Closing, opening and reopening: the difficult coexistence
Editorial

Closing, opening and reopening: the difficult coexistence

Massimo Ferluga, Umberto Lucangelo

Department of Perioperative Medicine, Intensive Care and Emergency, Cattinara Hospital, Trieste, Italy

Correspondence to: Prof. Umberto Lucangelo, MD, PhD. Chief of Department of Perioperative Medicine, Intensive Care and Emergency, Cattinara Hospital, Strada di Fiume 447, 34149 Trieste, Italy. Email: u.lucangelo@fmc.units.it.

Provenance: This is an invited Editorial commissioned by Section Editor Dr. Zhiheng Xu (State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, Department of Intensive Care, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China).

Comment on: Yoshida T, Nakahashi S, Nakamura MA, et al. Volume controlled ventilation does not prevent injurious inflation during spontaneous effort. Am J Respir Crit Care Med 2017. [Epub ahead of print].


Submitted Jun 09, 2017. Accepted for publication Jun 11, 2017.

doi: 10.21037/jtd.2017.06.93


Volume-controlled ventilation (VCV) has always been considered as protective ventilation, in particular during spontaneous breathing, being able to avoid the administration of injurious tidal volumes (Vt) to the patient. In fact, spontaneous efforts increase transpulmonary pressure (Pl) only during pressure-regulated ventilations (1). Despite this difference in terms of Pl, the conditions of lung parenchyma determine the damage to the lung tissue and the onset of ventilator induced lung injury (VILI).

In normal lung the pressures applied to a local region of the pleura are homogeneous and distributed over the whole lung (fluid-like behavior), whereas negative pleural pressures (Ppl) generated by diaphragmatic contraction are rather concentrated in dorsal parts (solid-like), once lung has been injured (2). Furthermore, when Pl is applied to the lung, a counterforce of equal intensity is developed (lung stress), whereas the associated lung deformation is called strain. These two forces are directly correlated by the specific elastance (Elsp), which reflects the intrinsic mechanical characteristics of the lung parenchyma (3). This concept is a recent introduction, but it has an important clinical relevance right away; in fact, Elsp is peculiar in each species: in pigs is about half that in human and consequently a plateau pressure (Pplat) of 30 cmH2O in pigs would approximately correspond to 60 cmH2O in humans. Therefore the differences on Elsp between species must be taken in account when considering the results of experimental studies (4,5).

In injured lung, dorsal zones are collapsed or cannot be inflated; therefore they can be stressed, but not strained. Consequently, in this inhomogeneous distribution of ventilation, the healthy regions have to sustain a greater stress that promotes the development of biotrauma. When the stress and strain from mechanical ventilation overcome the lung’s ability to adapt, mechanical ventilation becomes injurious, thus ventilator settings must take into account both gas exchange and stress and strain. The latters can be modified by different interfaces and positions. Lopez-Aguilar and colleagues found that the combination of low dose partial liquid ventilation with perfluorocarbons and prone positioning improved lung function while inducing minimal stress in an animal model of acute lung injury (ALI) (6).

The effects of spontaneous breathing in different severities of lung injury were recently investigated. Patient efforts generate negative change in Ppl, with a large difference between mild and severe lung injury. In the first, spontaneous efforts reduce just before peak airway pressure was reached; in contrast, in severe lung injury the respiratory muscles continue to contract until the end of inspiration, and patient active expiration increase airway pressure above plateau. Consequently, the highest Pl was generated in severe lung injury. These findings were supported by histological samples: the alveolar damage was less pronounced in mild lung injury models. On the contrary, in severe lung injury more hyaline membrane formation and alveolar hemorrhaging with more severe neutrophil infiltration into the alveoli and interstitium were observed (7).

Another important effect of spontaneous breathing is that local negative Ppl generated by diaphragmatic contraction is not uniformly transmitted. Using electrical impedance tomography during controlled ventilation, simultaneous inflation of the different lung regions was observed, whereas, when spontaneous efforts were present, they caused an early inflation of dependent lung regions. The latter was accompanied by simultaneous deflation of nondependent region, indicating movement of gas from nondependent to dependent lung regions; because this was not associated with alterations in tidal volume it indicates a pendelluft phenomenon. After induction of muscle paralysis a progressive reduction of inhomogeneity of ventilation was observed, confirming that extent of the pendelluft was proportional to the intensity of the respiratory effort (8).

Protti and colleagues introduced the difference between static and dynamic strain. Lung tissue deformation due to application of positive end-expiratory pressure (PEEP) is called static strain, whereas tidal ventilation is a dynamic process, as the energy is cyclically applied to the lungs; lung deformation due to tidal volume is called dynamic strain. In particular, if a large force is applied (dynamic strain), tension will concentrate and rupture will possibly occur. Conversely, if the force is applied on pre-stressed fibers (static strain), distension will be more uniform and rupture less common. Therefore PEEP-induced Vt may have had its own beneficial effect (9). Airway pressure release ventilation (APRV) is a ventilator mode characterized by an open-valve CPAP with a brief pressure release and that in previous animal studies was associated with higher Vt and Pplat. In an extrapulmonary lung injury model APRV was compared with low Vt ventilation and despite the greater Pplat and Vt in the APRV group, Pl was similar to that of protective ventilation group, demonstrating that the increases in Pplat in APRV reflects an increase in Ppl. The authors concluded that APRV represents a safe and effective ventilation mode in patients at risk for the development of extrapulmonary lung injury (10). The same group of authors recently studied the impact of dynamic strain on tissue injury in both normal and acutely injured lung tissue model ventilated in APRV. The normal tissue was not seriously injured as long as dynamic strain remained low. However, when high Pplat was combined with high dynamic strain, this caused significant damage to normal tissue and exacerbated damage to the injured tissue. This study reaffirmed that, even in the presence of high Pplat, the use of APRV promoted recruitment and stabilized the alveoli, reducing VILI (11).

Preserved spontaneous breathing during acute respiratory failure has been recently discussed. In ten patients equipped with esophageal catheters inspiratory muscle pressure (Pmus) was almost zero during controlled mechanical ventilation (CMV), although application of decreasing levels of pressure support led to a progressive increase of Pmus, under the assumption of identical mechanical properties of the respiratory system (compliance, resistance, flow and volume). As a result, Pl swings were similar overall between CMV and all the levels of pressure support ventilation (PSV) applied, although with a poor correlation. This difference was explained by the corresponding difference in the inspiratory flow rates between the different ventilator modalities, indicating that the resistive pressure drop caused this difference. If the analysis was focused only on values for which the inspiratory flow was similar, this resulted in a tight correlation. In the same way, the swings of esophageal pressure (Pes) were positive during CMV, but became negative during PSV and progressively lower for decreasing levels of support. Similarly, alveolar pressure (Palv) progressively decreased from CMV through the different levels of PSV and Palv was lower than the set PEEP, if a low level of support was applied. Finally, during spontaneous breathing, under identical mechanical properties of the respiratory system and for the same inspiratory flow, Pl will be the same during CMV and PSV. Similarly, if the lung is at the same volume, the pressure across the alveolar wall, which is due to the elastic recoil of the lung, will not differ between CMV and PSV. Consequently, a negative pressure will surround the alveoli and during PSV Palv will become very negative to overcome the resistive pressure drop; negative Palv values and their consequences on fluid shifts are potential mechanisms by which spontaneous breathing might induce lung injury (12).

Yoshida and colleagues reported that VCV prevented increases in Vt and in Pl calculated using Pes. The main findings were that the limitation of Vt and Pl by VCV could not eliminate harm from spontaneous breathing, unless the level of spontaneous effort was lowered and local dependent lung stress was reduced (13). We congratulate the authors and recognized the effort to provide more evidence in this field. In fact, these results confirmed that stress and strain are inadequately estimated by Pplat and Vt; therefore they must be taken in account when setting mechanical ventilation, especially in spontaneous breathing patients, to avoid further VILI.


Acknowledgements

None.


Footnote

Conflicts of Interest: The authors have no conflicts of interest to declare.


References

  1. Akoumianaki E, Maggiore SM, Valenza F, et al. The application of esophageal pressure measurement in patients with respiratory failure. Am J Respir Crit Care Med 2014;189:520-31. [Crossref] [PubMed]
  2. Hraiech S, Yoshida T, Papazian L. Balancing neuromuscular blockade versus preserved muscle activity. Curr Opin Crit Care 2015;21:26-33. [Crossref] [PubMed]
  3. Blankman P, Hasan D, Bikker IG, et al. Lung stress and strain calculations in mechanically ventilated patients in the intensive care unit. Acta Anaesthesiol Scand 2016;60:69-78. [Crossref] [PubMed]
  4. Gattinoni L, Carlesso E, Caironi P. Stress and strain within the lung. Curr Opin Crit Care 2012;18:42-7. [Crossref] [PubMed]
  5. Protti A, Cressoni M, Santini A, et al. Lung stress and strain during mechanical ventilation: any safe threshold? Am J Respir Crit Care Med 2011;183:1354-62. [Crossref] [PubMed]
  6. López-Aguilar J, Lucangelo U, Albaiceta GM, et al. Effects on lung stress of position and different doses of perfluorocarbon in a model of ARDS. Respir Physiol Neurobiol 2015;210:30-7. [Crossref] [PubMed]
  7. Yoshida T, Uchiyama A, Matsuura N, et al. The comparison of spontaneous breathing and muscle paralysis in two different severities of experimental lung injury. Crit Care Med 2013;41:536-45. [Crossref] [PubMed]
  8. Yoshida T, Torsani V, Gomes S, et al. Spontaneous effort causes occult pendelluft during mechanical ventilation. Am J Respir Crit Care Med 2013;188:1420-7. [Crossref] [PubMed]
  9. Protti A, Andreis DT, Monti M, et al. Lung stress and strain during mechanical ventilation: any difference between statics and dynamics? Crit Care Med 2013;41:1046-55. [Crossref] [PubMed]
  10. Kollisch-Singule M, Emr B, Jain SV, et al. The effects of airway pressure release ventilation on respiratory mechanics in extrapulmonary lung injury. Intensive Care Med Exp 2015;3:35. [Crossref] [PubMed]
  11. Jain SV, Kollisch-Singule M, Satalin J, et al. The role of high airway pressure and dynamic strain on ventilator-induced lung injury in a heterogeneous acute lung injury model. Intensive Care Med Exp 2017;5:25. [Crossref] [PubMed]
  12. Bellani G, Grasselli G, Teggia-Droghi M, et al. Do spontaneous and mechanical breathing have similar effects on average transpulmonary and alveolar pressure? A clinical crossover study. Crit Care 2016;20:142. [Crossref] [PubMed]
  13. Yoshida T, Nakahashi S, Nakamura MA, et al. Volume controlled ventilation does not prevent injurious inflation during spontaneous effort. Am J Respir Crit Care Med 2017. [Epub ahead of print]. [Crossref] [PubMed]
Cite this article as: Ferluga M, Lucangelo U. Closing, opening and reopening: the difficult coexistence. J Thorac Dis 2017;9(7):1808-1810. doi: 10.21037/jtd.2017.06.93