Poor Correlation between Diaphragm Thickening Fraction and Transdiaphragmatic Pressure in Mechanically Ventilated Patients and Healthy Subjects

Background The relationship between the diaphragm thickening fraction and the transdiaphragmatic pressure, the reference method to evaluate the diaphragm function, has not been clearly established. This study investigated the global and intraindividual relationship between the thickening fraction of the diaphragm and the transdiaphragmatic pressure. The authors hypothesized that the diaphragm thickening fraction would be positively and significantly correlated to the transdiaphragmatic pressure, in both healthy participants and ventilated patients. Methods Fourteen healthy individuals and 25 mechanically ventilated patients (enrolled in two previous physiologic investigations) participated in the current study. The zone of apposition of the right hemidiaphragm was imaged simultaneously to transdiaphragmatic pressure recording within different breathing conditions, i.e., external inspiratory threshold loading in healthy individuals and various pressure support settings in patients. A blinded offline breath-by-breath analysis synchronously computed the changes in transdiaphragmatic pressure, the diaphragm pressure-time product, and diaphragm thickening fraction. Global and intraindividual relationships between variables were assessed. Results In healthy subjects, both changes in transdiaphragmatic pressure and diaphragm pressure-time product were moderately correlated to diaphragm thickening fraction (repeated measures correlation = 0.40, P < 0.0001; and repeated measures correlation = 0.38, P < 0.0001, respectively). In mechanically ventilated patients, changes in transdiaphragmatic pressure and thickening fraction were weakly correlated (repeated measures correlation = 0.11, P = 0.008), while diaphragm pressure-time product and thickening fraction were not (repeated measures correlation = 0.04, P = 0.396). Individually, changes in transdiaphragmatic pressure and thickening fraction were significantly correlated in 8 of 14 healthy subjects (ρ = 0.30 to 0.85, all P < 0.05) and in 2 of 25 mechanically ventilated patients (ρ = 0.47 to 0.64, all P < 0.05). Diaphragm pressure-time product and thickening fraction correlated in 8 of 14 healthy subjects (ρ = 0.41 to 0.82, all P < 0.02) and in 2 of 25 mechanically ventilated patients (ρ = 0.63 to 0.66, all P < 0.01). Conclusions Overall, diaphragm function as assessed with transdiaphragmatic pressure was weakly related to diaphragm thickening fraction. The diaphragm thickening fraction should not be used in healthy subjects or ventilated patients when changes in diaphragm function are evaluated. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Additional work of breathing from trigger errors in mechanically ventilated children

Background Patient–ventilator asynchrony is associated with increased morbidity and mortality. A direct causative relationship between Patient–ventilator asynchrony and adverse clinical outcome have yet to be demonstrated. It is hypothesized that during trigger errors excessive pleural pressure swings are generated, contributing to increased work-of-breathing and self-inflicted lung injury. The objective of this study was to determine the additional work-of-breathing and pleural pressure swings caused by trigger errors in mechanically ventilated children. Methods Prospective observational study in a tertiary paediatric intensive care unit in an university hospital. Patients ventilated > 24 h and < 18 years old were studied. Patients underwent a 5-min recording of the ventilator flow–time, pressure–time and oesophageal pressure–time scalar. Pressure–time–product calculations were made as a proxy for work-of-breathing. Oesophageal pressure swings, as a surrogate for pleural pressure swings, during trigger errors were determined. Results Nine-hundred-and-fifty-nine trigger errors in 28 patients were identified. The additional work-of-breathing caused by trigger errors showed great variability among patients. The more asynchronous breaths were present the higher the work-of-breathing of these breaths. A higher spontaneous breath rate led to a lower amount of trigger errors. Patient–ventilator asynchrony was not associated with prolonged duration of mechanical ventilation or paediatric intensive care stay. Conclusions The additional work-of-breathing caused by trigger errors in ventilated children can take up to 30–40% of the total work-of-breathing. Trigger errors were less common in patients breathing spontaneously and those able to generate higher pressure–time–product and pressure swings. Trial registration Not applicable.

Volume targeting levels and work of breathing in infants with evolving or established bronchopulmonary dysplasia

ObjectivesTo assess the work of breathing at different levels of volume targeting in prematurely born infants with evolving or established bronchopulmonary dysplasia (BPD).DesignRandomised crossover study.SettingTertiary neonatal intensive care unit.PatientsEighteen infants born at <32 weeks gestation who remained ventilated at or beyond 1 week after birth, that is, they had evolving or established BPD.InterventionsInfants received ventilation at volume targeting levels of 4, 5, 6 and 7 mL/kg each for 20 minutes, the levels were delivered in random order. Baseline ventilation (without volume targeting) was delivered for 20 minutes between each epoch of volume-targeting.Main outcome measuresPressure-time product of the diaphragm (PTPdi), a measure of the work of breathing, at different levels of volume targeting.ResultsThe 18 infants had a median gestational age of 26 (range 24–30) weeks and were studied at a median of 18 (range 7–60) days. The mean PTPdi was higher at 4 mL/kg than at baseline, 5 mL/kg, 6 mL/kg and 7 mL/kg (all P≤0.001). The mean PTPdi was higher at 5 mL/kg than at 6 mL/kg (P=0.008) and 7 mL/kg (P<0.001) and higher at 6 mL/kg than 7 mL/kg (P=0.003). Only at 7 mL/kg was the PTPdi significantly lower than at baseline (P=0.001).ConclusionsOnly a tidal volume target of 7 mL/kg reduced the work of breathing below the baseline and may be more appropriate for infants with evolving or established BPD who remained ventilator dependent at or beyond 7 days of age.

Sex differences in exercise-induced diaphragmatic fatigue in endurance-trained athletes

There is evidence that female athletes may be more susceptible to exercise-induced arterial hypoxemia and expiratory flow limitation and have greater increases in operational lung volumes during exercise relative to men. These pulmonary limitations may ultimately lead to greater levels of diaphragmatic fatigue in women. Accordingly, the purpose of this study was to determine whether there are sex differences in the prevalence and severity of exercise-induced diaphragmatic fatigue in 38 healthy endurance-trained men ( n = 19; maximal aerobic capacity = 64.0 ± 1.9 ml·kg−1·min−1) and women ( n = 19; maximal aerobic capacity = 57.1 ± 1.5 ml·kg−1·min−1). Transdiaphragmatic pressure (Pdi) was calculated as the difference between gastric and esophageal pressures. Inspiratory pressure-time products of the diaphragm and esophagus were calculated as the product of breathing frequency and the Pdi and esophageal pressure time integrals, respectively. Cervical magnetic stimulation was used to measure potentiated Pdi twitches (Pdi,tw) before and 10, 30, and 60 min after a constant-load cycling test performed at 90% of peak work rate until exhaustion. Diaphragm fatigue was considered present if there was a ≥15% reduction in Pdi,tw after exercise. Diaphragm fatigue occurred in 11 of 19 men (58%) and 8 of 19 women (42%). The percent drop in Pdi,tw at 10, 30, and 60 min after exercise in men ( n = 11) was 30.6 ± 2.3, 20.7 ± 3.2, and 13.3 ± 4.5%, respectively, whereas results in women ( n = 8) were 21.0 ± 2.1, 11.6 ± 2.9, and 9.7 ± 4.2%, respectively, with sex differences occurring at 10 and 30 min ( P < 0.05). Men continued to have a reduced contribution of the diaphragm to total inspiratory force output (pressure-time product of the diaphragm/pressure-time product of the esophagus) during exercise, whereas diaphragmatic contribution in women changed very little over time. The findings from this study point to a female diaphragm that is more resistant to fatigue relative to their male counterparts.

Measurement of Pressure–Time Product during Spontaneous Assisted Breathing by Rapid Interrupter Technique

Background Measuring the work of breathing of patients undergoing spontaneous assisted ventilation can be useful to monitor and titrate ventilatory support. The aim of this study was to obtain measurements of the pressure generated by the respiratory muscles (PMUSC) and the derived pressure-time product (PTP; a good indicator of the metabolic work of breathing), performing the rapid interrupter technique with a commercial ventilator. Methods A Draeger Evita 4 ventilator (Draeger Medical, Lubeck, Germany) was controlled by a personal computer to rapidly interrupt the airway flow at different times and volumes of the respiratory cycle during pressure-support ventilation. From the airway pressure tracing after the occlusion, the authors estimated the alveolar pressure and PMUSC; the integration of PMUSC values over the inspiratory time yields the measurement of PTP. Esophageal pressure measurements were used as a reference. After a bench study of the valves' performance, the authors performed 11 measurement sequences in eight patients. Results The closure times for the inspiratory and expiratory valves were 74 +/- 10 and 61 +/- 13 ms, respectively. The interrupter technique provided a reliable estimate of PMUSC (PMUSC, occl = 1.00 . PMUSC, pes + 0.19; r = 0.88; 95% confidence interval for agreement, +5.49/-5.32 cm H2O). PTPoccl tightly correlated with PTPpes (PTPoccl = 0.95 . PTPpes + 0.13; r = 0.96; 95% confidence interval, 1.94/-1.61 cm H2O . s). Conclusion The rapid interrupter technique can be performed by means of a commercial ventilator, providing reliable measurement of PMUSC and PTP.

Physiological effects of intravenous fructose 1.6-diphosphate on diaphragmatic function in malnourished patients with COPD

Background. A low body mass index is one of the strongest predictors of mortality in Chronic Obstructive Pulmonary Disease (COPD) patients. Under-nutrition is often associated with skeletal muscle wasting and hypophosphatemia. Aim and Methods. In a pilot, randomised, doubleblind placebo-controlled study, we assessed the physiological effects of phosphorous administration in 17 stable undernourished COPD patients, on diaphragmatic function, breathing pattern, neuromuscular drive (P0.1) and dyspnea score. Fructose 1.6-diphosphate (FDP) or placebo was administered i.v. for 7 consecutive days. Results. FDP administration was associated with a marked increase in inspiratory time (Ti) that induced a significant rise (p&lt;0.05) in the Pressure Time Product of the diaphragm per breath (PTPdi/b). However, since breathing frequency also decreased, the Pressure Time Product per minute of the diaphragm (PTPdi/min), index of diaphragmatic energy expenditure was markedly reduced. The efficiency of the respiratory pump in clearing CO2 was also improved, although not significantly, in the FDP group (p=0.09) as well as the maximal transdiaphragmatic pressure during the sniff manoeuvre (Pdi,sniff). Conclusions. This pilot physiological study showed that phosphorus replacement in undernourished, stable COPD patients, may be associated with a complex modification in respiratory pattern and diaphragmatic functions, leading to a marked although not significant reduction in PTPdi/min.

Continuous Positive Airway Pressure in New-generation Mechanical Ventilators

Background A number of new microprocessor-controlled mechanical ventilators have become available over the last few years. However, the ability of these ventilators to provide continuous positive airway pressure without imposing or performing work has never been evaluated. Methods In a spontaneously breathing lung model, the authors evaluated the Bear 1000, Drager Evita 4, Hamilton Galileo, Nellcor-Puritan-Bennett 740 and 840, Siemens Servo 300A, and Bird Products Tbird AVS at 10 cm H(2)O continuous positive airway pressure. Lung model compliance was 50 ml/cm H(2)O with a resistance of 8.2 cm H(2)O x l(-1) x s(-1), and inspiratory time was set at 1.0 s with peak inspiratory flows of 40, 60, and 80 l/min. In ventilators with both pressure and flow triggering, the response of each was evaluated. Results With all ventilators, peak inspiratory flow, lung model tidal volume, and range of pressure change (below baseline to above baseline) increased as peak flow increased. Inspiratory trigger delay time, inspiratory cycle delay time, expiratory pressure time product, and total area of pressure change were not affected by peak flow, whereas pressure change to trigger inspiration, inspiratory pressure time product, and trigger pressure time product were affected by peak flow on some ventilators. There were significant differences among ventilators on all variables evaluated, but there was little difference between pressure and flow triggering in most variables on individual ventilators except for pressure to trigger. Pressure to trigger was 3.74 +/- 1.89 cm H(2)O (mean +/- SD) in flow triggering and 4.48 +/- 1.67 cm H(2)O in pressure triggering (P &lt; 0.01) across all ventilators. Conclusions Most ventilators evaluated only imposed a small effort to trigger, but most also provided low-level pressure support and imposed an expiratory workload. Pressure triggering during continuous positive airway pressure does require a slightly greater pressure than flow triggering.