Transpulmonary Pressure Describes Lung Morphology During Decremental Positive End-Expiratory Pressure Trials in Obesity

Carregando...
Imagem de Miniatura
Citações na Scopus
79
Tipo de produção
article
Data de publicação
2017
Título da Revista
ISSN da Revista
Título do Volume
Editora
LIPPINCOTT WILLIAMS & WILKINS
Autores
FUMAGALLI, Jacopo
BERRA, Lorenzo
ZHANG, Changsheng
PIRRONE, Massimiliano
MAGNI, Federico
BENNETT, Desmond
Citação
CRITICAL CARE MEDICINE, v.45, n.8, p.1374-1381, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Objectives: Atelectasis develops in critically ill obese patients when undergoing mechanical ventilation due to increased pleural pressure. The current study aimed to determine the relationship between transpulmonary pressure, lung mechanics, and lung morphology and to quantify the benefits of a decremental positive end-expiratory pressure trial preceded by a recruitment maneuver. Design: Prospective, crossover, nonrandomized interventional study. Setting: Medical and Surgical Intensive Care Units at Massachusetts General Hospital (Boston, MA) and University Animal Research Laboratory (Sao Paulo, Brazil). Patients/Subjects: Critically ill obese patients with acute respiratory failure and anesthetized swine. Interventions: Clinical data from 16 mechanically ventilated critically ill obese patients were analyzed. An animal model of obesity with reversible atelectasis was developed by placing fluid filled bags on the abdomen to describe changes of lung mechanics, lung morphology, and pulmonary hemodynamics in 10 swine. Measurements and Main Results: In obese patients (body mass index, 48 +/- 11 kg/m(2)), 21.7 +/- 3.7 cm H2O of positive end-expiratory pressure resulted in the lowest elastance of the respiratory system (18.6 +/- 6.1 cm H2O/L) after a recruitment maneuver and decremental positive end-expiratory pressure and corresponded to a positive (2.1 +/- 2.2 cm H2O) end-expiratory transpulmonary pressure. Ventilation at lowest elastance positive end-expiratory pressure preceded by a recruitment maneuver restored end-expiratory lung volume (30.4 +/- 9.1 mL/kg ideal body weight) and oxygenation (273.4 +/- 72.1 mm Hg). In the swine model, lung collapse and intratidal recruitment/derecruitment occurred when the positive end-expiratory transpulmonary pressure decreased below 2-4 cm H2O. After the development of atelectasis, a decremental positive end-expiratory pressure trial preceded by lung recruitment identified the positive end-expiratory pressure level (17.4 +/- 2.1 cm H2O) needed to restore poorly and nonaerated lung tissue, reestablishing lung elastance and oxygenation while avoiding increased pulmonary vascular resistance. Conclusions: In obesity, low-to-negative values of transpulmonary pressure predict lung collapse and intratidal recruitment/derecruitment. A decremental positive end-expiratory pressure trial preceded by a recruitment maneuver reverses atelectasis, improves lung mechanics, distribution of ventilation and oxygenation, and does not increase pulmonary vascular resistance.
Palavras-chave
electrical impedance tomography, lung CT scan, lung recruitment, positive end-expiratory pressure, transpulmonary pressure
Referências
  1. Amato MBP, 2015, NEW ENGL J MED, V372, P747, DOI 10.1056/NEJMsa1410639
  2. BAYDUR A, 1982, AM REV RESPIR DIS, V126, P788
  3. Behazin N, 2010, J APPL PHYSIOL, V108, P212, DOI 10.1152/japplphysiol.91356.2008
  4. BIONDI JW, 1988, ANESTH ANALG, V67, P144
  5. Borges JB, 2006, AM J RESP CRIT CARE, V174, P268, DOI 10.1164/rccm.200506-97OC
  6. Borges JB, 2012, J APPL PHYSIOL, V112, P225, DOI 10.1152/japplphysiol.01090.2010
  7. Chiumello D, 2008, CRIT CARE, V12, DOI 10.1186/cc7139
  8. Costa ELV, 2009, INTENS CARE MED, V35, P1132, DOI 10.1007/s00134-009-1447-y
  9. Ferretti A, 2001, CHEST, V119, P1401, DOI 10.1378/chest.119.5.1401
  10. Flegal KM, 2016, JAMA-J AM MED ASSOC, V315, P2284, DOI 10.1001/jama.2016.6458
  11. HEDENSTIERNA G, 1976, ACTA ANAESTH SCAND, V20, P248
  12. Jones RL, 2006, CHEST, V130, P827, DOI 10.1378/chest.130.3.827
  13. Kacmarek RM, 2016, CRIT CARE MED, V44, P32, DOI 10.1097/CCM.0000000000001383
  14. Lemyze M, 2013, CRIT CARE MED, V41, P2592, DOI 10.1097/CCM.0b013e318298637f
  15. Lumb AB, 2010, NUNNS APPL RESP PHYS
  16. Marshall RV, 2016, JAMA OTOLARYNGOL, V142, P772, DOI 10.1001/jamaoto.2016.1089
  17. MUSCEDERE JG, 1994, AM J RESP CRIT CARE, V149, P1327
  18. NIDEN AH, 1964, J CLIN INVEST, V43, P810, DOI 10.1172/JCI104967
  19. Pelosi P, 2001, AM J RESP CRIT CARE, V164, P122
  20. Pirrone M, 2016, CRIT CARE MED, V44, P300, DOI 10.1097/CCM.0000000000001387
  21. Protti A, 2013, CRIT CARE MED, V41, P1046, DOI 10.1097/CCM.0b013e31827417a6
  22. Reinius H, 2009, ANESTHESIOLOGY, V111, P979, DOI 10.1097/ALN.0b013e3181b87edb
  23. Steier J, 2014, THORAX, V69, P752, DOI 10.1136/thoraxjnl-2014-205148
  24. Suarez-Sipmann F, 2007, CRIT CARE MED, V35, P214, DOI 10.1097/01.CCM.0000251131.40301.E2
  25. Talmor D, 2008, NEW ENGL J MED, V359, P2095, DOI 10.1056/NEJMoa0708638
  26. Victorino JA, 2004, AM J RESP CRIT CARE, V169, P791, DOI 10.1164/rccm.200301-133OC
  27. Vieillard-Baron A, 2001, CRIT CARE MED, V29, P1551, DOI 10.1097/00003246-200108000-00009
  28. Yoshida T, 2016, CRIT CARE MED, V44, pE678, DOI 10.1097/CCM.0000000000001649
  29. ZAPOL WM, 1977, NEW ENGL J MED, V296, P476, DOI 10.1056/NEJM197703032960903
  30. ZERAH F, 1993, CHEST, V103, P1470, DOI 10.1378/chest.103.5.1470