Myorelaxants in ARDS patients

Abstract

Neuromuscular blocking agents (NMBAs) inhibit patient-initiated active breath and the risk of high tidal volumes and consequent high transpulmonary pressure swings, and minimize patient/ ventilator asynchrony in acute respiratory distress syndrome (ARDS). Minimization of volutrauma and ventilator-induced lung injury (VILI) results in a lower incidence of barotrauma, improved oxygenation and a decrease in circulating proinflammatory markers. Recent randomized clinical trials did not reveal harmful muscular effects during a short course of NMBAs. The use of NMBAs should be considered during the early phase of severe ARDS for patients to facilitate lung protective ventilation or prone positioning only after optimising mechanical ventilation and sedation. The use of NMBAs should be integrated in a global strategy including the reduction of tidal volume, the rational use of PEEP, prone positioning and the use of a ventilatory mode allowing spontaneous ventilation as soon as possible. Partial neuromuscular blockade should be evaluated in future trials.

Keywords: Corticosteroids; ECMO; Muscle relaxants; PEEP; Prone positioning; Protective ventilation; Sedation.

Fig. 1

Plausible beneficial effects of neuromuscular blocking agents (NMBAs) in ARDS patients

Fig. 2

Schema to explain the harm of vigorous spontaneous effort in ARDS. When vigorous spontaneous effort is preserved during mechanical ventilation, transpulmonary pressure (Paw—Ppl = PL) reaches injuriously high, thereby increasing tidal volume and causing global overdistension. In addition, negative Ppl distends pulmonary capillary vessels and increases perfusion; the transmural pressure across pulmonary capillary vessels is increased (Pcap—Ppl =  + 30), promoting interstitial edema formation (right magnified panel). In the presence of injury, permeability is increased and, therefore, alveolar edema formation is accelerated (Right magnified panel). In ARDS, atelectasis is often present in dorsal (dependent) lung regions (dotted black area in lung). Since the presence of atelectatic ‘solid-like’ lung tissue may block the pressure transmission of negative ∆Ppl following diaphragmatic contraction, more negative ∆Ppl is localized in dorsal lung regions (negative ∆Ppl − 20cmH2O vs. − 10cmH2O in dorsal vs. ventral lung regions). In this way, greater local (dorsal) lung stress causes local overdistension by drawing gas from other lung regions—e.g., ventral lung (blue line; this is called pendelluft phenomenon [45]) or directly from a ventilator. Thus, the bulk of effort-dependent lung injury occurs in dorsal lung regions, where vigorous spontaneous effort causes greater inspiratory lung stress and stretch (three red lines in lower panel). In addition, vigorous spontaneous effort causes patient–ventilator asynchrony and derecruitment with active exhalation. Abbreviations: ARDS acute respiratory distress syndrome; Pcap capillary pressure; Ppl pleural pressure

Fig. 3

Place of neuromuscular blocking agents in the ventilatory strategy of ARDS patients