You go and see a patient on the ward for pre-operative ...



You go and see a patient on the ward for pre-operative assessment. He starts to feel unwell, you attach an ECG monitor and he is in fast AF. What is atrial fibrillation?Supraventricular arrhythmia characterised by complete absence of coordinated atrial contractions. Seen on ECG as absence of p waves, presence of fibrillatory waves. How would you classify AF? First onset (<48hrs)Paroxysmal – recurrent episodesPersistent AF – non-terminating (need DCR/drugs to do so)Permanent AF – stopped trying to revert itWhat are the underlying physiological mechanisms in AF?Enhanced automaticity, trigger points for multiple atrial ectopicsChronically: re-entrant randomly circulating wavelets that collide and divide into ‘daughter wavelets’; plus electrical/structural remodelling of tissue shortening the refractory periods to maintain AF (becomes more and more difficult to revert).What are you pharmacological treatment options?Control of RVR – Digoxin, beta blockers, amiodarone, non-dihydripyridine CaCB (verapamil, diltizem)Reverting to SR - DCR, flecanide if nil IHD, newer class 3 agents ibutilide dofetilide increased risk torsades, amiodaronePreventing thromboembolic phenomenon – 3-7% annual risk ischaemic CVA from thromboembolism; warfarin, TTE to assess presence thrombus etcTell me about the pharmacology of amiodarone?PCBenzofuran derivative antiarrhtymic with primarily class 3 properties (also Class 1,3,4)Tablets 100-200mg, CCS 30-50mg/mL amiodarone hydrochlorideDilute with 5% glucosePKLoading dose IV 5mg/kg over 30 mins (central access), PO dose 200mg TDSVariable BO 20-80%, 98% PB – displacement reactions, LARGE VD (up to 65L/kg!)Metabolised liver CYP450 desmethyl amiodarone (active)Clearance 0.1/0.6L/min, t ? elim = 52 daysNot removed with CVVHFPDMOA: see belowCNS: Peripheral neuropathy, photosensitivity CVS: Hypotension bradycardia if rapid IV administration (resistant to Rx), AV block/dysrrhythmias (Torsades)RESP: Pulmonary fibrosis GIT/ENDO: Hypo/hyperthyroidism, cirrhosis, NVDOTHER: Corneal microdeposits, slate grey skin, CI in porphyriaHow does it work?Class III properties: blocks K channels, slows repolarisation thus prolongs APD and prolongs QT. Blocks Na cahnnels (decreased slope phase 0)Weak anti-adrenergic/Ca channel blocker actions (decreased HR, slowed AV conduction)What effects does it have on ion conductances?See aboveHow is this manifest on the ECG?Prolongations of the PR, QRS, and QT intervals and sinus bradycardia are frequent during chronic therapy. Amiodarone prolongs refractoriness in all cardiac tissues; Na+?channel block, delayed repolarization owing to K+?channel block, and inhibition of cell–cell coupling all may contribute to this effect.How do you commence treatment?Load 5mg/kg diluted in 250mL 5% glucose run over 30minsDoes it require loading, why?Yes, very lipid soluble, large VD.Would you stop amiodarone before anaesthesia if it had been running for 12 hours?NoWhat if the patient had been on it for 2 months?No t ? elim = 55 daysHow does amiodarone interact with other anaesthetic agents?Mild negative inotropy, drop SVR (additive effects volatiles/IV agents)Protein displacement reactions – NSAID, warfarin, phenytoin, propofolPotentiate effects CaCB, B-blockersIncrease plasma concentrations (via CYP450 inhibition) of digoxin, procainiamide, qunidine, warfarin and cyclosporin. ................
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