Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity
Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Submitted 10 October 2008 ; accepted in final form 11 November 2009 To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P Pl ) in severe obesity,...
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| Published in | Journal of applied physiology (1985) Vol. 108; no. 1; pp. 212 - 218 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Am Physiological Soc
01.01.2010
American Physiological Society |
| Series | Pulmonary Physiology and Pathophysiology in Obesity |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts
Submitted 10 October 2008
; accepted in final form 11 November 2009
To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P Pl ) in severe obesity, we studied 51 obese subjects (body mass index = 38–80.7 kg/m 2 ) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P Es , P Ga ) using a balloon-catheter, airway pressure (P AO ), flow, and volume. We compared P Es to another estimate of P Pl based on P AO and flow. Reasoning that the lungs would not inflate until P AO exceeded alveolar and pleural pressures (P AO > P Alv > P Pl ), we disconnected subjects from the ventilator for 10–15 s to allow them to reach relaxation volume (V Rel ) and then slowly raised P AO until lung volume increased by 10 ml, indicating the "threshold P AO " (P AO-Thr ) for inflation, which we took to be an estimate of the lowest P Alv or P Pl to be found in the chest at V Rel . P AO-Thr ranged from 0.6 to 14.0 cmH 2 O in obese and 0.2 to 0.9 cmH 2 O in control subjects. P Es at V Rel was higher in obese than control subjects (12.5 ± 3.9 vs. 6.9 ± 3.1 cmH 2 O, means ± SD; P = 0.0002) and correlated with P AO-Thr ( R 2 = 0.16, P = 0.0015). Respiratory system compliance (C RS ) was lower in obese than control (0.032 ± 0.008 vs. 0.053 ± 0.007 l/cmH 2 O) due principally to lower lung compliance (0.043 ± 0.016 vs. 0.084 ± 0.029 l/cmH 2 O) rather than chest wall compliance (obese 0.195 ± 0.109, control 0.223 ± 0.132 l/cmH 2 O). We conclude that many severely obese supine subjects at relaxation volume have positive P pl throughout the chest. High P Es suggests high P Pl in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes.
esophageal pressure; compliance; elastance; gastric pressure; pressure-volume curve
Address for reprint requests and other correspondence: S. H. Loring, Dept. of Anesthesia, Critical Care and Pain Medicine, Dana 715, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215 (e-mail sloring{at}bidmc.harvard.edu ). |
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| AbstractList | To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P(Pl)) in severe obesity, we studied 51 obese subjects (body mass index = 38-80.7 kg/m(2)) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P(Es), P(Ga)) using a balloon-catheter, airway pressure (P(AO)), flow, and volume. We compared P(Es) to another estimate of P(Pl) based on P(AO) and flow. Reasoning that the lungs would not inflate until P(AO) exceeded alveolar and pleural pressures (P(AO) > P(Alv) > P(Pl)), we disconnected subjects from the ventilator for 10-15 s to allow them to reach relaxation volume (V(Rel)) and then slowly raised P(AO) until lung volume increased by 10 ml, indicating the "threshold P(AO)" (P(AO-Thr)) for inflation, which we took to be an estimate of the lowest P(Alv) or P(Pl) to be found in the chest at V(Rel). P(AO-Thr) ranged from 0.6 to 14.0 cmH2O in obese and 0.2 to 0.9 cmH2O in control subjects. P(Es) at V(Rel) was higher in obese than control subjects (12.5 +/- 3.9 vs. 6.9 +/- 3.1 cmH2O, means +/- SD; P = 0.0002) and correlated with P(AO-Thr) (R(2) = 0.16, P = 0.0015). Respiratory system compliance (C(RS)) was lower in obese than control (0.032 +/- 0.008 vs. 0.053 +/- 0.007 l/cmH2O) due principally to lower lung compliance (0.043 +/- 0.016 vs. 0.084 +/- 0.029 l/cmH2O) rather than chest wall compliance (obese 0.195 +/- 0.109, control 0.223 +/- 0.132 l/cmH2O). We conclude that many severely obese supine subjects at relaxation volume have positive P(pl) throughout the chest. High P(Es) suggests high P(Pl) in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes.To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P(Pl)) in severe obesity, we studied 51 obese subjects (body mass index = 38-80.7 kg/m(2)) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P(Es), P(Ga)) using a balloon-catheter, airway pressure (P(AO)), flow, and volume. We compared P(Es) to another estimate of P(Pl) based on P(AO) and flow. Reasoning that the lungs would not inflate until P(AO) exceeded alveolar and pleural pressures (P(AO) > P(Alv) > P(Pl)), we disconnected subjects from the ventilator for 10-15 s to allow them to reach relaxation volume (V(Rel)) and then slowly raised P(AO) until lung volume increased by 10 ml, indicating the "threshold P(AO)" (P(AO-Thr)) for inflation, which we took to be an estimate of the lowest P(Alv) or P(Pl) to be found in the chest at V(Rel). P(AO-Thr) ranged from 0.6 to 14.0 cmH2O in obese and 0.2 to 0.9 cmH2O in control subjects. P(Es) at V(Rel) was higher in obese than control subjects (12.5 +/- 3.9 vs. 6.9 +/- 3.1 cmH2O, means +/- SD; P = 0.0002) and correlated with P(AO-Thr) (R(2) = 0.16, P = 0.0015). Respiratory system compliance (C(RS)) was lower in obese than control (0.032 +/- 0.008 vs. 0.053 +/- 0.007 l/cmH2O) due principally to lower lung compliance (0.043 +/- 0.016 vs. 0.084 +/- 0.029 l/cmH2O) rather than chest wall compliance (obese 0.195 +/- 0.109, control 0.223 +/- 0.132 l/cmH2O). We conclude that many severely obese supine subjects at relaxation volume have positive P(pl) throughout the chest. High P(Es) suggests high P(Pl) in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes. To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P Pl ) in severe obesity, we studied 51 obese subjects (body mass index = 38–80.7 kg/m 2 ) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P Es , P Ga ) using a balloon-catheter, airway pressure (P AO ), flow, and volume. We compared P Es to another estimate of P Pl based on P AO and flow. Reasoning that the lungs would not inflate until P AO exceeded alveolar and pleural pressures (P AO > P Alv > P Pl ), we disconnected subjects from the ventilator for 10–15 s to allow them to reach relaxation volume (V Rel ) and then slowly raised P AO until lung volume increased by 10 ml, indicating the “threshold P AO ” (P AO-Thr ) for inflation, which we took to be an estimate of the lowest P Alv or P Pl to be found in the chest at V Rel . P AO-Thr ranged from 0.6 to 14.0 cmH 2 O in obese and 0.2 to 0.9 cmH 2 O in control subjects. P Es at V Rel was higher in obese than control subjects (12.5 ± 3.9 vs. 6.9 ± 3.1 cmH 2 O, means ± SD; P = 0.0002) and correlated with P AO-Thr ( R 2 = 0.16, P = 0.0015). Respiratory system compliance (C RS ) was lower in obese than control (0.032 ± 0.008 vs. 0.053 ± 0.007 l/cmH 2 O) due principally to lower lung compliance (0.043 ± 0.016 vs. 0.084 ± 0.029 l/cmH 2 O) rather than chest wall compliance (obese 0.195 ± 0.109, control 0.223 ± 0.132 l/cmH 2 O). We conclude that many severely obese supine subjects at relaxation volume have positive P pl throughout the chest. High P Es suggests high P Pl in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes. Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Submitted 10 October 2008 ; accepted in final form 11 November 2009 To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P Pl ) in severe obesity, we studied 51 obese subjects (body mass index = 38–80.7 kg/m 2 ) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P Es , P Ga ) using a balloon-catheter, airway pressure (P AO ), flow, and volume. We compared P Es to another estimate of P Pl based on P AO and flow. Reasoning that the lungs would not inflate until P AO exceeded alveolar and pleural pressures (P AO > P Alv > P Pl ), we disconnected subjects from the ventilator for 10–15 s to allow them to reach relaxation volume (V Rel ) and then slowly raised P AO until lung volume increased by 10 ml, indicating the "threshold P AO " (P AO-Thr ) for inflation, which we took to be an estimate of the lowest P Alv or P Pl to be found in the chest at V Rel . P AO-Thr ranged from 0.6 to 14.0 cmH 2 O in obese and 0.2 to 0.9 cmH 2 O in control subjects. P Es at V Rel was higher in obese than control subjects (12.5 ± 3.9 vs. 6.9 ± 3.1 cmH 2 O, means ± SD; P = 0.0002) and correlated with P AO-Thr ( R 2 = 0.16, P = 0.0015). Respiratory system compliance (C RS ) was lower in obese than control (0.032 ± 0.008 vs. 0.053 ± 0.007 l/cmH 2 O) due principally to lower lung compliance (0.043 ± 0.016 vs. 0.084 ± 0.029 l/cmH 2 O) rather than chest wall compliance (obese 0.195 ± 0.109, control 0.223 ± 0.132 l/cmH 2 O). We conclude that many severely obese supine subjects at relaxation volume have positive P pl throughout the chest. High P Es suggests high P Pl in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes. esophageal pressure; compliance; elastance; gastric pressure; pressure-volume curve Address for reprint requests and other correspondence: S. H. Loring, Dept. of Anesthesia, Critical Care and Pain Medicine, Dana 715, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215 (e-mail sloring{at}bidmc.harvard.edu ). To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P Pl ) in severe obesity, we studied 51 obese subjects (body mass index = 38–80.7 kg/m 2 ) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P Es , P Ga ) using a balloon-catheter, airway pressure (P AO ), flow, and volume. We compared P Es to another estimate of P Pl based on P AO and flow. Reasoning that the lungs would not inflate until P AO exceeded alveolar and pleural pressures (P AO > P Alv > P Pl ), we disconnected subjects from the ventilator for 10–15 s to allow them to reach relaxation volume (V Rel ) and then slowly raised P AO until lung volume increased by 10 ml, indicating the “threshold P AO ” (P AO-Thr ) for inflation, which we took to be an estimate of the lowest P Alv or P Pl to be found in the chest at V Rel . P AO-Thr ranged from 0.6 to 14.0 cmH 2 O in obese and 0.2 to 0.9 cmH 2 O in control subjects. P Es at V Rel was higher in obese than control subjects (12.5 ± 3.9 vs. 6.9 ± 3.1 cmH 2 O, means ± SD; P = 0.0002) and correlated with P AO-Thr ( R 2 = 0.16, P = 0.0015). Respiratory system compliance (C RS ) was lower in obese than control (0.032 ± 0.008 vs. 0.053 ± 0.007 l/cmH 2 O) due principally to lower lung compliance (0.043 ± 0.016 vs. 0.084 ± 0.029 l/cmH 2 O) rather than chest wall compliance (obese 0.195 ± 0.109, control 0.223 ± 0.132 l/cmH 2 O). We conclude that many severely obese supine subjects at relaxation volume have positive P pl throughout the chest. High P Es suggests high P Pl in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes. To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P...) in severe obesity, we studied 51 obese subjects (body mass index = 38-80.7 kg/m...) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P..., P...) using a balloon-catheter, airway pressure (P...), flow, and volume. We compared P... to another estimate of P... based on P... and flow. Reasoning that the lungs would not inflate until P... exceeded alveolar and pleural pressures (P... > P... > P...), we disconnected subjects from the ventilator for 10-15 s to allow them to reach relaxation volume (V...) and then slowly raised P... until lung volume increased by 10 ml, indicating the "threshold P..." (P...) for inflation, which we took to be an estimate of the lowest P... or P... to be found in the chest at V... P... ranged from 0.6 to 14.0 cmH2O in obese and 0.2 to 0.9 cmH2O in control subjects. PEs at V... was higher in obese than control subjects (12.5 ± 3.9 vs. 6.9 ± 3.1 cmH2O, means ± SD; P = 0.0002) and correlated with PAO-Thr (R... = 0.16, P = 0.0015). Respiratory system compliance (CRS) was lower in obese than control (0.032 ± 0.008 vs. 0.053 ± 0.007 l/cmH2O) due principally to lower lung compliance (0.043 ± 0.016 vs. 0.084 ± 0.029 l/cmH2O) rather than chest wall compliance (obese 0.195 ± 0.109, control 0.223 ± 0.132 l/cmH2O). We conclude that many severely obese supine subjects at relaxation volume have positive P... throughout the chest. High P... suggests high P... in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes. (ProQuest: ... denotes formulae/symbols omitted.) To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P(Pl)) in severe obesity, we studied 51 obese subjects (body mass index = 38-80.7 kg/m(2)) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P(Es), P(Ga)) using a balloon-catheter, airway pressure (P(AO)), flow, and volume. We compared P(Es) to another estimate of P(Pl) based on P(AO) and flow. Reasoning that the lungs would not inflate until P(AO) exceeded alveolar and pleural pressures (P(AO) > P(Alv) > P(Pl)), we disconnected subjects from the ventilator for 10-15 s to allow them to reach relaxation volume (V(Rel)) and then slowly raised P(AO) until lung volume increased by 10 ml, indicating the "threshold P(AO)" (P(AO-Thr)) for inflation, which we took to be an estimate of the lowest P(Alv) or P(Pl) to be found in the chest at V(Rel). P(AO-Thr) ranged from 0.6 to 14.0 cmH2O in obese and 0.2 to 0.9 cmH2O in control subjects. P(Es) at V(Rel) was higher in obese than control subjects (12.5 +/- 3.9 vs. 6.9 +/- 3.1 cmH2O, means +/- SD; P = 0.0002) and correlated with P(AO-Thr) (R(2) = 0.16, P = 0.0015). Respiratory system compliance (C(RS)) was lower in obese than control (0.032 +/- 0.008 vs. 0.053 +/- 0.007 l/cmH2O) due principally to lower lung compliance (0.043 +/- 0.016 vs. 0.084 +/- 0.029 l/cmH2O) rather than chest wall compliance (obese 0.195 +/- 0.109, control 0.223 +/- 0.132 l/cmH2O). We conclude that many severely obese supine subjects at relaxation volume have positive P(pl) throughout the chest. High P(Es) suggests high P(Pl) in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes. |
| Author | Cohen, Robert I Behazin, Negin Loring, Stephen H Jones, Stephanie B |
| Author_xml | – sequence: 1 fullname: Behazin, Negin – sequence: 2 fullname: Jones, Stephanie B – sequence: 3 fullname: Cohen, Robert I – sequence: 4 fullname: Loring, Stephen H |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19910329$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1093/eurheartj/ehn573 10.1111/j.1464-5491.2004.01361.x 10.1378/chest.130.3.827 10.1152/jappl.1967.23.4.475 10.1046/j.1365-2796.1997.89104000.x 10.1111/j.1399-6576.1976.tb05036.x 10.1152/jappl.1998.85.4.1236 10.1152/jappl.1959.14.4.525 10.1152/jappl.1964.19.1.97 10.1152/jappl.1964.19.5.959 10.1152/jappl.1995.79.4.1199 10.1097/01.CCM.0000215515.49001.A2 10.1152/jappl.1960.15.3.377 10.1007/s00134-006-0349-5 10.1172/JCI104957 10.1016/0034-5687(79)90019-7 10.1152/jappl.1998.84.1.389 10.1152/jappl.1984.57.2.403 10.1023/A:1011491231934 10.1152/japplphysiol.00749.2006 10.1152/japplphysiol.00697.2005 10.1378/chest.109.1.144 10.1007/BF01711092 |
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| References | B20 B21 B22 B23 B24 B25 B26 B10 B11 B12 B13 B14 B15 B16 Smith JC (B17) 1986 Fry DL (B3) 1952; 40 B19 B1 B2 Steier J (B18) 2008; 177 B4 B5 B6 B7 B8 B9 16306256 - J Appl Physiol (1985). 2006 Mar;100(3):753-8 14104296 - J Appl Physiol. 1964 Jan;19:97-104 6053673 - J Appl Physiol. 1967 Oct;23(4):475-86 17110514 - J Appl Physiol (1985). 2007 Mar;102(3):841-6 12580216 - J Clin Monit Comput. 2000;16(5-6):329-35 12990893 - J Lab Clin Med. 1952 Nov;40(5):664-73 16967294 - Intensive Care Med. 2006 Nov;32(11):1722-32 14149924 - J Clin Invest. 1964 Apr;43:728-39 9451661 - J Appl Physiol (1985). 1998 Jan;84(1):389-95 441568 - Respir Physiol. 1979 Feb;36(2):121-9 14207752 - J Appl Physiol. 1964 Sep;19:959-66 6469810 - J Appl Physiol Respir Environ Exerc Physiol. 1984 Aug;57(2):403-7 8549177 - Chest. 1996 Jan;109(1):144-51 9042096 - J Intern Med. 1997 Jan;241(1):71-9 16540960 - Crit Care Med. 2006 May;34(5):1389-94 14425845 - J Appl Physiol. 1960 May;15:377-82 785930 - Acta Anaesthesiol Scand. 1976;20(3):248-54 9760311 - J Appl Physiol (1985). 1998 Oct;85(4):1236-43 16963682 - Chest. 2006 Sep;130(3):827-33 19136488 - Eur Heart J. 2009 Apr;30(7):850-6 8294633 - Intensive Care Med. 1993;19(8):478-80 8567562 - J Appl Physiol (1985). 1995 Oct;79(4):1199-205 15569138 - Diabet Med. 2004 Dec;21(12):1339-45 |
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| Snippet | Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts
Submitted 10 October 2008
; accepted in... To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P Pl ) in severe obesity, we studied 51 obese subjects (body mass index... To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P(Pl)) in severe obesity, we studied 51 obese subjects (body mass index... To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P...) in severe obesity, we studied 51 obese subjects (body mass index =... To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P Pl ) in severe obesity, we studied 51 obese subjects (body mass index... |
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| SubjectTerms | Adult Aged Comparative analysis Esophagus - physiopathology Female Highlighted Topic Humans Lung - physiopathology Lung Compliance Lung diseases Male Medical instruments Middle Aged Obesity Obesity, Morbid - physiopathology Pleural Cavity - physiopathology Pressure Pulmonary Gas Exchange Respiration Respiratory Mechanics Respiratory system Young Adult |
| Title | Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity |
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