Ventilator-associated lung injury
| Ventilator-associated lung injury | |
|---|---|
| Specialty | Pulmonology  |
Ventilator-associated lung injury (VALI) is an acute lung injury that develops during mechanical ventilation and is termed ventilator-induced lung injury (VILI) if it can be proven that the mechanical ventilation caused the acute lung injury. In contrast, ventilator-associated lung injury (VALI) exists if the cause cannot be proven. VALI is the appropriate term in most situations because it is virtually impossible to prove what actually caused the lung injury in the hospital.[1]
Cause
It is generally regarded, based on animal models and human studies, that volutrauma is the most harmful aspect of mechanical ventilation.[2][3][4] This may be regarded as the over-stretching of the airways and alveoli.
During mechanical ventilation, the flow of gas into the lung will take the path of least resistance. Areas of the lung that are collapsed (atelectasis) or filled with secretions will be underinflated, while those areas that are relatively normal will be overinflated. These areas will become overdistended and injured. This may be reduced by using smaller tidal volumes.[5][6]
During positive pressure ventilation, atelectatic regions will inflate, however, the alveoli will be unstable and will collapse during the expiratory phase of the breath (atelectotrauma). This repeated alveolar collapse and expansion (RACE) is thought to cause VALI. By opening the lung and keeping the lung open RACE (and VALI) is reduced.[7]
Another possible ventilator-associated lung injury is known as biotrauma. Biotrauma involves the lung suffering injury from any mediators of the inflammatory response or from bacteremia.
Finally oxygen toxicity contributes to ventilator-associated lung injury through several mechanisms including oxidative stress.
Possible reasons for predisposition to VALI include:
- An injured lung may be at risk for further injury
- Cyclic atelectasis is particularly common in an injured lung
Pathogenesis
Overdistension of alveoli and cyclic atelectasis (atelectotrauma) are the primary causes for alveolar injury during positive pressure mechanical ventilation. Severe injury to alveoli causes swelling of the tissues (edema) in the lungs, bleeding of the alveoli, loss of surfactant (decrease in lung compliance) and complete alveoli collapse (biotrauma).[1][8] High flow rates are associated with rheotrauma, high volumes with volutrauma and pressures with barotrauma. Collectively these may be converted into a single unit of mechanical power.
Diagnosis
VALI does not need to be distinguished from progressive ALI/ARDS because management is the same in both. Additionally, definitive diagnosis of VALI may not be possible because of lack of sign or symptoms.
Prevention
Preventing alveolar overdistension – Alveolar overdistension is mitigated by using small tidal volumes, maintaining a low plateau pressure, and most effectively by using volume-limited ventilation.
Preventing cyclic atelectasis (atelectotrauma) – Applied positive end-expiratory pressure (PEEP) is the principal method used to keep the alveoli open and lessen cyclic atelectasis.
Open lung ventilationn – Open lung ventilation is a ventilatory strategy that combines small tidal volumes (to lessen alveolar overdistension) and an applied PEEP above the low inflection point on the pressure-volume curve (to lessen cyclic atelectasis).
High frequency ventilation is thought to reduce ventilator-associated lung injury, especially in the context of ARDS and acute lung injury.[7]
Permissive hypercapnia and hypoxaemia allow the patient to be ventilated at less aggressive settings and can, therefore, mitigate all forms of ventilator-associated lung injury
Epidemiology
VALI is most common in people receiving mechanical ventilation for acute lung injury or acute respiratory distress syndrome (ALI/ARDS).[1]
24 percent of people mechanically ventilated will develop VALI for reasons other than ALI or ARDS.[1] The incidence is probably higher among people who already have ALI/ARDS, but estimates vary widely.[1] The variable estimates reflect the difficulty in distinguishing VALI from progressive ALI/ARDS.[1]
References
- ^ a b c d e f International consensus conferences in intensive care medicine: Ventilator-associated Lung Injury in ARDS. This official conference report was cosponsored by the American Thoracic Society, The European Society of Intensive Care Medicine, and The Societé de Réanimation de Langue Française, and was approved by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med 1999; 160:2118.
- ^ Attar MA, Donn SM. Mechanisms of ventilator-induced lung injury in premature infants. Semin Neonatol. 2002 Oct;7(5):353-60. PMID 12464497 [1]
- ^ Rahaman U. Mathematics of Ventilator-induced Lung Injury. Indian J Crit Care Med. 2017 Aug;21(8):521-524. PMID 28904482 [2]
- ^ Donn, S M (13 October 2005). "Minimising ventilator induced lung injury in preterm infants". Archives of Disease in Childhood: Fetal and Neonatal Edition. 91 (3): F226–F230. doi:10.1136/adc.2005.082271. PMC 2672704. PMID 16632652.
- ^ Calvin SH Ng, Ahmed A Arifi, Song Wan, Anthony MH Ho, Innes YP Wan, Eric MC Wong, Anthony PC Yim. Ventilation during Cardiopulmonary Bypass: Impact on Cytokine Response and Cardiopulmonary Function. Ann Thorac Surg 2008;85:154-62
- ^ Calvin SH Ng, Song Wan, Anthony MH Ho, Malcolm J Underwood. Gene Expression Changes with “Non-injurious” Ventilation Strategy. Crit Care 2009;13:403
- ^ a b Krishnan JA, Brower RG (2000). "High-frequency ventilation for acute lung injury and ARDS". Chest. 118 (3): 795–807. doi:10.1378/chest.118.3.795. PMID 10988205. Free Full Text.
- ^ Rouby JJ, Brochard L (2007). "Tidal recruitment and overinflation in acute respiratory distress syndrome: yin and yang". Am J Respir Crit Care Med. 175 (2): 104–6. doi:10.1164/rccm.200610-1564ED. PMID 17200505.