In patients with severe hypercapnia, the PaO2/FiO2 ratio was significantly lower and peak airway pressure, plateau airway pressure, and PEEP were higher than in patients with a maximum PaCO2 of <50 mmHg. The relationship between PaCO2 and ICU mortality demonstrated a U-shaped curve, with patients with very low and high PaCO2 having an increased risk of death. Mortality was significantly higher in patients with a maximum PaCO2 of ≥50 mmHg during the first 48 h of MV (62.5%) than in patients with a maximum PaCO2 of <50 mmHg (49.6%). The incidence of barotrauma, renal dysfunction, and cardiovascular dysfunction was significantly higher in patients with a maximum PaCO2 of ≥50 mmHg compared to patients with a maximum PaCO2 of <50 mmHg (p<0.05).
After adjustment for baseline variables including age, SAPS II at ICU admission, corrected minute ventilation, use of pressure/ volume limitation strategy (PLS), presence of acidosis, driving pressure, PaO2/FiO2 ratio, and study period, the presence of severe hypercapnia remained independently associated with a higher risk for ICU mortality (OR 1.93, 95% CI 1.32–2.81; p = 0.001). Even when limiting analysis to patients receiving PLS (and matched for all other variables), severe hypercapnia was associated with higher ICU mortality compared to patients with a maximum PaCO2 of <50 mmHg (OR 1.58, CI 95% 1.04–2.41; p = 0.032). Acidosis or the combination of hypercapnia and acidosis independently increased the risk of ICU mortality.
Conclusion:
Patients receiving lung-protective ventilation with a tidal volume of ≤6 ml/kg had a high incidence of severe hypercapnia. Although patients receiving lung-protective ventilation have a lower mortality, hypercapnia appears to be independently associated with worse outcomes in patients with ARDS. The authors challenge the notion that severe hypercapnia is safe and prospective trials are required to ascertain if hypercapnia is indeed ‘permissive’.
Link to original article in ESIM 2017
My comment:
Although a retrospective study, it raises the issue if we should apply early APRV - with benefits of improved oxygenation, circumventing the problem of 6 ml/kg Tv, and lower paCO2, as this is less of problem in this mode, This actually one of the points that Nader Habashi makes about APRV. It should not be used as a rescue mode. Its interesting to look at the animal long model in this mode, where there is no repeat collapsing and reopening of recruitable lung tissue and with in general little problem controlling paCO2. I think the time has come to compare in a RCT APRC versus VCV-AC and /or PC-AC in moderate to severe ARDS. My humble opinion and I tend to go very early to APRV already in ARDS. An RCT will give us the answer to this important question.
My comment:
Although a retrospective study, it raises the issue if we should apply early APRV - with benefits of improved oxygenation, circumventing the problem of 6 ml/kg Tv, and lower paCO2, as this is less of problem in this mode, This actually one of the points that Nader Habashi makes about APRV. It should not be used as a rescue mode. Its interesting to look at the animal long model in this mode, where there is no repeat collapsing and reopening of recruitable lung tissue and with in general little problem controlling paCO2. I think the time has come to compare in a RCT APRC versus VCV-AC and /or PC-AC in moderate to severe ARDS. My humble opinion and I tend to go very early to APRV already in ARDS. An RCT will give us the answer to this important question.
