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Although it has been postulated that central inhibition of respiratory drive may prevent development of diaphragm fatigue in patients with chronic obstructive pulmonary disease (COPD) during exercise, this premise has not been validated. We evaluated diaphragm electrical activation (EAdi) relative to maximum in 10 patients with moderately severe COPD at rest and during incremental exhaustive bicycle exercise. Flow was measured with a pneumotachograph and volume by integration of flow. EAdi and transdiaphragmatic pressures (Pdi) were measured using an esophageal catheter. End-expiratory lung volume (EELV) was assessed by inspiratory capacity (IC) maneuvers, and maximal voluntary EAdi was obtained during these maneuvers. Minute ventilation (V E) was 12.2 +/- 1.9 L/min (mean +/- SD) at rest, and increased progressively (p < 0.001) to 31.0 +/- 7.8 L/min at end-exercise. EELV increased during exercise (p < 0.001) causing end-inspiratory lung volume to attain 97 +/- 3% of TLC at end-exercise. Pdi at rest was 9.4 +/- 3.2 cm H(2)O and increased during the first two thirds of exercise (p < 0.001) to plateau at about 13 cm H(2)O. EAdi was 24 +/- 6% of voluntary maximal at rest and increased progressively during exercise (p < 0.001) to reach 81 +/- 7% at end-exercise. In conclusion, dynamic hyperinflation during exhaustive exercise in patients with COPD reduces diaphragm pressure-generating capacity, promoting high levels of diaphragm activation.

We compared crural diaphragm electrical activity (EAdi) with transdiaphragmatic pressure (Pdi) during varying levels of pressure support ventilation (PS) in 13 intubated patients. With changing PS, we found no evidence for changes in neuromechanical coupling of the diaphragm. From lowest to highest PS (2 cm H(2)O +/- 4 to 20 cm H(2)O +/- 7), tidal volume increased from 430 ml +/- 180 to 527 ml +/- 180 (p < 0.001). The inspiratory volume calculated during the period when EAdi increased to its peak did not change from 276 +/- 147 to 277 +/- 162 ml, p = 0.976. Respiratory rate decreased from 23.9 (+/- 7) to 21.3 (+/- 7) breaths/min (p = 0.015). EAdi and Pdi decreased proportionally by adding PS (r = 0.84 and r = 0.90, for mean and peak values, respectively). Mean and peak EAdi decreased (p < 0.001) by 33 +/- 21% (mean +/- SD) and 37 +/- 23% with the addition of 10 cm H(2)O of PS, similar to the decrease in the mean and peak Pdi (p < 0.001) observed (34 +/- 36 and 35 +/- 23%). We also found that ventilator assist continued during the diaphragm deactivation period, a phenomenon that was further exaggerated at higher PS levels. We conclude that EAdi is a valid measurement of neural drive to the diaphragm in acute respiratory failure.

Five awake previously tracheotomized mongrel dogs were challenged with inspiratory resistive breathing (IRB). The mean peak tracheal pressure = -35.4 +/- 1.1 cmH2O, ETCO2 = 39.8 +/- 1.5 mmHg was sustained for 2 h/d over 4 consecutive d. On the fourth day, following IRB, the dogs were placed under general anaesthesia, and the diaphragm was perfused via the internal mammary artery with a low molecular weight fluorescent tracer (Procion orange, FW = 631), to which normal muscle fibers are impermeable. Muscle fiber membrane damage was identified on tissue sections by using fluorescent microscopy showing the presence of the tracer in the cytoplasm. Four dogs undergoing the same protocol (except IRB) served as control. The dye was seen in 7.6 +/- 2.6% and in 0.3 +/- 0.1% of fibers in the IRB and control groups, respectively (p < 0.05). Via ATPase staining, it was found that fibers of type I were predominantly affected as compared to type II (p < 0.05). In addition, an increased area fraction of fibers demonstrating sarcomere disruption was found after IRB (2.4 +/- 0.5%) compared to pre-IRB (0.4 +/- 0.1%; p < 0.05). We conclude that resistive breathing of a magnitude similar to that seen in some respiratory diseases, or used in respiratory muscle training programs induces muscle membrane and sarcomere injury.

The present paper describes the influence of cross talk from the abdominal and intercostal muscles on the canine diaphragm electromyogram (EMG). The diaphragm EMG was recorded with bipolar surface electrodes placed on the costal portion of the diaphragm (abdominal side), aligned in the fiber direction, and positioned in a region with a relatively low density of motor end plates. The results indicated that cross talk may occur in the diaphragm EMG, especially during conditions of loaded breathing and light general anesthesia. The cross-talk signals showed characteristics that were entirely different from the diaphragm EMG. Although the diaphragm EMG was typical for signals recorded with electrodes aligned in the fiber direction, the cross-talk signals were characteristic of those obtained with electrode pairs not aligned in the direction of the muscle fibers. Alterations in electrode positioning, interelectrode distance, and/or electrode surface area cannot guarantee the elimination of cross-talk signals, whereas spinal anesthesia at a high thoracic level will paralyze the sources of the cross talk and hence eliminate the cross-talk signals. By taking advantage of the differences in EMG signal characteristics for the diaphragm EMG and cross-talk signals, an index that has the capability to detect cross talk was developed.

The goal of this study was to determine whether in the dog ATP-sensitive K+ channels blocked with glibenclamide affect diaphragmatic blood flow [phrenic arterial blood flow (Qpa)] during both spontaneous breathing at rest and increased diaphragmatic activity. A control group (no glibenclamide; n = 4) and an experimental group (50 mg/kg of glibenclamide; n = 5) were studied. During spontaneous breathing at rest, Qpa was 15.0 ml.min-1 x 100 g-1 and decreased by 5% in the presence of glibenclamide. Diaphragmatic pacing (30 min-1) generated by phrenic nerve pacing produced an initial diaphragmatic tension-time index of 0.25 in both groups. A 50% decay in transdiaphragmatic pressure was reached at 165 s in the experimental group compared with 421 s in the control group. Diaphragmatic pacing increased Qpa by 46% in the experimental group and 65% in the control group, yielding a 63% greater vascular resistance in the experimental group. Phrenic vein K+ content at rest was unchanged by the presence of glibenclamide, being 3.6 +/- 0.16 mmol/l compared with 3.5 +/- 0.19 mmol/l in the control group. Phrenic nerve pacing in the control group produced a 13% increase in phrenic vein K+ content, whereas in the experimental group a 16% decrease was observed. We suggest that ATP-sensitive K+ channels play an important role in the modulation of Qpa.

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Background Reverse triggering is a delayed asynchronous contraction of the diaphragm triggered by passive insufflation by the ventilator in sedated mechanically ventilated patients. The incidence of reverse triggering is unknown. This study aimed at determining the incidence of reverse triggering in critically ill patients under controlled ventilation. Methods In this ancillary study, patients were continuously monitored with a catheter measuring the electrical activity of the diaphragm. A method for automatic detection of reverse triggering using electrical activity of the diaphragm was developed in a derivation sample and validated in a subsequent sample. The authors assessed the predictive value of the software. In 39 recently intubated patients under assist-control ventilation, a 1-h recording obtained 24 h after intubation was used to determine the primary outcome of the study. The authors also compared patients’ demographics, sedation depth, ventilation settings, and time to transition to assisted ventilation or extubation according to the median rate of reverse triggering. Results The positive and negative predictive value of the software for detecting reverse triggering were 0.74 (95% CI, 0.67 to 0.81) and 0.97 (95% CI, 0.96 to 0.98). Using a threshold of 1 μV of electrical activity to define diaphragm activation, median reverse triggering rate was 8% (range, 0.1 to 75), with 44% (17 of 39) of patients having greater than or equal to 10% of breaths with reverse triggering. Using a threshold of 3 μV, 26% (10 of 39) of patients had greater than or equal to 10% reverse triggering. Patients with more reverse triggering were more likely to progress to an assisted mode or extubation within the following 24 h (12 of 39 [68%]) vs. 7 of 20 [35%]; P = 0.039). Conclusions Reverse triggering detection based on electrical activity of the diaphragm suggests that this asynchrony is highly prevalent at 24 h after intubation under assist-control ventilation. Reverse triggering seems to occur during the transition phase between deep sedation and the onset of patient triggering. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New