CRAMMER’S GUIDE TO ARRHYTHMIAS
Harrison’s IM 18th ed ren.sama
BRADYARRHYTHMIAS STRUCTURE, ETIOLOGY AND CLINICAL FEATURES
I. SA NODE DISEASES SA NODE: cluster of small fusiform cells in sulcus
terminalis on the epicardial surface of the heart
at the R atrial-superior caval junction, where
they envelop SA nodal artery (from R coronary
artery 55-60% and L circumflex artery 40-45%);
structurally heterogeneous but the central
prototypic nodal cells have fewer distinct
myofibrils than surroundings, NO IC DISK (on LM),
POOR SR AND NO T-TUBULES; richly innervated
by sympathetic and parasympathetic nerves
and ganglia; exhibits the most rapid phase 4
depolarization
SA node > compact AV node > AV bundle
(transverses central fibrous body, subject to
injury during surgery and VHD) > Bundle of His (in
the ventricular septum) > RBB and LBB > Purkinje
fiber network > ventricles
Extrinsic SA node dysfunction are often
reversible; most common causes: drugs and
autonomic NS influences that suppress
automaticity and/or compromise conduction
Intrinsic SA node dysfunction is degenerative,
characterized by pathologically fibrous
replacement of SA node or its connections; e.g.
SSS, MI, senile amyloidosis, inflammatory
diseases like pericarditis and myocarditis.
Specific indicator of intrinsic SA node disease:
abN SNRT, abN SACT, and low IHR
SSS – overdrive suppression of SA node result in
prolonged pauses and syncope upon
termination of tachycardia
AF – inc with advanced age, hpn, DM, LV
dilation, VHD and ventricular pacing
Greatest risk of thomboembolism: ≥65 yo, prior
history of stroke, VHD, LV dysfunction, or atrial
enlargement = should be tx with anticoagulants
See table 232-1 etiologies of SA node
dysfunction page 1868
ECG AND DIAGNOSTICS TREATMENT
ECG: sinus bradycardia (<60bpm benign and very NOT ASSOCIATED WITH INC MORTALITY
common in young healthy and physically conditioned pt;
<40bpm in awake state in the absence of physical AIM OF THERAPY: ALLEVIATE SYMPTOMS
conditioning is abN); sinus pauses (up to 3secs are PACEMAKER IMPLANTATION IS THE PRINCIPAL
common in awake athletes and longer in elderly); sinus THERAPEUTIC INTERVENTION IN PT WITH
arrest; sinus exit block; tachycardia (in SSS); and SYMPTOMS
chronotropic incompetence (inability to inc the HR in
response to exercise or stress or inability to reach 85% of BB and CCB – inc SNRT in pt with SA node
predicted maximal heart rate at peak exercise or failure to dysfunction
achieve HR of >100bpm with exercise or a maximal HR with
antiarrhythmic class I and III – promote SA node
exercise less than 2SD below that of age)
exit block
Type I second-degree SA block – progressive prolongation
Digitalis – shorten SNRT
of SA node conduction with intermittent failure of impulses
originating in the sinus node to conduct to surrounding Isoproterenol or atropine IV – inc sinus rate
atrial tissue acutely
Type II second-degree SA block – no change in SA node Theophylline – acutely and chronically inc HR but
conduction before a pause inc potential serious ventricular arrhythmias
Complete or third-degree SA block – no P waves Sinus bradycardia – common in pt with acute
inferior or posterior MI and can be exacerbated
Tachycardia-bradycardia syndrome – alternating sinus
by vagal activation induced by pain or other
bradycardia and atrial tachyarrhythmia
drugs like morphine. It is a prominent feature of
Autonomic NS testing – dx carotid sinus hypersensitivity; carotid sinus hypersensitivity and neutrally
pauses >3sec consistent with diagnosis. mediated hypotension associated with
vasovagal syncope and responds to pacemaker
Determining intrinsic heart rate (IHR) may distinguish SA
node dysfunction from slow HR that results from high vagal
tone. N IHR after administration of 0.2mg/kg propranolol
and 0.04mg/kg atropine is 117.2-(0.53xage) in beats/min;
slow IHR is indicative of SA disease
Electrophysiologic testing – assess presumed SA node
dysfunction and evaluation of syncope esp. in structural
heart disease
Invasive assessment of SA node: sinus node recovery time
(SNRT) is the longest pause after cessation of overdrive
pacing of the RA near SA node (N is <1500ms or corrected
for sinus cycle length <550ms) and sinoatrial conduction
time (SACT) is ½ the difference between intrinsic sinus cycle
length and a noncompensatory pause after premature
atrial stimulus (N is <125ms)
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II. AV NODE: subendocardial structure in the
ATRIOVENTRICULAR transitional zone, composed of aggregates of
CONDUCTION cells in the posterior-inferior RA; superior, medial
DISEASE and posterior transitional atrionodal zone
converge to form compact AV node
(~1x3x5mm) at the apex of the triangle of Koch
(coronary sinus ostium posteriorly, septal
tricuspid valve annulus anteriorly, tendon of
Todaro superiorly); highly innervated with
postganglionic sympathetic and
parasympathetic nerves
AV bundle: blood supply from AV nodal artery
and first septal perforator of the L anterior
descending coronary artery
Bundle branch: blood supply from the septal
perforators of L anterior descending coronary
arteries and branches of posterior descending
coronary arteries
Bundle of His and distal conducting system are
minimally influenced by autonomic tone;
insulated from ventricular myocardium (most
rapid conduction in the heart is observed here).
The action potentials (AP) exhibit very rapid
upstrokes (phase 0), prolonged plateaus (phase
2) and modest automaticity (phase 4)
Functional (autonomic, metabolic/endocrine
and drug-related) causes of AV node disease
tend to be reversible. Etiologies that produce
structural changes (fibrosis) are generally
permanent
Idiopathic progressive fibrosis of the conduction
system – one of the more common
degenerative (aging) cause of AV block
described as “sclerosing of the L cardiac
skeleton” typically 4th decade and accelerated
by atherosclerosis, hpn, and DM.
Acute MI – 10-25% develops AV block most
commonly 1st or 2nd AV block; 2nd and higher
degree tends to be INFERIOR which tends to be
more STABLE, narrow escape rhythms.
Acute ANTERIOR MI with block in distal AV
segments results in wide complex, UNSTABLE
escape and worse prognosis
For more info: See table 232-2 etiologies of AV
block page 1871
1ST deg AV block (PR interval >200ms) – slowing of
conduction through AV junction; typical site of delay is AV
NODE; WIDE QRS suggestive of delay in DISTAL conduction
system; NARROW QRS suggest delay in AV node or
(proximal) Bundle of His
2nd deg AV block – intermittent failure of electrical impulse
conduction system from atrium to ventricles
Mobitz type I (Wenckebach) – progressive lengthening PR
interval, shortening of RR interval and a pause that is less
than 2x the immediately preceding RR interval
Mobitz type II – intermittent failure of conduction of P wave
without changes in the preceding PR or RR interval;
typically occurs in distal or infra-His conduction system
(INFRANODAL), often associated with intraventricular
conduction delays; prolonged AH interval; associated with
series of nonconducted P waves after a period of sinus
bradycardia with N PR interval => PAROXYSMAL AV BLOCK
(indication of permanent pacing)
High-grade AV block – intermediate between 2nd deg and
3rd deg
3rd deg AV block – complete failure of conduction from
atrium to ventricle; block is distal to AV node, duration of
QRS is helpful in determining level of block
Without BBB: WIDE QRS escape rhythm – implies block is in
the DISTAL HIS or BUNDLE BRANCHES while NARROW QRS –
the block is in the AV NODE or PROXIMAL HIS and the
escape rhythm is in the AV junction; typically faster and
more stable
The difference of innervations of AV node and infranodal
conduction systems, vagal stimulation and carotid sinus
massage, slows conduction in AV node but have less
effect on infranodal tissue and may improve conduction
due to reduced rate of activation of distal tissue.
Atropine, isoproterenol and exercise improve conduction
though AV node and impair infranodal conduction.
Congenital CHB and narrow QRS – exercise inc HR
Acquired CHB and wide QRS – don’t respond to exercise
with an inc HR
Time from the most rapid deflection of the atrial
electrogram in the His bundle recording (AH interval)
represents conduction through the AV node. N is <130ms
Time from the His electrogram to the earliest onset of the
QRS on ECG (HV interval) represents the conduction time
through the His-Purkinje system. N is ≤55ms
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TEMPORARY OR PERMANENT ARTIFICIAL PACING
IS THE MOST RELIABLE TX FOR PT WITH SYMPTOMS
The most expeditious technique is the use of
transcutaneous pacing, where pacing patches
are placed anteriorly over cardiac apex
(cathode) and posteriorly between the spine
and scapula or above the R nipple (anode);
highly effective (acutely) but limited to pt
discomfort and longer-term failure to capture
the ventricle owing to changes in lead
impedance.
Permanent Pacemakers in adults access though
the subclavian-SVC venous system use a 5-letter
code:
First letter indicates chamber/s that is paced (O,
none; A, atrium; V, Ventricle; D, dual; S, single)
Second is the chamber/s in which sensing occurs
(O; A; V; D; S)
Third is the response to a sensed event (O, none;
I, inhibition; T, Triggered; D, inhibition +triggered)
Fourth refers to the programmability or rate of
response (R, Rate responsive)
Fifth refers to existence of antitachycardia
functions if present (O, None; P, antitachycardia
pacing; S, shock; D, pace+shock)
ACUTE complications of transvenous pacemaker
implantation: infection, hematoma,
pneumothorax, cardiac perforation,
diaphragmatic/phrenic nerve stimulation, and
lead dislodgement
Limitations of CHRONIC pacemaker therapy:
infection, erosion, lead failure, and abnormalities
due to inappropriate programming
Twiddler’s syndrome – rotation of pacemaker
pulse generator in its subcutaneous pocket
producing dislodgement with failure to
sense/pace the heart
Pacemaker syndrome – occurs when pacing
modes interrupts or fail to restore atrioventricular
synchrony include s/s of: neck pulsation, fatigue,
palpitations, cough, exertional dyspnea,
dizziness, syncope, inc JVP, canon A waves, and
stigma of CHF including edema, rales and S3
See table 234-3, 234-4, 234-5, 234-6 for
guidelines/indications for pacemaker
implantation pages 1876-1877
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 TACHYARRHYTHMIAS Standard definition: Ventricular rate of >100bpm
Palpitations and racing pulse
Premature beats – skipping pulse or pause or slowing of HR or dizziness
Dizziness or syncope due to dec CO or breathlessness due to marked inc in
cardiac filling pressure
24H Holter monitor – only for pts with daily symptoms
Patient-activated event monitor – intermittent symptoms that are of
prolonged duration; use with loop recorder to document short-live
episodes and the onset of arrhythmias; preferred monitoring technique for
symptomatic pt with less frequent arrhythmias but requires continuous
monitoring
12-lead ECG – important dx tool in identifying the mechanism and origin of
a tachycardia
I. SUPRAVENTRICULAR
TACHYARRHYTHMIAS (SVTs)
Atrial Premature Complexes MOST COMMON ARRHYTHMIA
(APCs)
Inc with age and + structural heart disease
Asymptomatic; palpitations
ECG: P wave before the anticipated sinus beat; PR interval lengthens;
characteristically reset the sinus node
Junctional Premature Extremely uncommon
Complexes (JPCs)
Complex originate from AV node and His bundle region
ECG: pseudo Q or S waves
Sinus Tachycardia Pathologic conditions: thyrotoxicosis, anemia, and hypotension
ECG: P wave upright in leads II, III, aVF and negative in aVR; biphashic in
V1
Diagnosis should NOT be based on PR interval or the presence of P wave
before every QRS
Inappropriate sinus tachycardia – HR inc either spontaneously or out of
proportion to the deg of physiologic stress; quite disabling; s/s: dizziness,
syncope, chest pain, headaches, GI upset; may occur after a viral illness
and may resolve spontaneously over 3-12 mos
Mechanisms:
1. ABN IMPULSE FORMATION
abN automaticity is due to inc in slope of phase 4 depolarization or dec
threshold for AP depolarization (phase 0) in myocardium other than sinus
node; responsible for most APCs and VPCs and some AT
Early afterdepolarization (EAD) – triggered activity during phase 3 of AP
due to alteration of plateau currents; may be responsible for VPC that
trigger polymorphic ventricular arrhythmias known as torsades des pointed
(TDP)
Late/Delayed afterdepolarization (DAD) – triggered activity during phase 4
of AP due to IC calcium accumulation; may be responsible for atrial,
junctional, fascicular tachyarrhythmia cause by digoxin toxicity and basis
for catecholamine-sensitive VT originating in outflow tract
2. ABN IMPULSE PROPAGATION
Reentry – is due to inhomogeneities in myocardial conduction and/or
recovery properties; anatomically driven (fixed) forms are more stable and
has monomorphic/uniform repetitive tachycardia; functional forms are
more dependent on dynamic changes, more unstable and polymorphic
NO INTERVENTION NEEDED
For extremely symptomatic:
BB may uncommonly exacerbate symptoms if AV block occurs with APC
and irregularity of pulse is more profound
Class IC antiarrhythmic agents – eliminate APC but should be avoided if
structural heart disease is present
Same as above
Treat underlying condition
Tx for inappropriate sinus tachycardia:
Inc hydration, salt loading, and careful titration of BB to max tolerated
dose in divided doses
If unresponsive to BB: catheter ablation and atrial pacing therapy
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Atrial Fibrillation (AF) MOST COMMON SUSTAINED ARRHYTHMIA
Marked disorganized, rapid and irregular atrial activation; ventricular
response is also irregular; 120-160bpm; if heightened vagal tone can be
<100bpm
Incidence inc with age (>70yo)
Acute AF common during early or acute recovery phase of major
vascular, abdominal, and thoracic surgery, in which autonomic fluxes
and/or direct mechanical irritation potentiate arrhythmia
Clinical importance of AF: (1) loss of atrial contractility, (2) inappropriate
fast ventricular response, and (3) loss of atrial appendage contractility and
emptying leading to inc risk of clot formation
Hallmarks of poor rate control with exertion: exercise intolerance and easy
fatigue
ECG: irregularly irregular ventricular response; PP interval (<200ms) and
chaotic P-wave morphology - confirmatory
Risk factors for stroke in AF: hx of stroke/TIA; MS; hpn; DM; >75yo; CHF; LV
dysfunction; marked LA enlargement (>5.0cm); spontaneous echo
contrast
ACUTE RATE CONTROL
Initial goals: establish ventricular rate and address antiagulation status and
begin IV heparin if duration of AF is >12H and risk of stroke is present
Ventricular rate control: BB, CCB, digoxin (can be used as stand-alone
agent)
Target INR 2-3; if pt hasn’t been anticoagulated for >1-2days perform TEE to
exclude presence of LA thrombus that may be lodge with attempted
restoration of sinus rhythm
Anticoagulation must be maintained for at least 1 mo after restoration of
sinus rhythm; heparin maintained until INR 1.8 with administration of
warfarin after TEE
For pt who don’t warrant early cardioversion: anticoagulants maintained
for at least 3 weeks with INR >1.8 on at least 2 separate occasion before
attempts of cardioversion
Termination of AF: direct current transthoracic cardioversion during short-
acting anesthesia; use 200J biphasic shock synchronously with QRS
complex
Drugs to maintain sinus rhythm: if (+) structural heart disease use sotalol,
amiodarone, dofetilide, or dronedarone; if depressed LV function with HF
symptoms precludes use of dronedarone and sotalol; if (-) structural heart
disease or hpn without sever hypertrophy used class IC agents like
flecainide or propafenone
CHRONIC RATE CONTROL
Acute rate control is inadequate if: HR >80bpm at rest or 100bpm with very
modest physical activity
Rate control + chronic anticoagulation must be coupled in all cases
CATHETER AND SURGICAL ABLATIVE THERAPY TO PREVENT RECURRENT AF
Alternative to additional drugs with recurrent symptomatic AF and poor
rate control; eliminates AF 50-80%
Surgical ablative therapy (Cox-Maze) is typically preformed at the time of
other cardiac surgery
If L appendage has been removed surgically, threshold for stopping
anticoagulants must be lowered
Antiarrhythmics are typically discontinued after catheter or surgical
ablation
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Atrial Flutter (AFL) and
Macroreentrant Atrial
Tachycardias (AT)
Multifocal Atrial Tachycardia
(MAT)
AV Nodal Tachycardias
1. AV nodal reentrant
tachycardia
(AVNRT)
Macroreentrant arrhythmias involving the atrial myocardium are
collectively called AFL – denotes nonfocal source of an atrial arrhythmia;
atrial rate 260-300bpm with ventricular response 2:1 or 130-150bpm
Most common AFL circuit rotates in a clockwise or counterclockwise
direction in the RA around tricuspid
Posterior boundary of R AFL circuit – crista teminalis, Eustachian ridge, IVC
and SVC
COUNTERCLOCKWISE R AFL 80% of all AFL with superiorly directed
activation of interatrial septum which produces SAW-TOOTHED
APPEARANCE of P waves
It is a signature tachycardia of pt with significant pulmonary disease
Atrial rhythm is at least 3 DISTINCT P WAVE MORPHOLOGIES and often at
least 3 different PR interval and associated with 100-150bpm
ABSENT INTERVENING SINUS RHYTHM – distinguishes MAT from normal sinus
rhythm with frequent multifocal APCs
MOST COMMON PAROXYSMAL REGUALR SVT
More common in women; 2nd-4th decade; tends to occur in the absences
of structural heart disease; well tolerated;
Frog sign – neck pulsations felt because of the simultaneous atrial and
ventricular contraction
Develops because of the presence of two electrophysiologically distinct
pathways for conduction in the AV node; fast pathway (only one
manifested resulting in a N PR interval)in more superior part has longer
refractory period; reentrant circuit can develop in response to premature
stimulation
ECG: narrow QRS; rate 120-250bpm; P wave buried in QRS
Atypical AVNRT: activation in the reverse direction producing prolonged
RP interval during tachycardia with negative P waves; easily precipitated
by ventricular stimulation
DC CARDIOVERSION – because of the anticipated rapid regular ventricular
rates
AFL terminated with low-energy cardioversion 50-100J; it is poorly tolerated
than AF
Risk of thromboembolism is high
In all patients, an effort to control ventricular rate pharmacologically
Recurrence rates >80% by 1 year; tx with catheter ablative therapy
Selected patients with high anesthesia risk, an attempt for pharmacologic
cardioversion is procainamide, amiodarone, or ibutilide is appropriate
Tx directed at underlying condition
CCB verapamil
Flecainide or Propafenone
Low dose amiodarone – control arrhythmia and minimize the risk of
pulmonary toxicity
FOCAL ATRIAL TACHYCARDIAS
Automatic ATs – start with “warm-up” period over 3-10 complexes, slow in
rate before termination; responds to adenosine not only with evidence of
AV block but with gradual slowing of atrial rhythm and termination;
provoked by isoproterenol infusion
Focal Reentrant AT – initiation of tachycardia with programmed atrial
stimulation or spontaneous premature beats; different P wave morphology;
don’t slow or terminate to adenosine; more common in the absence of
structural heart disease tends to have isolectric baseline between P wave
Tx directed at altering conduction within AV node
Vagal stimulation: valsalva maneuver or carotid sinus massage
Adenosine 6-12mg IV if unresponsive to physical maneuvers
IV BB or CCB – 2nd line
If hemodynamic compromised: R wave synchronous DC conversion using
100-200J
Prevention: digitalis, BB, CCB, class IA or IC
Catheter ablation – very effective in permanently eliminating AVNRT esp. if
with significant symptoms and HR of >200bpm
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 2. AV junctional The most common manifestation of digoxin intoxication is the sudden Tx directed at decreasing adrenergic stimulation and reversing digoxin
tachycardias regularization of response to AF. The junctional tachycardia due to this toxicity
doesn’t manifest retrograde conduction.
If due to abN automaticity: use BB or trail class IA or IC drugs
Accelerated junctional rhythm – HR >50bpm and <100bpm
For incessant automatic junctional tachycardia: use focal catheter
ablation

Tachycardias Associated with
Accessory AV Pathways
Accessory pathways (APs) – manifest as N QRS+short/long RP interval;
capable of conducting rapidly both ante/retrograde direction
Antegrade APs – bypasses AV node and pre-excites ventricles resulting in
shorter PR interval; “delta-waves” (initial QRS portion is slowed); has more
rapid conduction but longer refractory period than the AV node
MOST COMMON AP CONNECTS LA TO LV followed by posterior septal, R
free wall, and anterior septal
Tx is directed at altering conduction in the AV node
Adenosine – FIRST LINE DRUG
Others: IV CCB (verapamil or diltiazem) or BB; chronic oral use of these may
prevent recurrent supraventricular reentrant tachycardia associated with
AP
DC conversion – to terminate AF

Atriofascicular APs – ventricular insertion is at the site distant from the AV Non-life threatening situation: procainamide 15mg/kg IV over 20-30
groove in the fascicles which demonstrates decremental antegrade minutes to slow ventricular response and may organize or terminate AF;
conduction other: ibutilide

Mahaim fibers – other APs from AV node to the fascicles that manifest as N Caution for the use of digoxin (shorten refractory period of AP directly and
PR interval with delta waves inc ventricular rate) and verapamil (shorten refractory period indirectly by
vasodilatation and reflex inc in sympathetic tone) – inc risk for VF
Orthodromic AV reentry – most common macroeentrant tachycardia
associated with WPW syndrome Catheter ablation: hx of recurrent symptomatic SVT, incessant SVT, and HR
>200bpm with SVT
Echo beat – retrograde activation of atria via APs
Antidromic AV reentry and/or Preexcitation macroreentry – reentrant
circuit reverse so the impulse reaches ventricles via AP and conducts
retrogradely through to the atria via His-Purkinje system and AV node

The second most common and potentially more serious arrhythmia

associated with WPW syndrome is a rapidly conducting AF
CONCEALED APS

50% of APs, there’s no antegrade conduction but retrograde conduction is

preserve; AP will manifest as sustained tachycardia; more prone to AF but
not rapid ventricular response to AF

II. VENTRICULAR
TACHYARRHYMIAS

Ventricular Premature
Complexes (VPCs)
The origin of the premature beats in the ventricles at sites remote from the Threshold for tx of VPC is high and is directed at eliminating severe
Purkinje network produces slow ventricular activation and a wide QRS symptoms associated with palpitations.
complex >140ms in duration
If no structural heart disease – VPC don’t have prognostic significance
Common; inc with age and structural heart disease; associated with “fully
compensatory pause” (duration between last QRS before PVC and the If (+) structural heart disease – increased risk of SCD
next QRS is equal to 2x the sinus rate)
Bigeminy – every sinus beat is followed by VPC

Trigeminy – 2 sinus beats are followed by VPC

Mutiformed – different morphologic VPCs

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 Pairs/couplets – 2 successive VPCs
VT – ≥3 consecutive VPCs with rate >100bpm

Nonsustained VT – repetitive VPCs terminate spontaneously and are more

than 3 beats in duration

Interpolated VPCs – VPCs that fail to influence the incoming sinus impulse
Parasystolic focus – ventricular focus that fires repetitively at fixed interval
that produce variably coupled VPCs

Accelerated Idioventricular Ventricular rhythm characterized by ≥3 complexes at rate of >40bpm and

Rhythm (AIVR) <120bpm

Tends to be benign rhythm; characteristic gradual onset and offset and

more variability in cycle length; brief and self-limiting arrhythmia

Ventricular Tachycardia (VT)
Originates below the bundle of His at the rate >100bpm or >120bpm
QRS complex may be uniform (monomorphic) or vary from beat to beat
(polymorphic)
Polymorphic VT associated with long QT interval during their baseline
rhythm = TORSADES DES POINTES
Monomorphic VT suggest as stable tachycardia focus in the absence of a
structural heart disease or fixed anatomic abN that can create the
substrate for a stable reentrant VT circuit when structural disease is present;
tend to be reproducible and recurrent and initiated with pacing and
programmed ventricular stimulation
Sustained polymorphic VT and VF will result in hemodynamic collapse =
Emergency asynchronous defibrillation with at least 200-J monophasic or
100-J biphasic shock with IV lidocaine and/or amiodarone
For monomorphic wide complex rhythm that results in hemodynamic
compromise = prompt R-wave synchronous shock
If arrhythmia persists used R-wave synchronous cardioversion AFTER
administration of conscious sedation
Idiopathic LV septal VT – responds to IV verapamil
If VT + structural heart disease = implantation of ICD

TIME DURATION OF 30 SECONDS – used to distinguish sustained from Prevention of VT (not due to long QT syndrome: SOTALOL (associated with
unsustained VT decrease defibrillation threshold) or AMIODARONE (better tolerated with
marginal hemodynamic status and BP) are FIRST LINE
Sustained VT – hemodynamically unstable VT that requires termination
before 30sec Catheter ablative therapy: for pt without structural heart disease

Ventricular Flutter (VF) – sine wave on ECG and >250bpm; completely MANAGEMENT OF VT STORM: >2 episodes of VT in 24H
disorganized ventricular activation on ECG IV BB for polymorphic VT storm
SVT – (+) aberrant QRS pattern that matches exactly that of wide QRS Acute IV of lidocaine, procainamide, or amiodarone for recurrent
VT – BBB QRS pattern and doesn’t match up with QRS and/or wider in monomorphic VT
duration than QRS during wide complex tachycardia

Except some idiopathic outflow tract tachycardia – most VT DON’T

RESPOND TO VAGAL STIMULATION

PE: intermittent cannon a waves and variable S1 consistent with AV

dissociation (marked presence of sinus capture or fusion beats)

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Unique VT syndromes

1. Idiopathic Outflow VT in the absence of structural heart disease Tx is rarely required because it is hemodynamically tolerated and typically
Tract VT unsustained
80% originate in the R outflow tract; common in women; rarely associated
with SCD IV BB terminates tachycardia

Palpitations with exercise, stress, and caffeine ingestion; triggered Chronic BB or CCB prevents recurrence; Also responds to class IA or IC or
hormonally and timed to premenstrual period, gestation, and menopause; with sotalol
terminated by vagal maneuvers
Catheter ablation eliminate tachycardia

2. Idiopathic LV SECOND MOST COMMON IDIOPATHIC VT is linked anatomically to the VERAPAMIL

septal/fascicular VT Purkinje system in the LV
Catheter ablation is unresponsive to verapamil
ECG: narrow RBBB pattern and superior L axis or inferior R axis

3. VT associated with Most uniform and sustained VT are around areas of fibrosis around mitral Prophylactive ICD device reduce risk of SCD from first VT/VF episode
dilated and aortic valvular areas
cardiomyopathy

4. Bundle branch ECG: QRS morphology with LBBB type of pattern and L superior axis Catheter ablation and/ or adjunctive ICD therapy
reentrant VT

5. VT associated with High risk SCD ICD implantation

hypertrophic
cardiomyopathy Amiodarone, Sotalol and BB for control of recurrent VT

6. VT associated with Predicting risk of sudden death: AD, PR interval of >240ms, QRS 120ms or ICD implantation: LV EF <35% or history of unexplained syncope with
other infiltrative heart block and type 1 myotonic dystrophy significant LV dysfunction
cardiomyopathies
and neumuscular dx

7. Arrhythmogenic RV This is due to genetically determined dysplastic process or after a Threshold for ICD implantation is low
cardiomyopathy/dy suspected viral myocarditis
splasia (ARVCM/D) Other tx options: Sotalol, BB+other antiarrhythmias
Predominance of perivalvular fibrosis involving most free wall of RV in
proximity to tricuspid and pulmonic valves Catheter ablation directed at mappable sustained ventricular arrhythmias

ECG: RV activation, terminal notching of QRS complex (if distinct and

appears separated to QRS = epsilon waves) and inverted T waves

8. VT after operative Evidence of RV systolic dysfunction; typically macroreentrant circuit Catheter ablation
TOF repair around R ventriculotomy scar

9. Fascicular Digoxin toxicity will produce inc ventricular ectopy and bradyarrhythmias Correct electrolyte disorders and IV infusion of digoxin-specific Fab
tachycardia caused that predispose to ventricular arrhythmias and VF fragments (over the couse of 1H will bind digoxin and eliminate toxic
by digoxin toxicity effects)

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Genetically Determined
Abnormalities that Predispose
to Polymorphic Ventricular
Arrhythmias

1. Long QT syndrome Defects in cardiac ion channel responsible for cardiac repolarization; LQT 1 – restrict exercise; avoid swimming
enhanced sodium or calcium inward currents or inhibits outward potassium
currents during plateau lengthen AP duration and QT interval LQT 2 – BB

LQT1 – MOST COMMON GENOTYPIC ABN; fail to shorten or actually prolong LQT 3 – BB is not recommended and exercise is not restricted
QT interval with exercise; T wave is broad and QT is prolonged; most Prophylactic ICD implantation in: male pt with LQT3 and all pt with marked
common trigger is EXERCISE, followed by emotional stress; 80% of males QT prolongation (>500ms) particularly when coupled with family hx of SCD
have first cardiac event by 20yo

Jervell and Lange-Nielsen syndrome – 2 LQT1 alleles; more dramatic QT

prolongation and deafness and worse arrhythmia prognosis
LQT2 – SECOND MOST COMMON GENOTYPIC ABN; T waves notched and
bifid; most common trigger is EMOTIONAL STRESS, followed by sleep or
auditory stimulation

LQT3 – mutation in gene that encode sodium channel; late-onset peaked

biphasic T waves or asymmetric peaked T waves; POOREST PROGNOSIS OF
ALL LQTs; male has worst prognosis; most event occur during SLEEP

2. Acquired LQTS More common in women and manifest of subclinical LQTS Eliminate offending drug; reverse metabolic abN by infusion of magnesium
or potassium, preventing pause-dependent arrhythmias by temporary
Drug-induced LQT and polymorphic ventricular tachycardia (TDP) is pacing or isopreterenol
potentiated by hypokalemia and bradycardia; most are dose dependent

3. Short QT syndrome A gain of function of repolarization currents ICD implantation

ECG: T waves are tall and peaked; QT interval <320ms; predisposes to AF Quinidine – used to lengthen QT interval and reduce amplitude of T waves
and VF

4. Brugada Syndrome Major clinical features: transient or concealed ST segment elevation in V1 – Drug challenge with procainamide to establish diagnosis
V3 that is provoked with sodium blocking agents and a risk of polymorphic
ventricular arrhythmias Ajmaline and IV flecainide has higher sensitivity

Diminished inward sodium current in the region of RV outflow tract Tx: isoproterenol or quinidine
epicardium ICD implantation for those not benefited by BB and chronic quinidine
AD inheritance pattern; most common in young males (75%) and thought
to be responsible for sudden and unexpected nocturnal death syndrome
(SUDS)

5. Catecholaminergic Mutation of the myocardial ryanodine release channel which creates a Restrict exercise
polymorphic VT leak in calcium from SR
BB and ICD implantation
Manifest as bidirectional VT, nonsustained polymorphic VT or recurrent VF

Note: for any questions, comments, and typos please refer to the book :D

For more explanation and basic stuffs about ECG pls refer to chapter 228 & 231

ren.sama
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