Cardiac Arrhythmias

Carmen Chungunco, MD FPCP FPCC

Overview
The Beating Heart: Electrophysiology Review
Mechanisms of Arrhythmias
- Abnormal Impulse Generation
- Abnormal Impulse Conduction
Diagnostic Modalities : ECG
Treatment Modalities
Specific Arrhythmias: Diagnosis and Management
- Sinus Arrhythmia
- Sinus Bradycardia and Tachycardia
- AV Blocks
- Atrial Fibrillation/Flutter
- Ventricular Tachycardia
- Ventricular Fibrillation
The Beating Heart
Electrical impulses come before muscle contraction
Heart is endowed with special system:
- Automaticity/self-excitation generating rhythmical electrical impulses
to cause contraction of heart muscle
- Rapid conduction through the heart in only 1 specific direction
-

o AV bundle (His)
o left and right bundles of Purkinje fibers
Pacemaker vs Nonpacemaker
Ionic Basis of Membrane Electrical Activity
- determined by water-soluble ions Na, K, Ca
o Na and Ca primary carriers of depolarizing current
o K primary repolarizing current
- require aqueous channels to diffuse through lipid
membrane, ion-specific, voltage-gated
- Ion pumps and transporters
- movement of ions produce currents which form basis of action
potentials
Action Potentials in cardiac muscle:
- resting membrane potential = -85 to -95 mV
- caused by opening of 2 types of channels:
o fast Na channels
o slow Ca channels (slow to open, close)

Phases of Action Potential of Cardiac Cells

+)
Phase 0 rapid depolarization (inflow of Na
+
Phase 1 partial repolarization (inward Na current deactivated, outflow of
+
K)
Phase 2 plateau (slow inward calcium current)
+
Phase 3 repolarization (calcium current inactivates, K outflow)
+
+
Phase 4 pacemaker potential (Slow Na inflow, slowing of K outflow)
automaticity
Refractory period (phases 1-3)

Cardiac Electrophysiology AT A GLANCE

Electrophysiology Review
Cardiac myocytes are electrically excitable
Resting intracellular voltage of myocardial cell= negative -90mV (SA node
is -40mV)
- high intracellular K maintained by Na/K pump
+
+
+ +
Resting state: K inside and Na outside cell (Na /K pump)
+
Action potential occurs when Na enters the cell and sets up a depolarizing
current
Stimulation of a single muscle fibre causes electrical activity to spread
across the myocardium
Electrophysiology
3 major types of cardiac muscle:
- atrial muscle
- ventricular muscle
- specialized excitatory and conductive muscle fibers
o sino-atrial node
o internodal pathways
o AV node

Effective Refractory Period

time between Phase 0 and sufficient recovery of Na channels in Phase 3 to
permit a new propagated response
affected by altered recovery from inactivation, altered AP duration, or
prolongation of recovery time

SINUS NODE =DOMINANT PACEMAKER

exhibits self-excitation to greatest degree; most rapid phase 4 diastolic
depolarization
RMP = -55 to -60 mV due to cell membrane being leaky to Na ions
cyclic process: self-excitation, recovery from AP, hyperpolarization after
AP is over, upward drift of resting potential, re-excitation (Phase 4)

Pacemaker vs Nonpacemaker

Disorders of Impulse Generation

In pacemaker cells:
- interval between depolarizations = APD + duration of diastolic interval
Shortening of either factor will increase pacemaker firing rate
Diastolic interval is determined primarily by the slope of Phase 4
depolarization
- slowed by vagal discharge and B-blockers
- accelerated by hypokalemia, B-adrenoceptor stimulation, positive
chronotropic drugs

Impulse Generation: Automaticity

Property of a fiber to initiate an impulse spontaneously, without need for
prior stimulation
Inappropriate discharge rate of the normal pacemaker (sinus node)
Discharge of an ectopic or latent pacemaker (atrial sites, AV junction, HisPurkinje system)
- Due to slowing of sinus node OR inappropriate speeding up of ectopic
pacemaker
Abnormal automaticity arise from cells that have reduced maximum
diastolic potentials.

ARRHYTHMIAS
A change in the normal sinus cardiac rate and rhythm
Common cause of sudden cardiac death (SCD)
Usually occurs in the presence of preexisting heart disease

Mechanisms of Arrhythmia
Abnormalities in Impulse Generation
- Automaticity
- Triggered Activity/Afterdepolarizations
Abnormalities in Impulse Conduction
- Block
- Re-entry
Both

Impulse Generation: Triggered Activity

Triggered activity is initiated by afterdepolarizations, which are
depolarizing oscillations in the membrane voltage induced by one or more
preceding action potentials.
Not self-generating
Disorders of Impulse Generation
Afterdepolarizations interrupt Phase 3 (early afterdepolarization or
EADs) or Phase 4 (delayed afterdepolarization or DADs)
1. EADs exacerbated by longer AP (slow heart rate, hypokalemia,
hypomagnesemia, drugs like some antihistamines, antibiotics)
2. DADs occur when intracellular Ca is increased
- exacerbated by fast heart rates
- responsible for arrhythmias related to digitalis, catecholamines
and myocardial ischemia

Conditions that may lead to Re-entry:

Long pathway
- Ex. Dilated atrium or ventricle
Velocity of conduction becomes depressed, pathway length remains
constant
- Ex. Blocks, ischemia, high K levels
Refractory period of muscle has been shortened
- Ex. Response to various drugs like epinephrine
Disorders of Impulse Conduction
Blocks due to severely depressed conduction
- ex. AV nodal block or bundle branch bloc
Reentry (circus movement)
- Most common arrhythmia mechanism
- Property of networks of myocytes
- Defined as circulation of an activation wave around an inexcitable
obstacle
- one impulse reenters and excites areas of the heart more than once
- ex. Supraventricular tachycardia (SVT); Ventricular tachycardia (VT)

Diagnostics: ECG
primary tool in arrhythmia analysis
timed sum of the cellular APs in atria and ventricle
12-lead ECG with long continuous recording of lead II or V1
Shows rhythm, rate, axis, presence of chamber enlargement, ischemia or
injury
Normal ECG
Normal P, Q, R, S, T, U waves
Each cycle has a P wave followed by a QRS complex = SINUS rhythm
P-P intervals and R-R intervals are approximately the same
Normal rate (60-100)
Normal axis(-30 to +100)
Additional Tests: Holter Monitoring
non-invasive
24-hour ambulatory ECG for monitoring patients over longer periods of
time
If symptoms less frequent: event recorder (30 days) or implantable loop
recorder (months)

Additional Tests: Exercise Testing

Can induce various types of supraventricular and ventricular
tachyarrhythmias
For patients who have symptoms consistent with an arrhythmia induced
by exercise (syncope, palpitations)
Electrophysiologic Studies (EPS)
Invasive test which introduces multipolar catheter electrodes at various
intracardiac sites to record and/or stimulate cardiac electrical activity
Good diagnostic validity and reproducibility
Allows therapeutic intervention

Treatment Modalities
Antiarrhythmic Drugs
Pacemakers
- Temporary and Permanent
- Transcutaneous Pacing
Implantable Cardiac Defibrillators
Radiofrequency Ablation
Defibrillators
- Automatic External Defibrillators (AED)

Antiarrhythmics
Aim of Therapy:
1. to reduce ectopic pacemaker activity
2. to modify conduction or refractoriness in reentrant circuits to disable
the circular movement
ANTIARRHYTHMIC AGENTS
GENERALLY ALTER:
1. Diastolic potential in pacemaker cells and/or resting membrane
potential in ventricular cells (phase 4)
2. Phase 4 depolarization
3. Threshold potential
4. Action potential duration
Interval between depolarizations of a pacemaker cell =duration of action
potential + diastolic interval
Diastolic interval determined by phase 4 depolarization

Effect on Automaticity:
can slow spontaneous discharge by:
1. depressing diastolic depolarization
2. shifting threshold voltage to zero
3. hyperpolarizing resting membrane potential
affects ectopic sites more than sinus node

Class I Antiarrhythmics:
Lidocaine (Xylocaine)
low toxicity, high effectiveness in arrhythmias
associated with MI (main use: VT)
Cardiac Effects: blocks activated and inactivated Nachannels with rapid
kinetics
Toxicity: one of the least cardiotoxic drugs
- may precipitate hypotension by depressing myocardial contractility in
large doses in pts w/ heart failure
- neurologic: paresthesias, convulsions, dizziness
Class IC: Flecainide (Tambocor)
potent Na and K channel blocker
slow unblocking kinetics
very effective in suppressing premature ventricular contractions
may exacerbate arrhythmias in pts with ventricular arrhythmias + pts w/
previous MI and ventricular ectopy
oral route (100-200 mg BID), half-life 20 hrs
hepatic and renal metabolism
usually used in patients without structural heart disease
Class II Antiarrhythmics: Beta-blockers
Prototype: propranolol, esmolol
MOA:
- indirectly reduce the phase 4 slope by blocking positive chronotropic
action of norepinephrine
- Therapeutic Use: suppression of ventricular ectopic depolarizations
Beta-blocker effect on Pacemaker action potential

Effect on Reentry:
improves or depresses conduction
1. eliminate unidirectional block
2. facilitate conduction so returning wavefront reenters when cells still
refractory
3. depress conduction to transform unidirectional to bidirectional block
prolong refractoriness relative to action potential duration
Antiarrhythmics
As dosage increases, drugs also depress conduction in normal tissues,
producing drug-induced arrhythmias
Therapeutic doses may become proarrhythmic during fast heart rates,
acidosis, hyperkalemia or ischemia

Decrease slope of phase 4 depolarization (SA node)

Prolong repolarization (esp in AV node)
Used for VT and SVT precipitated by sympathetic stimulation

Vaughan Williams Classification of Antiarrhythmic Drugs

Class I: block sodium channels
- Ia (quinidine, procainamide, disopyramide)
- Ib (lidocaine)
- Ic (flecainide)
Class II: -adrenoceptor antagonists (atenolol, sotalol)
Class III: prolong action potential and prolong refractory period
(amiodarone, sotalol)
Class IV: Calcium channel antagonists (verapamil)

Class III Antiarrhythmics

Drugs which prolong ERP (effective refractory period) by prolonging
action potentials
Samples:
- Amiodarone
- Bretylium
- Sotalol
- Dofetilide
- Ibutilide

Class III: Amiodarone (Cordarone)

Cardiac Effects:
- broad spectrum of cardiac actions, high efficacy
- markedly prolongs APD (QT interval)
- significantly blocks inactivated Na channels
- has weak B-adrenergic and calcium channel blocking actions
Main Indications:
- maintaining sinus rhythm in atrial fibrillation
- preventing recurrent VT
- adjuvant therapy in patients with ICD
Cardiac Toxicity:
- symptomatic bradycardia and heart block in pts with preexisting sinus
or AV node disease
- prolongs QT interval
Toxicity:
- pulmonary fibrosis (dose-related)
- hypothyroidism or hyperthyroidism
- abnormal liver function tests and hepatitis
- skin deposits, photodermatitis
Class III: Sotalol
both Class II and III effects
not cardioselective
absorbed orally with 100% bioavailability
renal excretion, half-life 12 hrs
few direct drug interactions
Toxicities: further depression of LV function
Use: life-threatening ventricular arrhythmias
- maintaining sinus rhythm in AF
Class IV: Calcium channel blockers
Prototype: Verapamil (Isoptin)
Effects:
- block both activated and inactived L-type Ca channels
- prolongs AV nodal conduction time and ERP
- slows the SA node
- peripheral vasodilation
Indication:
- termination of SVT (if adenosine not available)
- control of heart rate in AF
Toxicity:
- dangerous in pts with VT misdiagnosed as SVT, may cause hypotension
and VF
- negative inotropic effects
- can induce AV block

Effects on pacemaker cells action potential

Others:
Adenosine
nucleoside which occurs naturally in the body
half-life <10 seconds
Cardiac Effect:
- marked hyperpolarization
- suppression of Ca-dependent AP
- directly inhibits AV nodal conduction
Use: DOC for prompt conversion of SVT to sinus
- due to high efficacy (90-95%) and very short duration of action
- 6 - 12 mg IV bolus
Magnesium
MOA: not well known
Use:
- digitalis-induced arrhythmias if low Mg
- torsade de pointes even if Mg normal (1 g/IV)
Potassium
Hypokalemia: increased risk of EAD and DAD ectopic pacemaker activity
(digitalis)
Hyperkalemia: depresses ectopic pacemakers, SA node
Digoxin
Cardiac Glycosides
Electrical effects due mainly to:
Inhibition of Na/K ATPase at the cell membrane
Enhanced vagal tone
Actions:
Slowing the sinus node discharge rate
Prolonging AV nodal refractoriness
Main Indication:
- slow the ventricular rate in chronic AF (not very
- effective in acute setting)
Digoxin is recommended for patients with symptomatic LV systolic
dysfunction and concomitant atrial fibrillation
Narrow therapeutic range so use with caution
- Increased risk of digitalis toxicity with low K levels,
- worsening renal function, advanced age
- Toxicity: Headache, nausea/vomiting, diarrheas and arrhythmias
Clinical Application
Pharmacologic Treatment of Arrhythmias:
1. Eliminate the cause if possible
2. Make a firm diagnosis
3. Determine baseline condition
4. Evaluate need for therapy
5. Weigh benefits vs risks of therapy
Remember: Antiarrhythmics can be proarrhythmics.
Treatment Modalities
Antiarrhythmic Drugs
Pacemakers
- Temporary and Permanent
- Transcutaneous Pacing
Implantable Cardiac Defibrillators

 Radiofrequency Ablation
Defibrillators
- Automatic External Defibrillators (AED)
Specific Arrhythmias
Arrhythmias
sinus arrhythmia
premature atrial contraction
premature ventricular contraction
Bradyarrhythmias
- sinus bradycardia
- sinus pause or arrest
- AV block
Tachyarrhythmias
- SVT
- atrial fibrillation
- atrial flutter
- ventricular tachycardia
- ventricular fibrillation
Sinus Node Dysfunction
One of the most common causes of pathologic bradycardia
SA node: blood supply comes from RCA (55-60%), LCX (40-45%), richly
innervated by sympathetic and parasympathetic nerves
Etiology of disease may be intrinsic or extrinsic (Table 225-1)
Includes sinus bradycardia, sinus pause/arrest

Sinus Tachycardia

AV Node Dysfunction
One of the most common cause of pathologic bradycardia
AV node: supplied by LAD and posterior descending coronary artery
Heterogenous cells with range of action potential profiles (fast and slow
pathways)
May be due to intrinsic and extrinsic causes (Table 225-2)
st
nd
Includes 1 deg, 2 deg and complete heart block
Sinus with First Degree AV Block

Sinus Arrhythmia

PR interval constant, >0.20 ms

no failure of conduction of P wave
nd

Sinus with 2 Degree AV Block (Wenkebach, Mobitz Type 1)

Sinus Bradycardia

PR interval progressively lengthening, then failure of conduction of P wave

nd

Sinus with 2 Degree AV Block (Mobitz Type 2)

PR interval constant
sudden failure of conduction of P wave

Sinus with 3rd Degree AV Block or Complete Heart Block

Mechanism: initiation and maintenance of multiple wavelets of reentry

(MICROREENTRY) due to interaction between atrial musculature near the
pulmonary veins and certain drivers

AV dissociation, P wave no relation to R wave

PP interval, RR interval constant
Sinus with PACs

common arrhythmia seen in ECG monitoring

usually benign, asymptomatic
P wave occurs before antiicipated beat, different contour
usually requires NO intervention

Sinus Rhythm with PVC

common in older age and those with structural heart disease

premature beat, associated with compensatory pause
may be benign
PVCs

Atrial Fibrillation
The most common sustained arrhythmia
Marked by disorganized, rapid and irregular atrial activation with irregular
ventricular response

Clinical Features:
- history of palpitations, easy fatigability, chest pain
- advanced age, (+) history of CHF, VHD, HPN, TIA or stroke
- PE: irregularly, irregularly cardiac rhythm
ECG:
- f waves at 350-600 beats/min with ventricular rate of 100-160
beats/min if untreated
- supraventricular complexes with irregular rhythm and NO obvious P
waves

 Significance:
- Loss of effective atrial contraction (atrial kick)
- AV node blocks transmission of impulses as a protective mechanism
- Heart rate control necessary to allow proper filling of ventricles
- Thromboembolic events high risk due to circulatory stasis

MANAGEMENT:
- Determine if hemodynamically stable patient.
o Unstable patients may need cardioversion.
- Determine if acute or chronic.
o If acute, possible role for cardioversion.
o If chronic, less chance for cardioversion.
The longer patient is in AF, less chance for cardioversion since
remodelling has occurred.
Chronic Atrial Fibrillation
Goals:
- Evaluate and treat contributing factors (thyrotoxicosis, electrolyte
imbalance, pulmonary emboli, pericarditis, etc)
- Control ventricular rate
- Prevent recurrences
- Prevent thromboembolic episodes
Rate versus Rhythm Control:
- no clear benefit of one over the other
- Rate Control: Beta blockers, CCB (verapamil and diltiazem), digoxin
- Rhythm Control:
o IC (flecainide) if no structural heart disease
o III (amiodarone, sotalol) if with heart disease
Radiofrequency Ablation aimed at isolation of the pulmonary veins
- 70-85% effective in persistent and paroxysmal AF
- Alternative to pharmacological therapy in pts with recurrent AF
Maze procedure surgical interruption of circuits
Prevention of thromboembolic events
- High Risk patients (CHADS2):
o age > 65 years
o left atrial enlargement
o CAD or CHF
o prior stroke or TIA
o significant valvular heart disease
o HPN
o DM
- MUST be treated with anticoagulation (warfarin, dabigatran)
Atrial Flutter

atrial rate of 260-300 beats/min with a ventricular response rate of 2:1

(130-150 beats/min)
may slow down to <200 beats/min with antiarrhythmics but ventricular
rate becomes 1:1 with adverse hemodynamic effects
typically poorly tolerated compared to AF
management:
- DC cardioversion
- rate control with verapamil, adenosine IA, IC or III antiarrhythmics
- catheter ablation

Supraventricular Tachycardia
Narrow complex tachycardias occurring at the AV node
Most common type is AVNRT (AV nodal reentry tachycardia)
nd
th
Observed in women more than men, manifests in 2 to 4 decade of life
Occurs in patient with NO STRUCTURAL HEART DISEASE, generally welltolerated, good prognosis
Presents as palpitations, syncope, feelings of anxiety
Develops from REENTRY mechanism

Management:
- Vagal maneuvers carotid sinus massage, Valsalva, exposure of face to
ice water
- Adenosine DOC, 6-12 mg/IV; terminates SVT in 90%
- Others: verapamil, BB, digoxin
- Radiofrequency ablation
Ventricular Tachycardia

MACROREENTRANT circuit
more commonly found in the right atrium around the tricuspid valve
can be caused by incisional scars from prior atrial surgery, fibrosis
ECG: identically recurring, regular, sawtooth flutter waves

 Arises distal to the bundle of His = wide complex

Heart rates >120 beats/min
Risk of SCD (sudden cardiac death) high in patients with structural heart
disease and low EF
- Ischemic heart disease (post-infarction)
- Cardiomyopathy

Occurrence of 3 or more consecutive premature ventricular contractions

whose QRS >120 ms
Wide complexes, bizarre-looking
May be sustained (>30 secs) or nonsustained (<30 secs)
May be monomorphic (same appearance) or polymorphic (vary beat to
beat)

Mechanism: enhanced automaticity and triggered activity, reentry

Management:
- Emergency asynchronous defibrillation (>200J)
- IV lidocaine or amiodarone as initial management, NO verapamil
- amiodarone for maintenance
- Implantation of ICD for those with EF<30%
- Catheter ablation for patients w/o structural heart disease
- Always treat underlying disease!

VT: Torsade de Pointes

Polymorphic VT associated with QT prolongation
Mechanism: generation of EADs
Oscillates around baseline: turning of the points stitching pattern
Management:
- Remove underlying QT-prolonging drugs
- Correct magnesium and potassium deficiencies
- Emergency pacing may be needed
Ventricular Fibrillation

completely disorganized ventricular activation

always produce hemodynamic collapse