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CARDIOLOGY

ARRHYTHMIAS

BRADYCARDIAS, AV BLOCK AND AV DISSOCIATION

Sinus bradycardia (SB) (NEJM 2000;342:703)

•  Etiologies: meds (incl bB, CCB, amio, Li, dig), ↑ vagal tone (incl. athletes, sleep, IMI), metabolic (hypoxia, sepsis, myxedema, hypothermia, ↓ glc), OSA, ↑ ICP

•  Treatment: usually none required; atropine, b1 agonists or temp. pacing if symptomatic

•  Most common cause of sinus pause is blocked premature atrial beat

Sick sinus syndrome (SSS)

•  Features may include: periods of unprovoked SB, SA arrest, paroxysms of SB and atrial

tachyarrhythmias (“tachy-brady” syndrome), chronotropic incompetence w/ ETT

•  Treatment: meds alone usually fail (adeq. control tachy → unacceptable brady); usually need combination of meds (bB, CCB, dig) for tachy & PPM for brady

AV dissociation

•  Default: slowing of SA node allows subsidiary pacemaker (eg, AV junction) to take over

•  Usurpation: acceleration of subsidiary pacemaker (eg, AV junctional tach, VT)

•  3° AV block: atrial pacemaker unable to capture ventricles, subsidiary pacemaker emerges distinguish from isorhythmic dissociation (A  V rate, some P waves nonconducting)

Temporary pacing wires

•  Consider w/ bradycardia with hemodyn instability or unstable escape rhythm when perm pacer not readily available. Risks: RV perf, VT, PTX, CHB if existing LBBB, etc.

•  Consider instead of PPM for sx bradycardia due to reversible cause (bB/CCB O/D, Lyme, myocarditis, SBE, s/p cardiac surgery/trauma), TdP, acute MI (sx brady, high grade AVB)

SUPRAVENTRICULAR TACHYCARDIAS (SVTS)

Arise above the ventricles, ∴ narrow QRS unless aberrant conduction or pre-excitation.

Figure 1-4 Approach to SVT (adapted from NEJM 2012;367:1438)

•  Catheter ablation: high overall success rate (AFL/AVNRT ~95%, AVRT ~90%, AF ~80%)

Complications: stroke, MI, bleeding, perforation, conduction block (JAMA 2007;290:2768)

ACCESSORY PATHWAYS (WOLFF-PARKINSON-WHITE)

Definitions

•  Accessory pathway (bypass tract) of conducting myocardium connecting atria & ventricles, allowing impulses to bypass normal AVN delay

•  Preexcitation (WPW) pattern: ↓ PR interval, ↑ QRS width w/ Δ wave (slurred onset, can be subtle), ST & Tw abnl (can mimic old IMI); only seen w/ pathways that conduct antegrade (if pathway only conducts retrograde then

ECG will be normal during SR; “concealed” bypass tract)

PAC can exaggerate preexcitation if AV node conduction slowed

•  WPW syndrome: accessory pathway + paroxysmal tachycardia

Classic tachycardias of WPW

•  Orthodromic AVRTnarrow-complex SVT (typically), conducting ↓ AVN & ↑ accessory pathway; requires retrograde conduction and ∴ can occur w/ concealed bypass tracts

•  Antidromic AVRT (rare): wide-complex SVT, conducting ↓ accessory pathway & ↑ AVN;

requires antegrade conduction and ∴ should see WPW pattern during SR

•  AF w/ rapid conduction down accessory pathway; ∴ wide-complex irregular SVT; requires antegrade conduction; ∴ should see WPW pattern in SR. Rarely can degenerate into VF.

Treatment

•  AVRT: vagal, bB, ? CCB; caution w/ adenosine (can precip. AF); have defibrillator ready

•  AF/AFL w/ conduction down accessory pathway: need to Rx arrhythmia and ↑ pathway

refractoriness; use procainamideibutilide, 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 V1 = RBBB-type vs. downward = LBBB-type

•  In structurally abnormal heart: prior MI (scar); CMPmyocarditis;

arrhythmogenic RV CMP (ARVC): incomplete RBBB,

ε wave (terminal notch in QRS) & TWI in V1–V3 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: ischemiaCMP; 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 V1–V3 (provoked w/ class IA or IC) on resting ECG

Diagnostic clues that favor VT (assume until proven o/w)

•  Prior MICHF 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 V1, r/S ratio <1 in V6 LBBB-type: onset to nadir >60–100 ms in V1, q wave in V6

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)