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Little history of Lung Protective Ventilation [LPV]
Ventilation first became widespread in the polio pandemics of the 20th century. Prior to that it has consisted more of using bellows to drive air into drowned victims/arrested people and causing barotrauma.
Polio used negative pressure iron lungs and boxes, then positive pressure ventilation was used. In the 1960's scientists became especially worried about oxygen toxicity, having observed the 100% lethality of animals breathing FiO2 100%.
Therefore they decided to start adopting high tidal volumes to allow lower FiO2. Then it was appreciated that high tidal volumes caused barotrauma and death. 1970s Bone and colleagues published an abstract in which they described patients with ARDS who were ventilated with PEEPs
of 16 ± 4 cm H2O and Vts of 22 ± 4 ml/kg; 40% of these patients developed severe barotrauma. I mean obviously silly to us now. But proves smart people never really knew any better, accepted at the time.
So barotrauma (pressure damage) became popular concept. However an elegant study on musicians showed us that having a high opening pressure did not necessitate lung damage because oboe/flute players could reach pressures that would horrify us but they don't tension pneumothorax.
Then, attention turned to volutrauma - lung overdistension was clearly an issue. Small lung volumes led to alveolar collapse and hypoxaemia but this could be mitigated by high PEEP to allow the FiO2 not to have to be increased.
The landmark ARDSnet trial in 2000 was stopped early at 800 patients because mortality in LPV arm was 31% vs control arm 40%. A huge difference for intensive care patients.
2 points to this - the control arm did have large tidal volumes (12ml/kg) vs average 6-8ml/kg in LPV group. But given that patients in standardised control arms of huge ARDS trials have terrible LPV compliance
Re-iterates the point no one is very good at LPV. Look nearly half of the control arms didn't have LPV
And then also intriguing extra point, evidence that having to increase RR in low tidal volumes generates more than the set PEEP, and may add a degree of protection. https://www.atsjournals.org/doi/pdf/10.1164/rccm.2105050
Furthermore multiple analyses have never found that having viral ARDS, or pancreatic ARDS, or trauma ARDS, or drowning ARDS, made you not benefit from LPV.
APRV is another nice strategy with some evidence, and again it is an open lung strategy that aims to maintain recruitment and prevent the rapid collapse-open that is very bad for alveolar cells.
So basically, it's always been clear we have to balance VOLUME and PRESSURE and FiO2 but....
When it comes to CPAP strategies I cannot see that large swings in transpulmonary pressure (Vt of 600/700), FiO2 80-100%, and PEEPs of 15, really help any of these things, and no wonder so much barotrauma.
