Arrhythmias

The Basics
of Arrhythmia

Basic Physiology reminder

Basic ECG reminder (1)

Rate
Rhythm
PR interval
QRS complex

Width
Any Q waves?
Axis
Lateral lead R wave progression

ST and T waves

Basic ECG reminder (2)

Determine heart rate

REGULAR RHYTHM count boxes
between 2 R waves and divide
into 300
5

300 / 5 = 60
1 small box = 0.04 second
1 large box = 0.20 second
15 large boxes = 3 seconds

30 large boxes = 6 seconds

300 large boxes = 1 minute
1 mm = 0.1 millivolt (mV)

Determine heart rate

Irregular rhythm count R - R intervals
on a 6 sec. strip and multiply by 10

Normal Sinus Rhythm (1)

NORMAL SINUS RHYTHM IS PRODUCED BY THE
SA NODE
P WAVE FOLLOWS QRS COMPLEX IN A
PREDICTABLE RELATIONSHIP
ALL P WAVES LOOK ALIKE, ALL QRS COMPLEXES
ARE NARROW
R R INTERVAL IS REGULAR
RATE: 60 100 bpm

Normal Sinus Rhythm (2)

Normal Sinus Rhythm (3)

Implies normal sequence of conduction, originating in the sinus node and

proceeding to the ventricles via the AV node and His-Purkinje system.

EKG Characteristics:

Regular narrow-complex rhythm

Rate 60-100 bpm

Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead aVR

Sinus / Atrial dysrhythmias

SINUS TACHYCARDIA
SINUS BRADYCARDIA
ATRIAL FIBRILLATION
ATRIAL FLUTTER
Premature atrial contractions
Paroxysmal atrial tachycardia
Supraventricular Tachycardia

What is an arrhythmia?
Abnormalities of electrical rhythm
Supraventricular
SVT, AF, Atrial flutter
Re-entrant tachycardia

Ventricular
VT, VF, Torsade de pointes

Asystole and PEA

Mechanisms of Arrhythmias
Automaticity

or

Ectopic Foci
Reentry / Conduction Block

Clinical manifestations
Palpitations
Syncope
If going fast enough, can precipitate cardiac
ischaemia and chest pain

Cardiac failure
Decreased level of consciousness
Hypoperfusion of all organs
Cardiac arrest

Common arrhythmias
Ventricular
Atrial
AF
VT
A Flutter
VF
Paroxs. SVT
Torsades
AVNRT
AVRT (WPW)
Multifocal atrial
tachycardia

Bradyarrhytmia
Medication
AV block
SSS

Examples of cardiac arrhythmias

Rhythms from the Sinus Node

Normal Sinus Rhythm (NSR)

Sinus Tachycardia: HR > 100 b/m

Causes:
Withdrawal of vagul tone & Sympathetic stimulation (exercise, fight or flight)
Fever & inflammation
Heart Failure or Cardiogenic Shock (both represent hypoperfusion states)
Heart Attack (myocardial infarction or extension of infarction)
Drugs (alcohol, nicotine, caffeine)

Sinus Bradycardia: HR < 60 b/m

Causes:
Increased vagul tone, decreased sympathetic output, (endurance training)
Hypothyroidism
Heart Attack (common in inferior wall infarction)
Vasovagul syncope (people passing out when they get their blood drawn)
Depression

Rhythms from the Sinus Node

Sinus Arrhythmia: Variation in HR by more than .16 seconds

Mechanism:
Most often: changes in vagul tone associated with respiratory reflexes
Benign variant

Causes
Most often: youth and endurance training

Sick Sinus Syndrome: Failure of the hearts pacemaking capabilities

Causes:
Idiopathic (no cause can be found)
Cardiomyopathy (disease and malformation of the cardiac muscle)
Implications and Associations
Associated with Tachycardia / Bradycardia arrhythmias
Is often followed by an ectopic escape beat or an ectopic rhythm

Recognizing and Naming Beats & Rhythms

Atrial Escape Beat

QRS is slightly different but still narrow,

indicating that conduction through the
ventricle is relatively normal

normal ("sinus") beats

sinus node doesn't fire leading

to a period of asystole (sick
sinus syndrome)

p-wave has different shape

indicating it did not originate in
the sinus node, but somewhere
in the atria. It is therefore called
an "atrial" beat

Recognizing and Naming Beats & Rhythms

Junctional Escape Beat

QRS is slightly different but still narrow,

indicating that conduction through the
ventricle is relatively normal

there is no p wave, indicating that it did

not originate anywhere in the atria, but
since the QRS complex is still thin and
normal looking, we can conclude that the
beat originated somewhere near the AV
junction. The beat is therefore called a
"junctional" or a nodal beat

Recognizing and Naming Beats & Rhythms

Ventricular
Escape Beat

QRS is wide and much different ("bizarre") looking

than the normal beats. This indicates that the beat
originated somewhere in the ventricles and
consequently, conduction through the ventricles did
not take place through normal pathways. It is
therefore called a ventricular beat

there is no p wave, indicating that the beat

did not originate anywhere in the atria
actually a "retrograde p-wave may sometimes be
seen on the right hand side of beats that
originate in the ventricles, indicating that
depolarization has spread back up through the
atria from the ventricles

Recognizing and Naming Beats & Rhythms

Ectopic Beats or Rhythms
beats or rhythms that originate in places other than the SA node
the ectopic focus may cause single beats or take over and pace
the heart, dictating its entire rhythm

they may or may not be dangerous depending on how they affect

the cardiac output

Causes of Ectopic Beats or Rhythms

hypoxic myocardium - chronic pulmonary disease, pulmonary embolus
ischemic myocardium - acute MI, expanding MI, angina
sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism

drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,

imbalances of calcium and magnesium

bradycardia - a slow HR predisposes one to arrhythmias

enlargement of the atria or ventricles producing stretch in pacemaker cells

The Re-Entry Mechanism of Ectopic Beats & Rhythms

Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery

Slow Conduction Path

Fast Recovery

Tissues with these type of circuits may exist:

in microscopic size in the SA node, AV node, or any type of heart tissue
in a macroscopic structure such as an accessory pathway in WPW

The Re-Entry Mechanism of Ectopic Beats & Rhythms

Premature Beat Impulse
Cardiac
Repolarizing Tissue
Conduction
(long refractory period)
Tissue
Fast Conduction Path
Slow Recovery

Slow Conduction Path

Fast Recovery

1. An arrhythmia is triggered by a premature beat

2. The beat cannot gain entry into the fast conducting
pathway because of its long refractory period and
therefore travels down the slow conducting pathway
only

The Re-Entry Mechanism of Ectopic Beats & Rhythms

Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery

Slow Conduction Path

Fast Recovery

3. The wave of excitation from the premature beat

arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast pathway

The Re-Entry Mechanism of Ectopic Beats & Rhythms

Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery

Slow Conduction Path

Fast Recovery

4. On arriving at the top of the fast pathway it finds the

slow pathway has recovered and therefore the wave of
excitation re-enters the pathway and continues in a
circular movement. This creates the re-entry circuit

Re-entry Circuits as Ectopic Foci and Arrhythmia Generators

Atrio-Ventricular Nodal Re-entry

supraventricular tachycardia
Atrial Re-entry

atrial tachycardia
atrial fibrillation
atrial flutter

Atrio-Ventricular Re-entry

Wolf Parkinson White

supraventricular tachycardia

Ventricular Re-entry

ventricular tachycardia

Recognizing and Naming Beats & Rhythms

Clinical Manifestations of Arrhythmias
many go unnoticed and produce no symptoms
palpitations ranging from noticing or being aware of ones heart
beat to a sensation of the heart beating out of the chest

if Q is affected (HR > 300) lightheadedness and syncope, fainting

drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,
imbalances of calcium and magnesium

very rapid arrhythmias u myocardial oxygen demand r ischemia

and angina

sudden death especially in the case of an acute MI

Recognizing and Naming Beats & Rhythms

Premature Ventricular Contractions (PVCs, VPBs, extrasystoles):
A ventricular ectopic focus discharges causing an early beat
Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre"
QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant)
In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion
PVCs are sometimes described by lay people as skipped heart beats

R on T
phenomemon

Multifocal
PVC's

Compensatory pause
after the occurance of a PVC

Recognizing and Naming Beats & Rhythms

Characteristics of PVC's
PVCs dont have P-waves unless they are retrograde (may be buried in T-Wave)
T-waves for PVCs are usually large and opposite in polarity to terminal QRS
Wide (> .16 sec) notched PVCs may indicate a dilated hypokinetic left ventricle
Every other beat being a PVC (bigeminy) may indicate coronary artery disease
Some PVCs come between 2 normal sinus beats and are called interpolated PVCs

The classic PVC note the

compensatory pause

Interpolated PVC note the sinus

rhythm is undisturbed

Recognizing and Naming Beats & Rhythms

PVC's are Dangerous When:
They are frequent (> 30% of complexes) or are increasing in frequency
The come close to or on top of a preceding T-wave (R on T)
Three or more PVC's in a row (run of V-tach)
Any PVC in the setting of an acute MI
PVC's come from different foci ("multifocal" or "multiformed")
These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:

Ventricular Tachycardia
Ventricular Fibrillation

The sooner defibrillation takes place,

the increased likelihood of survival

R on T phenomenon

time

sinus beats

V-tach

Unconverted V-tach r V-fib

Recognizing and Naming Beats & Rhythms

Notes on V-tach:
Causes of V-tach
Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause)
Typical V-tach patient
MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm)
V-tach complexes are likely to be similar and the rhythm regular
Irregular V-Tach rhythms may be due to to:
breakthrough of atrial conduction
atria may capture the entire beat beat
an atrial beat may merge with an ectopic ventricular beat (fusion beat)
Fusion beat - note pwave in front of PVC and
the PVC is narrower than
the other PVCs this
indicates the beat is a
product of both the sinus
node and an ectopic
ventricular focus

Capture beat - note that

the complex is narrow
enough to suggest normal
ventricular conduction.
This indicates that an
atrial impulse has made it
through and conduction
through the ventricles is
relatively normal.

Recognizing and Naming Beats & Rhythms

Premature Atrial Contractions (PACs):
An ectopic focus in the atria discharges causing an early beat
The P-wave of the PAC will not look like a normal sinus P-wave (different morphology)
QRS is narrow and normal looking because ventricular depolarization is normal
PACs may not activate the myocardium if it is still refractory (non-conducted PACs)
PACs may be benign: caused by stress, alcohol, caffeine, and tobacco
PACs may also be caused by ischemia, acute MIs, d electrolytes, atrial hypertrophy
PACs may also precede PSVT

PAC

Non conducted PAC

Non conducted PAC

distorting a T-wave

Recognizing and Naming Beats & Rhythms

Premature Junctional Contractions (PJCs):
An ectopic focus in or around the AV junction discharges causing an early beat
The beat has no P-wave
QRS is narrow and normal looking because ventricular depolarization is normal
PJCs are usually benign and require not treatment unless they initiate a more serious rhythm

PJC

Recognizing and Naming Beats & Rhythms

Atrial Fibrillation (A-Fib):
Multiple ectopic reentrant focuses fire in the atria causing a chaotic baseline
The rhythm is irregular and rapid (approx. 140 150 beats per minute)

Q is usually d by 10% to 20% (no atrial kick to ventricular filling)

May be seen in CAD (especially following surgery), mitral valve stenosis, LV hypertrophy, CHF
Treatment: DC cardioversion & O2 if patient is unstable
drugs: (rate control) b & Ca++ channel blockers, digitalis, to d AV Conduction

amiodarone to d AV conduction + prolong myocardial AP (u refractoriness of myocardium)

The danger of thromboembolic events are enhanced due to d flow in left atrial appendage
Treatment: anticoagulant drugs (Warfarin / Coumadin)
International Normalized Ratio (INR normalized PT time) should be between 2 and 3.

Recognizing and Naming Beats & Rhythms

Atrial Flutter:
A single ectopic macroreentrant focuses fire in the atria causing the fluttering baseline
AV node cannot transmit all impulses (atrial rate: 250 350 per minute)

ventricular rhythm may be regular or irregular and range from 150 170 beats / minute
Q may d, especially at high ventricular rates
A-fib and A-flutter rhythm may alternate these rhythms may also alternate with SVTs
May be seen in CAD (especially following surgery), VHD, history of hypertension, LVH, CHF

Treatment: DC cardioversion if patient is unstable

drugs: (goal: rate control) Ca++ channel blockers to d AV conduction
amiodarone to d AV conduction + prolong myocardial AP (u refractoriness of myocardium)
The danger of thromboembolic events is also high in A-flutter

Recognizing and Naming Beats & Rhythms

Multifocal Atrial Tachycardia (MAT):
Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles
QRS complexes are almost identical to the sinus beats

Rate is usually between 100 and 200 beats per minute

The rhythm is always IRREGULAR
P-waves of different morphologies (shapes) may be seen if the rhythm is slow
If the rate < 100 bpm, the rhythm may be referred to as wandering pacemaker

Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF

Treatments: Ca++ channel blockers, b blockers, potassium, magnesium, supportive therapy for
underlying causes mentioned above (antiarrhythmic drugs are often ineffective)

Note different P-wave

morphologies when the
tachycardia begins

Note IRREGULAR
rhythm in the tachycardia

Recognizing and Naming Beats & Rhythms

Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT):
A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted
normally to the ventricles (usually initiated by a PAC)

QRS complexes are almost identical to the sinus beats

Rate is usually between 150 and 250 beats per minute
The rhythm is always REGULAR
Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope (d Q)

Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter

May be terminated by carotid massage
u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction
Treatment: ablation of focus, Adenosine (d AV conduction), Ca++ Channel blockers

Rhythm usually begins

with PAC

Note REGULAR rhythm

in the tachycardia

Ventricular fibrillation

AV Nodal Reentrant Tachycardia

Rate 100-270
Normal QRS
Aberrancy possible

Acute Rx:
Vagal maneuvers
Adenosine 6-12 mg IV push beware of pro-arrhythmia
Ca++ channel blockers

Atrial Flutter

www.uptodate.com

Atrial flutter is caused by a reentrant circuit in the wall of the atrium

EKG Characteristics:

Typical: sawtooth flutter waves at a rate of ~ 300 bpm

Flutter waves have constant amplitude, duration, and
morphology through the cardiac cycle
There is usually either a 2:1 or 4:1 block at the AV node,
resulting in ventricular rates of either 150 or 75
bpm

Dx and Rx of Flutter
Unmasking of flutter
waves with adenosine.

Acute Rx:
ventricular rate control can be difficult
AV nodal blockers prevent 1:1 conduction
Ibutilide 1-2mg rapid IV infusion have paddles ready
Rapid pacing or low voltage DC cardioversion is effective
Anticoagulation as per atrial fibrillation

Ventricular Tachycardia
Rate 100-20
Wide QRS
Monomorphic vs
Polymorphic
Beware:
Accelerated idioventricular rhythm. Rate below 150, stable
hemodynamics, benign prognosis.
SVT with aberrancy. Look at the 12 lead not just a rhythm strip
Monomorphic vs. Polymorphic (long QT, bradycardia, ischemia)

Rx:
Unstable DC cardioversion
Stable monomorphic Procainamide, Amiodarone
Stable polymorphic - treat underlying etiology

Atrial Fibrillation

www.uptodate.com

Atrial fibrillation is caused by numerous waves of depolarization spreading

throughout the atria, leading to an absence of coordinated atrial contraction.
Classified as:
Recurrent: when AF occurs on 2 or more occasions
Paroxysmal: episodes that generally last </= 7 days (most last <24h)
Persistent: AF that last >/=7 days
Permanent: paroxysmal or persistent AF with failure to cardiovert or not
attempted

Dx and Rx of Atrial Fibrillation

Absent P waves
Irregularly irregular
ventricular response

Acute Rx:
rate control not rhythm control AFFIRM trial (NEJM 2002):
B-blockers, Ca++ channel blockers, digoxin, amiodarone
Ibutilide 1-2mg rapid IV infusion have paddles ready
Oral propafenone or flecainide beware pro-arrhythmia
Low voltage DC cardioversion
Anticoagulation as per atrial fibrillation
On the horizon: vernakalant, an atrial-selective Na and K channel
blocker for conversion of short-duration atrial fibrillation

Ventricular Fibrillation

www.uptodate.com

Ventricular fibrillation is caused by numerous waves of depolarization

spreading throughout the ventricles simultaneously, leading to disorganized
ventricular contraction and immediate loss of cardiac function.
EKG Characteristics:

Absent P waves

Disorganized electrical activity

Deflections continuously change in shape,
magnitude and direction

Rhythms Produced by Conduction

Block
AV Block (relatively common)
1st degree AV block
Type 1 2nd degree AV block
Type 2 2nd degree AV block
3rd degree AV block

SA Block (relatively rare)

1st Degree AV Block

The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/

EKG Characteristics:

Prolongation of the PR interval, which is constant

All P waves are conducted

Usually benign

2nd Degree AV Block

Mobitz 1

(Wenckebach)

EKG Characteristics:

Progressive prolongation of the PR interval

until a P wave is not conducted.

As the PR interval prolongs, the RR interval actually shortens

Usually benign unless associated with underlying pathology, i.e. MI

2nd Degree AV Block

Mobitz 2

EKG Characteristics:

Constant PR interval with intermittent failure

to conduct

Rhythm is dangerous as the block is lower in the conduction system

May cause syncope or may deteriorate into complete heart block

Causes: anterioseptal MI, fibrotic disease of the conduction system

Treatment: may require pacemaker in the case of fibrotic conduction
system

3rd Degree (Complete) AV Block

EKG Characteristics:

No relationship between P waves and QRS

complexes
Constant PP intervals and RR intervals

May be caused by inferior MI and its presence worsens the prognosis

May cause syncopal symptoms, angina, or CFH
Treatment: usually requires pacemaker

Right Bundle Branch Block (RBBB)

1.

Depolarization spreads from the left

ventricle to the right ventricle.

2.

This creates a second R-wave (R) in V1,

and a slurred S-wave in V5 - V6.

3.

The T wave should be deflected opposite

the terminal deflection of the QRS complex.
This is known as appropriate T wave
discordance with bundle branch block. A
concordant T wave may suggest ischemia
or myocardial infarction.

Left Bundle Branch Block (LBBB)

1.

Depolarization enters the right side of the right

ventricle first and simultaneously depolarizes the
septum from right to left.

2.

This creates a QS or rS complex in lead V1 and a

monophasic or notched R wave in lead V6.

3.

The T wave should be deflected opposite the

terminal deflection of the QRS complex. This is
known as appropriate T wave discordance with
bundle branch block. A concordant T wave may
suggest ischemia or myocardial infarction.

Antiarrhythmia Agents

Class 1A agents: Procainamide, quinidine

ses

Wide spectrum, but side effects limit usage

Quinidine : maintain sinus rhythms in atrial fibrillation and flutter
and to prevent recurrent tachycardia and fibrillation

Procainamide: acute treatment of supraventricular and ventricular

arrhythmias (no longer in production)
Side effects
Hypotension, reduced cardiac output
Proarrhythmia (generation of a new arrhythmia) eg.
Torsades de Points (QT interval)
Dizziness, confusion, insomnia, seizure (high dose)
Gastrointestinal effects (common)
Lupus-like syndrome (esp. procainamide)

Class 1B agents: Lidocaine, phenytoin

Uses
acute : Ventricular tachycardia and fibrillation (esp. during
ischemia)
Not used in atrial arrhythmias or AV junctional arrhythmias
Side effects
Less proarrhythmic than Class 1A (less QT effect)
CNS effects: dizziness, drowsiness

Class 1C agents: Flecainide, propafenone

Uses
Wide spectrum
Used for supraventricular arrhythmias (fibrillation and
flutter)
Premature ventricular contractions (caused problems)
Wolff-Parkenson-White syndrome
Side effects
Proarrhythmia and sudden death especially with chronic
use (CAST study)
Increase ventricular response to supraventricular
arrhythmias
CNS and gastrointestinal effects like other local
anesthetics

Class II agents: Propranolol, esmolol

Uses
treating sinus and catecholamine dependent tachy
arrhythmias

converting reentrant arrhythmias in AV

protecting the ventricles from high atrial rates (slow AV
conduction)

Side effects
bronchospasm
hypotension
beware in partial AV block or ventricular failure

Class III agents: Amiodarone, sotalol, ibutilide

Amiodarone
Uses
Very wide spectrum: effective for most arrhythmias
Side effects: many serious that increase with time
Pulmonary fibrosis
Hepatic injury
Increase LDL cholesterol
Thyroid disease
Photosensitivity

May need to reduce the dose of digoxin and class 1 antiarrhythmics

Class III agents: Amiodarone, sotalol, ibutilide

Sotalol
Uses
Wide spectrum: supraventricular and ventricular tachycardia
Side effects
Proarrhythmia, fatigue, insomnia

Class III agents: Amiodarone, sotalol, ibutilide

Ibutilide
Uses
conversion of atrial fibrillation and flutter with rapid IV infusion
Side effects
Torsades de pointes

Class IV agents: Verapamil and diltiazem

Uses
control ventricular rate during supraventricular tachycardia
convert supraventricular tachycardia (re-entry around AV)

Side effects
Caution when partial AV block is present. Can get asystole
if blocker is on board
Caution when hypotension, decreased CO or sick sinus
Some gastrointestinal problems

Additional agents

Adenosine
Administration
rapid i.v. bolus, very short T1/2 (seconds)
Cardiac effects
Slows AV conduction
Uses
convert re-entrant supraventricular arrhythmias
hypotension during surgery, diagnosis of CAD

Magnesium
treatment for tachycardia resulting from long QT

Additional agents

Digoxin (cardiac glycosides)

Mechanism
enhances vagal activity, inhibits Na/K ATPase
refractory period, slows AV conduction
Uses
treatment of atrial fibrillation and flutter

Atropine
Mechanism
selective muscarinic antagonist
Cardiac effects
blocks vagal activity to speed AV conduction and
increase HR
Uses
treat vagal bradycardia

Selected References:
ACC/AHA/ESC Practice Guidelines 2013-2014:
Supraventricular Arrhythmias.
Atrial Fibrillation
Ventricular Arrhythmias

Types

Sinus arrhythmia
Sinus bradycardia
Sinus tachycardia
Sinus arrest
Sinoatrial exit block
Sick sinus syndrome

Sinus arrhythmia

Sinus bradycardia

Sinus tachycardia

Sinus arrest

Sinoatrial exit block

Sick sinus syndrome