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VTPatho-physiologyRe-entrant (most common in 1st 30mins after MI) and incr automaticity (most common >12hrs after MI due to denervation hypersensitivity to NE and E in area beyond infarct)CausesMonomorphic: usually structural / IHDPolymorphic: usually poisoning / wide QTcRF: IHD, cardiomyopathy, meds (dig, type Ia antiarrhythmics, phenothiazides, TCA, sympathomimetics), hypo/hyperK , MI, MVPAssessmentOE: decr BP, canon a waves in JVP (AV dissocation, like in HB), variable intensity of S1; hypotension common; VT more likely if >35yrs, active angina, prev MIECGECG (general) Rate >100 (usually >150; 100-150 if on anti-arrhythmics)3+ consecutive ventricular beats (non-sustained = <30secs)QRS >120-140 (>100 in children)RS >100 (>95% spec)Morphology of V1 and V6QRS >140 with RBBB morphology (V1 positive = L sided ectopic focus) or QRS >160 with LBBB morphology (V1 negative = R sided ectopic focus); if ectopic focus is high in septum, QRS may be surprisingly narrowConcordance of QRS vectors in all precordial leads (20% sens, 90% spec)LAD/RAD: the more abnormal the axis, the more likely VTQRS pattern / axis different to baselineRegular rhythmEvidence of AV dissociation (absent if underlying AF) Notching of QRS at different positions = different P wave rate to QRS rate (40% sens; less in paeds; >75% spec) Fusion beats: QRS with features of narrow atrial and wide ventricular Capture beats: normal QRS amongst broad complexesBrugada’s criteria for VT: this is easiestAbsent RS in any precordial lead (100% spec) = VT (ie. All leads are just an R wave or an S wave) --< ie. Soley +ive or solely –ive)RS >100 in any precordial lead = VTAV dissociation as above = VT; (seen in <25%; more likely to be seen in slower rhythm)If no, look at Wellen’s criteriaWellen’s criteria for VT: RBBB pattern = V1 positive = L sided ectopic focus V1: Monophasic / biphasic complex in V1V1: Left side up rabbit ear = triphasic rSR in V1V6: RS ratio <1V6: QS wave LBBB pattern = V1 negative = R sided ectopic focusV1: R wave >0.03V1: RS >0.06V1: Notched downslope of S waveV6: RS ratio <1V6: any Q waveQRS / RS in V1 (50% VT, 2% SVT)Suggestive of SVT with aberrancy: RSR / QS in V1 (85% SVT, 10% VT); slows with carotid massage; varying BBBDifferential diagnosisSVT with BBB, SVT with aberrant conduction, pre-excited SVT, metabolic derangement (hyperK), toxin-related, pacemaker-relatedMngElectrical cardioversion: indicated if severe chest pain / APO, hypotension Synchronised unless pulseless; 90% success rate; use 50-70J biphasic 120J 150J 170JOverdrive pacingDrugs: Amiodarone: 150mg IV over 5-10mins rpt over 10-20mins if needed 600mg/24hrs 30% effective in 1hr; best if poor LV function Procainamide: 100mg IV 50mg/min IV unti reversion (max 500mg) Most effective (75%); but CI if MI / LV dysfunction due to negative inotrope Sotalol: 1.5mg/kg over 5mins 65% effective; CI if CV compromise (ie. Poor LV function) or long QTc Lignocaine: 1-1.5mg/kg IV Q5mins (max 300mg/hr) 50mg bolus if needed Use if ischaemic VT; less effective than procainamide/sotalol (20% with intial bolus; further 10% with 2nd) otherwiseChloral hydrate toxicity beta-blockersNa channel blocker (eg. TCA) NaHCO3Stimulants alpha and beta blockerSVT vs VTMore likely VT if:Absence of typical RBBB/LBBB morphologyExtreme axisQRS >160AV dissociation changes + P waves at different rate to QRSConcordance of chest leadsRSR with taller L rabbit ear>35yrs, IHD, prev MI, CCF, HOCM, FH sudden cardiac deathMore likely SVT if:BBB / WPW on prev ECG’sPMH SVT ................
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