This report summarizes current physiological and technical knowledge on esophageal pressure (Pes) measurements in patients receiving mechanical ventilation. The respiratory changes in Pes are representative of changes in pleural pressure. The difference between airway pressure (Paw) and Pes is a valid estimate of transpulmonary pressure. Pes helps determine what fraction of Paw is applied to overcome lung and chest wall elastance. Pes is usually measured via a catheter with an air-filled thin-walled latex balloon inserted nasally or orally. To validate Pes measurement, a dynamic occlusion test measures the ratio of change in Pes to change in Paw during inspiratory efforts against a closed airway. A ratio close to unity indicates that the system provides a valid measurement. Provided transpulmonary pressure is the lung-distending pressure, and that chest wall elastance may vary among individuals, a physiologically based ventilator strategy should take the transpulmonary pressure into account. For monitoring purposes, clinicians rely mostly on Paw and flow waveforms. However, these measurements may mask profound patient–ventilator asynchrony and do not allow respiratory muscle effort assessment. Pes also permits the measurement of transmural vascular pressures during both passive and active breathing. Pes measurements have enhanced our understanding of the pathophysiology of acute lung injury, patient–ventilator interaction, and weaning failure. The use of Pes for positive end-expiratory pressure titration may help improve oxygenation and compliance. Pes measurements make it feasible to individualize the level of muscle effort during mechanical ventilation and weaning. The time is now right to apply the knowledge obtained with Pes to improve the management of critically ill and ventilator-dependent patients.

Purpose Esophageal pressure (Pes) is a minimally invasive advanced respiratory monitoring method with the potential to guide management of ventilation support and enhance specific diagnoses in acute respiratory failure patients. To date, the use of Pes in the clinical setting is limited, and it is often seen as a research tool only. Methods This is a review of the relevant technical, physiological and clinical details that support the clinical utility of Pes. Results After appropriately positioning of the esophageal balloon, Pes monitoring allows titration of controlled and assisted mechanical ventilation to achieve personalized protective settings and the desired level of patient effort from the acute phase through to weaning. Moreover, Pes monitoring permits accurate measurement of transmural vascular pressure and intrinsic positive end-expiratory pressure and facilitates detection of patient–ventilator asynchrony, thereby supporting specific diagnoses and interventions. Finally, some Pes-derived measures may also be obtained by monitoring electrical activity of the diaphragm. Conclusions Pes monitoring provides unique bedside measures for a better understanding of the pathophysiology of acute respiratory failure patients. Including Pes monitoring in the intensivist’s clinical armamentarium may enhance treatment to improve clinical outcomes.

Background: Prolonged controlled mechanical ventilation depresses diaphragmatic efficiency. Assisted modes of ventilation should improve it. We assessed the impact of pressure support ventilation versus neurally adjusted ventilator assist on diaphragmatic efficiency. Method: Patients previously ventilated with controlled mechanical ventilation for 72 hours or more were randomized to be ventilated for 48 hours with pressure support ventilation (n =12) or neurally adjusted ventilatory assist (n = 13). Neuro-ventilatory efficiency (tidal volume/diaphragmatic electrical activity) and neuro-mechanical efficiency (pressure generated against the occluded airways/diaphragmatic electrical activity) were measured during three spontaneous breathing trials (0, 24 and 48 hours). Breathing pattern, diaphragmatic electrical activity and pressure time product of the diaphragm were assessed every 4 hours. Results: In patients randomized to neurally adjusted ventilator assist, neuro-ventilatory efficiency increased from 27 ± 19 ml/μV at baseline to 62 ± 30 ml/μV at 48 hours (p <0.0001) and neuro-mechanical efficiency increased from 1 ± 0.6 to 2.6 ± 1.1 cmH₂O/μV (p = 0.033). In patients randomized to pressure support ventilation, these did not change. Electrical activity of the diaphragm, neural inspiratory time, pressure time product of the diaphragm and variability of the breathing pattern were significantly higher in patients ventilated with neurally adjusted ventilatory assist. The asynchrony index was 9.48 [6.38– 21.73] in patients ventilated with pressure support ventilation and 5.39 [3.78– 8.36] in patients ventilated with neurally adjusted ventilatory assist (p = 0.04). Conclusion: After prolonged controlled mechanical ventilation, neurally adjusted ventilator assist improves diaphragm efficiency whereas pressure support ventilation does not. Trial registration: ClinicalTrials.gov study registration: NCT0247317, 06/11/2015.

Background: A lung-protective ventilatory strategy with low tidal volume (VT) has been proposed for use in acute respiratory distress syndrome (ARDS). Alveolar derecruitment may occur during the use of a lung-protective ventilatory strategy and may be prevented by recruiting maneuvers. This study examined the hypothesis that the effectiveness of a recruiting maneuver to improve oxygenation in patients with ARDS would be influenced by the elastic properties of the lung and chest wall. Methods: Twenty-two patients with ARDS were studied during use of the ARDSNet lung-protective ventilatory strategy: VT was set at 6 ml/kg predicted body weight and positive end-expiratory pressure (PEEP) and inspiratory oxygen fraction (Fio2) were set to obtain an arterial oxygen saturation of 90-95% and/or an arterial oxygen partial pressure (Pao2) of 60- 80 mmHg (baseline). Measurements of Pao2/Fio2, static volume-pressure curve, recruited volume (vertical shift of the volume-pressure curve), and chest wall and lung elastance (EstW and EstL: esophageal pressure) were obtained on zero end-expiratory pressure, at baseline, and at 2 and 20 min after application of a recruiting maneuver (40 cm H2O of continuous positive airway pressure for 40 s). Cardiac output (transesophageal Doppler) and mean arterial pressure were measured immediately before, during, and immediately after the recruiting maneuver. Patients were classified a priori as responders and nonresponders on the basis of the occurrence or nonoccurrence of a 50% increase in Pao2/Fio2 after the recruiting maneuver. Results: Recruiting maneuvers increased Pao2/Fio2 by 20 +/- 3% in nonresponders (n = 11) and by 175 +/- 23% (n = 11; mean +/- standard deviation) in responders. On zero end-expiratory pressure, EstL (28.4 +/- 2.2 vs. 24.2 +/- 2.9 cm H2O/l) and EstW (10.4 +/- 1.8 vs. 5.6 +/- 0.8 cm H2O/l) were higher in nonresponders than in responders (P < 0.01). Nonresponders had been ventilated for a longer period of time than responders (7 +/- 1 vs. 1 +/- 0.3 days; P < 0.001). Cardiac output and mean arterial pressure decreased by 31 +/- 2 and 19 +/- 3% in nonresponders and by 2 +/- 1 and 2 +/- 1% in responders (P < 0.01). Conclusions: Application of recruiting maneuvers improves oxygenation only in patients with early ARDS who do not have impairment of chest wall mechanics and with a large potential for recruitment, as indicated by low values of EstL.

Patients with relatively normal pulmonary function at the time of brain death may have declines in functioning, and only 15% to 20% of these patients' lungs are subsequently suitable for transplantation.^1-3 This may result from the pulmonary damage associated with brain injury⁴ or the iatrogenic effects of mechanical ventilation.^5,6

To evaluate whether the shape of the airway pressure-time (Paw-t) curve during constant flow inflation corresponds to radiologic evidence of tidal recruitment or tidal hyperinflation in an experimental model of acute lung injury. Prospective randomized laboratory animal investigation. Department of Clinical Physiology, University of Uppsala, Sweden. Anesthetized, paralyzed, and mechanically ventilated pigs. Acute lung injury was induced by lung lavage. During constant inspiratory flow, the Paw-t curve was fitted to a power equation: airway pressure =a · timeb+c,where coefficient b (stress index) describes the shape of the curve:b = 1, straight curve; b < 1, progressive increase in slope; and b > 1, progressive decrease in slope. Tidal volume (Vt) was 6 mL/kg, and positive end-expiratory pressure was set to obtain a b value between 0.9 and 1.1 before (b = 1) and after (b = 1 after recruiting maneuver) application of a recruiting maneuver. Positive end-expiratory pressure was decreased and Vt increased to obtain 0.9 >b > 0.8 and 0.8 >b > 0.6, whereas positive end-expiratory pressure and Vt were both increased to obtain 1.3 >b > 1.1 and 1.5 >b > 1.3. Experimental conditions sequence was random. Pulmonary computed tomography was obtained during end-expiratory and end-inspiratory occlusions. Tidal recruitment was quantified as nonaerated (between −100 and +100 Hounsfield units) lung area at end-expiration minus end-inspiration. Tidal hyperinflation was quantified as hyperinflated (between −900 and −1000 Hounsfield units) lung area at end-inspiration minus end-expiration. Computed tomography images showed that tidal recruitment and tidal hyperinflation corresponded to b < 1 and b > 1, respectively. Stress index values and tidal recruitment and tidal hyperinflation values were significantly correlated (R2 = .917 and R2 = .911, p < .0001, respectively). Shape of the Paw-t curve detects tidal recruitment and tidal hyperinflation.