Avoid common mistakes on your manuscript.
Introduction
Spontaneous breathing during mechanical ventilation balances important advantages including improved oxygenation [1] and less diaphragm disuse [2] against serious disadvantages including increased injury to the lung and diaphragm [2,3,4,5] and potentially lower survival [6]. Of course, spontaneous breathing is an absolute requirement for successful weaning, and so it must ultimately be a goal in all patients. While the traditional focus in acute respiratory distress syndrome (ARDS) is on controlling and monitoring ventilator breaths, recent advances point to important differences between spontaneous and mechanical breaths in terms of pathophysiology and monitoring [3, 4, 7]. This paper reviews these insights and provides suggestions for bedside monitoring of spontaneous effort in patients with ARDS during mechanical ventilation, focusing on the use of esophageal manometry.
Monitoring mechanical breaths
During a mechanical breath (i.e., without spontaneous effort), ventilation is preferentially distributed to the non-dependent “baby” lung, in part because of the predominance of atelectasis in the dependent lung; this explains why, during paralysis, the non-dependent “baby” lung is one of the regions more susceptible to stretch-induced injury [8,9,10]. In order to avoid such injury, physicians attempt to limit tidal volume (VT) or airway pressure (Paw), or in some cases, the transpulmonary pressure (PL) [7, 11].
Paw consists of two components: resistive pressure, which generates airflow through the airways and/or relates to tissue resistance and the endotracheal tube; and, alveolar pressure, which distends the alveoli and chest wall [11, 12]. Peak Paw comprises resistive and alveolar components. At end-inspiration airflow has ceased, and because there is now no “resistive” component, the resulting “plateau” pressure reflects the pressure distending the alveoli and chest wall [11, 12]. Therefore, plateau phase, either Paw, or PL, e.g., plateau Paw, driving pressure, or plateau PL, and not peak phase, best reflects the maximal stretch of distended alveoli (Fig. 1a)—and their propensity to injury, and for this reason clinicians target plateau Paw to less than 30 cmH2O (or plateau PL to less than 25 cmH2O) to prevent ventilator-induced lung injury [7, 11]. The relationships among pressures (peak and plateau, airway and transpulmonary) and regional lung distension during a mechanical breath are illustrated in Fig. 1a.
Monitoring spontaneous breaths
The context is more complicated during spontaneous effort for several reasons. First, the addition of spontaneous effort to a mechanical breath involves a (negative) deflection in pleural pressure (Ppl) combined with a (positive) deflection in Paw, which results in an additive increase in the distending pressure (i.e., PL = Paw − Ppl). Therefore, reliance on Paw (plateau Paw or driving pressure) is not sufficient to limit injurious stretch; instead, esophageal pressure (Pes) can be measured to assess the intensity of the effort, i.e., the negative deflection (or “swing”) in Pes caused by the effort, and to calculate the PL [7, 13]. Second, spontaneous effort exerts its impact differently on the non-dependent vs. the dependent lung. The plateau phase of PL is associated with maximal stretch in the non-dependent lung, but not the dependent lung. When peak PL occurs at the time that Pes is most negative as a result of vigorous effort, peak PL could correspond to time of maximal distension in the dependent lung (Fig. 1b). Therefore, in contrast to mechanical breaths, plateau PL (i.e., at end-inspiration) potentially underestimates maximal dependent lung stress/stretch during vigorous effort in ventilated patients with ARDS. Third, vigorous effort appears to increase injury in the dependent lung—the same region in which spontaneous effort increases inspiratory distension [4].
The key mechanism is inhomogeneous pressure transmission in the presence of “solid-like” injured lung (Supplemental Figure). Here, the negative deflection in Ppl resulting from diaphragm contraction is poorly transmitted to the remainder of the pleural surface, and thus “confined” to the dependent lung [3, 4, 14]. The higher distending pressure in the local lung will tend to draw gas from the non-dependent lung (this is called pendelluft [14]), or from the trachea and ventilator, towards the dependent lung. This causes a transient overdistension [3, 4, 14] and tidal recruitment in the dependent lung [3, 4] during early inspiration (i.e., the peak phase of PL), corresponding, in space and time, to maximal intensity of the diaphragm contraction and the peak negative value of deflection (swing) in Pes. Importantly, such injurious inflation is likely observed in the presence of vigorous effort, and “solid-like” atelectatic lung tissue due to insufficient PEEP [4, 5, 15].
Clinical implications
Limitations of VT and Paw are validated clinical approaches to lessen ventilator-induced lung injury during ventilator breaths, but effort-dependent lung injury is not preventable using such global parameters [3, 4, 14]. Instead monitoring PL and Pes may be preferable during spontaneous breaths, especially when spontaneous effort is vigorous. First, here plateau PL (at end-inspiration) corresponds to time of maximal distension in the non-dependent lung, but this is not always a good surrogate for dependent lung stress. When peak PL occurs at the time that Pes is most negative as a result of vigorous effort, (even with residual inspiratory flow) it is important to note that peak PL could correspond to time of maximal distension in the dependent lung—the region most at risk during spontaneous effort. Thus, the limitation of peak PL as well as plateau PL may become an important target in preventing effort-dependent lung injury. In future, we might carefully evaluate the safe upper limit of PL (or ∆PL) calculated using esophageal balloon manometry in order to minimize effort-dependent lung injury. This is because the assessment using Pes (i.e., ∆PL or PL) could misrepresent the “true” PL in the dependent lung due to “solid-like” dependent lung behavior and a vertical gradient of Ppl. Second, monitoring the degree of negative “swing” in Pes (i.e., intensity of spontaneous effort) can facilitate a balance between avoiding diaphragm disuse (from absence of effort) and overuse injury (from excess effort), thereby preventing ventilator-induced diaphragm dysfunction [2]. Third, Pes is useful to monitor patient–ventilator asynchronies and to estimate vascular distending pressures, which are potentially related to effort-dependent lung injury [7]. Finally, although regional pressure measurements are of increasing interest, they might ultimately best be assessed in conjunction with real-time regional lung imaging.
Conclusion
Emerging insights into the pathophysiology of spontaneous effort during mechanical ventilation are not intuitive but can be better understood with bedside monitoring such as esophageal manometry. Subsequent studies will determine the validity of—and identify thresholds for—titration of peak and plateau PL, as well as swings in Pes, in best protecting the lungs and diaphragms of patients with ARDS.
References
Putensen C, Zech S, Wrigge H, Zinserling J, Stuber F, Von Spiegel T, Mutz N (2001) Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Respir Crit Care Med 164:43–49
Goligher EC, Dres M, Fan E, Rubenfeld GD, Scales DC, Herridge MS, Vorona S, Sklar MC, Rittayamai N, Lanys A, Murray A, Brace D, Urrea C, Reid WD, Tomlinson G, Slutsky AS, Kavanagh BP, Brochard LJ, Ferguson ND (2018) Mechanical ventilation-induced diaphragm atrophy strongly impacts clinical outcomes. Am J Respir Crit Care Med 197:204–213
Yoshida T, Nakahashi S, Nakamura MAM, Koyama Y, Roldan R, Torsani V, De Santis RR, Gomes S, Uchiyama A, Amato MBP, Kavanagh BP, Fujino Y (2017) Volume-controlled ventilation does not prevent injurious inflation during spontaneous effort. Am J Respir Crit Care Med 196:590–601
Morais CCA, Koyama Y, Yoshida T, Plens GM, Gomes S, Lima C, Ramos OP, Pereira SM, Kawaguchi N, Yamamoto H, Uchiyama A, Borges JB, Vidal Melo MF, Tucci MR, Amato MBP, Kavanagh BP, Costa ELV, Fujino Y (2018) High positive end-expiratory pressure renders spontaneous effort non-injurious. Am J Resp Crit Care Med. https://doi.org/10.1164/rccm.201706-1244OC
Magalhaes PAF, Padilha GA, Moraes L, Santos CL, Maia LA, Braga CL, Duarte M, Andrade LB, Schanaider A, Capellozzi VL, Huhle R, Gama de Abreu M, Pelosi P, Rocco PRM, Silva PL (2018) Effects of pressure support ventilation on ventilator-induced lung injury in mild acute respiratory distress syndrome depend on level of positive end-expiratory pressure: a randomised animal study. Eur J Anaesthesiol 35:298–306
Papazian L, Forel JM, Gacouin A, Penot-Ragon C, Perrin G, Loundou A, Jaber S, Arnal JM, Perez D, Seghboyan JM, Constantin JM, Courant P, Lefrant JY, Guerin C, Prat G, Morange S, Roch A (2010) Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med 363:1107–1116
Mauri T, Yoshida T, Bellani G, Goligher EC, Carteaux G, Rittayamai N, Mojoli F, Chiumello D, Piquilloud L, Grasso S, Jubran A, Laghi F, Magder S, Pesenti A, Loring S, Gattinoni L, Talmor D, Blanch L, Amato M, Chen L, Brochard L, Mancebo J (2016) Esophageal and transpulmonary pressure in the clinical setting: meaning, usefulness and perspectives. Intensive Care Med 42:1360–1373
Tsuchida S, Engelberts D, Peltekova V, Hopkins N, Frndova H, Babyn P, McKerlie C, Post M, McLoughlin P, Kavanagh BP (2006) Atelectasis causes alveolar injury in nonatelectatic lung regions. Am J Respir Crit Care Med 174:279–289
Bellani G, Guerra L, Musch G, Zanella A, Patroniti N, Mauri T, Messa C, Pesenti A (2011) Lung regional metabolic activity and gas volume changes induced by tidal ventilation in patients with acute lung injury. Am J Respir Crit Care Med 183:1193–1199
Borges JB, Costa EL, Suarez-Sipmann F, Widstrom C, Larsson A, Amato M, Hedenstierna G (2014) Early inflammation mainly affects normally and poorly aerated lung in experimental ventilator-induced lung injury. Crit Care Med 42:e279–e287
Henderson WR, Chen L, Amato MB, Brochard LJ (2017) Fifty years of research in ARDS. Respiratory mechanics in acute respiratory distress syndrome. Am J Resp Crit Care Med 196:822–833
Bellani G, Grasselli G, Teggia-Droghi M, Mauri T, Coppadoro A, Brochard L, Pesenti A (2016) Do spontaneous and mechanical breathing have similar effects on average transpulmonary and alveolar pressure? A clinical crossover study. Crit Care 20:142
Yoshida T, Fujino Y, Amato MB, Kavanagh BP (2017) Fifty years of research in ARDS. Spontaneous breathing during mechanical ventilation. Risks, mechanisms, and management. Am J Respir Crit Care Med 195:985–992
Yoshida T, Torsani V, Gomes S, De Santis RR, Beraldo MA, Costa EL, Tucci MR, Zin WA, Kavanagh BP, Amato MB (2013) Spontaneous effort causes occult pendelluft during mechanical ventilation. Am J Respir Crit Care Med 188:1420–1427
Guldner A, Pelosi P, Gama de Abreu M (2014) Spontaneous breathing in mild and moderate versus severe acute respiratory distress syndrome. Curr Opin Crit Care 20:69–76
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Conflicts of interest
TY and BPK have applied for a patent on a CNAP (continuous negative abdominal pressure) device.
Electronic supplementary material
Below is the link to the electronic supplementary material.
Rights and permissions
About this article
Cite this article
Yoshida, T., Amato, M.B.P. & Kavanagh, B.P. Understanding spontaneous vs. ventilator breaths: impact and monitoring. Intensive Care Med 44, 2235–2238 (2018). https://doi.org/10.1007/s00134-018-5145-5
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00134-018-5145-5