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 accessanesthesiology.mhmedical.com/content.aspx?aid=57065609
RD 2024/04/19
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.