Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (21 page)

• 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
(rheumatic MV disease, prosthetic valve or valve repair) vs.
nonvalvular
•
Lone AF
= age <60 y and w/o clinical or echo evidence of cardiac disease (including HTN)
Epidemiology and etiologies (
Annals
2008;149:ITC5-2)

• 1–2% of pop. has AF (8% of elderly); lifetime risk 25%; mean age at presentation ~75 y • Acute (up to 50% w/o identifiable cause)

Cardiac
: HF, myo/pericarditis, ischemia/MI, hypertensive crisis, cardiac surgery

Pulmonary
: acute pulmonary disease or hypoxia (eg, COPD flare, PNA), PE, OSA

Metabolic
: high catecholamine states (stress, infection, postop, pheo), thyrotoxicosis

Drugs
: alcohol (“holiday heart”), cocaine, amphetamines, theophylline, caffeine

Neurogenic
: subarachnoid hemorrhage, ischemic stroke

• Chronic: ↑ age, HTN, ischemia, valve dis. (MV, TV, AoV), CMP, hyperthyroidism, obesity
Evaluation

• H&P, ECG, CXR, TTE (LA size, thrombus, valves, LV fxn, pericardium), K, Mg, FOBT before anticoag, TFTs; r/o MI not necessary unless other ischemic sx

Figure 1-5 
Approach to acute AF

(Adapted from
NEJM
2004;351:2408;
JACC
2006;48:e149)

Strategies for recurrent AF (
Circ
2011;123:104;
Lancet
2012;379:648)

•
Rate control
: goal HR <110 at rest if EF >40% and asx (
NEJM
2010;362:1363)

AV node ablation + PPM as a last resort (
NEJM
2001;344:1043; 2002;346:2062)

•
Rhythm control
: no clear survival benefit vs. rate cntl (
NEJM
2002;347:1825 & 2008;358:2667)

Consider if
sx
w/ rate cntl, difficult to cntl rate, ? unable to anticoag, ? benefit in CRT