Spontaneous breathing: a double-edged sword to handle with care

Abstract

In acute hypoxemic respiratory failure (AHRF) and acute respiratory distress syndrome (ARDS) patients, spontaneous breathing is associated with multiple physiologic benefits: it prevents muscles atrophy, avoids paralysis, decreases sedation needs and is associated with improved hemodynamics. On the other hand, in the presence of uncontrolled inspiratory effort, severe lung injury and asynchronies, spontaneous ventilation might also worsen lung edema, induce diaphragm dysfunction and lead to muscles exhaustion and prolonged weaning. In the present review article, we present physiologic mechanisms driving spontaneous breathing, with emphasis on how to implement basic and advanced respiratory monitoring to assess lung protection during spontaneous assisted ventilation. Then, key benefits and risks associated with spontaneous ventilation are described. Finally, we propose some clinical means to promote protective spontaneous breathing at the bedside. In summary, early switch to spontaneous assisted breathing of acutely hypoxemic patients is more respectful of physiology and might yield several advantages. Nonetheless, risk of additional lung injury is not completely avoided during spontaneous breathing and careful monitoring of target physiologic variables such as tidal volume (Vt) and driving transpulmonary pressure should be applied routinely. In clinical practice, multiple interventions such as extracorporeal CO₂ removal exist to maintain inspiratory effort, Vt and driving transpulmonary pressure within safe limits but more studies are needed to assess their long-term efficacy.

Keywords: Spontaneous breathing; acute respiratory distress syndrome (ARDS); esophageal pressure (Pes); physiology; ventilator-induced lung injury (VILI).

Figure 1

Monitoring of esophageal and transpulmonary pressure during PSV. Waveforms of airway pressure (Pao), airflow, tidal volume (Vol), esophageal (Pes) and transpulmonary pressure (P_L) recorded in a severe acute respiratory distress syndrome patients undergoing protective PSV while on ECMO. Positive end expiratory pressure is set at 15 cmH₂O, support is 8 cmH₂O, obtaining tidal volume ≈340 mL (≈5 mL/kg IBW) and respiratory rate 16 bpm. The dashed line on the left denotes maximal dynamic driving PL (∆P_L,dyn) during inspiration, while the second, positioned at end inspiration (zero flow), identify end-inspiratory PL (∆P_L,ei). PSV, pressure support ventilation; ECMO, extracorporeal membrane oxygenation.

Figure 2

Effects of controlled ventilation vs. spontaneous breathing on ventilation inhomogeneity. Functional map of distribution of regional tidal ventilation in the chest assessed by electric impedance tomography (EIT): (A) volume controlled ventilation in an intubated patient with set Vt of 500 mL, respiratory rate 16 bpm and PEEP 5 cmH₂O. The dependent regions are distended by only 25% of the global Vt, resulting in highly inhomogeneous ventilation distribution; (B) spontaneously breathing non-intubated patient with respiratory rate of 20 bpm and no PEEP. Notice the equal distribution of ventilation between the non-dependent and the dependent lung regions, yielding almost perfectly homogeneous distribution. Vt, tidal volume.