Noninvasive respiratory support and patient self-inflicted lung injury in COVID-19: a narrative review

Abstract

COVID-19 pneumonia is associated with hypoxaemic respiratory failure, ranging from mild to severe. Because of the worldwide shortage of ICU beds, a relatively high number of patients with respiratory failure are receiving prolonged noninvasive respiratory support, even when their clinical status would have required invasive mechanical ventilation. There are few experimental and clinical data reporting that vigorous breathing effort during spontaneous ventilation can worsen lung injury and cause a phenomenon that has been termed patient self-inflicted lung injury (P-SILI). The aim of this narrative review is to provide an overview of P-SILI pathophysiology and the role of noninvasive respiratory support in COVID-19 pneumonia. Respiratory mechanics, vascular compromise, viscoelastic properties, lung inhomogeneity, work of breathing, and oesophageal pressure swings are discussed. The concept of P-SILI has been widely investigated in recent years, but controversies persist regarding its mechanisms. To minimise the risk of P-SILI, intensivists should better understand its underlying pathophysiology to optimise the type of noninvasive respiratory support provided to patients with COVID-19 pneumonia, and decide on the optimal timing of intubation for these patients.

Keywords: ARDS; COVID-19; P-SILI; SARS-CoV-2; high-flow nasal oxygen therapy; lung injury; noninvasive ventialtion; spontaneous breathing.

Fig 1

Interstitial and capillary pressure and lung stress. Interstitial pressure is normally higher than pleural pressure, and higher when stress is greater. This suggests that transpulmonary pressure measured by oesophageal pressure (P_oes) may underestimate actual trans-alveolar and trans-capillary pressure and its potential injurious effects on the lung. (a–d) Different interstitial and capillary pressures after changes of extravascular pressure and their effects. Fluid movement from the capillary bed to the interstitium (Jv)=Kf([Pc–Pi]–σ[πc–πi]). (a) Jv_A=([1.47–{–0.98}]–[1.96–1.18])=1.67 kPa. (b) Jv_B=([1.96–{–2.45}]–[1.96–0.78])=3.24 kPa. In this case, a greater passage of fluid from the capillary to the interstitial space is present. (c) Jv_C=([0.98–{–0.49}]–[1.96–0.98])=0.49 kPa. (d) Jv_D=([0.98–{–0.98}]–[1.96–0.98])=0.98 kPa. Pc, hydrostatic oncotic pressure; Pi, hydrostatic interstitial pressure; P_pl, pleural pressure; πc, capillary oncotic pressure; πi, capillary hydrostatic pressure.

Fig 2

Spontaneous breathing effort at ZEEP or CPAP and spontaneous breathing with pressure support in COVID-19. Representative example of spontaneous breathing in patients with severe COVID-19. During spontaneous breathing at ZEEP or CPAP, the airway pressure (P_AW) is zero (at zero PEEP, ZEEP) or equal to PEEP (if CPAP) in the non-dependent regions of the lung, while it is equal to the superimposed pressure plus PEEP (CPAP) or ZEEP in the dependent (more ventilated) regions. The transpulmonary pressure (P_TP) is higher in dependent lung regions and increases as the oesophageal pressure becomes more negative (Poes) (Part a, b). Conversely, in non-dependent lung areas, when a positive support pressure is applied to mechanically ventilated lungs (even if the patient is breathing spontaneously), the resulting P_AW will be equal to the selected support plus PEEP, while the Poes and P_TP will be lower than during spontaneous breathing (Part c). In dependent regions, when a support pressure is applied to mechanically ventilated but spontaneously breathing lungs, the P_AW will be equal to the difference of PEEP, pressure support (Ps), minus superimposed pressure, with a lower value of PTP and Poes with regard to spontaneously breathing, non-ventilated patients (Part d). CPAP, continuous positive pressure ventilation; PEEP, positive end-expiratory pressure; MV, mechanical ventilation; ZEEP, zero PEEP; P_TP, transpulmonary pressure; Poes, oesophageal pressure; P_AW, airway pressure.

Fig 3

Normal and high respiratory drive and effort during passive, active, or active (plus support) ventilation. Representation of the possible response of patients with COVID-19 to passive, active, or active (plus pressure support) ventilation. Oesophageal pressure (P_oes) swings are higher during active breathing.

Fig 4

Identification and first-line management of noninvasive respiratory support failure. One of the most sensitive and specific scores for the detection of noninvasive respiratory support failure in acute hypoxaemic respiratory failure is the HACOR (sensitivity: 72%; specificity: 90% 1 h after initiation). Along with the HACOR, several parameters should be considered before proceeding to tracheal intubation. No specific score for COVID-19 has been validated to date, but promising scores are reported in the figure. EPAP, end-expiratory airway pressure; GCS, Glasgow Coma Scale; HFNOT, high-flow nasal oxygen therapy; NPPV, noninvasive positive-pressure ventilation; Pao₂/FiO₂, partial pressure of oxygen/fraction of inspired oxygen; P_oes, oesophageal pressure; ROX, rate oxygenation index; SpO₂, peripheral oxygen saturation; V_T, tidal volume.