Narrative review: ventilator-induced respiratory muscle weakness

Abstract

Clinicians have long been aware that substantial lung injury results when mechanical ventilation imposes too much stress on the pulmonary parenchyma. Evidence is accruing that substantial injury may also result when the ventilator imposes too little stress on the respiratory muscles. Through adjustment of ventilator settings and administration of pharmacotherapy, the respiratory muscles may be rendered almost (or completely) inactive. Research in animals has shown that diaphragmatic inactivity produces severe injury and atrophy of muscle fibers. Human data have recently revealed that 18 to 69 hours of complete diaphragmatic inactivity associated with mechanical ventilation decreased the cross-sectional areas of diaphragmatic fibers by half or more. The atrophic injury seems to result from increased oxidative stress leading to activation of protein-degradation pathways. Scientific understanding of ventilator-induced respiratory muscle injury has not reached the stage where meaningful controlled trials can be done, and thus, it is not possible to give concrete recommendations for patient management. In the meantime, clinicians are advised to select ventilator settings that avoid both excessive patient effort and excessive respiratory muscle rest. The contour of the airway pressure waveform on a ventilator screen provides the most practical indication of patient effort, and clinicians are advised to pay close attention to the waveform as they titrate ventilator settings. Research on ventilator-induced respiratory muscle injury is in its infancy and portends to be an exciting area to follow.

Figure 1

The upper-left panel shows the instrumentation for measurement of transdiaphragmatic pressure is response to stimulation of the phrenic nerves. Balloon catheters are passed through the nose to record esophageal pressure (Pes) and gastric pressure (Pga); transdiaphragmatic pressure (Pdi) is calculated by subtracting Pes from Pga. A special magnet is used to stimulate the phrenic nerves. The bottom-left panel shows the fall in Pes and rise in Pga and Pdi in response to phrenic-nerve stimulation (indicated by arrows). The right panel shows values of transdiaphragmatic pressure in response to stimulation of the phrenic nerves in patients requiring mechanical ventilation. The boxed area represents the 95% confidence interval of values obtained in healthy subjects. Data represented by open and closed symbols are taken respectively from Cattapan et al (29) and Watson et al (30).

Figure 2

Patient effort during the time that the ventilator is delivering a breath (measured as inspiratory pressure-time product per breath in cm H₂O.s) is closely related to a patient’s respiratory drive (measured as dP/dt in cm H₂O/sec) at the moment that a patient triggers the ventilator (r=0.78). The inspiratory muscles of patient who has a low respiratory drive at the time of triggering the ventilator will perform very little work during the remainder of inspiration when the ventilator is providing assistance. Conversely, the inspiratory muscles of a patient who has a high respiratory drive will expend considerable effort throughout the period of inspiration even though the mechanical ventilator is providing assistance. (Based on data published in (31))

Figure 3

Airway-pressure waveforms recorded in a patient shortly after the initiation of mechanical ventilation (left), in patient making no respiratory effort (controlled mechanical ventilation, middle), and in a patient receiving an appropriate level of assist-control mechanical ventilation (right). The dashed lines on the left and right panels reproduce the tracing achieved by passive, controlled mechanical ventilation as occurs in a patient receiving neuromuscular blocking agents. The left waveform depicts a patient in respiratory distress who has an excessive work of breathing; this can be inferred from the initial concavity, which results from vigorous inspiratory effort, and the spike at the end of ventilator assistance, which is the result of expiratory muscle recruitment. The middle waveform depicts a patient making no respiratory effort and thus is at risk of developing ventilator-induced respiratory muscle weakness. The right waveform depicts a patient performing an appropriate amount of respiratory work: the small downward dip at the start of the breath indicates the small inspiratory effort required to trigger the ventilator, and the distance between the solid line (actual airway pressure) and dashed line (expected tracing during controlled ventilation, as in the middle panel) is proportional to the amount of work performed by the patient’s inspiratory muscles while the ventilator is providing assistance. The patient in the right panel is performing much more respiratory work than the patient in the middle panel and much less work than the patient in the left panel.