Arrhythmias

BRADYCARDIA AND AV BLOCK

BRADYCARDIAS

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

Etiologies: meds (incl βB, CCB, amio, Li, dig), → vagal tone (incl. in athletes, sleep, IMI), metabolic (hypoxia, sepsis, myxedema, hypothermia, ↓ glc), OSA, ↑ ICP
Treatment: if no sx, none; atropine, β₁ agonists or long-term permanent pacing if sx
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 of tachy → unacceptable brady); usually need combination of meds (βB, CCB, dig) for tachy & PPM for brady

Pseudobradycardia

Intermittent PVCs (with low stroke volume and hence low pulse wave) followed by compensatory pause can cause ascertainment of HR by palpation of radial pulse to be artifactually low

AV BLOCK AND AV DISSOCIATION

AV Block
Type	Features
1°	Prolonged PR (>200 ms), all atrial impulses conducted (1:1)
2° Mobitz I (Wenckebach)	Progressive ↑ PR until impulse not conducted (↑ “grouped beating”) Due to AV node conduction delay: ischemia (IMI), inflammation (myocarditis, MV surgery), high vagal tone (athletes), drug-induced QRS duration most often normal AVB usually worsens w/ carotid sinus massage, improves w/ atropine & exercise Often paroxysmal/nocturnal/asymptomatic; no Rx required
2° Mobitz II	Occasional or repetitive blocked impulses w/ consistent PR interval. Nb, do not confuse with APBs in bigeminal pattern; to dx AVB, atrial rate should be regular and P waves should be the same. Due to His-Purkinje conduction delay: ischemia (AMI), degeneration of conduction system, infiltrative disease, inflammation/valve surgery QRS duration most often prolonged AVB usually improves w/ carotid sinus massage, worsens w/ atropine & exercise (both of which should be avoided if dx suspected) Risk of progression to 3° AVB. Zoll at bedside when recognized; temp pacing wire or PPM often required.
3° (complete)	No AV conduction, with ventricular rhythm slower than atrial rhythm Escape, if present is regular and can be narrow (jxnal) or wide (vent.) Urgent temporary pacing as bridge to permanent pacing is appropriate in most scenarios, especially when syncope present
Nb, if 2:1 block, cannot distinguish type I vs II 2° AVB (no chance to observe PR prolongation); usually categorize based on other ECG & clinical data. High-grade AVB usually refers to block of ≥2 successive impulses. All categories above assume SR in atrium, criteria do not apply during rapid atrial rates, such as in atrial flutter or tachycardia.

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 (βB/CCB O/D, Lyme, myocarditis, SBE, s/p cardiac surgery/trauma), TdP, acute MI (sx brady, high-grade AVB)

SUPRAVENTRICULAR TACHYCARDIAS

PALPITATIONS

Etiologies

PACs, PVCs; SVT, AF, VT, respiratory sinus arrhythmia; pauses; noncardiac

Workup

History: duration & frequency; initiating & aggravating factors: exercise, alcohol, stimulants (caffeine, pseudoephedrine, other prescription & recreational drugs); h/o presyncope or syncope; FHx of arrhythmia, CMP, SCD
Structural evaluation w/ echo; consider ETT if exercise-induced or other RF; TFTs
Ambulatory cardiac monitoring: must monitor during symptoms to diagnose! Holter (worn continuously): if sx typically occur within a 24-48-hr period Looping event monitor (worn continuously): if sx fleeting Nonlooping event monitor (put on during sx): if rarer episodes lasting minutes

SUPRAVENTRICULAR TACHYCARDIAS (SVTS)

Arise above the ventricles,

narrow QRS unless aberrant conduction or pre-excitation

Common Etiologies of SVT (NEJM 2006;354:1039 & 2012;367:1438)
	Type	Features
Atrial	Sinus tachycardia (ST)	Caused by pain, fever, hypovolemia, hypoxia, anemia, anxiety, β-agonists, etc.
	Atrial tachycardia (AT)	Originate at site in atria other than SA node. Seen w/ CAD, COPD, ↑ catechols, EtOH, dig.
	Multifocal atrial tachycardia (MAT)	↑ automaticity at multiple sites in the atria. Seen with underlying pulmonary disease.
	Atrial flutter (AFL)	Macroreentry, usually w/in right atrium
	Atrial fibrillation (AF)	Chaotic atrial activation and rapid, irregular bombardment of AVN
AV Jxn	AV nodal reentrant tach (AVNRT)	Reentrant circuit using dual pathways w/in AVN
	AV reciprocating tachycardia (AVRT)	Reentrant circuit using AVN antegrade and accessory pathway retrograde. When in sinus rhythm may show pre-excitation (WPW) or not (concealed accessory pathway).
	Paroxysmal junctional reciprocating tachycardia (PJRT)	Reentry using AVN & slowly conducting concealed posterosept acc path. More common in peds, at times w/ tachy-induced CMP.
	Nonparoxysmal junctional tachycardia (NPJT)	↑ jxnal automaticity. May see retrograde P’s & AV dissoc. A/w myo/endocarditis, cardiac surg, IMI, dig.

Diagnosis of SVT Type (NEJM 2006;354:1039 & 2012;367:1438)
Onset	Abrupt on/off argues against sinus tachycardia
Rate	Not dx as most can range from 140-250 bpm, but: ST usually <150; AFL often conducts 2:1 → vent. rate 150; AVNRT & AVRT usually >150
Rhythm	Irregular → AF, AFL w/ variable block, or MAT
P wave	Long RP: ST (P same as sinus), AT, MAT (≥3 morphologies), PJRT Short RP, P inverted in inf. leads → retrograde atrial activation via AVN AVNRT: buried in or distort terminal portion of QRS (pseudo-RSR’ in V₁) AVRT: slightly after QRS (RP interval > 100 ms favors AVRT vs AVNRT) NPJT: either no P wave or retrograde P wave similar to AVNRT Fibrillation or no P waves → AF Saw-toothed “F” waves (best seen in inferior leads & V₁) → AFL
Response to vagal stim. or adenosine	Slowing of HR often seen with ST, AF, AFL, AT, whereas reentrant rhythms (AVNRT, AVRT) may abruptly terminate (classically w/ P wave after last QRS) or no response. Occ AT may terminate. AFL & AF → ↑ AV block → unmasking of “F” waves or fibrillation
Short RP: P wave closer to preceding than following QRS (ie, RP < PR). Long RP: P wave closer to following than preceding QRS (ie, PR < RP).

Figure 1-8 Approach to SVT

Treatment of SVT
Rhythm	Acute treatment	Long-term treatment
Unstable	Cardioversion per ACLS	n/a
ST	Treat underlying stressor(s)	n/a
AT	βB, CCB or amiodarone; ? vagal maneuvers or adenosine	βB or CCB, ± antiarrhythmics, possibly radiofrequency ablation (RFA)
AVNRT or AVRT	Vagal maneuvers Adenosine (caution in AVRT^) CCB* or βB	For AVNRT (see next section for AVRT): RFA. CCB or βB (chronic or prn) ± Class IC antiarrhythmics (if nl heart)
NPJT	CCB, βB, amiodarone	Rx underlying dis. (eg, dig tox, ischemia)
AF	βB, CCB, digoxin, AAD	See “Atrial Fibrillation”
AFL	βB, CCB, digoxin, AAD	RFA; βB or CCB ± antiarrhythmics
MAT	CCB or βB if tolerated	Treat underlying disease process AVN ablation + PPM if refractory to meds
^Avoid adenosine & nodal agents if accessory pathway + preexcited tachycardia, see below (JACC* 2003;42:1493)

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 AVRT: narrow-complex SVT (typically), conducting ↑ AVN & ↑ accessory pathway; requires retrograde conduction and can occur w/ concealed bypass tracts
Antidromic AVRT (less common): wide-complex regular tachycardia, conducting ↓ accessory pathway & ↑ AVN. Can meet many ECG morphology criteria for VT. 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, βB; caution w/ adenosine (can precip. AF); have defibrillator ready
AF/AFL w/ conduction down accessory pathway: need to Rx arrhythmia and ↑ pathway refractoriness; use procainamide, ibutilide, or DCCV; avoid CCB & βB, 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) or if rapid conduction possible ([check mark] w/ EPS if preexcitation persists despite exercise testing).

Risk of SCD related to how short RR interval is in AF and # of accessory pathways present. Exercise testing to look for loss of pre-excitation can be used as a proxy for short RR interval in AF: if pathway still present at peak exercise, more concerning.

ATRIAL FIBRILLATION

Classification (Circ 2014;130:2071)

Paroxysmal (terminates spontaneously or w/ Rx w/in 7 d) vs persistent (sustained >7 d) vs long-standing persistent (>1 y) vs permanent (no plan to restore or maintain SR)
Nonvalvular (AF absent rheumatic MS, prosthetic valve or mitral valve repair) vs valvular
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 1-9 Approach to acute AF

Rate control

If sx, goal HR <80; if asx & EF >40%, goal HR <110 at rest (NEJM 2010;362:1363)
AV node ablation + PPM if pharmacologic Rx inadequate (NEJM 2001;344:1043; 2002;346:2062)

Rate Control for AF
Agent		Acute (IV)	Maint. (PO)	Comments
CCB	Verapamil	5-10 mg over 2′ may repeat in 30′	120-360 mg/d in divided doses	↓ BP (Rx w/ Ca gluc) Can worsen HF Preferred if severe COPD Can ↑ dig levels
CCB	Diltiazem	0.25 mg/kg over 2′ may repeat after 15′ 5-15 mg/h infusion	120-360 mg/d in divided doses
βB	Metoprolol	2.5-5 mg over 2′ may repeat q5′ × 3	25-100 mg bid or tid	↓ BP (Rx w/ glucagon) Preferred if CAD Risks: HF & bronchospas.
Digoxin^* (onset >30 min)		0.25 mg q2h up to 1.5 mg	0.125-0.375 mg qd (adj for CrCl)	Consider in HF or low BP Poor exertional HR ctrl
Amiodarone		300 mg over 1 h → 0.5-1 mg/min × 24 h	100-200 mg QD	Consider in HF or low BP Long-term potential tox
IV βB, CCB and digoxin *contraindicated* if evidence of WPW (ie, pre-excitation or WCT) since may facilitate conduction down accessory pathway leading to VF; use procainamide, ibutilide or amiodarone
^*Many meds incl. amio, verapamil, quinidine, propafenone, macrolides & azole antifungals ↑ digoxin levels.

Cardioversion

Consider pharm or electrical cardioversion w/ 1^st AF episode or if sx; if AF >48 h, 2-5% risk stroke w/ cardioversion (pharmacologic or electric) either TEE to r/o thrombus or ensure therapeutic anticoagulation for ≥3 wk prior if need to cardiovert urgently, anticoagulate acutely (eg, IV UFH)
Likelihood of success ∝ AF duration & atrial size; control precip. (eg, vol status, thyroid)
Consider pre-Rx w/ antiarrhythmic drugs (eg, ibutilide), espec if 1^st cardioversion fails
For pharmacologic cardioversion, class III and IC drugs have best proven efficacy
If SR returns (spont. or w/ Rx), atria may be mech. stunned; also, high risk of recurrent AF over next 3 mo. Anticoag postcardioversion ≥4 wk (? unless <48 h and low risk).

Rhythm control (Lancet 2012;379:648; Circ 2014;130:2071)

No clear survival benefit or ↓ stroke risk vs rate control (NEJM 2002;347:1825 & 2008;358:2667)
Consider if symptomatic w/ rate control (eg, heart failure), difficult to control rate, or tachycardia-mediated cardiomyopathy

Antiarrhythmic Drugs (AAD) for AF (Circ 2011;123:104 & 2012;125:381; EHJ 2012;33:2719)
Agent		Conversion	Maintenance	Comments
III	Amiodarone	5-7 mg/kg IV over 30-60′ → 1 mg/min, 10 g load	200-400 mg qd (most effective AAD for SR)	↑ QT, but TdP rare Low rate of acute conversion. May convert wks after load, attention to anticoag Pulm, liver, thyroid toxicity [check mark] PFTs, LFTs, TFTs Potentiates warfarin, → warfarin by ˜50%
	Dronedarone	n/a	400 mg bid	↓ side effects but also ↓ effic. c/w amio; contraindic. in perm AF or sx HF / ↓ EF; risk of liver toxicity
	Ibutilide	1 mg IV over 10′ may repeat × 1	n/a	Contraindic. if ↓ K or ↑ QT ↑ QT, 3-8% risk of TdP Mg 1-2 g IV to ↓ risk TdP Lasts 4-6 h
	Dofetilide	500 mcg PO bid	500 mcg mg bid	↑ QT, ↑ risk of TdP; renal adj
	Sotalol	n/a	80-160 mg bid	[check mark] for ↓ HR, ↑ QT; renal adj
IC	Flecainide	300 mg PO × 1	100-150 mg bid	PreRx w/ AVN blocker Contraindic. if structural or ischemic heart disease
	Propafenone	600 mg PO × 1	150-300 mg tid
IA	Procainamide	10-15 mg/kg IV over 1 h	n/a	↓ BP; ↑ QT ± PreRx w/ AVN blocker
Underlying disease			Maintenance AAD of choice
None or minimal (incl HTN w/o LVH)			class IC (“pill in pocket”), sotalol, dronedarone
HTN w/ LVH			amiodarone
CAD			sotalol, dofetilide, amiodarone, dronedarone
HF			amiodarone, dofetilide