Is Carbon Dioxide Harmful or Helpful in ARDS?

Arterial CO2 tensions (PaCO2) represents a balance between CO2 production and elimination via the lungs, and in health is maintained within a tight range (3.5 – 4.5 kPa). Traditional approaches to CO2 management in the critically ill focused maintaining tidal and minute ventilation to avoid the risks of hypercapnia. The demonstration that high lung stretch directly injures the lungs heralded the use of more protective ventilatory strategies that reduce lung stretch, and have been proven to improve survival in patients with ARDS). Consequently, hypercapnia– and its associated hypercapnic acidosis (HCA) - is prevalent in the critically ill, ‘permitted’ order to realize the benefits of lower lung stretch. Experimental and clinical investigations have generated key advances in our understanding of the effects of hypercapnia. Hypercapnia to be a potent biologic agent, with the potential to exert both beneficial and potentially harmful effects. Hypercapnia modulates the innate immune response, with inhibition of nuclear factor kappa-B, is a key transcriptional protein in injury, inflammation and repair, mediating diverse effects of hypercapnia. Advances in extracorporeal technologies have made possible the direct removal of CO2 while maintaining lung protective ventilation, a promising, though as yet unproven approach. Consequently, it is important to understand the biology of hypercapnia, in order to best understand when hypercapnia should be encouraged, tolerated or avoided in patients with ARDS.