RT Book, Section A1 Laffey, John G. A1 Kavanagh, Brian P. A2 Tobin, Martin J. SR Print(0) ID 57065609 T1 Chapter 14. Permissive Hypercapnia T2 Principles and Practice of Mechanical Ventilation, 3e YR 2013 FD 2013 PB The McGraw-Hill Companies PP New York, NY SN 978-0-07-173626-8 LK accessmedicine.mhmedical.com/content.aspx?aid=57065609 RD 2024/11/10 AB Carbon dioxide (CO2) is the “waste product” of aerobic respiration. In health, arterial carbon dioxide tension (PaCO2) is tightly regulated, with minute ventilation potently enhanced in response to small elevations in CO2 tension. In critical illness its role is becoming better understood; indeed, in survivors of cardiac arrest, elevated CO2 is associated with a higher incidence of reported near-death experiences.1 Although usually well tolerated, hypercapnia traditionally has been considered to be an adverse event. In fact, the extent and severity of acidosis are predictive of adverse outcome in diverse clinical contexts, including cardiac arrest,2,3 sepsis,4–6 and in neonatal practice.7 Traditional approaches to CO2 management in the operating room and for patients with acute respiratory failure generally focused on the deleterious effects of hypercapnia, traditionally targeting therefore normocapnia or even hypocapnia.