UNSWAGATI, CIREBON

dr. Irwan M. Loebis, SpJP.

Intrinsic Cardiac Conduction System
Phases of action potential of myocytes

• Phase 0 rapid depolarisation

(inflow of Na+)
• Phase 1 partial repolarisation
(inward Na+ current deactivated,
Phase 1
outflow of K+)
• Phase 2 plateau (slow inward Phase 2
calcium current) 0 mV
• Phase 3 repolarisation (calcium
current inactivates, K+ outflow) Phase 0
Phase 3
• Phase 4 pacemaker potential
(Slow Na+ inflow, slowing of K+
outflow) ‘autorhythmicity’ -90mV Phase 4
• Refractory period
Pacemaker Cells

Cells with natural automaticity; and do not have a

static resting potential
 Latent Pacemaker
Sinoatrial Node
Native Pacemaker;
Rate: 60 – 100x /min

Junctional
Latent / Ectopic
Pacemaker;
Rate: 40-60x /min

Ventricular
Latent/ Ectopic Pacemaker;
Rate: 30-40x /min

Latent Pacemaker will initiate impulses and take over the pacemaking function
if the SA node slows or fails to fire, or if conduction abnormalitites block the
normal wave of depolarization from reaching them (Escape Rhythm)
 DEFINITION

Arrhythmias ( also termed dysrhythmias ) is

defined as abnormalities of the electrical
rhythm caused by disorders in impulse
formation or disorders in impulse conduction,
or combination of both.
I. Disorders in impulse formation

1. Automaticity:
-Normal Automaticity
example: in sinus node
Clinical examples: Sinus tachycardia or bradycardia
-Abnormal activity
example: Depolarization-induced automaticity in Purkinje
fibers or ventricular muscle
Clinical example: possibly accelerated ventricular rhythms
after myocardial infarction
 Normal Automaticity…

• SA nodes Cells fastest inherent discharge rate 

dominant pacemaker
• Overdrive suppression: phenomenon that prevents
competition among the cells capable of pacemaker
activity in the heart  normal response of a normal
pacemaker cell to remain inhibited when it is driven
faster than its own spontaneous rate.
• Mediated by continous Na, K ATPase pump
 Overdrive suppression (OS)
Inhibition is mediated by:
- activity>> Na+/K+ pump

IF SINUS discharge rate SLOWS below the intrinsic

rate of the LATENT PACEMAKER LATENT.PM
becomes the dominant pacemaker.
Ex: Ectopic Impulse Formation (by normal
automaticity>> of latent. pacemakers)
 Overdrive suppression (OS)…

Other Inhibition:
- Sympathetic autonomic tone <<
- Sinus node dysfunction
- Impaired sinoatrial conduction
- Excessive local or circulating cathecolamines
AbNormal Automaticity (AbN A)

• AbN A  when spontaneous diastolic depolarization or automaticity in

working atrial and ventricular muscle (N= do not possess this property)
• Ex: N Resting Pot. (RP) = -90 mV, threshold pot. -50-(55) mV
• Ab N  RP << (less negative)  near threshold
• Ex: - MCI/ischemia
- autonomic >>, electrolyt, drugs, hypoxia, inflammation, fever
 Accelarated Automaticity (symphatetic)

• SA node and non SA node

• Sites, Terms, and rates of pacemaker tachs

site terms rate

Sinus node Sinus tachycardia 100-200

Atria Atrial tachycardia 100-200
Common bundle Accelarated junctional rythym 60-130
Accelarated ventricular rythm
Bundle branch 50-110
Accelarated Automaticity (symphatetic)

• Stimulate β1 reseptor to increases peacemaker channel

open (if)
• Shift the action potential thresold to more negative
Deccelarated Automaticity
(parasymphatetic)
• Three causes:
1. Physiologic slowing the sinus rate
2. Physiologic or pathologic enhancement of
parasymphatetic nervous activity
3. Pathologic pacemaker failure
Deccelarated Automaticity
(parasymphatetic)
• Cholinergic stimulation via teh vagus nerve
• Decreased of the probability of the pacemaker channel
being open (If)
• Shift the action potential thresold to less negative
• Increases of the K channel being open at rest
2. Triggered activity
-Early after depolarization
examples: EADs produced by barium, hypoxia, high
concentration of catecholamines, drugs such so sotalol, N-
acetyl procainamide, cesium
Clinical examples: possibly idiopathic and acquired long QT
syndroms and associated ventricular arrhytmias
-Delayed after depolarization
example: DADs produced in Purkinje fibers by digitalis
Clinical example: possibly some digitalis-induced arrythmias
 Triggered activity

Initiation of impulse by an After Depolarization (incompletely

cellular repolarization) :
A. Early after depolarization)
B. Delayed after depolarization

Caused:
1. Hypoxia, hypercarbia, local catecholamine cons.>,
ischemia, AMI
2. Stretching of myocardial cells, which unquestionably
occurs in failing hearts
3. Antiarrhytmial drugs  prolong repolarization
4. Digitalis glycosides<<Na+/K+ pump activity
II. Disorders in Impulse Conduction

Block:
1. normal conduction
2. Unidirectional block
3. Normal retrogade conduction
4. Slowed retrograde conduction
Arrhythmogenesis

ALTERED ALTERED
IMPULSE IMPULSE
FORMATION CONDUCTION
 Arrhythmogenesis (2)
Abnormality
Bradyarrhytmias
Altered Impulse Formation
 Decreased Automaticity
Altered Impulsed Conduction
 Conduction Blocks
Tachyarrhytmias
Altered Impulse Formation
 Sinus Node
 Ectopic Focus
Triggered Activity
 Early Afterdepolarization
 Delayed Afterdepolarization
Altered Impulsed Conduction
 Reentry
Anatomical
Functional
Mechanism Examples
Decreased phase 4 depolarization (i.e. Sinus Bradycardia
parasymphatetic stimulation)
Ischemic, Anatomic, drug induced First, Second, and Third
Degree AV Block
Increased phase 4 depolarization (i.e. Sinus Tachycardia
symphatetic stimulation)
Acquires phase 4 depolarization Ectopic Atrial Tachycardia
Prolonged action potential duration Torsade de Pointes
Intracellular calcium overload APBs, VPBs, Digitalis
Induced
Unidirectional Block plus slowed Atrial Flutter, AV Nodal
conduction reentrant tachycardia
Atrial Fibrilation,
Ventricular Fibrilation
Mechanism of Reentry (2)

Usually occurs in: Fibrosis, infarction scars

Reentry could happen through:
• Certain and fixed path  Monomorphic tachycardia
• No stable, fixed path  Polymorphic Ventricular
Tachycardia, i.e. fibrilation or Atrium or Ventricle
Reentry mechanism is responsible for Paroxysmal
Supraventicular Tachycardia, Atrial Flutter &
Fibrillation, Ventricular Tachycardia & Fibrilation.
 AVNRT and AVRT
AVNRT
presence of dual AV node
pathways (designated a and b or
slow and fast, respectively) each
with slightly differing conduction
and refractory periods. An
extrasystole exposes the
differing properties of the two
pathways and often initiates
tachycardia
AVRT
Presence of a second
connection between the atria
and ventricles (normally, the AV
node is the only connection
between atria and ventricles).
This connection is called an
accessory atrioventricular (AV)
pathway
Wolf Parkinson White (WPW) Syndrome
Sinus Bradycardia

• HR< 60 bpm; every QRS narrow, preceded by p wave

• Can be normal in well-conditioned athletes
• HR can be<30 bpm in children, young adults during
sleep, with up to 2 sec pauses
Sinus bradycardia--etiologies

• Normal aging
• 15-25% Acute MI, esp. affecting inferior wall
• Hypothyroidism, infiltrative diseases
(sarcoid, amyloid)
• Hypothermia, hypokalemia
• SLE, collagen vasc diseases
• Situational: micturation, coughing
• Drugs: beta-blockers, digitalis, calcium channel
blockers, amiodarone, cimetidine, lithium
Sinus bradycardia--treatment

• No treatment if asymptomatic
• Sxs include chest pain (from coronary
hypoperfusion), syncope, dizziness
• Office: Evaluate medicine regimen—stop all
drugs that may cause
• Bradycardia associated with MI will often
resolve as MI is resolving; will not be the sole
sxs of MI
• ER: Atropine if hemodynamic compromise,
syncope, chest pain
• Pacing
Sinus Arrhythmia

• Variations in the cycle lengths between p waves/ QRS

complexes
• Will often sound irregular on exam
• Normal p waves, PR interval, normal, narrow QRS
Sinus arrhythmia

• Usually respiratory--Increase in heart rate

during inspiration
• Exaggerated in children, young adults and
athletes—decreases with age
• Usually asymptomatic, no treatment or
referral
• Can be non-respiratory, often in normal or
diseased heart, seen in digitalis toxicity
• Referral may be necessary if not clearly
respiratory, history of heart disease
Sick Sinus Syndrome

•All result in bradycardia

•Sinus bradycardia (rate of ~43 bpm) with a sinus
pause
•Often result of tachy-brady syndrome: where a burst of
atrial tachycardia (such as afib) is then followed by a
long, symptomatic sinus pause/arrest, with no
breakthrough junctional rhythm.
Sick Sinus Syndrome--etiology

• Often due to sinus node fibrosis, SNode

arterial atherosclerosis, inflammation
(Rheumatic fever, amyloid, sarcoid)
• Occurs in congenital and acquired heart
disease and after surgery
• Hypothyroidism, hypothermia
• Drugs: digitalis, lithium, cimetidine,
methyldopa, reserpine, clonidine, amiodarone
• Most patients are elderly, may or may not
have symptoms
Sick sinus syndrome--treatment

• Address and treat cardiac conditions

• Review med list, TSH
• Pacemaker for most is required
Approach to Tachycardia
Sinus Tachycardia

• HR > 100 bpm, regular

• Often difficult to distinguish p and t waves
Sinus tachycardia--etiologies

• Fever • Hypotension and shock

• Hyperthyroidism • Pulmonary embolism
• Effective volume • Acute coronary
depletion ischemia and
• Anxiety myocardial infarction
• Pheochromocytoma • Heart failure
• Sepsis • Chronic pulmonary
• Anemia disease
• Exposure to stimulants • Hypoxia
(nicotine, caffeine) or
illicit drugs
Sinus Tachycardia--treatment

• Office: evaluate/treat potential etiology :check TSH, CBC,

optimize CHF or COPD regimen, evaluate recent OTC
drugs
• Verify it is sinus rhythm
• If no etiology is found and is bothersome to patients, can
treat with beta-blocker
Paroxysmal Supraventricular Tachycardia

• Refers to supraventricular tachycardia other than

afib, aflutter and MAT
• Occurs in 35 per 100,000 person-years
• Usually due to reentry—AVNRT or AVRT
Management of PSVTs
Atrial Fibrillation

• Irregular rhythm
• Absence of definite p waves
• Narrow QRS
• Can be accompanied by rapid ventricular response
PAC

• P wave from another atrial focus

• Occurs earlier in cycle
• Different morphology of p wave
PAC

• Benign, common cause of perceived irregular rhythm

• Can cause sxs: “skipping” beats, palpitations
• No treatment, reassurance
• With sxs, may advise to stop smoking, decrease caffeine
and ETOH
• Can use beta-blockers to reduce frequency
1st Degree AV Block

• PR interval >200ms
• If accompanied by wide QRS, refer to cardiology, high
risk of progression to 2nd and 3rd deg block
• Otherwise, benign if asymptomatic
2nd Degree AV Block Mobitz type I
(Wenckebach)

• Progressive PR longation, with eventual non-

conduction of a p wave
• May be in 2:1 or 3:1
Wenckebach, Mobitz type I

• Usually asymptomatic, but with accompanying

bradycardia can cause angina, syncope esp in elderly—
will need pacing if sxs
• Also can be caused by drugs that slow conduction (BB,
CCB, dig)
• 2-10% long distance runners
• Correct if reversible cause, avoid meds that block
conduction
2 nd degree block Type II (Mobitz 2)

• Normal PR intervals with sudden failure of a p wave to

conduct
• Usually below AV node and accompanied by BBB or
fascicular block
• Often causes pre/syncope; exercise worsens sxs
• Generally need pacing, possibly urgently if symptomatic
3rd Degree AV Block

• Complete AV disassociation, HR is a ventricular rate

• Will often cause dizziness, syncope, angina, heart
failure
• Can degenerate to Vtach and Vfib
• Will need pacing, urgent referral
PVC

• Extremely common throughout the population, both with

and without heart disease
• Usually asymptomatic, except rarely dizziness or fatigue
in patients that have frequent PVCs and significant LV
dysfunction
PVC

• No treatment is necessary, risk outweighs benefit

• Reassurance
• Optimize cardiac and pulmonary disease management
 Non-sustained Ventricular tachycardia

• Defined as 3 or more consecutive ventricular beats

• Rate of >120 bpm, lasting less than 30 seconds
• May be discovered on Holter, or other exercise testing
Non-sustained ventricular
tachycardia
• Need to exclude heart disease with Echo and
stress testing
• If normal, there is no increased risk of death
• May need anti-arrhythmia treatment if sxs
• In presence of heart disease, increased risk
of sudden death
• Need referral for EPS and/or prolonged Holter
monitoring
Ventricular fibrillation

• Defibrillation
Vaughan Williams classification of
antiarrhythmic drugs

• Class I: block sodium channels

– Ia (quinidine, procainamide,
disopyramide) AP
– Ib (lignocaine) AP Phase 1
IV
– Ic (flecainide) AP Phase 2
• Class II: ß-adrenoceptor 0 mV
antagonists (atenolol, sotalol)
• Class III: prolong action Phase III
I Phase 3
potential and prolong refractory 0
period (suppress re-entrant
rhythms) (amiodarone, sotalol) -80mV Phase 4
• Class IV: Calcium channel II
antagonists. Impair impulse
propagation in nodal and
damaged areas (verapamil)
Proarrhythmia

• Ventricular
– Torsades de pointes (class IA, III)
– Sustained monomorphic VT (class IC)
– Sudden death in coronary disease
(class IC)
• Atrial
– Increased arrhythmias
– Conversion to atrial flutter (usually
class IC)
• Abnormal conduction/impulse formation
– Increased ventricular rate during AF
(class IA, IC)
– Sinus/AV-nodal dysfunction (nearly all
drugs)
• Altered defibrillation thresholds (class I)
Indications for Pacemaker
Intracardiac Defibrillators (ICD)