Inotropic Drugs Flashcards
Cardiac Glycosides
Agents: Digoxin
Mechanims: inhibiton of sarcolemmal NaK-ATPase (mechanical effect) and enhanced vagal tone (electrical effect).
Uses: Heart failure with reduced ejection fraction, SVTs (supraventricular tachycardias)
Side Effects: **Cardiac **AV block, SVT or Ventricular reentrant arrythmias (delayed afterdepolarizations and increased automaticity, Gastrointestinal nausea, vomitting
Sympathomimetic Amines
Agents: dopamine (HF with hypotension), dobutamine (HF), epinepherine (cardiac arrest), norepinepherine (HF with peripheral vasodilation aka warm shock), isoproterenol (bradycardia/heart block)
Mechanism: all bind to beta1 receptors. Gs protein activates adenylate cyclase, increase in cAMP activates a protein kinase that increases Ca influx thru L-type calcium channels. This increase phase 2
Uses:
Dopamine (low conc: vasodilation of renal and mesentric vessel via dopaminergic receptors promoting diruesis by increaing GFR; medium dose: increase inotrophy of heart Beta 1 receptors and promotes release of norepinephrine from nerve terminals; high dose: systemic vasoconstriction alpha 1 receptors in addition to beta 1.
Dobutamine: synthetic analog of dopamine but does promote vasoconstriction
Norepinephrine: chronotropic and ionotropic effect plus vasocontrictor
Side effects: precipatation of tachyarrythmias
dobutamine, dopamine, epinepherine (precipatation of tachyarrythmias)
norepinepherine (myocardial ischemia due to increase afterload/contractility of heart and precipatation of tachyarrythmias)
Phosphodiesterase-3 Inhibitors
Agent: Milrinone
Mechanism: by inhibiting phosphodiesterase-3, prevents breakdown of cAMP which promotes Ca influx in cardiomyoctes (force of contraction increases) and promotes vasodilation in vascular smooth muscle
Uses: hospital setting acute heat failure when standard therapy has not worked
Vasopressin
Mechanism: at high IV doses potent vasoconstrictor binding vascular smooth muscle V1 receptors.
Uses: vasodilatory shock (e.g. sepsis)
