PHASES OF ACTION POTENTIAL

Phase 2
Phase 1
>Plateau Stage
>Limited depolarization
>Cell less permeable to Na+ Phase 3
>Inactivation of fast
>Ca++ influx through slow >Rapid repolarization
Na+ channels→ Na+
Ca++ channels >Na+ gates closed
ion conc equalizes
>K+ begins to leave cell >K+ efflux
>↑ K+ efflux & Cl- influx
>Inactivation of slow
Ca++ channels

Phase 0
Phase 4
>Rapid depolarization
>Resting Membrane Potential
>Opening fast Na+
>High K+ efflux
channels→ Na+ rushes in
>Ca++ influx
→depolarization
Electrical Properties
of Cardiac cells

Property Discharge Resting Velocity Fiber AP

Rate Potentials Diameter Morphology
x/mnt mV m/sec μm
SA Node 60 – 100 -50 to -60 <0.05 5 – 10

Atrial -80 to -90 0.3 – 0.4 10 – 15

Myocard

AV Node 45 – 50 -60 to -70 0.1 1 – 10

Purkinje 25- 40 -90 to -95 2–3 100

Fibers

Ventricle 25 – 40 -80 to -90 0.3 – 0.4 10 – 15

Myocard
 Gelombang P
• Depolarisasi atrium
• Menentukan apa iramanya (rhytm)

5
6
PR Interval

7
Kompleks QRS

8
QRS Complex
ST Segment
 Periode ventrikel dalam fase recovery, diukur dari akhir
gelombang S (J point) sampai awal gelombang T.
 Normal berada pada garis isoelektrik dan menandakan awal
repolarisasi ventrikel
Mechanism of Cardiac
Arrhythmias

Tachyarrhythmias
 Automaticity
 Automaticity Abnormal Triggered Unidirectional
of Latent
of SA Node Automaticity activity block & reentry
Pacemakers

Enhanced
Automaticity

 Automaticity Conduction Block

of SA Node

Bradyarrhythmias

Issa, Ziad. Clinical Arrhythmology and Electrophysiology.

Leonard S. Lilly Pathophysiology of Heart Disease 4th Ed.
Sinus Node Dysfunction
Classified as :
Intrinsic
Degenerative, iatrogenic, ischemic
Extrinsic
Neurogenic, pharmacologic, electrolyte disturbances

Manifested as syncope, dizziness. Commonly due to tachycardic-

bradycardic syndrome, age >50 yo
ECG should be obtained while symptoms occurs
If frequent use holter monitoring, if infrequent, use cardiac event
monitoring or implantable loop
Other tests : autonomic modulation using drugs or valsava manuvre
(>3 s of sinus pause). EP required only the non invasive testing
results in unconclusive
ECG on SND
SB < 60bpm is abN when persistent and inapropriate to activity whereas < 40 bpm considered abN
Sinus arrest/pause > 3seconds considered abN
Sinus exit block has fixed P-P interval
Wekenbach type has periodicity
 AV Block
Etiologies :
Congenital (VSD AV, TGA, Epstein)
Acquired
Drugs (Digoxin, BB, CCB, Antiarrhythmics agents)
MI
Type I, II.1 benign, due to hypertonic vagal
Type II.2, III due to AVN ischemia/infarction
In inferior MI  hypertonic vagal tone
Anterior MI  BB infarction
Degenerative
Rheumatic disease
Iatrogenic
Vagally mediated
 AV Block
Diagnosis
ECG
Autonomic modulation
Exercise test
Exercise/atropine improve supranodal block
While it worsens infranodal block
EP study
Only for symptomatic who had uncaptured bradycardic
episodes
 AV Block
Classification
Type I
Prolongation in atrial, AVN,
or HBS
Type II.1
Prolonged RP of the AVN
RP dependent PR interval
Type II.2
Fixed PR intervals
Type III
AV dissociation
Narrow Complex
Tachycardias

Sinus Tachycardia SVT Atrial Atrial

Flutter Fibrilation
Sinus Rate > 100 Reentrant Automatic Atrial Rate Atrial Rate
-AVNRT -Atrial 300±50 400±50
-AVRT - Unifocal
-Intraatrial - Multifocal
-Sinoatrial -Junctional
- Paroxysmal
- Nonparoxysmal
Atrial Rate 200 ±50

Baltazar. Basic and Bedside Electrocardiography.

Atrial Tachycardia

Regular atrial rhythms 100 – 240 bpm originating outside the SA node
Most focal AT originated form RA and 2/3 of this along crista terminalis from SA to CS-AV
junction (line of fire)
Non paroxysmal AT frequently found in pts with digitalis toxicity or structural heart disease,
theophyline, beta agonist, COPD.
Often related with some acute event such as pulmonary infection, hypoxia, AMI, alcohol
excess
23 % of all SVTs in pts>70 yo
Frequently associated with structural heart disease and AV block
Atrial Tachycardia

Narrow QRS >100 bpm

Ectopic uniform P waves
P wave flat baseline
Can occur with AV block
terminates with QRS complex
PR int < RP int
Commonly appears in short
periods
Multifocal Atrial
Tachycardia

At least 3 consecutive p waves in different morphology

Irregular PR and RR intervals with isoelectric baseline between p waves
Commonly seen in elderly with COPD exacerbation, electrolyte imbalances, pulmonary infection
Junctional Tachycardia

If p wave preceeds QRS,

PR interval < 0.12 s
HR 100 – 120 bpm
If p wave follows QRS, RP
duration < 0.20 s
Self limitting in most
cases
Frequently comes with SND
or structural heart disease,
electrolyte imbalance
Incessant type can cause
tachymyopathy
SVT  AVNRT
The most commont of the PSVT
(50 to 60 %)
Classified as typical and atypical form
Slow-fast path (short RP interval)
Fast-slow path (long RP interval)
Often become manifest in teenager
Frequently paroxysmal in nature
and not associated with structural
heart disease
Chronic management needed for
those who develop highly symptomtic
SVT and need ER visit for termination
Catheter ablation is the first choice
Infrequent AVNRT can be treated
using pill in pocket method
AVNRT
WPW Low Risk
WPW syndrome characterized by : Intermittent
Short PR interval Delta waves disappear in stress test
Delta waves
Asymptomatic
ST-T segment abnormalities
Disappear with procainamide
Paroxysmal AF occurs in 5-% on WPW patients
High Risk
Most patients are asymptomatic and discoered accidentally
Mortality due to SCD in WPW syndrome is low (0.39%) Short ERP
Presence of delta waves in stress test
History of VF
Ebstein anomaly
Multiple BT
AVRT
Consist of :
Ortodromic conduction
Antidromic conduction
Bypass tract involvement
RP interval > 80 ms
Retrograde unembeded p
wave in inferior leads
Not associated with AV block
RP int<PR int on typical
form
Ussualy no apparent
structural heart disease
Atrial Flutter
Atrial activity present with obvious flutter waves in a
sawtooth pattern negative in inferior leads and + in V1
2:1 conduction mostly occurs
Paroxysmal AFL can occur in pts with no structural
heart disease (lone AFL) but it is rare 1.7%
Chronic AFL ussualy comes with structural heart
disease
AFL contributes 15% of all SVT and 25-30%
frequently coexist with AF

60 % occurs as part of exacerbation of pulmonary

disease, AMI, cardiopulmonary surgery
Th/ using ibutilide, amiodarone, sotalol, class IC
Rate control using AVN blocking agents
Chronic th/ RF ablation
Stroke prevention needed, using same score as AF
Macroreentrant AT/atypical AFL commonly found in
adults with congenital heart disease
Atypical AFL is difficult to distinguished with typical
AFL, thus requires EP study
Approach on Narrow
Complex Tachycardias
Post MI Ventricular Tachycardia
Sustained VT : VT runs > 30s or requires intervention
< 30s due to hemodynamic compremise
Non-sustained VT : VT runs > 3 complexes< 30s
Sustained Monomorphic VT most commonly caused by
post MI myocardial scar
STEMI pts had VT alone in 3.5% of all and VT/VF in
2% of cases

SMVT that develops 2 days post AMI indicated a a

large infarction, LV dysfunction and a worse prognosis
First line treatment with amiodarone, lidocaine is not
effective in the absence of ischemia
Chronic therapy with ICD and amiodarone
Idiopathic VT accounts for 10% of VTs has no proved
structural heart disease
Idiopathic VT
Idiopathic VT accounts for 10% of VTs
has no prove for structural heart disease,
CAD, ARVD
Adenosine sensitive VT caused by cAMP
mediated DADs
90% of idiopathic VT are adenosine
sensitive, whereas 60-80% originated
from RVOT

Acute Management using DC

cardioversion or Adenosine, Verapamil if
good LV function
Chronic management: BB, CCB NDHP,
catheter ablation if symptomatic, drug-
refractory VT, drug intolerant, undesired
long term drug therapy
BBR VT is the reentrant arrhythmias
usually occurs in DCM (45%)
Present as non specific intraventricular
conduction delay an LBBB pattern
 Atrial Fibrilation
The most common of
sustained cardiac arrhythmias
Accounts for 20% of stroke
etiology
Pathophysiology of AF
Triggers
Mostly EADs or DADs
from PVs inlet
Maintenance
Short AP duration
slowed conduction
AF begets AF
electrical remodelling
structural remodelling
Contractile remodelling
atrial endothelial
remodelling
 Initial Evaluation • hh
Determination of the AF
pattern
Determining underlying
cause
Echocardiogram
Thyroid function test
Renal Function test
Defining associated
cardiac and non cardiac
conditions
Acute Treatment
Rate Control
BB, NDP CCB, Digoxin,
Amiodarone
Cardioversion
Pharmacologic
Flecainide, Ibutilide,
Propafenone,
Amiodarone,
Vernakalant
DC conversion
Pretreatment on
antiarrhythmic agents
prior DCC increase the
successs rate
Long Term Management

Prevention of systemic embolization

Warfarin therapy and/or
antithrombotic agents
Symptom relieve
Optimal management on
concomitant disease
Rate control
Optimal resting HR (<80-110
bpm)
AVN blocking agents
Amiodarone in hemodynamic
comprise
Rhythm control
Antiarrhythmic agents
Rate vs. Rhythm control
• SELAMAT BELAJAR