Editorial Views  |   March 2016
The Goldilocks Principle, Carbon Dioxide, and Acute Respiratory Distress Syndrome: Too Much, Too Little, or Just Right?
Author Notes
  • From the Departments of Anesthesia and Critical Care and Critical Illness and Injury Research Centre, Keenan Research Centre for Biomedical Science of St Michael’s Hospital, Toronto, Ontario, Canada.
  • Corresponding article on page 674.
    Corresponding article on page 674.×
  • Accepted for publication December 2, 2015.
    Accepted for publication December 2, 2015.×
  • Address correspondence to Dr. Curley: curleyg@smh.ca
Article Information
Editorial Views / Critical Care / Respiratory System
Editorial Views   |   March 2016
The Goldilocks Principle, Carbon Dioxide, and Acute Respiratory Distress Syndrome: Too Much, Too Little, or Just Right?
Anesthesiology 3 2016, Vol.124, 532-534. doi:10.1097/ALN.0000000000000996
Anesthesiology 3 2016, Vol.124, 532-534. doi:10.1097/ALN.0000000000000996
ON the face of it, we have blown hot, then cold when it comes to carbon dioxide. We have tolerated it (permissive hypercapnia), considered adding it (therapeutic hypercapnia), and even at times deliberately or inadvertently decreased it.1  Advances in extracorporeal therapies, as reported in this month’s Anesthesiology,2  mean that if we wish, we can just remove it. Should we?
Careful science, rather than caprice, has guided our understanding of the biology of carbon dioxide and the fundamental role it plays in normal physiology, adaptation to, and modulation of disease. Carbon dioxide is essentially a “waste product” of aerobic cellular respiration. Arterial carbon dioxide tension (Paco2) represents the balance between carbon dioxide produced and eliminated. Hypercapnia has been an unavoidable component of lung protection strategies in several key clinical studies over the past four decades. Hickling et al.3,4  first described the concept of “permissive hypercapnia” in two case series, wherein low tidal volume, pressure-limited mechanical ventilation in patients with acute respiratory distress syndrome (ARDS) led to substantial elevations in Paco2 and a mortality that was significantly lower than that predicted by Apache II scores. Comparable findings had been reported a decade before, whereby lowering tidal volumes in status asthmaticus5  and in neonatal pulmonary hypertension6  was associated with improved survival. Eventually, two pivotal large randomized controlled trials indicated that low tidal volume mechanical ventilation improves survival in patients with ARDS.7,8  In all these studies, the relative contribution of lung-protective ventilation or an increase in Paco2 could not be ascertained, although a post hoc analysis of one revealed an association between hypercapnia and improved survival.9 
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