Mechanical ventilation can be delivered with two extreme approaches: (a) by dictating a flow, volume, pressure, or respiratory timing (or some combination), or (b) by delivering assistance synchronized to and regulated by the patient’s neural breathing efforts. Whereas the former approach is advantageous in patients who do not breathe, the latter approach is advantageous in spontaneously breathing patients.
Almost 50 years ago, Gunaratna1 demonstrated that the problem of patients fighting the ventilator during controlled ventilation could be overcome by the use of patient-triggered ventilation. The patient-triggered ventilation was associated with immediate relief of the respiratory distress, apprehension, and agitation.
Since the 1970s, numerous modes of mechanical ventilation that aim to synchronize the ventilator and the patient have been introduced. Patient-triggered or cycled modes of ventilation are controlled by airway pressure, flow, and/or volume measured in the respiratory circuit. Significant limitations of these signals to trigger and cycle-off the assist have been documented for decades.2–12 Despite the term patient-triggered ventilation, severe patient–ventilator asynchrony occurs in at least 25% of ventilated patients13–15 and is associated with prolonged duration of ventilation. Patients with frequent ineffective triggering also tend to receive excessive levels of ventilator support13 and/or sedation.16 In newborns, compared to controlled ventilation, patient-triggered ventilation is associated with shorter duration of ventilation.17–20 Excessive assistance can cause muscle fiber injury and atrophy of the diaphragm.21,22 Conventional ventilation can induce loss of inspiratory muscle force, as much as 75%.22,23–27 Promoting spontaneous breathing28–33 and reducing sedation,34–39 alone or together,40 shortens the duration of mechanical ventilation.
Last, but not least, regulation of spontaneous breathing constitutes a very complex interaction between motor-nerve output and sensory feedback.
In summary, conventional modes of ventilation have limitations with regards to (a) synchronizing assist delivery to the patient’s neural breathing efforts; (b) bedside monitoring of patient respiratory drive and/or interaction with the ventilator; (c) adjusting the level of assist in response to patient demand; and (d) taking advantage of intrinsic lung protective reflexes.
An ideal approach, therefore, is to connect the patient’s respiratory centers to the ventilator, as naturally as the respiratory muscles are connected to the brainstem via the phrenic nerves. This notion is what set the spirit for developing the mode known as neurally adjusted ventilatory assist (NAVA).41
Figure 13-1 (left) describes schematically the hierarchy of the steps involved in generating a spontaneous breath. Respiratory neurons originating in the brainstem of the central nervous system send their signals to the diaphragm via the phrenic nerves. After neuromuscular transmission, diaphragmatic excitation occurs, where action potentials propagate along the diaphragm muscle fibers. This is the source of the diaphragmatic electrical activity (Edi) (see “Electrical Activity of the Diaphragm” below). The Edi ...