RT Book, Section
A1 Butterworth IV, John F.
A1 Mackey, David C.
A1 Wasnick, John D.
SR Print(0)
ID 1161427055
T1 Adrenergic Agonists & Antagonists
T2 Morgan & Mikhail's Clinical Anesthesiology, 6e
YR 2018
FD 2018
PB McGraw-Hill Education
PP New York, NY
SN 9781259834424
LK accessmedicine.mhmedical.com/content.aspx?aid=1161427055
RD 2024/04/20
AB KEY  CONCEPTS  Adrenergic  agonists  can  be  categorized  as  direct  or  indirect.  Direct  agonists  bind  to  the  receptor,  whereas  indirect  agonists  increase  endogenous  neurotransmitter  activity.  The  primary  effect  of  phenylephrine  is  peripheral  vasoconstriction  with  a  concomitant  rise  in  systemic  vascular  resistance  and  arterial  blood  pressure.  Clonidine  decreases  anesthetic  and  analgesic  requirements  and  provides  sedation  and  anxiolysis.  Dexmedetomidine  has  a  higher  affinity  for  α2-receptors  than  clonidine.  It  has  sedative,  analgesic,  and  sympatholytic  effects  that  blunt  many  of  the  cardiovascular  responses  seen  during  the  perioperative  period.  Long-term  use  of  these  agents,  particularly  clonidine  and  dexmedetomidine,  leads  to  super-sensitization  and  upregulation  of  receptors;  with  abrupt  discontinuation  of  either  drug,  an  acute  withdrawal  syndrome  including  hypertensive  crisis  can  occur.  Ephedrine  is  commonly  used  as  a  vasopressor  during  anesthesia.  As  such,  its  administration  should  be  viewed  as  a  temporizing  measure  while  the  cause  of  hypotension  is  determined  and  remedied.  At  low  doses  (0.5–3  mcg/kg/min),  dopamine  (DA)  primarily  activates  dopaminergic  receptors.  Stimulation  of  these  receptors  (specifically,  DA1  receptors)  vasodilates  the  renal  vasculature  and  promotes  diuresis.  Labetalol  lowers  blood  pressure  without  reflex  tachycardia  because  of  its  combination  of  α  and  β  effects.  Esmolol  is  an  ultrashort-acting  selective  β1-antagonist  that  reduces  heart  rate  and,  to  a  lesser  extent,  blood  pressure.  Abrupt  discontinuation  of  β-blocker  therapy  for  24  to  48  h  may  trigger  a  withdrawal  syndrome  characterized  by  hypertension,  tachycardia,  and  angina  pectoris.