dr M.

Arman Nasution SpPD

ARITMIA
• A-RHYTHM –IA
• Defn- Arrhythmia is deviation of heart from
normal RHYTHM.

• RHYTHM
1) HR- 60-100
2) Should origin from SAN
3) Cardiac impulse should propagate through
normal conduction pathway with normal
velocity.
CLASSIFICATION OF
ARRHYTHMIAS
. Atrial fibrillation
500

Atrial flutter
350

Paroxysmal TA
200
Simple tachyarrythmia
150

100
Normal range

60 Mild bradyarrhythmias
40
moderate BA
20
Severe BA
ARRHYTHMIAS

Sinus arrythmia

Atrial arrhythmia SVT

Nodal arrhythmia
(junctional)

Ventricular arrhytmia
ELECTROPHYSIOLOGY OF CARDIAC TISSUE

 Impulse generation and transmission

 Myocardial action potential

 Depolarization and repolarization waves as

seen in ECG
 Types of cardiac tissue
(on the basis of impulse generation)
• AUTOMATIC/ PACEMAKER/ CONDUCTING FIBRES
(Ca++ driven tissues)
 Includes SA node, AV node, bundle of His,
Purkinje fibres
 Capable of generating their own impulse
 Normally SA node acts as Pacemaker of heart
• NON-AUTOMATIC MYOCARDIAL CONTRACTILE FIBRES
(Na+ driven tissues)
 Cannot generate own impulse
 Includes atria and ventricles
IMPULSE GENERATION AND TRANSMISSION
 MYOCARDIAL ACTION POTENTIAL

In automatic tissues In non-automatic

tissues
ACTION POTENTIAL IN NON AUTOMATIC
MYOCARDIAL CONTRACTILE TISSUE
 Early Inactivated
+30 mV Plateau phase
repolarization 1
2
0 mV
Rapid
Na+ Repolarization
Phase zero phase
open
depolarization0
3

Phase 4
Resting depolarization
4
-80 mV
-90 mV
Ca++ K+ K+ K+
Na+ K+
OUTSIDE Na+ Ca++

MEMBRANE Atp
INSIDE Na+
K+
ACTION POTENTIAL IN NODAL TISSUES
+30 mV
1
2
0 mV

0
3

4
-80 mV
-90 mV
Ca++ K+ K+ K+
Na+ K+
OUTSIDE Na+ Ca++

MEMBRANE Atp
INSIDE Na+
K+
FAST CHANNEL AP SLOW CHANNEL AP

 Occurs in atria, ventricles,  Occurs in SA node, A-V

PF node
 Predominant ion in phase-0  Predominant ion in phase-
is Na+ 0 is Ca2+
 Conduction velocity more  Less
 Selective channel blocker is  Selective channel blockers
tetradotoxin , LA are calcium channel
blockers

FAST CHANNEL VS SLOW CHANNEL AP

COMMON TERMS
 Automaticity
 Capacity of a cell to undergo spontaneous diastolic
depolarization
 Excitability
 Ability
of a cell to respond to external stimulus by
depolariztion
 Threshold potential
 Level
of intracellular negativity at which abrupt and
complete depolarization occurs
COMMON TERMS

 Conduction velocity of impulse

 Determined primarily by slope of action potential
and amplitude of phase-0, any reduction in slope
leads to depression of conduction
 Propagation of impulse
 Depends on ERP & Conduction velocity
Refractory period
Depolarization
&
Repolarization
waves seen in
ECG
 ECG is used as a rough guide to some
cellular properties of cardiac tissue
• P wave: atrial depolarization
• PR-Interval reflects AV nodal conduction time
• QRS DURATION reflects conduction time in
ventricles
• T-wave: ventricular repolarization
• QT interval is a measure of ventricular APD
Mechanisms of cardiac arrythmia

• Abnormal impulse generation:

• Depressed automaticity
• Enhanced automaticity
• Triggered activity (after depolarization):
• Delayed after depolarization
• Early after depolarization
• Abnormal impulse conduction:
• Conduction block
• Re-entry phenomenon
• Accessory tract pathways
 a) Enhanced automaticity
Automatic behavior in sites ordinarily lacking
pacemaker activity
CAUSES:
Ischaemia/digitalis/catecholamines/acidosis/
hypokalemia/stretching of cardiac cells

Nonpacemaker nodal tissues: membrane potential

comes to -60mv

Increased slope of phase 4 depolarisation

Become ECTOPIC PACEMAKERS.(AV nodal rhythm,

idioventricular rhythm, ectopic beats)
ECTOPIC PACEMAKER ACTIVITY ENCOURAGED BY

Less negative
RMP

More negative TP
 b) Trigerred automaticity
+30 mV

0 mV

Early After
Depolarisation
(EAD)

-80 mV
-90 mV
 b) Trigerred automaticity
+30 mV

0 mV

Delayed After
Depolarisation
(DAD)

-80 mV
-90 mV
C. ABNORMAL IMPULSE CONDUCTION

 Conduction block
 Firstdegree block
 Second degree block

 Third degree block

 Re-entry phenomenon
 Accessory tract pathways
RE-ENTRY

INEXCITABLE
TISSUE

2
1
Re-entry
Counterclockwise
right atrial reentry

LA is passively
activated
REQUIREMENTS FOR RE-ENTRY CIRCUIT

 Presence of anatomically defined circuit

 Region of unidirectional block

 Re-entry impulse with slow conduction

ACCESSORY TRACT PATHWAYS
 ANATOMY & PHYSIOLOGY

 Blood Flow through

heart
 Superior and Inferior
Vena Cava
 Right Atrium
 Right Ventricle
 Pulmonary Artery
 Lungs
 Pulmonary Vein
 Left Atrium
 Left Ventricle
 Aorta
 Body
 CONDUCTION SYSTEM
 The heart has a conduction system separate
from any other system
 The conduction system makes up the PQRST
complex we see on paper
 An arrhythmia is a disruption of the
conduction system
Understanding how the
heart conducts normally is
essential in understanding
and identifying arrhythmias
 CONDUCTION SYSTEM

 SA Node
 Inter-nodal and
inter-atrial pathways
 A-V Node
 Bundle of His
 Perkinje Fibers
 SA NODE
 The primary pacemaker of the
heart
 Each normal beat is initiated by
the SA node
 Inherent rate of 60-100 beats per
minute
 Represents the P-wave in the
QRS complex or atrial
depolarization (firing)
 AV NODE
 Located in the septum of
the heart
 Receives impulse from
inter-nodal pathways and
holds the signal before
sending on to the Bundle
of His
 Represents the PR
segment of the QRS
complex
 AV NODE
 Represents the PR segment of the cardiac
cycle
 Has an inherent rate of 40-60 beats per
minute
 Acts as a back up when the SA node fails

 Where all junctional rhythms originate

 QRS COMPLEX

 Represents the
ventricles depolarizing
(firing) collectively.
(Bundle of His and
Perkinje fibers)
 Origin of all ventricular
rhythms
 Has an inherent rate
of 20-40 beats per
minute
 EKG TRACE

 Isoelectric
line (baseline)
 P-wave
 Atria firing
 PR interval
 Delay at AV
 EKG TRACE

 QRS
 Ventricles
firing
 T-wave
 Ventricles
repolarizing
 EKG TRACE

 ST segment
 Ventricle
contracting
 Should be at
isoelectric line
 Elevation or
depression may be
important
 U wave
 Perkinje fiber
repolarization?
 WAVEFORM ANALYSIS
 For each strip it is necessary to go through steps
to correctly identify the rhythm
1. Is there a P-wave for every QRS?
 P-waves are upright and uniform
 One P-wave preceding each QRS
2. Is the rhythm regular?
 Verify by assessing R-R interval
 Confirm by assessing P-P interval
3. What is the rate?
 Count the number of beats occuring in one minute
 Counting the p-waves will give the atrial rate
 Counting QRS will give ventricular rate
 Summary
 Normal
 Heart rate = 60 – 100 bpm
 PR interval = 0.12 – 0.20 sec

 QRS interval <0.12

 SA Node discharge = 60 – 100 / min

 AV Node discharge = 40 – 60 min

 Ventricular Tissue discharge = 20 – 40 min

 Summary

 Cardiac cycle
P wave = atrial depolarization
 PR interval = pause between atrial and ventricular
depolarization
 QRS = ventricular depolarization

 T wave = ventricular depolarization

 Sinus Rhythms
Normal Sinus Rhythm

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

60 - Before each QRS,

Regular .12 - .20 <.12
100 Identical
 Sinus Rhythms

 Normal Sinus Rhythm

 Sinus Node is the primary pacemaker
 One upright uniform p-wave for every QRS

 Rhythm is regular

 Rate is between 60-100 beats per minute

 Sinus Rhythms
Sinus Bradycardia

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Before each QRS,

<60 Regular .12 - .20 <.12
Identical
 Sinus Rhythms

 Sinus Bradycardia
 One upright uniform p-wave for every QRS
 Rhythm is regular

 Rate less than 60 beats per minute

 SA node firing slower than normal
 Normal for many individuals

 Identify what is normal heart rate for patient

 Sinus Rhythms
Sinus Tachycardia

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Before each QRS,

>100 Regular .12 - .20 <.12
Identical
 Sinus Rhythms

 Sinus Tachycardia
 One upright uniform p-wave for every QRS
 Rhythm is regular

 Rate is greater than 100 beats per minute

 Usually between 100-160 (>160 SVT)
 Can be high due to anxiety, stress, fever, medications
(anything that increases oxygen consumption)
 Sinus Rhythms
Sinus Arrhythmia

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Before each QRS,

Var. Irregular .12 - .20 <.12
Identical
 Sinus Rhythms

 Sinus Arrhythmia
 One upright uniform p-wave for every QRS
 Rhythm is irregular
 Rate increases as the patient breathes in
 Rate decreases as the patient breathes out

 Rate is usually 60-100 (may be slower)

 Variation of normal, not life threatening
 Sinus Rhythms
Sinus Arrest

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Before each QRS,

NA Irregular .12 - .20 <.12
Identical
 Sinus Rhythms
Sinus Arrest

Stop of sinus rhythm

New rhythm starts

Sinus Pause
One dropped beat is a sinus pause
Beats walk through
 Atrial Rhythms
Premature Atrial Contraction (PAC)

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Premature &
NA Irregular abnormal or .12 - .20 <.12
hidden
 Atrial Rhythms
 Premature Atrial Contraction (PAC)
 One P-wave for every QRS
 P-wave may have different morphology on ectopic beat, but it
will be present
 Single ectopic beat will disrupt regularity of underlying
rhythm
 Rate will depend on underlying rhythm

 Underlying rhythm must be identified

 Classified as rare, occasional, or frequent PAC’s based

on frequency
 Atrial Rhythms
Atrial Fibrillation

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Var. Irregular Wavy irregular NA <.12

 Atrial Rhythms
 Atrial Fibrillation
 No discernable p-waves preceding the QRS complex
 The atria are not depolarizing effectively, but fibrillating
 Rhythm is grossly irregular
 If the heart rate is <100 it is considered controlled a-fib, if
>100 it is considered to have a “rapid ventricular response”
 AV node acts as a “filter”, blocking out most of the
impulses sent by the atria in an attempt to control the heart
rate
 Atrial Rhythms

 Atrial Fibrillation (con’t)

 Often a chronic condition, medical attention only
necessary if patient becomes symptomatic
 Patient will report history of atrial fibrillation.
 Atrial Rhythms
Atrial Flutter

PR Interval QRS
Heart Rate Rhythm P Wave
(sec.) (Sec.)
Atrial=250
Not
– 400
Irregular Sawtooth Measur- <.12
Ventricular
able
Var.
 Atrial Rhythms
 Atrial Flutter
 More than one p-wave for every QRS complex
 Demonstrate a “sawtooth” appearance
 Atrial rhythm is regular. Ventricular rhythm will be regular if
the AV node conducts consistently. If the pattern varies, the
ventricular rate will be irregular
 Rate will depend on the ratio of impulses conducted through
the ventricles
 ATRIAL RHYTHMS

 Atrial Flutter
 Atrialflutter is classified as a ratio of p-waves per
QRS complexes (ex: 3:1 flutter 3 p-waves for each
QRS)
 Not considered life threatening, consult physician is
patient symptomatic
 Junctional Rhythms
 Rhythms that originate at the AV junction
 Junctional rhythms do not have characteristic
p-waves.
 Junctional Rhythms
Premature Junctional Contraction PJC

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Premature,
Usually Short Normal
Irregular abnormal, may be
normal <.12 <.12
inverted or hidden
 Junctional Rhythms
 Premature Junctional Contraction (PJC)
 P-wave can come before or after the QRS complex, or it
may lost in the QRS complex
 If visible, the p-wave will be inverted
 Rhythm will be irregular due to single ectopic beat
 Heart rate will depend on underlying rhythm
 Underlying rhythm must be identified
 Classify as rare, occasional, or frequent PJC based on
frequency
 Atria are depolarized via retrograde conduction
 Junctional Rhythms
Accelerated Junctional

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Inverted, absent or
Var. Regular <.12 <.12
after QRS
 Junctional Rhythms
 Accelerated Junctional Rhythm
 P-wave can come before or after the QRS complex,
or lost within the QRS complex
 If p-waves are seen they will be inverted
 Rhythm is regular
 Heart rate between 60-100 beats per minute
 Within the normal HR range
 Fast rate for the junction (normally 40-60 bpm)
 Junctional Rhythms
Junctional Tachycardia

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

May be inverted or Short Normal

>100 Regular
hidden <.12 <.12
 Junctional Rhythms
 Junctional Tachycardia
 P-wave can come before or after the QRS complex or lost
within the QRS entirely
 If a p-wave is seen it will be inverted
 Rhythm is regular
 Rate is between 100-180 beats per minute
 In the tachycardia range, but not originating from SA node
 AV node has sped up to override the SA node for control of
the heart
 JUNCTIONAL RHYTHMS
Junctional Escape

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

40 – Absent, inverted Short Normal

Regular
60 or after QRS <.12 <.12
 JUNCTIONAL RHYTHMS

 Junctional Escape Rhythm

 P-wave may come before or after the QRS or may
be hidden in the QRS entirely
 If p-waves are seen, they will be inverted
 Rhythm is regular
 Rate 40-60 beats per minute
 The SA node has failed; the AV junction takes over
control of the heart
 VENTRICULAR RHYTHMS
Premature Ventricular Contraction (PVC)

PR
Heart QRS
Rhythm P Wave Interval
Rate (Sec.)
(sec.)
No P waves
Wide
Var. Irregular associated with NA
>.12
premature beat
 VENTRICULAR RHYTHMS

 Premature Ventricular Contraction (PVC)

 The ectopic beat is not preceded by a p-wave
 Irregular rhythm due to ectopic beat
 Rate will be determined by the underlying rhythm
 QRS is wide and may be bizarre in appearance
 Caused by a irritable focus within the ventricle which fires
prematurely
 Must identify an underlying rhythm
 VENTRICULAR RHYTHM

 Premature Ventricular Contraction

 Classify as rare, occasional, or frequent
 Classify as unifocal, or multifocal PVC’s
 Unifocal-originating from same area of the
ventricle; distinguished by same morphology
 VENTRICULAR RHYTHM

 Premature Ventricular Contraction

 Classify as unifocal, or multifocal PVC’s
 Unifocal-originating from same area of the ventricle;
distinguished by same morphology
 Multifocal-originating from different areas of the
ventricle; distinguished by different morphology
 VENTRICULAR RHYTHM

 Premature Ventricular Contraction

 Bigeminy
A PVC occurring every other beat
 Also seen as Trigeminy, Quadrigeminy
 VENTRICULAR RHYTHM
 Dangerous PVC’s
 R on T

 Runs of PVC’s
 3 or more
considered Vtach
 VENTRICULAR RHYTHMS

Ventricular Tachycardia

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

No P waves
100 –
Regular corresponding to QRS, NA >.12
250
a few may be seen
 VENTRICULAR RHYTHMS

 Ventricular Tachycardia
 No discernable p-waves with QRS
 Rhythm is regular
 Atrial rate cannot be determined, ventricular rate is
between 150-250 beats per minute
 Must see 4 beats in a row to classify as v-tach
 VENTRICULAR RHYTHMS

 Ventricular Tachycardia
 THIS IS A DEADLY RHYTHM
 Check patient:
 If patient awake and alert, monitor patient and call physician
 If patient has no vital signs, call code and start CPR
 Defibrillate
 VENTRICULAR RHYTHMS

Ventricular Fibrillation

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

0 Chaotic None NA None

 VENTRICULAR RHYTHMS

 Ventricular Fibrillation
 No discernable p-waves
 No regularity

 Unable to determine rate

 Multiple irritable foci within the ventricles all

firing simultaneously
 May be coarse or fine

 This is a deadly rhythm

 Patient will have no pulse
 Call a code and begin CPR
 ASYSTOLE

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

None None None None None

 ASYSTOLE

 No p-waves
 No regularity

 No Rate

 This rhythm is associated with death

 Check patient and leads
 No pulse

 Begin CPR
 HEART BLOCK
First Degree Heart Block

Heart PR Interval QRS

Rhythm P Wave
Rate (sec.) (Sec.)

Before each QRS,

Norm. Regular > .20 <.12
Identical
 HEART BLOCK

 First Degree Heart Block

 P-wave for every QRS
 Rhythm is regular

 Rate may vary

 Av Node hold each impulse longer than normal before

conducting normally through the ventricles
 Prolonged PR interval
 Looks just like normal sinus rhythm
 HEART BLOCK
Second Degree Heart Block
Mobitz Type I (Wenckebach)

QRS
Heart PR Interval
Rhythm P Wave (Sec.
Rate (sec.)
)
Norm. Present but some
Progressively
can be Irregular not followed by <.12
longer
slow QRS
 HEART BLOCK

 Second Degree Heart Block

 Mobitz Type I (Wenckebach)
 Some p-waves are not followed by QRS complexes
 Rhythm is irregular
 R-R interval is in a pattern of grouped beating
 Rate 60-100 bpm
 Intermittent Block at the AV Node
 Progressively prolonged p-r interval until a QRS is blocked
completely
 HEART BLOCK
Second Degree Heart Block
Mobitz Type II (Classical)

PR
Heart QRS
Rhythm P Wave Interval
Rate (Sec.)
(sec.)
Regular
Usually 2 3 or 4 before each <.12
or .12 - .20
slow QRS, Identical depends
irregular
 HEART BLOCK

 Second Degree Heart Block

 Mobitz Type II (Classical)
 More p-waves than QRS complexes
 Rhythm is irregular
 Atrial rate 60-100 bpm; Ventricular rate 30-100 bpm
(depending on the ratio on conduction)
 Intermittent block at the AV node
 AV node normally conducts some beats while blocking others
 HEART BLOCK
Third Degree Heart Block
(Complete)

PR
Heart QRS
Rhythm P Wave Interval
Rate (Sec.)
(sec.)
Present but no
30 – <.12
Regular correlation to QRS Varies
60 depends
may be hidden
 HEART BLOCK

 Third Degree Heart Block (Complete)

 There are more p-waves than QRS complexes
 Both P-P and R-R intervals are regular
 Atrial rate within normal range; Ventricular rate
between 20-60 bpm
 The block at the AV node is complete
 Thereis no relationship between the p-waves and QRS
complexes
WPW: INITIATION OF SVT

Supraventricular tachycardia
• initiated by a closely
coupled premature atrial
complex (PAC)
• blocks in the accessory
pathway
• but conducts through the
AV node
• retrograde conduction via
accessory pathway
• inverted P wave produced
by retrograde conduction
visible in the inferior ECG
leads
 Regulation by autonomic tone
Parasympathetic/Vagus Nerve
stimulation:

• Ach binds to M2 receptors

• Activate Ach dependent outward K+

conductance (thus hyperpolarisation)

• ↓ phase 4 AP

Sympathetic stimulation:
• Activation of β1 receptors

• Augmentation of L-type Ca2+ current

• Phase 4 AP more steeper

+30 mV
Possible MOA of antiarrythmic agents
1
2
0 mV

RATE
0 SLOPE 3

THRESHOLD POTENTIAL
4
-80 mV Effective Refractory Period
-90 mV RMP
Ca++ K+ K+ Na+ Ca++ K+
Na+ K+
OUTSIDE Na+ Ca++

MEMBRANE Atp
INSIDE Na+
K+
 Classification of Anti-Arrhythmic Drugs
(Vaughan-Williams-Singh..1969)
Class I: block Na+ channels
Ia (quinidine, procainamide,
disopyramide) (1-10s)
Ib (lignocaine) (<1s) Phase 1

Ic (flecainide) (>10s) IV
Phase 2
0 mV
Class II: ß-adrenoceptor
antagonists (atenolol, sotalol) Phase 0
III
I Phase 3

Class III: prolong action potential

and prolong refractory period -
(amiodarone, dofetilide, sotalol) 80m
Phase 4
II
V
Class IV: Ca2+ channel antagonists
(verapamil, diltiazem)
CLASSIFICATION BASED ON CLINICAL USE

 Drugs used for supraventricular

arrhythmia`s
 Adenosine, verapamil, diltiazem
 Drugs used for ventricular arrhythmias
 Lignocaine, mexelitine, bretylium
 Drugs used for supraventricular as well as
ventricular arrhythmias
 Amiodarone, - blockers, disopyramide,
procainamide
Na+ channel blocker
• Bind to and block Na+ channels (and K+ also)
• Act on initial rapid depolarisation (slowing
effect)
• Local Anaesthetic (higher concentration): block
nerve conduction
• Do not alter resting membrane potential
(Membrane Stabilisers)
• At times, post repolarization refractoriness.
• Bind preferentially to the open channel state
• USE DEPENDENCE : The more the channel is in
use, the more drug is bound
 Ia Ib Ic
Moderate Na channel Mild Na channel Marked Na channel
blockade blockade blockade
Slow rate of rise of Limited effect on Markedly reduces
Phase 0 Phase 0 rate of rise of phase
0
Prolong refractoriness Little effect on Prolong refractoriness
by blocking several refractoriness as by blocking delayed
types of K channels there is minimal rectifier K channels
effect on K channels
Lengthen APD & Shorten APD & No effect on APD &
repolarization repolarization repolarization
Prolong PR, QRS QT unaltered or Markedly prolong PR
slightly shortened & QRS
 Class I: Na+ Channel Blockers

• IA: Ʈrecovery moderate (1-10sec)

Prolong APD

• IB: Ʈrecovery fast (<1sec)

Shorten APD in some heart
tissues

• IC: Ʈrecovery slow(>10sec)

Minimal effect on APD
Class IA
QUINIDINE

 Historically first antiarrhythmic drug used.

 In 18th century, the bark of the cinchona plant
was used to treat "rebellious palpitations“

pharmacological effects

threshold for excitability

automaticity
prolongs AP
QUINIDINE

Clinical Pharmacokinetics
 well absorbed

 80% bound to plasma proteins (albumin)

 extensive hepatic oxidative metabolism

 3-hydroxyquinidine,

 is nearly as potent as quinidine in blocking

cardiac Na+ channels and prolonging cardiac
action potentials.
QUINIDINE

 Uses

 to maintain sinus rhythm in patients with atrial

flutter or atrial fibrillation

 to prevent recurrence of ventricular

tachycardia or VF
QUINIDINE
ADVERSE EFFECTS-

Non cardiac
Diarrhea, thrombocytopenia,
 cinchonism & skin rashes.

cardiac
marked QT-interval prolongation &torsades
de pointes (2-8% )
hypotension
tachycardia
DRUG INTERACTIONS

 Metabolized by CYP450
 Increases digoxin levels

 Cardiac depression with beta blockers

 Inhibits CYP2D6
DISOPYRAMIDE
 Exerts electrophysiologic effects very similar to
those of quinidine.
 Better tolerated than quinidine

 exert prominent anticholinergic actions

 Negative ionotropic action.

 A/E-

 precipitation of glaucoma,

 constipation, dry mouth,

 urinary retention
PROCAINAMIDE

 Lesser vagolytic action , depression of

contractility & fall in BP
 Metabolized by acetylation to N-acetyl
procainamide which can block K+ channels
 Doesn’t alter plasma digoxin levels
 Cardiac adverse effects like quinidine
 Can cause SLE not recommended > 6
months
 Use: Monomorphic VT, WPW Syndrome
 Ia Ib Ic
Moderate Na channel Mild Na channel Marked Na channel
blockade blockade blockade
Slow rate of rise of Limited effect on Markedly reduces
Phase 0 Phase 0 rate of rise of phase
0
Prolong refractoriness Little effect on Prolong refractoriness
by blocking several refractoriness as by blocking delayed
types of K channels there is minimal rectifier K channels
effect on K channels
Lengthen APD & Shorten APD & No effect on APD &
repolarization repolarization repolarization
Prolong PR, QRS QT unaltered or Markedly prolong PR
slightly shortened & QRS
CLASS IB DRUGS

Lignocaine, phenytoin,
mexiletine

Block sodium
channels also shorten
repolarization
CLASS IB
LIGNOCAINE

 Blocks inactivated sodium channels more

than open state
 Relatively selective for partially depolarized
cells
 Selectively acts on diseased myocardium

 Rapid onset & shorter duration of action

 Useful only in ventricular arrhythmias ,

Digitalis induced ventricular arrnhythmias
 Lidocaine is not useful in atrial arrhythmias???
 atrial action potentials are so short that the
Na+ channel is in the inactivated state only
briefly compared with diastolic (recovery) times,
which are relatively long
 Pharmacokinetics

• High first pass metabolism

• Metabolism dependent on hepatic blood
flow
• T ½ = 8 min – distributive, 2 hrs –
elimination
• Propranolol decreases half life of lignocaine
• Dose= 50-100 mg bolus followed by 20-40
mg every 10-20 min i.v
 Adverse effects

• Relatively safe in recommended doses

• Drowsiness, disorientation, muscle
twitchings
• Rarely convulsions, blurred vision,
nystagmus
• Least cardiotoxic antiarrhythmic
 Local anaesthetic
 Inactive orally

 Given IV for antiarrhythmic action

 Na+ channel blockade which occurs

 Only in inactive state of Na+ channels

 CNS side effects in high doses

 Action lasts only for 15 min

 Inhibits purkinje fibres and ventricles but

 No action on AVN and SAN so

 Effective in Ventricular arrhythmias only

MEXILETINE

 Oral analogue of lignocaine

 No first pass metabolism in liver

 Use:
 chronic treatment of ventricular arrhythmias
associated with previous MI
 Unlabelled use in diabetic neuropathy

 Tremor is early sign of mexiletine toxicity

 Hypotension, bradycardia, widened QRS ,
dizziness, nystagmus may occur
TOCAINIDE

 Structurally similar to lignocaine but can be

administered orally
 Serious non cardiac side effects like pulmonary
fibrosis, agranulocytosis, thrombocytopenia
limit its use
 Class I C drugs
Encainide, Flecainide, Propafenone

Have minimal effect on

repolarization
Are most potent sodium
channel blockers

• Risk of cardiac arrest ,

sudden death so not used
commonly
• May be used in severe
ventricular arrhythmias
CLASS IC
PROPAFENONE CLASS 1C

 Structural similarity with propranolol & has

-blocking action
 Undergoes variable first pass metabolism

 Reserve drug for ventricular arrhythmias, re-

entrant tachycardia involving accesory
pathway
 Adverse effects: metallic taste, constipation
and is proarrhythmic
 Flecainde (Class Ic)
• Potent blocker of Na & K channels with slow
unblocking kinetics
• Blocks K channels but does not prolong APD &
QT interval
• Maintain sinus rhythm in supraventricular
arrhythmias
• Cardiac Arrhythmia Suppression Test (CAST
Trial):
When Flecainide & other Class Ic given
prophylactically to patients convalescing from
Myocardial Infarction it increased mortality by 2½
fold. Therefore the trial had to be prematurely
terminated
 Class II: Beta blockers
• -receptor stimulation:
• ↑ automaticity,
• ↑ AV conduction velocity,
• ↓ refractory period
• -adrenergic blockers competitively block
catecholamine induced stimulation of
cardiac - receptors
BETA BLOCKERS
 Depress phase 4 depolarization of pacemaker
cells,
 Slow sinus as well as AV nodal conduction :
↓ HR, ↑ PR
 ↑ ERP, prolong AP Duration by ↓ AV conduction
 Reduce myocardial oxygen demand

 Well tolerated, Safer

 β Adrenergic β Blockers
Stimulation
↑ magnitude of Ca2+ current & ↓ Intracellular Ca2+ overload
slows its inactivation

↑ Pacemaker current→↑ ↓Pacemaker current→↓ heart

heart rate rate
↑ DAD & EAD mediated Inhibits after-depolarization
arrhythmias mediated automaticity

Epinephrine induces Propranolol blocks this action

hypokalemia (β2 action)
• Control supraventricular arrhythmias
• Atrial flutter, fibrillation, PSVT
• Treat tachyarrhythmias caused by adrenergic+
• Hyperthyroidism Pheochromocytoma,
during anaesthesia with halothane
• Digitalis induced tachyarrythmias
• Prophylactic in post-MI
• Ventricular arrhythmias in prolonged QT
syndrome
• β1 selective agent
• Very short elimination t1/2 :9 mins
• Metabolized by RBC esterases
• Rate control of rapidly conducted AF
• Use:
• Arrythmia associated with anaesthesia
• Supraventricular tachycardia
 Class III drugs
↑APD & ↑RP by
blocking the K+
channels
 ↑ APD
Block IK

0mV

Vm
(mV)

-80mV
 Amiodarone
• Iodine containing long acting drug
• Mechanism of action: (Multiple actions)
– Prolongs APD by blocking K+ channels
– blocks inactivated sodium channels
– β blocking action , Blocks Ca2+ channels
– ↓ Conduction, ↓ectopic automaticity
 Amiodarone
 Pharmacokinetics:
 Variableabsorption 35-65%
 Slow onset 2days to several weeks
 Duration of action : weeks to months

 Dose
 Loading dose: 150 mg over 10min
 Then 1 mg/min for 6 hrs
 Then maintenance infusion of 0.5
mg/min for 24 hr
 Amiodarone
• Uses:
– Can be used for both supraventricular and
ventricular tachycardia
• Adverse effects:
– Cardiac: heart block , QT prolongation,
bradycardia, cardiac failure, hypotension
– Pulmonary: pneumonitis leading to pulmonary
fibrosis
– Bluish discoloration of skin, corneal microdeposits
– GIT disturbances, hepatotoxicity
– Blocks peripheral conversion of T4to T3 can
cause hypothyroidism or hyperthyroidism
 Antiarrhythmic
 Multiple actions
 Iodine containing
 Orally used mainly
 Duration of action is very long (t ½ = 3-8 weeks)
 APD & ERP increases
 Resistant AF, V tach, Recurrent VF are
indications
 On prolonged use- pulmonary fibrosis
 Neuropathy may occur
 Eye : corneal microdeposits may occur
• Bretylium:
– Adrenergic neuron blocker used in resistant
ventricular arrhythmias
• Sotalol:
– Beta blocker
• Dofetilide, Ibutilide :
– Selective K+ channel blocker, less adverse
events
– use in AF to convert or maintain sinus rhythm
– May cause QT prolongation
 Dronedarone
 Vernakalant

 Azimilide

 Tedisamil
Calcium channel blockers (Class IV)
• Inhibit the inward
movement of calcium
↓ contractility,
automaticity , and AV
conduction.
• Verapamil & diltiazem
 Verapamil

• Uses:
– Terminate PSVT
– control ventricular rate in atrial flutter or
fibrillation
• Drug interactions:
– Displaces digoxin from binding sites
– ↓ renal clearance of digoxin
 Other antiarrhythmics
• Adenosine :
– Purine nucleoside having short and rapid action
– IV suppresses automaticity, AV conduction and
dilates coronaries
– Drug of choice for PSVT
– Adverse events:
• Nausea, dyspnoea, flushing, headache
Adenosine

0mV

Vm
(mV)

↓ APD

Hyperpolarization

-80mV
 Adenosine
• Acts on specific G protein-coupled adenosine
receptors
• Activates AcH sensitive K+ channels channels in SA
node, AV node & Atrium

• Shortens APD, hyperpolarization & ↓ automaticity

• Inhibits effects of ↑ cAMP with sympathetic

stimulation

• ↓ Ca currents

• ↑AV Nodal refractoriness & inhibit DAD’s

 Other antiarrhythmics

 Atropine: Used in sinus bradycardia

 Digitalis: Atrial fibrillation and atrial flutter

 Magnesium SO4: digitalis induced arrhythmias

 Magnesium
• Its mechanism of action is unknown but may
influence Na+/K+ATPase, Na+ channels,
certain K+ channels & Ca2+ channels
• Use: Digitalis induced arrhythmias if
hypomagnesemia present, refractory
ventricular tachyarrythmias, Torsade de
pointes even if serum Mg2+ is normal
• Given 1g over 20mins
 Drugs of choices
S. Arrhythmia Drug
No
1 Sinus tachycardia Propranolol
2 Atrial extrasystole Propranolol,
3 AF/Flutter Esmolol, verapamil ,digoxin
4 PSVT Adenosine ,esmolol
5 Ventricular Lignocaine , procainamide ,
Tachycardia Amiodarone
6 Ventricular fibrillation Lignocaine, amiodarone
7 A-V block Atropine , isoprenaline
Definition of Arrhythmia:
The Origin, Rate, Rhythm, Conduct velocity
and sequence of heart activation are
abnormally.
Anatomy of the conducting system
ARRHYTHMIA PRESENTATION

 Palpitation.
 Dizziness.

 Chest Pain.

 Dyspnea.

 Fainting.

 Sudden cardiac death.

PATHOGENESIS AND INDUCEMENT
OF ARRHYTHMIA
 Some physical condition

 Pathological heart disease

 Other system disease

 Electrolyte disturbance and acid-base

imbalance
 Physical and chemical factors or toxicosis
MECHANISM OF ARRHYTHMIA

 Abnormal heart pulse formation

1. Sinus pulse
2. Ectopic pulse
3. Triggered activity
 Abnormal heart pulse conduction
1. Reentry
2. Conduct block
CLASSIFICATION OF ARRHYTHMIA
 Abnormal heart pulse formation
1. Sinus arrhythmia
2. Atrial arrhythmia
3. Atrioventricular junctional arrhythmia
4. Ventricular arrhythmia
 Abnormal heart pulse conduction
1. Sinus-atrial block
2. Intra-atrial block
3. Atrio-ventricular block
4. Intra-ventricular block
 Abnormal heart pulse formation and
conduction
DIAGNOSIS OF ARRHYTHMIA

 Medical history

 Physical examination

 Laboratory test
THERAPY PRINCIPAL

 Pathogenesis therapy
 Stop the arrhythmia immediately if the
hemodynamic was unstable
 Individual therapy
ANTI-ARRHYTHMIA AGENTS

 Anti-tachycardia agents

 Anti-bradycardia agents
ANTI-TACHYCARDIA AGENTS

 Modified Vaugham Williams classification

1. I class: Natrium channel blocker
2. II class: ß-receptor blocker
3. III class: Potassium channel blocker
4. IV class: Calcium channel blocker
5. Others: Adenosine, Digital
ANTI-BRADYCARDIA AGENTS

1. ß-adrenic receptor activator

2. M-cholinergic receptor blocker
3. Non-specific activator
CLINICAL USAGE

Anti-tachycardia agents:
 Ia class: Less use in clinic
1. Guinidine
2. Procainamide
3. Disopyramide: Side effect: like M-cholinergic
receptor blocker
Anti-tachycardia agents:
 Ib class: Perfect to ventricular
tachyarrhythmia
1. Lidocaine
2. Mexiletine
Anti-tachycardia agents:
 Ic class: Can be used in ventricular and/or
supra-ventricular tachycardia and
extrasystole.
1. Moricizine
2. Propafenone
ANTI-TACHYCARDIA AGENTS:

 II class: ß-receptor blocker

1. Propranolol: Non-selective
2. Metoprolol: Selective ß1-receptor
blocker, Perfect to hypertension and
coronary artery disease patients
associated with tachyarrhythmia.
ANTI-TACHYCARDIA AGENTS:
 III class: Potassium channel blocker, extend-
spectrum anti-arrhythmia agent.
 Amioarone: Perfect to coronary artery disease
and heart failure patients
 Sotalol: Has ß-blocker effect

 Bretylium
ANTI-TACHYCARDIA AGENTS:
 IV class: be used in supraventricular
tachycardia
1. Verapamil
2. Diltiazem
 Others:
Adenosine: be used in supraventricular
tachycardia
ANTI-BRADYCARDIA AGENTS
 Isoprenaline
 Epinephrine

 Atropine

 Aminophylline
PROARRHYTHMIA EFFECT OF
ANTIARRHYTHMIA AGENTS
 Ia, Ic class: Prolong QT interval, will cause VT
or VF in coronary artery disease and heart
failure patients
 III class: Like Ia, Ic class agents

 II, IV class: Bradycardia

NON-DRUG THERAPY

 Cardioversion: For tachycardia especially

hemodynamic unstable patient
 Radiofrequency catheter ablation (RFCA):
For those tachycardia patients (SVT, VT, AF,
AFL)
 Artificial cardiac pacing: For bradycardia,
heart failure and malignant ventricular
arrhythmia patients.
SINUS ARRHYTHMIA
SINUS TACHYCARDIA
 Sinus rate > 100 beats/min (100-180)
 Causes:
1. Some physical condition: exercise,
anxiety, exciting, alcohol, coffee
2. Some disease: fever, hyperthyroidism,
anemia, myocarditis
3. Some drugs: Atropine, Isoprenaline
 Needn’t therapy
SINUS TACHYCARDIA
 Rate: 101-160/min
 P wave: sinus
 QRS: normal
 Conduction: normal
 Rhythm: regular or slightly irregular
 The clinical significance of this dysrhythmia depends on the
underlying cause. It may be normal.
 Underlying causes include:
 increased circulating catecholamines
 CHF
 hypoxia
 PE
 increased temperature
 stress
 response to pain
 Treatment includes identification of the underlying cause and
correction.
 SINUS BRADYCARDIA
 Sinus rate < 60 beats/min
 Normal variant in many normal and older people
 Causes: Trained athletes, during sleep, drugs (ß-
blocker) , Hypothyriodism, CAD or SSS
 Symptoms:
1. Most patients have no symptoms.
2. Severe bradycardia may cause dizziness, fatigue,
palpitation, even syncope.
 Needn’t specific therapy, If the patient has severe
symptoms, planted an pacemaker may be needed.
SINUS BRADYCARDIA
 Rate: 40-59 bpm
 P wave: sinus
 QRS: Normal (.06-.12)
 Conduction: P-R normal or slightly prolonged at slower rates
 Rhythm: regular or slightly irregular
 This rhythm is often seen as a normal variation in athletes, during sleep, or in
response to a vagal maneuver. If the bradycardia becomes slower than the SA
node pacemaker, a junctional rhythm may occur.
 Treatment includes:
 treat the underlying cause,
 atropine,
 isuprel, or
 artificial pacing if patient is hemodynamically
compromised.
SINUS ARRHYTHIMIA
 Rate: 45-100/bpm
 P wave: sinus
 QRS: normal
 Conduction: normal
 Rhythm: regularly irregular
 The rate usually increases with inspiration and decreases with expiration.
 This rhythm is most commonly seen with respiration due to fluctuations in
vagal tone.
 The non respiratory form is present in diseased hearts and sometimes confused
with sinus arrset (also known as "sinus pause").
 Treatment is not usually required unless symptomatic bradycardia is present.
WANDERING PACEMAKER
 Rate: variable depending on the site of the pacemaker; usually 45-100/ bpm.
 P wave: also variable in morphology
 QRS: normal
 Conduction: P-R interval varies depending on the site of the pacemaker
 Rhythm: irregular
 This dysrhythmia may occur in normal hearts as a result of fluctuations in vagal
tone. It may also be seen in patients with heart disease or COPD.
 Wandering atrial pacemaker may also be a precursor to multifocal atrial
tachycardia.
 There is usually no treatment required.
 SINUS ARREST OR SINUS STANDSTILL

 Sinus arrest or standstill is recognized by a

pause in the sinus rhythm.
 Causes: myocardial ischemia, hypoxia,
hyperkalemia, higher intracranial pressure,
sinus node degeneration and some drugs
(digitalis, ß-blocks).
 Symptoms: dizziness, amaurosis, syncope

 Therapy is same to SSS

SINUS PAUSE, ARREST
 Rate: normal
 P wave: those that are present are normal
 QRS: normal
 Conduction: normal
 Rhythm: The basic rhythm is regular. The length of the pause is not a multiple
of the sinus interval.
 This may occur in individuals with healthy hearts. It may also occur with
increased vagal tone, myocarditis, MI, and digitalis toxicity.
 If the pause is prolonged, escape beats may occur.
 The treatment of this dysrhythmia depends on the underlying cause.
 If the cause is due to increased vagal tone and the patient is symptomatic, atropine
may be indicated.
SINOATRIAL EXIT BLOCK (SAB)

 SAB: Sinus pulse was blocked so it couldn’t

active the atrium.
 Causes: CAD, Myopathy, Myocarditis, digitalis
toxicity, et al.
 Symptoms: dizziness, fatigue, syncope

 Therapy is same to SSS

SINOATRIAL BLOCK
 Rate: normal or bradycardia
 P wave: those present are normal
 QRS: normal
 Conduction: normal
 Rhythm: basic rhythm is regular.
 In a type I SA block, the P-P interval shortens until one P wave is dropped.
 In a type II SA block, the P-P intervals are an exact multiple of the sinus cycle,
and are regular before and after the dropped P wave.
 This usually occurs transiently and produces no symptoms. It may occur in
healthy patients with increased vagal tone. It may also be found with CAD,
inferior MI, and digitalis toxicity.
SINOATRIAL EXIT BLOCK (SAB)

 Divided into three types: Type I, II, III

 Only type II SAB can be recognized by EKG.
SICK SINUS SYNDROME (SSS)
 SSS: The function of sinus node was
degenerated. SSS encompasses both
disordered SA node automaticity and SA
conduction.
 Causes: CAD, SAN degeneration, myopathy,
connective tissue disease, metabolic disease,
tumor, trauma and congenital disease.
 With marked sinus bradycardia, sinus arrest,
sinus exit block or junctional escape rhythms
 Bradycardia-tachycardia syndrome
 SICK SINUS SYNDROME (SSS)
 EKG Recognition:
1. Sinus bradycardia, ≤40 bpm;
2. Sinus arrest > 3s
3. Type II SAB
4. Nonsinus tachyarrhythmia ( SVT, AF or Af).
5. SNRT > 1530ms, SNRTc > 525ms
6. Instinct heart rate < 80bmp
SICK SINUS SYNDROME (SSS)

 Therapy:
1. Treat the etiology
2. Treat with drugs: anti-bradycardia agents,
the effect of drug therapy is not good.
3. Artificial cardiac pacing.
ATRIAL ARRHYTHMIA
PREMATURE CONTRACTIONS

 The term “premature contractions” are

used to describe non sinus beats.
 Common arrhythmia

 The morbidity rate is 3-5%

ATRIAL PREMATURE CONTRACTIONS
(APCS)
 APCs arising from somewhere in either the left or
the right atrium.
 Causes: rheumatic heart disease, CAD,
hypertension, hyperthyroidism, hypokalemia
 Symptoms: many patients have no symptom,
some have palpitation, chest incomfortable.
 Therapy: Needn’t therapy in the patients
without heart disease. Can be treated with ß-
blocker, propafenone, moricizine or verapamil.
PREAMATURE ATRIAL CONTRACTIONS
 Rate: normal or accelerated
 P wave: usually have a different morphology than sinus P waves because they
originate from an ectopic pacemaker
 QRS: normal
 Conduction: normal, however the ectopic beats may have a different P-R
interval.
 Rhythm: PAC's occur early in the cycle and they usually do not have a
complete compensatory pause.
 PAC's occur normally in a non diseased heart.
 However, if they occur frequently, they may lead to a more serious atrial
dysrhythmias.
 They can also result from CHF, ischemia and COPD.
 ATRIAL TACHYCARDIA

 Classify by automatic atrial tachycardia (AAT);

intra-atrial reentrant atrial tachycardia (IART);
chaotic atrial tachycardia (CAT).
 Etiology: atrial enlargement, MI; chronic
obstructive pulmonary disease; drinking;
metabolic disturbance; digitalis toxicity;
electrolytic disturbance.
ATRIAL TACHYCARDIA

 May occur transient; intermittent; or

persistent.
 Symptoms: palpitation; chest uncomfortable,
tachycardia may induce myopathy.
 Auscultation: the first heart sound is variable
INTRA-ATRIAL REENTRY TACHYCARDIA
(IART)
 ECG characters:
1. Atrial rate is around 130-150bpm;
2. P’ wave is different from sinus P wave;
3. P’-R interval ≥ 0.12”
4. Often appear type I or type II, 2:1 AV block;
5. EP study: atrial program pacing can induce
and terminate tachycardia
 AUTOMATIC ATRIAL TACHYCARDIA
(AAT)
 ECG characters:
1. Atrial rate is around 100-200bpm;
2. Warmup phenomena
3. P’ wave is different from sinus P wave;
4. P’-R interval≥ 0.12”
5. Often appear type I or type II, 2:1 AV block;
6. EP study: Atrial program pacing can’t
induce or terminate the tachycardia
 CHAOTIC ATRIAL TACHYCARDIA (CAT)
 Also termed “Multifocal atrial tachycardia”.
 Always occurs in COPD or CHF,
 Have a high in-hospital mortality ( 25-56%).
Death is caused by the severity of the underlying
disease.
 ECG characters:
1. Atrial rate is around 100-130bpm;
2. The morphologies P’ wave are more than 3
types.
3. P’-P’, P’-R and R-R interval are different.
4. Will progress to af in half the cases
5. EP study: Atrial program pacing can’t induce or
terminate the tachycardia
 THERAPY
 IRAT: Esophageal Pulsation Modulation,
RFCA, Ic and IV class anti-tachycardia agents
 AAT: Digoxin, IV, II, Ia and III class anti-
tachycardia agents; RFCA
 CAT: treat the underlying disease, verapamil
or amiodarone.
 Associated with SSS: Implant pace-maker.
PAROXYSMAL ATRIAL TACHYCARDIA
 Rate: atrial 160-250/min: may conduct to ventricles 1:1, or 2:1, 3:1, 4:1 into the
presence of a block.
 P wave: morphology usually varies from sinus
 QRS: normal (unless associated with aberrant ventricular conduction).
 Conduction: P-R interval depends on the status of AV conduction tissue and
atrial rate: may be normal, abnormal, or not measurable.
 PAT may occur in the normal as well as diseased heart.
 It is a common complication of Wolfe-Parkinson-White syndrome.

 This rhythm is often transient and doesn't require treatment.

 However, it can be terminated with vagal maneuvers.
 Digoxin, antiarrhythmics, and cardioversion may be used.
ATRIAL FLUTTER

 Etiology:
1. It can occur in patients with normal
atrial or with abnormal atrial.
2. It is seen in rheumatic heart disease
(mitral or tricuspid valve disease), CAD,
hypertension, hyperthyroidism,
congenital heart disease, COPD.
3. Related to enlargement of the atria
4. Most AF have a reentry loop in right
atrial
ATRIAL FLUTTER

 Symptoms: depend on underlying disease,

ventricular rate, the patient is at rest or is
exerting
 With rapid ventricular rate: palpitation,
dizziness, shortness of breath, weakness,
faintness, syncope, may develop angina and
CHF.
ATRIAL FLUTTER
 Therapy:
1. Treat the underlying disease
2. To restore sinus rhythm: Cardioversion,
Esophageal Pulsation Modulation, RFCA,
Drug (III, Ia, Ic class).
3. Control the ventricular rate: digitalis. CCB, ß-
block
4. Anticoagulation
 ATRIAL FIBRILLATION
 Subdivided into three types: paroxysmal,
persistent, permanent.
 Etiology:
1. Morbidity rate increase in older patients
2. Etiology just like atrial flutter
3. Idiopathic
 Mechanism:
1. Multiple wavelet re-entry;
2. Rapid firing focus in pulmonary vein, vena
cava or coronary sinus.
ATRIAL FIBRILLATION
 Rate: atrial rate usually between 400-650/bpm.
 P wave: not present; wavy baseline is seen instead.
 QRS: normal
 Conduction: variable AV conduction; if untreated the ventricular response is
usually rapid.
 Rhythm: irregularly irregular. (This is the hallmark of this dysrhythmia).
 Atrial fibrillation may occur paroxysmally, but it often becomes chronic. It is
usually associated with COPD, CHF or other heart disease.
 Treatment includes:
 Digoxin to slow the AV conduction rate.
 Cardioversion may also be necessary to terminate this rhythm.
 ATRIAL FIBRILLATION
 Manifestation:
 Affected by underlying diseases, ventricular rate and
heart function.
 May develop embolism in left atrial. Have high
incidence of stroke.
 The heart rate, S1 and rhythm is irregularly irregular
 If the heart rhythm is regular, should consider about
(1) restore sinus rhythm; (2) AF with constant the
ratio of AV conduction; (3) junctional or ventricular
tachycardia; (4) slower ventricular rate may have
complete AV block.
ATRIAL FIBRILLATION
 Therapy:
1. Treat the underlying disease
2. Restore sinus rhythm: Drug, Cardioversion,
RFCA, Maze surgery
3. Rate control: digitalis. CCB, ß-block
4. Antithrombotic therapy: Aspirine, Warfarin
ATRIOVENTRICULAR JUNCTIONAL
ARRHYTHMIA
ATRIOVENTRICULAR JUNCTIONAL
PREMATURE CONTRACTIONS

 Etiology and manifestation is like APCs

 Therapy the underlying disease

 Needn’t anti-arrhythmia therapy.

PREMATURE JUNCTIONAL
CONTRACTION
 Rate: normal or accelerated.
 P wave: as with junctional rhythm.
 QRS: normal
 Conduction: P-R interval < .12 secs if P waves are present.
 Rhythm: PJC's occur early in the cycle of the baseline rhythm. A
full compensatory pause may occur.
 PJCs may occur in both healthy and diseased hearts. If they are
occasional, they are insignificant. If they are frequent, junctional
tachycardia may result.
 Treatment is usually not required.
JUCTIONAL TACHYCARDIA
 Rate: faster than 60/bpm
 P wave: as with junctional rhythm.
 QRS: normal or widened with aberrant ventricular conduction.
 Conduction: P-R interval usually < .12 seconds if present
 Rhythm: usually regular
 The clinical significance of this rhythm depends upon the basic rhythm
disturbance. If the ventricular rate is rapid, cardiac output may decrease.
 Treatment includes:
 finding and correcting the underlying cause,
 vagal maneuvers,
 verapamil, and
 cardioversion.
NONPAROXYSMAL AV JUNCTIONAL
TACHYCARDIA
 Mechanism: relate to hyper-automaticity
or trigger activity of AV junctional tissue
 Etiology: digitalis toxicity; inferior MI;
myocarditis; acute rheumatic fever and
postoperation of valve disease
 ECG: the heart rate ranges 70-150 bpm or
more, regular, normal QRS complex,
may occur AV dissociation and
wenckebach AV block
NONPAROXYSMAL AV JUNCTIONAL
TACHYCARDIA

 Therapy:
 Treat underlying disease; stopping
digoxin, administer potassium,
lidocaine, phenytoin or propranolol.
 Not for DC shock

 It can disappear spontaneously. If had

good tolerance, not require therapy.
JUNCTIONAL ESCAPE RHYTHM
 Rate: 40-60/bpm
 P wave: inverted in leads where they are normally upright; this happens
when the atrial depolarization wave moves towards a negative (-)
lead.P waves may occur before, during or after the QRS, depending on
where the pacemaker is located in the AV junction.
 QRS: normal
 Conduction: P-R interval < .12 seconds if present.
 Rhythm: irregular as a result of the escape beats.
 The most common cause of this rhythm in healthy individuals is sinus
bradycardia.
 It may also be seen in the presence of a high degree or complete AV
block. If the ventricular rate is slow, hemodynamic compromise may
occur.
 Treatment depends upon the underlying cause and the baseline
dysrhythmias.
 Atropine or a pacemaker may be used to
increase the ventricular rate.
PAROXYSMAL TACHYCARDIA
 Most PSVT (paroxysmal supraventricular
tachycardia) is due to reentrant mechanism.
 The incidence of PSVT is higher in AVNRT
(atrioventricular node reentry tachycardia) and
AVRT (atioventricular reentry tachycardia), the
most common is AVNRT (90%)
 Occur in any age individuals, usually no
structure heart disease.
PAROXYSMAL TACHYCARDIA
 Manifestation:
 Occur and terminal abruptly.
 Palpitation, dizziness, syncope,
angina, heart failure and shock.
 The sever degree of the
symptom is related to ventricular
rate, persistent duration and
underlying disease
PAROXYSMAL TACHYCARDIA

 ECG characteristic of AVNRT

1. Heart rate is 150-250 bpm, regular
2. QRS complex is often normal, wide
QRS complex is with aberrant
conduction
3. Negative P wave in II III aVF, buried into
or following by the QRS complex.
4. AVN jump phenomena
PAROXYSMAL TACHYCARDIA

 ECG characteristic of AVRT

1. Heart rate is 150-250 bpm, regular

2. In orthodromic AVRT, the QRS complex is

often normal, wide QRS complex is with
antidromic AVRT
3. Retrograde P’ wave, R-P’>110ms.
PAROXYSMAL TACHYCARDIA
 Therapy:
 AVNRT & orthodromic AVRT
1. Increase vagal tone: carotid sinus massage,
Valsalva maneuver.if no successful,
2. Drug: verapamil, adrenosine, propafenone
3. DC shock
 Antidromic AVRT:
1. Should not use verapamil, digitalis, and
stimulate the vagal nerve.
2. Drug: propafenone, sotalol, amiodarone
 RFCA
 PRE-EXCITATION SYNDROME
(W-P-W SYNDROME)
 There are several type of accessory
pathway
1. Kent: adjacent atrial and ventricular
2. James: adjacent atrial and his bundle
3. Mahaim: adjacent lower part of the
AVN and ventricular
 Usually no structure heart disease,
occur in any age individual
WPW SYNDROME

 Manifestation:
 Palpitation, syncope, dizziness

 Arrhythmia: 80% tachycardia is AVRT,

15-30% is AFi, 5% is AF,
 May induce ventricular fibrillation
 WPW SYNDROME
 Therapy:
1. Pharmacologic therapy: orthodrome
AVRT or associated AF, AFi, may use Ic
and III class agents.
2. Antidromic AVRT can’t use digoxin and
verapamil.
3. DC shock: WPW with SVT, AF or Afi
produce agina, syncope and hypotension
4. RFCA
VENTRICULAR ARRHYTHMIA
VENTRICULAR PREMATURE
CONTRACTIONS (VPCS)
 Etiology:
1. Occur in normal person
2. Myocarditis, CAD, valve heart disease,
hyperthyroidism, Drug toxicity (digoxin,
quinidine and anti-anxiety drug)
3. electrolyte disturbance, anxiety, drinking,
coffee
VPCS

 Manifestation:
1. palpitation
2. dizziness
3. syncope
4. loss of the second heart sound
 PVCS
 Therapy: treat underlying disease, antiarrhythmia
 No structure heart disease:
1. Asymptom: no therapy
2. Symptom caused by PVCs: antianxiety agents, ß-
blocker and mexiletine to relief the symptom.
 With structure heart disease (CAD, HBP):
1. Treat the underlying diseas
2. ß-blocker, amiodarone
3. Class I especially class Ic agents should be avoided
because of proarrhytmia and lack of benefit of
prophylaxis
VENTRICULAR TACHYCARDIA

 Etiology: often in organic heart disease

CAD, MI, DCM, HCM, HF,
long QT syndrome
Brugada syndrome
 Sustained VT (>30s), Nonsustained VT

 Monomorphic VT, Polymorphic VT

VENTRICULAR TACHYCARDIA
 Torsades de points (Tdp): A special type of
polymorphic VT,
 Etiology:
1. congenital (Long QT),
2. electrolyte disturbance,
3. antiarrhythmia drug proarrhythmia (IA or IC),
4. antianxiety drug,
5. brain disease,
6. bradycardia
VENTRICULAR TACHYCARDIA

 Accelerated idioventricular rhythm:

1. Related to increase automatic tone
2. Etiology: Often occur in organic heart
disease, especially AMI reperfusion periods,
heart operation, myocarditis, digitalis
toxicity
 VT

 Manifestation:
1. Nonsustained VT with no symptom
2. Sustained VT : with symptom and
unstable hemodynamic, patient may
feel palpitation, short of breathness,
presyncope, syncope, angina,
hypotension and shock.
 VT

 ECG characteristics:
1. Monomorphic VT: 100-250 bpm, occur and
terminate abruptly,regular
2. Accelerated idioventricular rhythm: a runs of 3-10
ventricular beats, rate of 60-110 bpm, tachycardia
is a capable of warm up and close down, often seen
AV dissociation, fusion or capture beats
3. Tdp: rotation of the QRS axis around the baseline,
the rate from 160-280 bpm, QT interval prolonged
> 0.5s, marked U wave
 TREATMENT OF VT

1. Treat underlying disease

2. Cardioversion: Hemodynamic unstable
VT (hypotension, shock, angina, CHF)
or hemodynamic stable but drug was
no effect
3. Pharmacological therapy: ß-blockers,
lidocain or amiodarone
4. RFCA, ICD or surgical therapy
 THERAPY OF SPECIAL TYPE VT
 Accelerated idioventricular rhythm:
 usually no symptom, needn’t therapy.
 Atropine increased sinus rhythm
 Tdp:
1. Treat underlying disease,
2. Magnesium iv, atropine or isoprenaline, ß-
block or pacemaker for long QT patient
3. temporary pacemaker
VENTRICULAR FLUTTER AND
FIBRILLATION
 Often occur in severe organic heart disease:
AMI, ischemia heart disease
 Proarrhythmia (especially produce long QT
and Tdp), electrolyte disturbance
 Anaesthesia, lightning strike, electric shock,
heart operation
 It’s a fatal arrhythmia
VENTRICULAR FLUTTER AND
FIBRILLATION
 Manifestation:
Unconsciousness, twitch, no blood pressure
and pulse, going to die
 Therapy:
1. Cardio-Pulmonary Resuscitate (CPR)
2. ICD
CARDIAC CONDUCTION BLOCK

 Block position:
Sinoatrial; intra-atrial; atrioventricular; intra-
ventricular
 Block degree
1. Type I: prolong the conductive time
2. Type II: partial block
3. Type III: complete block
ATRIOVENTRICULAR BLOCK

 AV block is a delay or failure in transmission

of the cardiac impulse from atrium to
ventricle.
 Etiology:

Atherosclerotic heart disease; myocarditis;

rheumatic fever; cardiomyopathy; drug
toxicity; electrolyte disturbance, collagen
disease, lev’s disease.
AV BLOCK

 AV block is divided into three categories:

1. First-degree AV block
2. Second-degree AV block: further
subdivided into type I and type II
3. Third-degree AV block: complete block
 AV BLOCK

 Manifestations:
 First-degree AV block: almost no symptoms;

 Second degree AV block: palpitation, fatigue

 Third degree AV block: Dizziness, agina, heart

failure, lightheadedness, and syncope may
cause by slow heart rate, Adams-Stokes
Syndrome may occurs in sever case.
 First heart sound varies in intensity, will appear
booming first sound
FIRST DEGREE A-V HEART BLOCK
 Rate: variable
 P wave: normal
 QRS: normal
 Conduction: impulse originates in the SA node but has prolonged
conduction in the AV junction; P-R interval is > 0.20 seconds.
 Rhythm: regular
 This is the most common conduction disturbance. It occurs in both
healthy and diseased hearts.
 First degree AV block can be due to:
 inferior MI,
 digitalis toxicity
 hyperkalemia
 increased vagal tone
 acute rheumatic fever
 myocarditis.
 Interventions include treating the underlying cause and observing for
progression to a more advanced AV block.
SECOND DEGREE A-V BLOCK MOBITZ TYPE I
(WENCKEBACK)
 Rate: variable
 P wave: normal morphology with constant P-P interval
 QRS: normal
 Conduction: the P-R interval is progressively longer until one P wave is
blocked; the cycle begins again following the blocked P wave.
 Rhythm: irregular
 Second degree AV block type I occurs in the AV node above the Bundle of His.
 It is often transient and may be due to acute inferior MI or digitalis toxicity.
 Treatment is usually not indicated as this rhythm usually produces no
symptoms.
SECOND DEGREE A-V BLOCK MOBITZ
TYPE II
 Rate: variable
 P wave: normal with constant P-P intervals
 QRS: usually widened because this is usually associated with a bundle branch
block.
 Conduction: P-R interval may be normal or prolonged, but it is constant until
one P wave is not conducted to the ventricles.
 Rhythm: usually regular when AV conduction ratios are constant
 This block usually occurs below the Bundle of His and may progress into a
higher degree block.
 It can occur after an acute anterior MI due to damage in the bifurcation or the
bundle branches.
 It is more serious than the type I block.
 Treatment is usually artificial pacing.
THIRD DEGREE (COMPLETE)
A-V BLOCK
 Rate: atrial rate is usually normal; ventricular rate is usually less than 70/bpm.
The atrial rate is always faster than the ventricular rate.
 P wave: normal with constant P-P intervals, but not "married" to the QRS
complexes.
 QRS: may be normal or widened depending on where the escape pacemaker is
located in the conduction system
 Conduction: atrial and ventricular activities are unrelated due to the complete
blocking of the atrial impulses to the ventricles.
 Rhythm: irregular
 Complete block of the atrial impulses occurs at the A-V junction, common
bundle or bilateral bundle branches.
 Another pacemaker distal to the block takes over in order to activate the
ventricles or ventricular standstill will occur.
 May be caused by:
 digitalis toxicity
 acute infection
 MI and
 degeneration of the conductive tissue.
 Treatment modalities include:
 external pacing and atropine for acute, symptomatic episodes and
 permanent pacing for chronic complete heart block.
AV BLOCK

 Treatment:
1. I or II degree AV block needn’t
antibradycardia agent therapy
2. II degree II type and III degree AV block
need antibradycardia agent therapy
3. Implant Pace Maker
INTRAVENTRICULAR BLOCK

 Intraventricular conduction system:

1. Right bundle branch
2. Left bundle branch
3. Left anterior fascicular
4. Left posterior fascicular
INTRAVENTRICULAR BLOCK
 Etiology:
 Myocarditis, valve disease, cardiomyopathy,
CAD, hypertension, pulmonary heart
disease, drug toxicity, Lenegre disease,
Lev’s disease et al.
 Manifestation:
 Single fascicular or bifascicular block is
asymptom; tri-fascicular block may have
dizziness; palpitation, syncope and Adams-
stokes syndrome
 INTRAVENTRICULAR BLOCK

 Therapy:
1. Treat underlying disease
2. If the patient is asymptom; no treat,
3. bifascicular block and incomplete
trifascicular block may progress to
complete block, may need implant pace
maker if the patient with syncope
RIGHT BUNDLE BRANCH BLOCK
 Rate: variable
 P wave: normal if the underlying rhythm is sinus
 QRS: wide; > 0.12 seconds
 Conduction: This block occurs in the right or left bundle branches or in both.
The ventricle that is supplied by the blocked bundle is depolarized abnormally.
 Rhythm: regular or irregular depending on the underlying rhythm.
 Left bundle branch block is more ominous than right bundle branch block
because it usually is present in diseased hearts. Both may be caused by
hypertension, MI, or cardiomyopathy. A bifasicular block may progress to third
degree heart block.
 Treatment is artificial pacing for a bifasicular block that is associated with an
acute MI.
PVC BIGEMNY
 Rate: variable
 P wave: usually obscured by the QRS, PST or T wave of the PVC
 QRS: wide > 0.12 seconds; morphology is bizarre with the ST segment and the T wave
opposite in polarity. May be multifocal and exhibit different morphologies.
 Conduction: the impulse originates below the branching portion of the Bundle of His;
full compensatory pause is characteristic.
 Rhythm: irregular. PVC's may occur in singles, couplets or triplets; or in bigeminy,
trigeminy or quadrigeminy.

 PVCs can occur in healthy hearts. For example, an increase in circulating

catecholamines can cause PVCs. They also occur in diseased hearts and from
drug (such as digitalis) toxicities.
 Treatment is required if they are:
 associated with an acute MI,
 occur as couplets, bigeminy or trigeminy,
 are multifocal, or
 are frequent (>6/min).
 Interventions include:
 lidocaine,
 pronestyl, or
 quinidine.
VENTRICULAR TACHYCARDIA
 Rate: usually between 100 to 220/bpm, but can be as rapid as 250/bpm
 P wave: obscured if present and are unrelated to the QRS complexes.
 QRS: wide and bizarre morphology
 Conduction: as with PVCs
 Rhythm: three or more ventricular beats in a row; may be regular or irregular.
 Ventricular tachycardia almost always occurs in diseased hearts.
 Some common causes are:
 CAD
 acute MI
 digitalis toxicity
 CHF
 ventricular aneurysms.
 Patients are often symptomatic with this dysrhythmia.
 Ventricular tachycardia can quickly deteriorate into ventricular fibrillation.
 Electrical countershock is the intervention of choice if the patient is
symptomatic and rapidly deteriorating.
 Some pharmacological interventions include lidocaine, pronestyl, and
bretylium.
TORSADE DE POINTES
 Rate: usually between 150 to 220/bpm,
 P wave: obscured if present
 QRS: wide and bizarre morphology
 Conduction: as with PVCs
 Rhythm: Irregular
 Paroxysmal –starting and stopping suddenly
 Hallmark of this rhythm is the upward and downward deflection of the QRS
complexes around the baseline. The term Torsade de Pointes means "twisting
about the points."
 Consider it V-tach if it doesn’t respond to antiarrythmic therapy or treatments
 Caused by:
 drugs which lengthen the QT interval such as quinidine
 electrolyte imbalances, particularly hypokalemia
 myocardial ischemia
 Treatment:
 Synchronized cardioversion is indicated when the patient is unstable.
 IV magnesium
 IV Potassium to correct an electrolyte imbalance
 Overdrive pacing
VENTRICULAR FIBRILLATION
 Rate: unattainable
 P wave: may be present, but obscured by ventricular waves
 QRS: not apparent
 Conduction: chaotic electrical activity
 Rhythm: chaotic electrical activity
 This dysrhythmia results in the absence of cardiac output.
 Almost always occurs with serious heart disease, especially acute MI.
 The course of treatment for ventricular fibrillation includes:
 immediate defibrillation and ACLS protocols.
 Identification and treatment of the underlying cause is also needed.
 IDIOVENTRICULAR RHYTHM
 Rate: 20 to 40 beats per minute
 P wave: Absent
 QRS: Widened
 Conduction: Failure of primary pacemaker
 Rhythm: Regular
 Absent P wave
Widened QRS > 0.12 sec.
Also called " dying heart" rhythm
Pacemaker will most likely be needed to re-establish a normal heart rate.
 Causes:
 Myocardial Infarction
 Pacemaker Failure
 Metabolic imbalance
 Myoardial Ischemia
 Treatment goals include measures to improve cardiac output and establish a normal
rhythm and rate.
 Options include:
 Atropine
 Pacing
 Caution: Supressing the ventricular rhythm is contraindicated because that rhythm
protects the heart from complete standstill.
VENTRICULAR STANDSTILL (ASYSTOLE)
 Rate: none
 P wave: may be seen, but there is no ventricular response
 QRS: none
 Conduction: none
 Rhythm: none
 Asystole occurs most commonly following the termination of atrial, AV
junctional or ventricular tachycardias. This pause is usually insignificant.
 Asystole of longer duration in the presence of acute MI and CAD is frequently
fatal.
 Interventions include:
 CPR,
 artificial pacing, and
 atropine.
 Recognizing and Naming Beats & Rhythms

QRS is slightly different but still narrow,

Atrial Escape Beat 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

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
Ventricular
through the ventricles did not take place through normal
Escape Beat
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 Conduction Path

Slow Recovery 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
Conduction
Repolarizing Tissue
Tissue
(long refractory period)

Fast Conduction Path Slow Conduction Path

Slow Recovery 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 Conduction Path

Slow Recovery 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 Conduction Path

Slow Recovery 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 Ventricular Re-entry
• atrial tachycardia • ventricular tachycardia
• atrial fibrillation
• atrial flutter

Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular 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 (PVC’s, VPB’s, 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
• PVC’s are sometimes described by lay people as “skipped heart beats”

R on T
phenomemon

Multifocal Compensatory pause

PVC's after the occurance of a PVC
 Recognizing and Naming Beats & Rhythms
Characteristics of PVC's
• PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave)
• T-waves for PVC’s are usually large and opposite in polarity to terminal QRS
• Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle
• Every other beat being a PVC (bigeminy) may indicate coronary artery disease
• Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s

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

Unconverted V-tach r V-fib

sinus beats V-tach
 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 p-wave Capture beat - note that

in front of PVC and the PVC the complex is narrow
is narrower than the other enough to suggest normal
PVC’s – this indicates the ventricular conduction.
beat is a product of both This indicates that an
the sinus node and an atrial impulse has made it
ectopic ventricular focus through and conduction
through the ventricles is
relatively normal.
 Recognizing and Naming Beats & Rhythms

Premature Atrial Contractions (PAC’s):

• 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
• PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s)
• PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco
• PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy
• PAC’s may also precede PSVT

Non conducted PAC Non conducted PAC

PAC
distorting a T-wave
 Recognizing and Naming Beats & Rhythms

Premature Junctional Contractions (PJC’s):

• 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
• PJC’s 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 SVT’s
• 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 Note IRREGULAR

morphologies when the rhythm in the tachycardia
tachycardia begins
 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

Note REGULAR rhythm

Rhythm usually begins in the tachycardia
with PAC
ECG ARTIFACT
 Artifact occurs when something causes a disruption in
monitoring.

 Some common causes are:

 AC interference -causes 60 cycle artifact
 Muscle tremors
 Respiratory artifact-wandering baseline
 Loose electrode
 Broken lead wire
CARDIOVERSION

Synchronized shock with the QRS complex

PSVT

 TREAT UNDERLYING CAUSE

 DRUGS: ADENOSINE, β-BLOCKERS,
DIGOXIN, MS, QUINIDINE
 CAROTID / VAGAL MANEUVERS

 SYNCHRONIZED CARDIOVERSION IF UNSTABLE

VENTRICULAR ARRHYTHMIAS

 ORIGINATES IN VENTRICLES
 PATIENT MAY BE SYMPTOMATIC, REQUIRES
IMMEDIATE ATTENTION
 PVC, couplet, bigeminy, trigeminy

 V-TACH (ventricular tachycardia)

 V-Fib (Ventricular fibrillation)

PREMATURE VENTRICULAR CONTRACTION
(PVC)
 EARLY IRREGULAR VENTRICULAR BEATS
 QRS IS WIDE /BIZZARE

 CAN BE CHRONIC ASYMPTOMATIC

ABNORMALITY OR WARNING OF SERIOUS
DYSRHYTHMIA
PREMATURE VENTRICULAR CONTRACTION
(PVC)
 ETIOLOGY:

HYPOXIA
DIGOXIN TOXICITY
MECHANICAL STIMULATION
ELECTROLYTE (K) IMBALANCE
MI
PVCS
PREMATURE VENTRICULAR CONTRACTION
(PVC)
 CLINICAL SIGNS:
 DEPEND ON FREQUENCY
 PVC  SHORT DIASTOLIC FILLING TIME

 C.O.
 FREQUENT PVC – SENSATION OF PALPATIONS,
SKIPPED BEATS
 BIGEMINY – PVC EVERY OTHER BEAT

 TRIGEMINY – PVC EVERY 3RD BEAT

PREMATURE VENTRICULAR CONTRACTION
(PVC)

 TREATMENT:
 TREAT IMPAIRED HEMODYNAMICS
 ANTIARRHYTHMICS

 OXYGEN

 MONITOR FOR PVC LANDING ON

T-WAVE
 OBSERVE FOR UNIFOCAL (VS) MULTIFOCAL
VENTRICULAR ARRHYTHMIAS

 VENTRICULAR TACHYCARDIA
 3 OR MORE PVC’s
 QRS IS WIDE/ BIZARRE

EXTREMELY SERIOUS
MAY LEAD TO LETHAL RHYTHMS

 ETIOLOGY: SAME CAUSES AS PVC, ALSO

CARDIOMYOPATHY, MYOCARDIAL IRRITABILITY
VENTRICULAR TACHYCARDIA
TREATMENT

 VT /W PULSE - CARDIOVERT
 MONITOR MORE CLOSELY

 PREPARE FOR CARDIOVERSION

(O2, LIDOCAINE, TREAT CAUSE)

 VT W/O PULSE - DEFIBRILLATE
VENTRICULAR FIBRILLATION
TOTAL UNORGANIZED MULTIFOCAL
RHYTHM, VENTRICLES QUIVER,
NO CARDIAC OUTPUT
V-FIB

 ETIOLOGY:
SAME AS VT, PVC
SURGICAL MANIPULATION OF HEART
FAILED CARDIOVERSION
 CLINICAL SIGNS:
SAME AS CARDIAC ARREST
EKG SHOWS DISORGANIZED
RHYTHM
V-FIB

 TREATMENT

IMMEDIATE DEFIBRILLATION X3
CPR
SURVIVAL IS < 10% FOR EVERY MINUTE
THE PATIENT REMAINS IN V-fib
SCREAM FOR VFIB AND PULSELESS
VTACH
1.Shock360J* monophasic, 1st and subsequent
shocks.(Shock every 2 minutes if indicated)
2.CPR After shock, immediately begin chest
compressions followed by respirations (30:2
ratio) for 2 minutes.
3.Rhythm check after 2 minutes of CPR (and
after every 2 minutes of CPR thereafter) and
shock again if indicated. Check pulse only if an
organized or non-shockable rhythm is present.
SCREAM
CARDIAC ARREST
 VENTRICULAR ASYSTOLE
 80 – 90% DUE TO V-fib
 TOTAL ABSENCE OF ELECTRICAL AND
MECHANICAL ACTIVITY
 ETIOLOGY
TRAUMA
OVERDOSE
MI
 CLINICAL SIGNS
 ASYSTOLE or V-fib
 NO DEFINABLE WAVE FORMS
 ABSENCE OF VITAL SIGNS
VENTRICULAR ASYSTOLE

Acronym Comments
T Transcutaneous Only effective with early
Pacemaker implementaion
E Epinephrine 1 mg IV q3-5 min
A Atropine 1 mg IV q3-5 min
PEA- PULSELESS ELECTRICAL ACTIVITY

 Asystole Algorithm
PEA

 Problem search

 Epinephrine – 1mg IV/IO q3-5min

 Atropine- with a slow HR, I mg IV/IO q3-5min

 Consider termination of efforts if asystole

persists despite appropriate interventions.
CARDIAC ARREST
REVIEW ACLS GUIDELINES 2005
TREATMENT: IMMEDIATE CPR

A. AIRWAY/ ADVANCED AIRWAY CONTROL

B. BREATHING/ POSITIVE PRESSURE
VENTILATION
C. CIRCULATION/ CPR, START IV

D. DEFIBRILLATE (V-fib, V-tach ONLY)

E. DRUGS-Antidysrhythmic tx
CARDIAC ARREST

 EPINEPHRINE 1:10,000 IV PUSH

REPEAT Q 5 MIN.
 AMIODORONE:
 ATROPINE:
 VASOPRESSIN:
 CONSIDER ANTIARRHYTHMICS
 USE ACLS ALGORITHMS
CARDIAC ARREST

 TREATMENT: POST CARDIAC ARREST

MONITOR -
CARDIAC STATUS
RESPIRATORY STATUS
TREAT UNDERLYING CAUSE
EMOTIONAL SUPPORT
SAFE ENVIRONMENT
DEFBRILLATION (VS)
CARDIOVERSION

 DEFIBRILLATION
ASYNCHRONOUS ELECTRICAL DISCHARGE THAT
CAUSES DEPOLARIZATION OF ALL MYOCARDIAL CELLS
AT ONCE.
THIS ALLOWS (HOPEFULLY) THE SA NODE TO RESTORE
ITS PACEMAKER FUNCTION AND DICTATE A REGULAR
SINUS RHYTHM.
USED FOR PULSELESS V-tach AND V-fib
VOLTAGE: 200 – 360 joules (“stacked shock”)
or AED
CARDIOVERSION (AKA)
SYNCHRONIZED CONVERSION

ELECTRICAL IMPULSE IS DISCHARGED DURING QRS

(VENTRICULAR DEPOLARIZATION)
USUALLY TIMED /W CARDIAC MONITOR TO PREVENT
SHOCK ON
T-WAVE
USED FOR RAPID A-fib, V-tach /W PULSE AND
PERSISTENT PAT / PSVT
VOLTAGE: 50 – 100 joules
EQUIPMENT REVIEW
 DEFIBRILLATOR
SELECT ENERGY LEVEL, THEN CHARGE
 PADDLES
USE 25 POUNDS OF PRESSURE WHEN APPLIED TO CHEST,
Placed 2nd RICS and 5th LAAS
 CONDUCTING AGENT
GEL OR PAD WHICH ESTABLISHES SKIN CONTACT, REDUCES
SKIN BURNS
 JOULES
MEASUREMENT OF ELECTRICAL ENERGY
 DISCHARGES
NO ONE SHOULD COME IN CONTACT WITH PATIENT OR BED
DURING DISCHARGE
HEART BLOCK

 DEPRESSED CONDUCTION OF IMPULSE FROM ATRIA

TO VENTRICLES
 AV NODE BECOMES DEFECTIVE AND IMPULSES (P-
WAVES) ARE BLOCKED FROM BEING TRANSMITTED
TO VENTRICLES
FIRST DEGREE
SECOND DEGREE
TYPE I
TYPE II
THIRD DEGREE
1° HEART BLOCK

 PR INTERVAL > 0.20 SECONDS

 CAUSES:MAY BE NORMAL VARIANT
INFERIOR WALL MI
DRUGS: DIGOXIN
VERAPAMIL
 TREATMENT:
MONITOR
OBSERVE FOR SYMPTOMS
FIRST DEGREE HEART BLOCK
2° HEART BLOCK

 ONE OR MORE P-WAVES ARE NOT

CONDUCTED THROUGH THE VENTRICLE

 HEART RATE - VENTRICULAR RATE SLOW TO

NORMAL
ATRIAL RATE MAY BE 2 – 4 X’s
FASTER THAN VENTRICULAR
2° HEART BLOCK
CAUSES: ORGANIC HEART DISEASE
MI, Dig toxicity, B and Ca Channel Blockers
DIGOXIN TOXICITY
SYMPTOMS
 Tx:
Monitor HR
Atropine
Temporary pacemaker
Avoid meds that decrease conductivity
2 TYPES OF 2° HEART BLOCK
MOBITZ TYPE I- Wenkeback
MOBITZ TYPE II
SECOND DEGREE HEART BLOCK
MOBITZ I
 PRI becomes progressively longer until drops
QRS
SECOND DEGREE HEART BLOCK
MOBITZ TYPE II
 PRI constant and regular, but in a 2:1 , 3:1
pattern
3° HEART BLOCK
(COMPLETE HEART BLOCK)

 ATRIAL IMPULSES & VENTRICULAR RESPONSE ARE IN

TOTAL DISASSOCIATION
 P-WAVES ARE SEEN & ARE IRREGULAR
 QRS COMPLEX ARE SEEN & ARE IRREGULAR
(ESCAPE RHYTHM)
 NO CORRELATION BETWEEN P-WAVES & QRS
(RATE IS SLOW) – independent rhythms
3° HEART BLOCK
(COMPLETE HEART BLOCK)
 CAUSES
ORGANIC HEART DISEASE
MI
DRUGS
ELECTROLYTE IMBALANCE
EXCESS VAGAL TONE
 SIGNS & SYMPTOMS
EXTREME DIZZINESS
HYPOTENSION
SYNCOPE
S/S OF  C.O.
ALTERED MENTAL STATUS
NSR VS 3RD DEGREE BLOCK
3° HEART BLOCK
(COMPLETE HEART BLOCK)
 TREATMENT
PACEMAKER
TEMPORARY
OR
PERMANENT
PACEMAKER

 Indications: Speed up a slow HR or Slow down a rapid

HR
 ELECTRICAL DEVICE THAT DELIVERS CONTROLLED
ELECTRICAL STIMULUS THROUGH ELECTRODES
PLACED IN CONTACT WITH HEART MUSCLE
 2 PIECES
PULSE GENERATOR IMPLANTED IN CHEST WALL
UNDER R CLAVICLE
PACEMAKER ELECTRODES IMPLANTED IN
MYOCARDIAL TISSUE
PACED RHYTHM

 Pacemaker spike
PACEMAKER
 TEMPORARY
PACEMAKER
 USED IN EMERGENCY
SITUATION
 FIXED (COMPETITIVE)
PACEMAKER SENDS
STIMULUS TO
VENTRICLE AT A FIXED
RATE, REGARDLESS OF
VENTRICULAR ACTIVITY
TYPES OF PACEMAKERS

Use a 5 letter code

system, first 3 used
more often:
1. Chamber being
paced: A, V, D
2. Chamber being
sensed: A, V, D, O
3. Type of response by
the PM to the
sensing: I, T, D, O
PATIENT TEACHING
 Carry PM ID card
 MEDI ALERT BRACELET
 Avoid swimming, golf and weight lifting
 AVOID MRI
 Check PM q3-6 mos.
 PACEMAKER SURVEILANCE
 Monitor pulse rates
 Don’t hold cell phones over generators
AUTOMATIC IMPLANTABLE
CARDIOVERSION DEFIBRILLATOR (AICD)
 PROVIDES INTERNAL SHOCKS WHEN SERIOUS ARRHYTHMIA
IS DETECTED (V-tach OR V-fib)
 Has a pulse generator and a sensor that monitors the heart
 If pt has dysrhythmia it delivers a shock which the pt will feel

 USEFUL WHEN ARRHYTHMIA IS UNRESPONSIVE TO MEDS

OR SURGICAL ABLATION OR IRRITABLE MYOCARDIAL TISSUE
Ass Wr Wb

TERIMA KASIH