Avoiding Ventilator-Induced lund injury (VILI)
The term Ventilator-Induced Lung Injury (VILI) was introduced in 1993. It includes a group of noxious stimuli that - through variable mechanisms - cause damage to the lung parenchyma.
Causes of VILI
- Excessive pressure leading to lung parenchymal damage
- Includes: Pneumothorax, subcutaneous emphysema, interstitial emphysema,
pneumomediastinum and gas embolism
- Effective pressure distending the parenchyma is the trans-pulmonary pressure which is not
necessarily the same as the pressure applied to the airway (--> TPP)
- The relationship between airway pressure and TPP is strictly linear in an individual patient
- One must consider the relationship between the elastance of the lungs and the whole respiratory
system. The higher the chest wall's relative component to total elastance - the less predictive of
trans-pulmonary pressure will the airway pressure be
- This means that the plateau pressure needs to be interpreted in the context of the resulting TPP
This is the case in normal lung and chest wall elastance. A plateau airway pressure of 30cmH2O would yield a TPP of 15cmH2O.
This is the case with increased lung elastance in the presence of normal chest wall elastance (eg. ARDS patient). A plateau airway pressure of 30cmH2O would yield a TPP > 15cmH2O.
This is the case with increased chest wall elastance (eg. obese patient, burns) with normal lung elastance. A plateau airway pressure of 30cmH2O would yield a TPP < 15cmH2O.
- Excessive volumes leading to lung parenchymal damage
- There has been a long-standing debate whether volutrauma or the associated changes in
pressure result in parenchymal injury
- This debate becomes less meaningful if we consider TV in the context of TPP, stress and strain
- Stress is equal to TPP while Strain is the TV normalised to the lung resting volume (TV/FRC)
Stress is defined as TPP and is therefore the same.
Stress increases with increased elastance / poor compliance and vice versa.
Stress increases with increases strain and vice versa.
Strain increases with increasing ratios of TV to FRC.
Stress follows accordingly.
Clinically this means that the tidal volume needs to be appreciated on the background of the FRC which itself is altered by pathological states.
Ultimately, by limiting Stress / TPP one will incorporate the above concept into their clinical decisions.
- Refers to damage induced by cyclic collapse and reinflation of lung tissue
- Associated with increased secretion of cytokines and therefore inflammatory response
- The model by Mead et al. suggests an underlying mechanism including unequal distribution of
stress and strain within diseased lung
- Please refer to the PHYSICS section on "Stress Raisers" for more detail
- The take-home message is that an unequally aerated lung generates focal areas of high stress due to adjacent open and collapsed areas.
- Refers to detrimental effects of excessive flow on the lung parenchyma during positive pressure
- Flow can be seen as the rate at which a given strain occurs in the lung
- The higher the rate of strain, the greater the resistance within the extracellular matrix. This
process requires energy which is then dissipated into the lung parenchyma
- We do currently not understand if and where the threshold is for those forces to become harmful
Referring back to the concept of mechanical power one can see that the applied power during positive pressure ventilation increases most significantly with changes in flow, TV and driving pressure.
- Refers to parenchymal damage caused by a high respiratory rate
- The above graph shows that mechanical power increases significantly with respiratory rate
- Assuming every delivered breath generates a certain amount of stress/strain then the respiratory rate acts as a stress/strain multiplier. This can act as a cumulative stress effect over time.
- We do not know whether there is a threshold for a "safe rate" but animal data shows that at a given strain the damage to the parenchyma is less with lower rates
- Clinically one may use this information to support the concept of permissive hypercapnia while minimising the stress on the lung
- Refers to iatrogenic induction of increased cytokine release from lung parenchyma
- Associated with systemic inflammatory changes (ARDS causing SIRS)
- Also local pulmonary bio-trauma such as rupture causing air leak, altered capillary permeability, oedema, surfactant degradation and paracrine effects of alveolar cells