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Vasoactive and anti-arrhythmic medications (Anti-arrhythmics (Class III…
Vasoactive and anti-arrhythmic
medications
Definitions
Vasopressor
Cause vasoconstriction, increasing SVR
Inodilators
Inotropes with vasodilatation effect (reduced SVR)
Inotropes
Increase cardiac contractility
Catecholamines
MOA
Act on a and B receptors of blood vessels and
on the SAN affecting HR
Short t1/2, given via central line as a result
a1 agonists cause vasoconstriction
B1 agonists increase cardiac contractility (HR, SV)
B2 agonists cause vasodilation
Types
Adr
B1 agonist at low dose (inotrope)
a1 agonist at high dose (vasoconstriction)
Dobutamine
B1 agonist (inotrope)
B2 agonist (vasodilation)
NA
a1 and B1 agonist (mainly vasoconstriction)
DA
B1 agonist at low dose (inotrope)
a1 agonist at high dose (vasoconstriction)
Indication
Commonly used inotropes/vasopressors
Non-catecholamines
Troponin sensitisers
E.g. levosimendon, glucagon
MOA: inotrope (cardiac contractility)
Vasopressors
E.g. ADH, phenyephrine
MOA: vasoconstriction
PDE III inhibitors
E.g. enoxamine, milrinone
MOA: inotropic (contractility, SV)
Anti-arrhythmics
Class III (K+ blockers)
E.g. amiodarone, sotolol
MOA: block K+ channels, slowing repolarisation,
increasing refractory period, slowing HR
Class IV (CCBs)
E.g. verapamil, diltiazem
MOA: voltage gated L-type Ca channels, block
cardioselectively to reduce cardiac conductivity at AVN
Class II (B-blockers)
E.g. propanolol
MOA: target B1-R in heart, slow the pacemaker
potential of conduction cells in the SAN
Non-classifieds
Adenosine
Digoxin
Class I (Na blockers)
E.g. flecainide, lidocaine
MOA: block fast Na+ channels in ventricular AP
(funny Na channels), slowing depolarisation