In their clear overview on ventilator-induced lung injury (VILI) in Intensive Care Medicine, Gattinoni and colleagues1 call to mind that mechanical ventilation (MV) should provide sufficient gas exchange without generating additional injury. However, current MV does cause VILI1. We would like to draw attention again to a neglected MV method: negative pressure ventilation (NPV). NPV is not only effective and safe2, it also avoids the development of VILI.
VILI is not caused by MV itself, but by the supra-atmospheric pressure generated in positive pressure ventilation (PPV). In contrast, NPV applies sub-atmospheric pressure around the chest and abdomen. Although the driving pressure (the pressure difference between lung and outside of the thorax) is the same in these two methods, their effect on the pressure in the inter-pleural space is quite different: PPV increases it whereas NPV decreases it. This difference is neglected in most discussions, although high pleural pressure is a probable cause of VILI, as we explain below.
Normally, the pressure in the inter-pleural space is sub-atmospheric, with the lung pulling the visceral pleura inward, and the chest wall pulling the parietal pleura outward. This, together with lubricant between the pleurae, minimizes friction between the lung and the thoracic wall. By expanding the chest, natural inspiration decreases the pressure in the thorax. This drop in pressure is distributed over the lungs and inter-pleural space, causing air to flow into the lungs, and further reducing friction between lung and thoracic wall. NPV mimics spontaneous breathing: the reduced pressure outside the thorax wall will again lower the pressure in both lung and inter-pleural space.
Barotrauma
The supra-atmospheric pressure from PPV raises the pressure in the lung and presses the pleurae together, raising the pleural pressure and increasing the friction between them. This increased friction causes shear stress which can result in alveolar rupture, pneumomediastinum, subcutaneous emphysema and pneumothorax [reference [1] in Gattinoni et al.1. In contrast, NPV substantially lowers the risk of air leaks.
Volutrauma and atelectasis
Whereas airways normally close only during deep expiration below the functional residual capacity, high pleural pressure can cause lung closure before the tidal volume has been expired3. Subsequent tidal volumes delivered by PPV then cause hyperinflation in a vicious cycle. Sustained airway closure leads to absorption atelectasis4. In contrast, NPV will prevent lung closure, hyperinflation and atelectasis.
Haemodynamic consequences
Haemodynamic consequences are also highlighted in the article by Gattinoni et al.1: the cardiovascular system suffers from raised intrathoracic pressure. Pulmonary hypertension, heart failure, lung edema (with subsequent lung closure), and compression atelectasis are well documented side effects of PPV. In contrast, NPV spares the cardiovascular system, improves ventricular filling and cardiac index2.
Gattinoni and colleagues conclude that “the impossibility of ‘safe ventilation’ is the rationale for resorting to extracorporeal support”. NPV, for the reasons outlined above, may, by potentially preventing VILI and thus preventing patients deteriorating to such an acute respiratory distress syndrome (ARDS), be that ‘safe ventilation’ strategy we seek. NPV deserves investigation and the development of torso-only modern, lightweight, practicable devices2,5.
References.
- Gattinoni L, Collino F, Camporota L (2024) Ventilator induced lung injury: a case for a larger umbrella? Intensive Care Med 50:275–278. https://doi.org/10.1007/s00134-023-07296-1 ↩︎
- Howard D, Coulthard MG, Speight C, Grocott M (2022) Negative pressure ventilation for COVID-19 respiratory failure: a phoenix from the ashes? Arab Board Med J 23(1):5–13. https://doi.org/10.4103/abmj.abmj_7_22 ↩︎
- Grasso F, Engelberts D, Helm E, Frndova H, Jarvis S, Talakoub O, McKerlie C, Babyn P, Post M, Kavanagh BP (2008) Negative-pressure ventilation. Better oxygenation and less lung injury. Am J Respir Crit Care Med 177:412–418. https://doi.org/10.1164/rccm.200707-1004OC ↩︎
- Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G (2003) Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 98:28–33. https://doi.org/10.1097/00000542-200301000-00008 ↩︎
- Coulthard MG, The Exovent Development Group (2021) Exovent: a study of a new negative-pressure ventilatory support device in healthy adults. Anaesthesia 76(5):623–628. https://doi.org/10.1111/anae.15350 ↩︎