal volume/diaphragmatic electrical activity) and neuro-mechanical efficiency (pressure generated against the occluded airways/diaphragmatic electrical activity) were measured during three spontaneous breathing trials (0, 24 and 48 hours). Breathing pattern, diaphragmatic electrical activity and pressure time product of the diaphragm were assessed every 4 hours. Results: In patients randomized to neurally adjusted ventilator assist, neuro-ventilatory efficiency increased from 27 ± 19 ml/μV at baseline to 62 ± 30 ml/μV at 48 hours (p <0.0001) and neuro-mechanical efficiency increased from 1 ± 0.6 to 2.6 ± 1.1 cmH₂O/μV (p = 0.033). In patients randomized to pressure support ventilation, these did not change. Electrical activity of the diaphragm, neural inspiratory time, pressure time product of the diaphragm and variability of the breathing pattern were significantly higher in patients ventilated with neurally adjusted ventilatory assist. The asynchrony index was 9.48 [6.38– 21.73] in patients ventilated with pressure support ventilation and 5.39 [3.78– 8.36] in patients ventilated with neurally adjusted ventilatory assist (p = 0.04). Conclusion: After prolonged controlled mechanical ventilation, neurally adjusted ventilator assist improves diaphragm efficiency whereas pressure support ventilation does not. Trial registration: ClinicalTrials.gov study registration: NCT0247317, 06/11/2015.

Dynamic hyperinflation and intrinsic positive end-expiratory pressure (PEEPi) are observed in patients with chronic obstructive pulmonary disease (COPD) and flow limitation. Several reports suggest that PEEP levels approaching PEEPi reduce inspiratory load due to PEEPi, without further hyperinflation. Hence PEEP should not increase intrathoracic pressure or affect hemodynamics and gas exchange. To verify this hypothesis, the effects of PEEP (0 to 15 cm H2O) on respiratory mechanics, hemodynamics, and gas exchange were studied in nine COPD patients during controlled mechanical ventilation. PEEP levels approaching PEEPi (9.8 ± 0.5 cm H2O) did not affect the expiratory flow/volume relationship, confirming the presence of flow limitation. PEEP levels of 5 and 10 cm H2O did not change lung volume and PEEPi in the respiratory system (PEEPtot,rs) and chest wall (PEEPtot,cw) or affect hemodynamics and gas exchange. When applied PEEP overcame PEEPi, changes in lung volume and the expiratory flow/volume relationship were observed. PEEPtot,rs and PEEPtot,cw also increased. Under these circumstances, PEEP increased static elastance in both the respiratory system and the chest wall, reducing cardiac index and affecting hemodynamics and gas exchange. Our data show that in mechanically ventilated COPD patients with PEEPi due to flow limitation, PEEP levels exceeding the 85% of PEEPi (Pcrit) caused further hyperinflation and compromised hemodynamics and gas exchange.

Background: Limited data suggest that increased resistance to flow within endotracheal tubes (ETT) may occur in patients whose lungs are mechanically ventilated for more than 48 h, especially when airway humidification is inadequate. This could lead to sudden ETT obstruction or induce excessive loading during spontaneous breathing. Methods: Twenty-three such patients were randomly assigned to three types of airway humidifier based on three different working principles: a Fisher Paykell hot water system (n = 7), a Pall BB2215 heat and moisture exchanger (HME) hydrophobic filter (n = 8), and a Dar Hygrobac 35254111 HME hygroscopic filter (n = 8). The decrease in internal pressure along the ETT and the flow rate were measured in each patient every 2 days. An "effective inner diameter" was derived from these measurements and allowed the inner ETT configuration to be monitored. Results: On the first day of intubation, the mean diameter was similar in the three groups, and was slightly smaller than the in vitro diameter (mean +/- SD: 7.6 +/- 0.6 mm for Fisher-Paykell, 7.7 +/- 0.4 for Pall, and 7.5 +/- 0.4 for Dar). The mean diameter tended to decrease from day to day. At the end of the study, the overall reduction in mean diameter was significantly greater with the hydrophobic HME (Pall) than with the two other systems (Pall: -6.5 +/- 4% vs. 2.5 +/- 2.5% for Dar and 1.5 +/- 3% for Fisher-Paykell; P < 0.01 with analysis of variance). The same was true of the mean reduction in effective inner ETT diameter expressed per day of ventilation (-1.6 +/- 1.5% per day for Pall vs. -0.5 +/- 0.4% for Dar and -0.2 +/- 0.4% for Fisher-Paykell; P < 0.01). In four patients, the ETT became obstructed and emergency repeated tracheal intubation was required. The Pall HME and the Fisher-Paykell system were being used in three and one patient, respectively. Before obstruction, the reduction in ETT diameter was significantly greater for these four patients than for the remaining 23 patients (7.8 +/- 1.4% vs. 3.1 +/- 4.1%; P < 0.01). Conclusions: During prolonged mechanical ventilation, significant alterations in inner ETT configuration occur frequently and are influenced by the type of humidification device used. In vivo monitoring of ETT mechanical properties might be clinically useful.

The authors tested the hypothesis that during laparoscopic surgery, Trendelenburg position and pneumoperitoneum may worsen chest wall elastance, concomitantly decreasing transpulmonary pressure, and that a protective ventilator strategy applied after pneumoperitoneum induction, by increasing transpulmonary pressure, would result in alveolar recruitment and improvement in respiratory mechanics and gas exchange. In 29 consecutive patients, a recruiting maneuver followed by positive end-expiratory pressure 5 cm H(2)O maintained until the end of surgery was applied after pneumoperitoneum induction. Respiratory mechanics, gas exchange, blood pressure, and cardiac index were measured before (T(BSL)) and after pneumoperitoneum with zero positive end-expiratory pressure (T(preOLS)), after recruitment with positive end-expiratory pressure (T(postOLS)), and after peritoneum desufflation with positive end-expiratory pressure (T(end)). Esophageal pressure was used for partitioning respiratory mechanics between lung and chest wall (data are mean ± SD): on T(preOLS), chest wall elastance (E(cw)) and elastance of the lung (E(L)) increased (8.2 ± 0.9 vs. 6.2 ± 1.2 cm H(2)O/L, respectively, on T(BSL); P = 0.00016; and 11.69 ± 1.68 vs. 9.61 ± 1.52 cm H(2)O/L on T(BSL); P = 0.0007). On T(postOLS), both chest wall elastance and E(L) decreased (5.2 ± 1.2 and 8.62 ± 1.03 cm H(2)O/L, respectively; P = 0.00015 vs. T(preOLS)), and Pao(2)/inspiratory oxygen fraction improved (491 ± 107 vs. 425 ± 97 on T(preOLS); P = 0.008) remaining stable thereafter. Recruited volume (the difference in lung volume for the same static airway pressure) was 194 ± 80 ml. Pplat(RS) remained stable while inspiratory transpulmonary pressure increased (11.65 + 1.37 cm H(2)O vs. 9.21 + 2.03 on T(preOLS); P = 0.007). All respiratory mechanics parameters remained stable after abdominal desufflation. Hemodynamic parameters remained stable throughout the study. In patients submitted to laparoscopic surgery in Trendelenburg position, an open lung strategy applied after pneumoperitoneum induction increased transpulmonary pressure and led to alveolar recruitment and improvement of E(cw) and gas exchange.