Two Similar Averages for Respiratory Muscle Activity
Two Similar Averages for Respiratory Muscle Activity
To the Editor: In the recent article of Corne et al. (1) a method (which we will designate A) is used for the removal of the electrocardiogram (ECG) artifact present in the esophageal diaphragmatic electromyogram (EMG) waveform. The QRS artifact (typically 100 ms long) was first removed from the signal. The EMG signal was then rectified. The deleted 100-ms segment was replaced with a straight line starting with the average of the signal over 40 ms before the QRS artifact and ending with the average over 40 ms after the QRS artifact. The EMG signal was then averaged (100-ms moving average). Their Fig. 1 in Ref. 1 shows a signal example of the process. The resulting signal called EMGdi is of good quality and detail with minimal ECG artifact (mainly P-wave residual). In 1981, L. A. van Eykern already patented (US patent 4,248,240) a method (which we will designate asB) for transcutaneous diaphragmatic EMG that works in a similar way. Here, the deleted (gated) 100-ms segment corresponding to the ECG artifact is replaced with the ongoing average, by switching from the rectified signal to the output of the averager during the gate. In recent studies, this method was used and described by Maarsingh et al. (2) and Sprikkelman et al. (4).
We were intrigued to see the difference between the two methods. Besides the difference in filling of the QRS gap, there is a significant difference in process delay time. For our method (B), 40 ms are necessary to align the detected QRS complex with the ECG artifact. Corne et al. (1) used a pregate average of 40 ms, a 100-ms gate, and a further 40-ms average after the gate, adding up to a process time of 180 ms. If we delay the outcome of our method with 140 ms, the only difference between the two processes will be the filling of the gate. We compared methods A andB with an EMG averager without gating. For a test signal, we used an artificial respiratory EMG signal (30 breaths/min); for time keeping and QRS detection, we used a genuine ECG signal of one of our recordings (68–80 beats/min). In 37 breaths the root mean square error was 5.7 % for method A and 6.4 % for method B, the first being slightly better.
In 1987, O'Brien et al. (3) showed the feasibility and value of noninvasive transcutaneous diaphragm EMG in a group of infants using two prototype respiratory EMG monitors. With a second method available that produces almost ECG artifact-free averaged respiratory EMG waveforms from either esophageal or surface EMG recordings, the question arises of when we will see applications of respiratory EMG implemented in the clinical practice. Up until now, little has happened.
REFERENCES
- 1 Effects of inspiratory flow on diaphragmatic motor output in normal subjects.J Appl Physiol892000481492
Link | ISI | Google Scholar - 2 Respiratory muscle activity measured with a noninvasive EMG technique: technical aspects and reproducibility.J Appl Physiol88200019551961
Link | ISI | Google Scholar - 3 Transcutaneous respiratory electromyographic monitoring.Crit Care Med15/41987294299
Crossref | ISI | Google Scholar - 4 Respiratory muscle activity in the assessment of bronchial responsiveness in asthmatic children.J Appl Physiol841998897901
Link | ISI | Google Scholar
REPLY
To the Editor: We would like to thank the authors for their letter and their interest in our publication. There seems to have been some misunderstanding of what we were doing. We were not concerned with on-line processing. All analysis was done post hoc. Delays were, therefore, not an issue. Because we were not concerned about processing delays, we could interpolate with impunity, between the average values before and after the electrocardiogram (ECG). This probably accounts for the slightly better performance of our method.
We share the authors' interest in the potential utility of diaphragmatic electromyogram (EMG) for clinical respiratory monitoring. However, removal of the ECG artifact is not the only or most difficult hurdle in achieving this goal. Changes in relation between electrode and muscle, and extraneous artifacts related to motion, cross talk from other muscles, electrical noise, and esophageal peristalsis, as well as problems with long-term stability of the signal are among the many problems that need to be addressed before EMG can be used reliably in the clinical arena. We refer the authors to numerous publications from Sinderby's laboratory that deal with these issues (1-1-1-3).
The following is the abstract of the article discussed in the subsequent letter:
Corne, S., K. Webster, and M. Younes. Effects of inspiratory flow on diaphragmatic motor output in normal subjects. J Appl Physiol 89: 481–492, 2000.—Increasing inspiratory flow (V˙) has been shown to shorten neural inspiratory time (Tin) in normal subjects breathing on a mechanical ventilator, but the effect ofV˙ on respiratory motor output before inspiratory termination has not previously been studied in humans. While breathing spontaneously on a mechanical ventilator, eight normal subjects were intermittently exposed to 200-ms-duration positive pressure pulses of different amplitudes at the onset of inspiration. Based on the increase inV˙ above control breaths (ΔV˙), trials were grouped into small, medium, and large groups (mean ΔV˙: 0.51, 1.11, and 1.65 l/s, respectively). We measured Tin, transdiaphragmatic pressure (Pdi), and electrical activity (electromyogram) of the diaphragm (EMGdi). Transient increases inV˙ caused shortening of Tin from 1.34 to 1.10 (not significant), 1.55 to 1.11 (P < 0.005), and 1.58 to 1.17 s (P < 0.005) in the small, medium, and large ΔV˙ groups, respectively. EMGdi measured at end Tin of the pulse breaths was 131 (P < 0.05), 142, and 155% (P < 0.05) of the EMGdi of the control breaths at an identical time point in the small, medium, and large trials, respectively. The latency of the excitation was 126 ± 42 (SD) ms, consistent with a reflex effect. Increasing V˙ had two countervailing effects on Pdi: 1) a depressant mechanical effect due primarily to the force-length (11.2 cmH2O/l) relation of the diaphragm, and 2) an increase in diaphragm activation. For the eight subjects, mean peak Pdi did not change significantly, but there was significant intersubject variability, reflecting variability in the strength of the excitation reflex. We conclude that increasing inspiratory V˙ causes a graded facilitation of EMGdi, which serves to counteract the negative effect of the force-length relation on Pdi.
REFERENCES
| 1-1. | Sinderby C, Beck JC, Lindström LH, Grassino AE.Enhancement of signal quality in esophageal recordings of diaphragm EMG.J Appl Physiol82199713701377 Link | ISI | Google Scholar |
| 1-2. | Sinderby C, Beck JC, Weinberg J, Spahija J, Grassino A.Voluntary activation of the human diaphragm in health and disease.J Appl Physiol85199821462158 Link | ISI | Google Scholar |
| 1-3. | Beck J, Sinderby J, Lindström L, Grassino A.Influence of bipolar electrode positioning on measurements of human crural diaphragm EMG.J Appl Physiol81199614341449 Link | ISI | Google Scholar |
