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Noradrenaline Ephedrine

Pharmaceutics
 MOA  Direct agonist, at lower  Direct and indirect action,
doses alpha selectivity, at mainly alpha1, some beta
higher doses beta activity  Not metabolised by COMT –
 Structure  Metabolised by COMT – OH no C3 OH group
group on C3  Not metabolised by MAO –
 Metabolised by MAO – no alkyl group on alpha C
alkyl group on alpha C  Indirect activity – alkyl group
 Less beta effect – no group on alpha C
on terminal amine  Increased lipid solubility/CNS
effects – no substitutions on
benzene ring
 Alkyl substitution on
terminal amine – beta effect
Pharmacokinetics  IV only (metabolised in GIT)  IV, IM, PO
 Poorly lipid soluble, does  More lipid soluble, can cross
not cross BBB BBB
 Metabolised by COMT and  Not metabolised by MAO or
MAO COMT, 35% hepatic
 97% excreted renally as metabolism, 65% excreted
VMA, 3% normetanephrine unchanged in urine
 T1/2b 2 mins  T1/2b 5 hrs
 Onset <1 min, duration 5  Onset 1 min, duration 1hr
mins
Pharmacodynamics
 CVS  Alpha effects low dose –  Alpha and beta effects,
vasoconstriction, decrease in increase vasoconstriction,
HR due to BRR, potential inotropy, HR. Indirect action
decrease in CO. Beta effects can cause tachyphylaxis if
at higher dose – increased NAdr stores depleted
inotropy and HR
 Respiratory  Increased PVR,  Similar
bronchodilator, respiratory
stimulant
 CNS  Decreased CBF from  Does cross BBB, thus can get
vasoconstriction. Mydriasis. agitation, confusion,
Does not cross BBB increased MAC requirement
 Other  Decreases RBF, splanchnic BF  Similar
flow, uterine BF. Increases
BGL, FFA, renin release
 Side effects  Tissue necrosis if  Can be given IM and
extravasation (thus use CVC), peripherally, HTN crisis if on
effects prolonged if on MAOi
MAOis, metabolic acidosis,
HTN crisis, tachyarrythmia,
MI
 Uses  Vasopressor in critically  treat hypotension (e.g. with
ill/vasodilatory shock GA or regional),
bronchospasm, nasal
decongestant, narcolepsy

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