Observational study of the effect of obesity on lung volumes
Background Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood. Patients and methods We undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seate...
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| Published in | Thorax Vol. 69; no. 8; pp. 752 - 759 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
BMJ Publishing Group LTD
01.08.2014
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0040-6376 1468-3296 1468-3296 |
| DOI | 10.1136/thoraxjnl-2014-205148 |
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| Abstract | Background Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood. Patients and methods We undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (PL) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory PL volume curves were measured. Results The obese group had a body mass index (BMI) of 46.8 (17.2) kg/m2, and the normal group had a BMI of 23.2 (1.6) kg/m2 (p=0.001). Obese and normals were matched for age (p=0.233), gender (p=0.637) and height (p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) %predicted, p=0.033; FEV1/FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cm H2O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cm H2O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs −2.0 (3.5) cm H2O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cm H2O, p=0.008). BMI correlated with end-expiratory gastric (seated R2=0.43, supine R2=0.66, p<0.01) and oesophageal pressures (seated R2=0.51, supine R2=0.62, p<0.01). Conclusions Obese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing. |
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| AbstractList | Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood.BACKGROUNDSevere obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood.We undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (PL) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory PL volume curves were measured.PATIENTS AND METHODSWe undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (PL) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory PL volume curves were measured.The obese group had a body mass index (BMI) of 46.8 (17.2) kg/m(2), and the normal group had a BMI of 23.2 (1.6) kg/m(2) (p=0.001). Obese and normals were matched for age (p=0.233), gender (p=0.637) and height (p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) %predicted, p=0.033; FEV1/FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cm H2O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cm H2O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs -2.0 (3.5) cm H2O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cm H2O, p=0.008). BMI correlated with end-expiratory gastric (seated R(2)=0.43, supine R(2)=0.66, p<0.01) and oesophageal pressures (seated R(2)=0.51, supine R(2)=0.62, p<0.01).RESULTSThe obese group had a body mass index (BMI) of 46.8 (17.2) kg/m(2), and the normal group had a BMI of 23.2 (1.6) kg/m(2) (p=0.001). Obese and normals were matched for age (p=0.233), gender (p=0.637) and height (p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) %predicted, p=0.033; FEV1/FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cm H2O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cm H2O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs -2.0 (3.5) cm H2O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cm H2O, p=0.008). BMI correlated with end-expiratory gastric (seated R(2)=0.43, supine R(2)=0.66, p<0.01) and oesophageal pressures (seated R(2)=0.51, supine R(2)=0.62, p<0.01).Obese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing.CONCLUSIONSObese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing. Background Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood. Patients and methods We undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (PL) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory PL volume curves were measured. Results The obese group had a body mass index (BMI) of 46.8 (17.2) kg/m2, and the normal group had a BMI of 23.2 (1.6) kg/m2 (p=0.001). Obese and normals were matched for age (p=0.233), gender (p=0.637) and height (p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) %predicted, p=0.033; FEV1/FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cm H2O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cm H2O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs −2.0 (3.5) cm H2O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cm H2O, p=0.008). BMI correlated with end-expiratory gastric (seated R2=0.43, supine R2=0.66, p<0.01) and oesophageal pressures (seated R2=0.51, supine R2=0.62, p<0.01). Conclusions Obese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing. BackgroundSevere obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood.Patients and methodsWe undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (PL) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory PL volume curves were measured.ResultsThe obese group had a body mass index (BMI) of 46.8 (17.2) kg/m2, and the normal group had a BMI of 23.2 (1.6) kg/m2 (p=0.001). Obese and normals were matched for age (p=0.233), gender (p=0.637) and height (p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) %predicted, p=0.033; FEV1/FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cmH2O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cmH2O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs -2.0 (3.5) cmH2O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cmH2O, p=0.008). BMI correlated with end-expiratory gastric (seated R2=0.43, supine R2=0.66, p<0.01) and oesophageal pressures (seated R2=0.51, supine R2=0.62, p<0.01).ConclusionsObese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing. Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood. We undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (PL) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory PL volume curves were measured. The obese group had a body mass index (BMI) of 46.8 (17.2) kg/m(2), and the normal group had a BMI of 23.2 (1.6) kg/m(2) (p=0.001). Obese and normals were matched for age (p=0.233), gender (p=0.637) and height (p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) %predicted, p=0.033; FEV1/FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cm H2O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cm H2O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs -2.0 (3.5) cm H2O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cm H2O, p=0.008). BMI correlated with end-expiratory gastric (seated R(2)=0.43, supine R(2)=0.66, p<0.01) and oesophageal pressures (seated R(2)=0.51, supine R(2)=0.62, p<0.01). Obese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing. Background Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood. Patients and methods We undertook a comprehensive observational study of lung volumes and elasticity in nine obese and nine normal weight subjects, seated and supine, during spontaneous breathing. Seated and supine total lung capacity (TLC) and subdivisions were measured by multibreath helium dilution method. Using balloon catheters, oesophageal (Poes) and gastric (Pgas) pressures were recorded. Transpulmonary pressure (PL ) was calculated as mouth pressure (Pmouth)-Poes, and complete expiratory PL volume curves were measured. Results The obese group had a body mass index (BMI) of 46.8 (17.2) kg/m2 , and the normal group had a BMI of 23.2 (1.6) kg/m2 (p=0.001). Obese and normals were matched for age (p=0.233), gender (p=0.637) and height (p=0.094). The obese were more restricted than the normals (TLC 88.6 (16.9) vs 104.4 (12.3) %predicted, p=0.033; FEV1 /FVC 79.6 (7.3) vs 82.5 (4.2) %, p=0.325), had dramatically reduced expiratory reserve volume (ERV 0.4 (0.4) vs 1.7 (0.6) L, p<0.001) and end-tidal functional residual capacity (FRC) was smaller (37.5 (6.9) vs 46.9 (4.6) %TLC, p=0.004) when seated, but was similar when supine (39.4 (7.7) vs 41.5 (4.3) %TLC, p=0.477). Gastric pressures at FRC were significantly elevated in the obese (seated 19.1 (4.7) vs 12.1 (6.2) cm H2 O, p=0.015; supine 14.3 (5.7) vs 7.1 (2.6) cm H2 O, p=0.003), as were end-expiratory oesophageal pressures at FRC (seated 5.2 (6.9) vs -2.0 (3.5) cm H2 O, p=0.013; supine 14.0 (8.0) vs 5.4 (3.1) cm H2 O, p=0.008). BMI correlated with end-expiratory gastric (seated R2 =0.43, supine R2 =0.66, p<0.01) and oesophageal pressures (seated R2 =0.51, supine R2 =0.62, p<0.01). Conclusions Obese subjects have markedly increased gastric and oesophageal pressures, both when upright and supine, causing dramatically reduced FRC and ERV, which increases work of breathing. |
| Author | Hart, Nicholas Steier, Joerg Moxham, John Lunt, Alan Polkey, Michael I |
| Author_xml | – sequence: 1 givenname: Joerg surname: Steier fullname: Steier, Joerg email: joerg.steier@gstt.nhs.uk organization: Lane Fox Unit, Sleep Disorders Centre, Guy's & St Thomas’ NHS Foundation Trust, London, UK – sequence: 2 givenname: Alan surname: Lunt fullname: Lunt, Alan email: joerg.steier@gstt.nhs.uk organization: King's College London School of Medicine, King's Health Partners, King's College Hospital, London, UK – sequence: 3 givenname: Nicholas surname: Hart fullname: Hart, Nicholas email: joerg.steier@gstt.nhs.uk organization: Lane Fox Unit, Sleep Disorders Centre, Guy's & St Thomas’ NHS Foundation Trust, London, UK – sequence: 4 givenname: Michael I surname: Polkey fullname: Polkey, Michael I email: joerg.steier@gstt.nhs.uk organization: NIHR Respiratory Biomedical Research Unit, The Royal Brompton Hospital and Imperial College, London, UK – sequence: 5 givenname: John surname: Moxham fullname: Moxham, John email: joerg.steier@gstt.nhs.uk organization: King's College London School of Medicine, King's Health Partners, King's College Hospital, London, UK |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24736287$$D View this record in MEDLINE/PubMed |
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| Snippet | Background Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood. Patients and... Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood. We undertook a... Severe obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood.BACKGROUNDSevere obesity... BackgroundSevere obesity causes respiratory morbidity and mortality. The impact of obesity on the mechanics of breathing is not fully understood.Patients and... |
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| SubjectTerms | Abdomen Adult Anthropometry Body mass index Case-Control Studies Compliance Female Gastrointestinal surgery Gender Health care Humans Lung Volume Measurements - methods Male Mechanics Middle Aged Obesity Obesity - physiopathology Posture Pressure Pulmonary Gas Exchange - physiology Spirometry Work of Breathing - physiology |
| Title | Observational study of the effect of obesity on lung volumes |
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