Although not usually classed as an ‘anti-dysrhythmic’ drug (it is, of course, powerfully pro-dysrhythmogenic in healthy individuals), adrenaline (also called epinephrine) is used in the emergency treatment of patients with cardiac arrest (whether due to asystole or ventricular fibrillation). For these indications it is administered intravenously (or sometimes directly into the heart or down an endotracheal tube, as discussed in the above section on cardiac arrest). It has important uses other than in cardiac arrest, being essential for the treatment of anaphylactic shock and useful in combination with local anaesthetics to reduce the rate of removal from the injection site.
Mechanism of Action
Adrenaline is a potent and non-selective agonist at both α- and β-adrenoceptors. It causes an increased rate of depolarization of cardiac pacemaker potential, thereby increasing heart rate, in addition to increasing the force of contraction of the heart and intense α1-mediated peripheral vasoconstriction (thereby producing a very marked pressor response), which is partly offset by β2-mediated arterial vasodilation.
Adverse Effects
Adrenaline is powerfully pro-dysrhythmogenic and increases the work of the heart (and hence its oxygen requirement). Its peripheral vasoconstrictor effect can reduce tissue perfusion. For these reasons, it is only used systemically in emergency situations.
Pharmacokinetics
Adrenaline is rapidly eliminated from the circulation by a high-affinity/low-capacity uptake process into sympathetic nerve terminals (‘uptake 1’) and by a lower-affinity/highercapacity process into a variety of tissues (‘uptake 2’). It is subsequently metabolized by monoamine oxidase and catechol-O-methyl transferase, and is excreted in the urine as inactive metabolites, including vanillyl mandelic acid (VMA).
Drug Interactions
Tricyclic antidepressants block uptake 1 and so may potentiate the action of adrenaline. Adrenoceptor antagonists, both α and β, block its actions at these receptors.
Mechanism of Action
Adrenaline is a potent and non-selective agonist at both α- and β-adrenoceptors. It causes an increased rate of depolarization of cardiac pacemaker potential, thereby increasing heart rate, in addition to increasing the force of contraction of the heart and intense α1-mediated peripheral vasoconstriction (thereby producing a very marked pressor response), which is partly offset by β2-mediated arterial vasodilation.
Adverse Effects
Adrenaline is powerfully pro-dysrhythmogenic and increases the work of the heart (and hence its oxygen requirement). Its peripheral vasoconstrictor effect can reduce tissue perfusion. For these reasons, it is only used systemically in emergency situations.
Pharmacokinetics
Adrenaline is rapidly eliminated from the circulation by a high-affinity/low-capacity uptake process into sympathetic nerve terminals (‘uptake 1’) and by a lower-affinity/highercapacity process into a variety of tissues (‘uptake 2’). It is subsequently metabolized by monoamine oxidase and catechol-O-methyl transferase, and is excreted in the urine as inactive metabolites, including vanillyl mandelic acid (VMA).
Drug Interactions
Tricyclic antidepressants block uptake 1 and so may potentiate the action of adrenaline. Adrenoceptor antagonists, both α and β, block its actions at these receptors.
Post a Comment