Created by Andrew Street
about 8 years ago
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Question | Answer |
Indications for adrenaline. | • Cardiac arrest • Anaphylaxis • It may be injected directly into tissues to induce local vasoconstriction - eg during endoscopy to control mucosal bleeding. It is sometimes mixed with local anaesthetic drugs (eg lidocaine) to prolong local anaesthesia. |
MOA of adrenaline. | MOA: Adrenaline is a potent agonist of the α1, α2, β1 & β2 adrenoceptors, & correspondingly has a multitude of sympathetic (‘fight or flight’) effects. These include: vasoconstriction of vessels supplying skin, mucosa & abdominal viscera (mainly α1-mediated); ^HR, force of contraction & myocardial excitability (β1); & vasodilatation of vessels supplying the heart & muscles (β2). These explain its use in cardiac arrest, where the redistribution of blood flow in favour of the HT is desirable, at least theoretically, & may improve the chances of restoring an organised rhythm. Additional effects of adrenaline, mediated by β2 receptors, are bronchodilatation & suppression of inflammatory mediator release from mast cells. Together with its vascular effects, these underpin its use in anaphylaxis, where widespread release of inflammatory mediators from mast cells produces generalised vasodilatation, profound hypotension & often bronchoconstriction. |
SE's of adrenaline. | • Adrenaline-induced HT • Anxiety • Tremor • Headache • Palpitations • Angina, MI, arrhythmias - especially in pt's with HT DS |
CI's, cautions, & important interactions of adrenaline. | CI's: • Combination adrenaline-anaesthetic preparations shouldn't be used in areas supplied by end arteries (eg fingers and toes) as it may cause tissue necrosis Cautions: • HT DS Important interactions: In pt's receiving treatment with a β-blocker, adrenaline may induce widespread vasoconstriction, because its α1-mediated vasoconstricting effect is not opposed by β2-mediated vasodilatation. |
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