The physiological underpinnings of life-saving respiratory support

Abstract

Treatment of respiratory failure has improved dramatically since the polio epidemic in the 1950s with the use of invasive techniques for respiratory support: mechanical ventilation and extracorporeal respiratory support. However, respiratory support is only a supportive therapy, designed to "buy time" while the disease causing respiratory failure abates. It ensures viable gas exchange and prevents cardiorespiratory collapse in the context of excessive loads. Because the use of invasive modalities of respiratory support is also associated with substantial harm, it remains the responsibility of the clinician to minimize such hazards. Direct iatrogenic consequences of mechanical ventilation include the risk to the lung (ventilator-induced lung injury) and the diaphragm (ventilator-induced diaphragm dysfunction and other forms of myotrauma). Adverse consequences on hemodynamics can also be significant. Indirect consequences (e.g., immobilization, sleep disruption) can have devastating long-term effects. Increasing awareness and understanding of these mechanisms of injury has led to a change in the philosophy of care with a shift from aiming to normalize gases toward minimizing harm. Lung (and more recently also diaphragm) protective ventilation strategies include the use of extracorporeal respiratory support when the risk of ventilation becomes excessive. This review provides an overview of the historical background of respiratory support, pathophysiology of respiratory failure and rationale for respiratory support, iatrogenic consequences from mechanical ventilation, specifics of the implementation of mechanical ventilation, and role of extracorporeal respiratory support. It highlights the need for appropriate monitoring to estimate risks and to individualize ventilation and sedation to provide safe respiratory support to each patient.

Development and validation of a mechanical power-oriented prediction model of weaning failure in mechanically ventilated patients: a retrospective cohort study

“…FiO 2 levels before weaning reflect the severity of hypoxia, as well as the state of circulatory function and oxygen transport capacity. 29 Our results are consistent with those of Yan Jia et al, 30 but differ from the findings of Savi et al, 31 showing that FiO 2 is a better predictor of the risk of weaning failure than PO 2 / FiO 2 . This discrepancy may be related to significant influence of FiO 2 and PEEP levels on PO 2 /FiO 2 .…”

Oxygenation thresholds for invasive ventilation in hypoxemic respiratory failure: a target trial emulation in two cohorts

“…Affected patients have a 20–40% mortality risk and survivors may experience decreased quality of life [ 1 , 4 – 6 ]. Invasive ventilation is a potentially lifesaving intervention that restores compensated gas exchange [ 7 , 8 ]. However, invasive ventilation exposes patients to the risks of peri-intubation cardiac arrest, ventilator-induced lung injury, pneumonia, delirium, and ICU-acquired weakness [ 9 – 13 ].…”

“…However, invasive ventilation exposes patients to the risks of peri-intubation cardiac arrest, ventilator-induced lung injury, pneumonia, delirium, and ICU-acquired weakness [ 9 – 13 ]. The best physiologic thresholds for the initiation of invasive ventilation are unknown [ 8 ].…”

Time-controlled adaptive ventilation in patients with ARDS—lack of protocol adherence: a systematic review

“…Since the ARMA trial, there has been no multicenter randomized controlled trial that has been able to assign further mortality benefit to a particular ventilatory strategy [ 2 ]. The main goals of invasive ventilation strategies are to ensure an acceptable gas exchange while preventing ventilator-induced lung injury (VILI) therefore buying time for the lung to heal [ 3 ]. VILI is mainly attributed to repetitive opening and closing of lung units (atelectrauma) and/or cyclic overdistension of the lung (volutrauma) [ 4 ].…”

“…Currently, lung protective ventilation is defined as using low tidal volume (TV) (6 ml/kg predicted body weight) and a plateau pressure lower than 30 cmH 2 O to reduce VILI [ 5 ]. This approach significantly reduced mortality compared to a strategy with high TV and higher plateau pressures [ 3 ].…”