RT Book, Section
A1 Forman, Stuart A.
A1 Benkwitz, Claudia
A2 Longnecker, David E.
A2 Mackey, Sean C.
A2 Newman, Mark F.
A2 Sandberg, Warren S.
A2 Zapol, Warren M.
SR Print(0)
ID 1144117553
T1 Inhalational Anesthetics
T2 Anesthesiology, 3e
YR 2017
FD 2017
PB McGraw-Hill Education
PP New York, NY
SN 9780071848817
LK accessanesthesiology.mhmedical.com/content.aspx?aid=1144117553
RD 2024/04/18
AB KEY  POINTSThe  most  useful  definition  of  dose  for  inhaled  anesthetics  is  the  partial  pressure  in  alveoli,  which  can  be  monitored  in  end-tidal  gases.All  halogenated  anesthetics  decompose  when  they  contact  desiccated  alkaline  chemicals  in  CO2  adsorbents,  producing  carbon  monoxide  (CO)  and  heat.  Proper  use  and  maintenance  of  anesthesia  equipment  and  less-alkaline  CO2  adsorbents  reduce  potential  harm  to  patients.The  rate  at  which  the  alveolar  anesthetic  concentration  (FA  or  Palv)  approaches  the  inspired  (circuit)  concentration  (FI  or  Pcirc)  depends  on  FI  (the  concentration  effect),  minute  alveolar  ventilation  (increased  ventilation  accelerates  equilibration),  cardiac  output  (increased  output  slows  equilibration),  and  the  anesthetic  blood-gas  partition  coefficient  (high  solubility  slows  equilibration).Nitrous  oxide  (N2O)  diffuses  into  air-filled  spaces  in  the  body,  causing  expansion,  increased  pressure,  or  both.The  minimum  alveolar  concentration  (MAC)  is  the  alveolar  concentration  of  inhaled  anesthetic  that  blocks  movement  in  half  of  subjects  in  response  to  a  surgical  incision.  MAC  is  influenced  by  age,  pharmacologic,  physiologic,  and  genetic  factors.MAC-awake  is  the  alveolar  concentration  of  anesthetic  causing  loss  of  response  to  verbal  commands  in  half  of  subjects.  Amnesia  is  produced  by  inhalational  anesthetic  concentrations  lower  than  MAC-awake.Awareness  and  explicit  recall  of  intraoperative  events  are  attributable  to  inadequate  delivery  of  anesthetics  for  the  patient’s  needs.  Without  preventive  measures,  awareness  during  anesthesia  occurs  in  about  1  of  750  patients,  and  about  1%  of  patients  are  at  high  risk  for  this  complication.  Intraoperative  awareness  may  cause  psychological  disturbances  leading  to  post-traumatic  stress  disorder.All  potent  volatile  anesthetics  in  current  use  decrease  mean  arterial  pressure  in  a  dose-dependent  manner.  Severe  cardiovascular  and  respiratory  depression  can  occur  even  at  low  volatile  anesthetic  concentrations  in  elderly,  hypovolemic,  or  critically  ill  patients.  Avoidance  of  these  toxicities  requires  vigilant  monitoring  and  anticipation  of  anesthetic  requirements.Volatile  anesthetics  all  attenuate  baroreceptor  reflex  control  to  a  varying  degree  and  may  increase  heart  rate,  by  both  indirect  and  direct  vagolytic  effect  on  the  heart.Volatile  anesthetics  tend  to  increase  the  respiratory  rate  and  decrease  tidal  volume  and  blunt  ventilatory  responses  to  hypercapnia  and  hypoxia.Desflurane  is  very  pungent  and  associated  with  airway  irritability,  bronchoconstriction,  and  laryngospasm  when  used  for  induction.  Among  volatile  anesthetics,  sevoflurane  causes  the  least  amount  of  airway  irritation.Volatile  anesthetics  inhibit  cerebrovascular  autoregulation  by  vasodilating  vessels,  increasing  blood  flow  and  potentially  intracranial  pressure.  Cerebrovascular  responses  to  altered  Pco2  are  maintained.  Cerebral  metabolic  oxygen  consumption  is  reduced  by  volatile  anesthetics  and  increased  by  N2O.Halothane  undergoes  the  most  hepatic  metabolism  of  the  inhaled  agents.  Whereas  enflurane,  isoflurane,  and  sevoflurane  are  also  metabolized  in  the  liver,  desflurane  and  nitrous  oxide  are  minimally  metabolized.  The  oxidative  metabolism  of  halothane  and  other  volatile  agents  can  induce  severe  immune-mediated  hepatitis.All  potent  volatile  agents  may  trigger  malignant  hyperthermia  in  susceptible  individuals.Preclinical  evidence  suggests  that  volatile  anesthetics  exert  neurotoxic  effects  that  may  impair  cognitive  development  in  the  very  young  or  accelerate  cognitive  decline  in  the  elderly.  However,  definitive  clinical  evidence  of  significant  sequelae  remains  absent,  while  ongoing  prospective  trials  are  expected  to  clarify  the  risks.