Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine by Marc Sabatine

pathway
refractoriness; use procainamide , ibutilide , amio, flecainide or DCCV; avoid CCB & bB (ineffective), dig/adenosine (can ↓ refractoriness of pathway → ↑ vent. rate → VF)
• Long term : Rx sx tachycardias w/ RFA, antiarrhythmics (IA, IC) if not candidate for RFA;
consider RFA if asx but AVRT or AF inducible on EPS ( NEJM 2003;349:1803) of if rapid conduction possible (✓ w/ EPS if preexcitation persists despite exercise testing)
risk of SCD related to how short RR interval is in AF and if SVT inducible w/ exercise

WIDE-COMPLEX TACHYCARDIAS (WCTS)
    Etiologies ( Lancet 2012;380:1520)
• Ventricular tachycardia (VT) • SVT conducted with aberrancy : either fixed BBB, rate-dependent BBB (usually RBBB), conduction via an accessory pathway or atrially triggered ventricular pacing Monomorphic ventricular tachycardia (MMVT)
• All beats look similar; predominantly upward in V 1 = RBBB-type vs. downward = LBBB-type

• In structurally abnormal heart: prior MI (scar); CMP ; myocarditis ;
arrhythmogenic RV CMP (ARVC) : incomplete RBBB,
ε wave (terminal notch in QRS) & TWI in V 1 –V 3 on resting ECG, LBBB-type VT, dx w/ MRI ( Lancet 2009;373:1289)
• In structurally normal heart (w/ normal resting ECG):
RVOT VT : LBBB-type VT w/ inferior axis; typically ablate
idiopathic LV VT : RBBB-type VT w/ superior axis; responds to verapamil
    Polymorphic ventricular tachycardia (PMVT)
• QRS morphology changes from beat to beat • Etiologies: ischemia ; CMP ; catecholaminergic;
torsades de pointes (TdP = “twisting of the points,” PMVT + ↑ QT): ↑ QT acquired (meds, lytes, stroke, see "ECG") w/ risk ↑ w/ ↓ HR, freq PVCs (pause dependent) or congenital (K/Na channelopathies) w/ resting Tw abnl & TdP triggered by sympathetic stimulation (eg, exercise, emotion, sudden loud noises) ( Lancet 2008;372:750).
Brugada syndrome (Na channelopathy):>; pseudo-RBBB w/ STE in V 1 –V 3 (provoked w/ class IA or IC) on resting ECG

    Diagnostic clues that favor VT (assume until proven o/w)
• Prior MI , CHF or LV dysfunction best predictors that WCT is VT ( Am J Med 1998;84:53) • Hemodynamics and rate do not reliably distinguish VT from SVT
• MMVT is regular, but initially it may be slightly irregular, mimicking AF w/ aberrancy; grossly irregularly irregular rhythm suggests AF w/ aberrancy • ECG features that favor VT ( Circ 1991;83:1649)
AV dissociation (independent P waves, capture or fusion beats) proves VT
very wide QRS (>140 ms in RBBB-type or >160 in LBBB-type); extreme axis deviation
QRS morphology atypical for BBB RBBB-type: absence of tall R′ (or presence of monophasic R) in V 1 , r/S ratio <1 in V 6 LBBB-type: onset to nadir >60–100 ms in V 1 , q wave in V 6
concordance (QRS in all precordial leads w/ same pattern/direction)
    Long-term management (  JACC 2006;48:1064)
• Workup: echo to ✓ LV fxn, cath or stress test to r/o ischemia, ? MRI and/or RV bx to
look for infiltrative CMP or ARVC, ? EP study to assess inducibility
• ICD : 2° prevention after documented VT/VF arrest (unless due to reversible cause)
1° prev. if high risk, eg, EF <30–35%, ARVC, Brugada, certain LQTS, severe HCMP. See “Intracardiac Devices.” ? Wearable vest if revers. etiol. waiting for ICD ( Circ 2013;127:854).
Antitachycardia pacing (ATP = burst pacing faster than VT) can terminate VT w/o shock
• Meds : bB, antiarrhythmics (eg, amio, mexiletine) to suppress VT which could trigger shock • If med a/w TdP → QT >500 ± VPBs: d/c med, replete K, give Mg, ± pacing ( JACC 2010;55:934) • Radiofrequency ablation if isolated VT focus or if recurrent VT triggering ICD firing; ablation before ICD implantation ↓ discharge rate by 40% ( Lancet 2010;375:31)

ATRIAL FIBRILLATION
    Classification ( Circ 2006;114:e257 & 2011;123:104)
• Paroxysmal (self-terminating, usually <48 h) vs. persistent (sustained >7 d or terminated after Rx) vs. permanent (typically >1 y and when cardioversion has failed or is foregone) • Valvular