Spontaneous Effort During Mechanical Ventilation: Maximal Injury With Less Positive End-Expiratory Pressure
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Citações na Scopus
129
Tipo de produção
article
Data de publicação
2016
Título da Revista
ISSN da Revista
Título do Volume
Editora
LIPPINCOTT WILLIAMS & WILKINS
Autores
YOSHIDA, Takeshi
LIMA, Raul G.
KAVANAGH, Brian P.
Citação
CRITICAL CARE MEDICINE, v.44, n.8, p.E678-E688, 2016
Resumo
Objectives: We recently described how spontaneous effort during mechanical ventilation can cause ""pendelluft,"" that is, displacement of gas from nondependent (more recruited) lung to dependent (less recruited) lung during early inspiration. Such transfer depends on the coexistence of more recruited (source) liquid-like lung regions together with less recruited (target) solid-like lung regions. Pendelluft may improve gas exchange, but because of tidal recruitment, it may also contribute to injury. We hypothesize that higher positive end-expiratory pressure levels decrease the propensity to pendelluft and that with lower positive end-expiratory pressure levels, pendelluft is associated with improved gas exchange but increased tidal recruitment. Design: Crossover design. Setting: University animal research laboratory. Subjects: Anesthetized landrace pigs. Interventions: Surfactant depletion was achieved by saline lavage in anesthetized pigs, and ventilator-induced lung injury was produced by ventilation with high tidal volume and low positive end-expiratory pressure. Ventilation was continued in each of four conditions: positive end-expiratory pressure (low or optimized positive end-expiratory pressure after recruitment) and spontaneous breathing (present or absent). Tidal recruitment was assessed using dynamic CT and regional ventilation/perfusion using electric impedance tomography. Esophageal pressure was measured using an esophageal balloon manometer. Measurements and Results: Among the four conditions, spontaneous breathing at low positive end-expiratory pressure not only caused the largest degree of pendelluft, which was associated with improved ventilation/perfusion matching and oxygenation, but also generated the greatest tidal recruitment. At low positive end-expiratory pressure, paralysis worsened oxygenation but reduced tidal recruitment. Optimized positive end-expiratory pressure decreased the magnitude of spontaneous efforts (measured by esophageal pressure) despite using less sedation, from -5.6 +/- 1.3 to -2.0 +/- 0.7 cm H2O, while concomitantly reducing pendelluft and tidal recruitment. No pendelluft was observed in the absence of spontaneous effort. Conclusions: Spontaneous effort at low positive end-expiratory pressure improved oxygenation but promoted tidal recruitment associated with pendelluft. Optimized positive end-expiratory pressure (set after lung recruitment) may reverse the harmful effects of spontaneous breathing by reducing inspiratory effort, pendelluft, and tidal recruitment.
Palavras-chave
electric impedance tomography, esophageal pressure, lung injury, pendelluft, positive end-expiratory pressure, spontaneous breathing
Referências
- Akoumianaki E, 2014, AM J RESP CRIT CARE, V189, P520, DOI 10.1164/rccm.201312-2193CI
- Amato MBP, 2015, NEW ENGL J MED, V372, P747, DOI 10.1056/NEJMsa1410639
- BAYDUR A, 1982, AM REV RESPIR DIS, V126, P788
- Borges JB, 2006, AM J RESP CRIT CARE, V174, P268, DOI 10.1164/rccm.200506-97OC
- Borges JB, 2012, J APPL PHYSIOL, V112, P225, DOI 10.1152/japplphysiol.01090.2010
- Costa ELV, 2009, INTENS CARE MED, V35, P1132, DOI 10.1007/s00134-009-1447-y
- DANGELO E, 1974, J APPL PHYSIOL, V37, P311
- DANGELO E, 1973, RESP PHYSIOL, V19, P356, DOI 10.1016/0034-5687(73)90039-X
- de Matos GFJ, 2012, CRIT CARE, V16, DOI 10.1186/cc10602
- De Troyer A, 2009, J APPL PHYSIOL, V107, P315, DOI 10.1152/japplphysiol.91472.2008
- Dreyfuss D, 1998, AM J RESP CRIT CARE, V157, P294
- Evans CL, 1914, J PHYSIOL-LONDON, V49, P10
- Haberthur C, 2005, CRIT CARE, V9, pR407, DOI 10.1186/cc3735
- Hedenstierna G, 2006, MINERVA ANESTESIOL, V72, P183
- HOPPIN FG, 1969, J APPL PHYSIOL, V27, P863
- KIM MJ, 1976, J APPL PHYSIOL, V41, P369
- KRUEGER JJ, 1961, J APPL PHYSIOL, V16, P465
- Levine S, 2008, NEW ENGL J MED, V358, P1327, DOI 10.1056/NEJMoa070447
- MARINI JJ, 1990, CRIT CARE CLIN, V6, P635
- Marini JJ, 2011, CURR OPIN CRIT CARE, V17, P24, DOI 10.1097/MCC.0b013e328342726e
- Markstaller K, 2001, BRIT J ANAESTH, V87, P459, DOI 10.1093/bja/87.3.459
- MARSHALL R, 1962, J APPL PHYSIOL, V17, P917
- Neumann P, 1998, AM J RESP CRIT CARE, V158, P1636
- Papazian L, 2010, NEW ENGL J MED, V363, P1107, DOI 10.1056/NEJMoa1005372
- PENGELLY LD, 1971, J APPL PHYSIOL, V30, P797
- PUTENSEN C, 1994, ANESTHESIOLOGY, V81, P921, DOI 10.1097/00000542-199410000-00018
- Putensen C, 2001, AM J RESP CRIT CARE, V164, P43
- ROSSI A, 1990, EUR RESPIR J, V3, P818
- STOCK MC, 1987, CRIT CARE MED, V15, P462, DOI 10.1097/00003246-198705000-00002
- Wrigge H, 2003, ANESTHESIOLOGY, V99, P376, DOI 10.1097/00000542-200308000-00019
- Yoshida T, 2012, CRIT CARE MED, V40, P1578, DOI 10.1097/CCM.0b013e3182451c40
- Yoshida T, 2013, AM J RESP CRIT CARE, V188, P1420, DOI 10.1164/rccm.201303-0539OC
- Yoshida T, 2013, CRIT CARE MED, V41, P536, DOI 10.1097/CCM.0b013e3182711972