This study provides direct electromyographic evidence of persistent diaphragmatic contractile activity in patients with a variety of diseases requiring mechanical ventilation in the assist/control mode. Persistent diaphragmatic contraction during ventilator-assisted breaths has been indirectly demonstrated in normal animals and humans by measuring airway pressure and in ill humans by measuring the mechanical work of breathing. Inspection of the diaphragmatic EMG allows precise determination of contraction duration thus facilitating the study of tidal volume and flow rate alteration on the contractions duration. We chose to express the duration of electromyographic activity in terms of inspired tidal volume because available evidence suggests that volume feedback from stretch receptors, in part, controls inspiratory duration. review
We found that diaphragmatic contractile activity ceased during ventilator-assisted breaths at a volume close to each patients measured spontaneous tidal volume, except in two patients with possible diaphragmatic fatigue. In these two patients, Voff was consistently less than spontaneous tidal volume. Increasing ventilator-delivered inspiratory flow rate led to increases in VoflF; however, a clear statement about the effect of delivered tidal volume on Voflf cannot be made. During controlled breaths initiated by the ventilator, there is no electromyographic activity present except when the delivered tidal volume approaches the patients spontaneous tidal volume. At low tidal volumes, controlled breaths are assisted late in the breath. The pressure waveform often appears similar in contour to other controlled breaths, but the peak pressure is lower.
A current model for control of phasic breathing has been constructed primarily from observations in animals and suggests that increasing flow rate should affect Voff. In its simplest form (refer to Fig 4), the model proposes a central threshold for inspiratory oflf-switch. The central off-switch interacts with stretch receptor volume information transmitted by the vagi to determine the volume of inspiratory termination. Threshold for off-switch decreases with time after the onset of inspiration; a region of graded inhibition follows the off-switch threshold and produces a snowball effect, with some inhibition allowing greater inhibition until inspiration terminates. Inspiratory flow rate appears to feed back as well, probably at a submedullary level, resulting in reflex changes in phrenic output and diaphragmatic EMG. The model posits a higher off-switch volume with increasing flow rates, since volume feedback would intersect the off-switch threshold prior to significant decrease. Our results provide human data to support this model.
Figure 4. Tidal volume and time interactions at inspiratory off-switch threshold. Model for central respiratory control proposes stretch receptor feedback intersecting off-switch threshold at higher point on its descent when delivered flow rate is higher. Inspiratory tidal volume at off-switch (Voff) will therefore be greater.