Pleural Pressure Targeted Positive Airway Pressure Improves Cardiopulmonary Function in Spontaneously Breathing Patients With Obesity

Abstract

Background: Increased pleural pressure affects the mechanics of breathing of people with class III obesity (BMI > 40 kg/m2).

Research question: What are the acute effects of CPAP titrated to match pleural pressure on cardiopulmonary function in spontaneously breathing patients with class III obesity?

Study design and methods: We enrolled six participants with BMI within normal range (control participants, group I) and 12 patients with class III obesity (group II) divided into subgroups: IIa, BMI of 40 to 50 kg/m2; and IIb, BMI of ≥ 50 kg/m2. The study was performed in two phases: in phase 1, participants were supine and breathing spontaneously at atmospheric pressure, and in phase 2, participants were supine and breathing with CPAP titrated to match their end-expiratory esophageal pressure in the absence of CPAP. Respiratory mechanics, esophageal pressure, and hemodynamic data were collected, and right heart function was evaluated by transthoracic echocardiography.

Results: The levels of CPAP titrated to match pleural pressure in group I, subgroup IIa, and subgroup IIb were 6 ± 2 cmH2O, 12 ± 3 cmH2O, and 18 ± 4 cmH2O, respectively. In both subgroups IIa and IIb, CPAP titrated to match pleural pressure decreased minute ventilation (IIa, P = .03; IIb, P = .03), improved peripheral oxygen saturation (IIa, P = .04; IIb, P = .02), improved homogeneity of tidal volume distribution between ventral and dorsal lung regions (IIa, P = .22; IIb, P = .03), and decreased work of breathing (IIa, P < .001; IIb, P = .003) with a reduction in both the work spent to initiate inspiratory flow as well as tidal ventilation. In five hypertensive participants with obesity, BP decreased to normal range, without impairment of right heart function.

Interpretation: In ambulatory patients with class III obesity, CPAP titrated to match pleural pressure decreased work of breathing and improved respiratory mechanics while maintaining hemodynamic stability, without impairing right heart function.

Trial registry: ClinicalTrials.gov; No.: NCT02523352; URL: www.clinicaltrials.gov.

Keywords: CPAP; hypertension; obesity; pleural pressure.

Copyright © 2021. Published by Elsevier Inc.

Figures

Figure 1

A, B, Graphs showing analyses of tracings of airway pressure, EP, and airflow during titration of CPAP in a participant with normal BMI (A) and BMI of > 50 kg/m2 (B). The orange dotted line indicates the zero-flow level. SwingAOP is defined as the difference EPE0 – EPS0 at atmospheric pressure and as the difference EPECPAP – EPSCPAP while undergoing CPAP. SwingTV is defined as the difference EPS0 – EPI0 at atmospheric pressure and as the difference EPSCPAP – EPICPAP while breathing with CPAP. SwingTOT is the sum of the two previous components. Please see the text for details. EP = esophageal pressure; EPE0 = esophageal pressure at the end of exhalation during spontaneous breathing; EPECPAP = esophageal pressure at the end of exhalation during CPAP; EPI0 = esophageal pressure at the end of inspiration during spontaneous breathing; EPICPAP = esophageal pressure at the end of inspiration during CPAP; EPS0 = esophageal pressure at the start of inspiration during spontaneous breathing; EPSCPAP = esophageal pressure at the start of inspiration during CPAP; SwingAOP = swing needed to reach the opening airway pressure, ie, the onset of inspiratory flow; SwingTOT = total swing; SwingTV = esophageal pressure change during the generation of a tidal volume.

Figure 2

A, B, Graphs showing EP swings during spontaneous breathing at atmospheric pressure and with CPAP in participants with normal BMI (group I, red), BMI of 41 to 49 kg/m2 (group IIa, blue), and BMI of > 50 kg/m2 (group IIb, gray). Data are shown as median and range. A, Total EP swing. B, EP swing needed to reach opening airway pressure. C, EP swing during tidal ventilation. Atm P = atmospheric pressure; AOP = airway opening pressure; EP = esophageal pressure.

Figure 3

A, B, Graphs showing analyses of changes in airway pressure (blue trace) and EP (red trace) when titrated CPAP was applied in participant 6 (A) and participant 3 (B). Within a few seconds of CPAP initiation, a decrease in EP swing was detected. Work of breathing, calculated as pressure-time product (see text and e-Appendix 1 for details) and highlighted in gray in the figures, decreased as well. EP = esophageal pressure.

Figure 4

Graph showing effects of CPAP on respiratory pressures and volumes during spontaneous breathing in participants with normal BMI (group I, red), BMI of 41 to 49 kg/m2 (group IIa, blue), and BMI of > 50 kg/m2 (group IIb, gray). Data are shown as median and range. Atm P = atmospheric pressure; PTP = pressure-time product; SB = spontaneous breathing; SpO2 = peripheral saturation of oxygen; VE = minute ventilation.

Figure 5

Analysis of tidal ventilation distribution by electrical impedance tomography (EIT) during spontaneous breathing at Atm P and with CPAP. EIT shows that at Atm P in patients with class III obesity, ventilation distributes predominantly to the most ventral lung regions. Titrating CPAP according to end-expiratory esophageal pressure leads to a more homogeneous distribution of ventilation by increasing the amount of tidal volume directed to the dorsal, gravity-dependent lung areas (group I, P = .22; group IIa, P = .22; and group IIb, P = .03). Atm P = atmospheric pressure.

Figure 6

Diagram showing BP during spontaneous breathing at Atm P and with CPAP in each participant. Colors in the cells are consistent with the hypertension classification according to the American Heart Association. Atm P = atmospheric pressure.