Aritmia

Content
 Physiology of normal cardiac
rhythm
 Definition and mechanisms of
arrhythmias
 Classification of drugs to treat
arrhythmias
 Important anti-arrhythmic drugs
(mechanism and pharmacological
characteristics)
 Arrhythmias in clinical practice
 Physiology of cardiac rate
and rhythm
 Cardiac myocytes are electrically excitable
 Resting intracellular voltage of myocardial
cells is negative -90mV (SA node is -40mV)
 Resting state - K+ inside and Na+ outside cell
(Na+/K+ pump)
 Action potential occurs when Na+ enters the
cell and sets up a depolarising current
 Stimulation of a single muscle fibre causes
electrical activity to spread across the
myocardium
 Phases of action potential of
cardiac cells
 Phase 0 rapid depolarisation
(inflow of Na+)
 Phase 1 partial repolarisation
(inward Na+ current Phase 1
deactivated, outflow of K+) IV
Phase 2
 Phase 2 plateau (slow inward0 mV
calcium current)
 Phase 3 repolarisation Phase 0 III
I Phase 3
(calcium current inactivates,
K+ outflow)
 Phase 4 pacemaker potential -80mV
Phase 4
(Slow Na+ inflow, slowing of II
K outflow) ‘autorhythmicity’
+

 Refractory period (phases

1-3)
 Sinus rhythm
 Sinoatrial node is
cardiac pacemaker
 Normal sinus rhythm
60-100 beats/min
 Depolarisation
triggers
depolarisation of
atrial myocardium
(‘forest fire’)
 Conducts more
slowly through AV
node
 Conducts rapidly
through His bundles
and Purkinje fibres
 Sinus rhythm
 Sinoatrial rate controlled by autonomic
nervous system
 Parasympathetic system predominates
(M2 muscarinic receptors)
 Sympathetic system (ß1 receptors)
• Increased heart rate (positive
chronotropic effect)
• Increased automaticity
• Facilitation of conduction of AV node
 ECG
 Recording of electrical activity of the heart
 Net sum of depolarisation and
repolarisation potentials of all myocardial
cells
 P-QRS-T pattern
 P - atrial depolarisation
 QRS - ventricular depolarisation
 T - ventricular repolarisation
 Definition of arrhythmia
 Cardiac arrhythmia is an abnormality
of the heart rhythm
 Bradycardia – heart rate slow (<60
beats/min)
 Tachycardia – heart rate fast (>100
beats/min)
 Mechanisms of arrhythmia
production
 Re-entry (refractory tissue reactivated
due to conduction block, causes abnormal
continuous circuit. eg accessory pathways
linking atria and ventricles in Wolff-
Parkinson-White syndrome)
 Abnormal pacemaker activity in non-
conducting/conducting tissue (eg
ischaemia)
 Delayed after-depolarisation
(automatic depolarisation of cardiac cell
triggers ectopic beats, can be caused by
drugs eg digoxin)
 CARDIAC ARRHYTHMIAS
 ETIOLOGY

• Sympathetic over-activity
• Electrolytes disturbances ( K, Ca, Mg )
• Acid – Base disturbances (Acidosis)
• Myocardial Ischemia
• Drugs (Cardiac & Non-cardiac)
• Myocardial diseases
• Over-stretching of myocardial fibers
• Other
 CARDIAC ARRHYTHMIAS
 IMPULSE PROPAGATION ARRHYTHMIAS

• RE-ENTRY ARRHYTHMIA:
 It´s the most common mechanism

• FACTORS REQUIRED:

 Unidirectional block

 A circuit length long enough to delay the impulse

propagation significantly to permit to the
previously depolarized cells recovery from the
A.R.P. to be in R.R.P. or repolarized.
 CARDIAC ARRHYTHMIAS
 IMPULSE PROPAGATION ARRHYTHMIAS

• PRE-EXCITATION SYNDROMES

• Occurrence: 1 in 1000

• Wolf-Parkinson-White Syndrome

• Long-Ganong-Levine Syndrome
 CARDIAC ARRHYTHMIAS
 TRIGGERED ACTIVITY

• Requires previous excitation by other action

potential

• Is associated with elevated intracellular Calcium

concentration

• Increased intracellular Calcium concentration

causes release of sarcoplasmic Calcium and
these increases the Sodium and Potassium
mebrane conductance
 CARDIAC ARRHYTHMIAS
 TRIGGERED ACTIVITY
Repeated Action Potential Stimuli

Calcium release from Sarcoplasmic Reticulum

Increase intracellular concentration of Ca

Incresed Membrane Conductance to Na & K

Progressive depolarization until Threshold

Potential is reached

Induction of an Action Potential development

“Premature Beat”
 Jenis Aritmia
 Sinus takikardi/sinus bradikardi
 Venticular -/Atrial – extrasystole
 Supra-ventricular tachycardia
 Ventricular tachycardia
 Atrial fibrillation
 Block
 Atrial fibrillation / Flutter

• Valvular heart disease (+++ mitral valve)

• Manipulation of right atrium (canulation)
• Electrolyte disturbances
• Hypovolemia
• Hyperthyroidism http://www.emedu.org
 Atrial fibrillation / Flutter

• Valvular heart disease (+++ mitral valve)

• Manipulation of right atrium (canulation)
• Electrolyte disturbances
• Hypovolemia
• Hyperthyroidism http://www.emedu.org
 Atrial fibrillation / Flutter

• Valvular heart disease (+++ mitral valve)

• Manipulation of right atrium (canulation)
• Electrolyte disturbances
• Hypovolemia
• Hyperthyroidism http://www.emedu.org
 Sinus tachycardia

• Awake patient ( + Hypertension)

• Hypovolemia
• Hypoxia
• Hyperthyroidism
http://www.emedu.org
 Supraventricular tachycardia

• Abnormal rhythm after weaning from CPB

• May be poorly tolerated
• Amiodarone

http://www.emedu.org
 Supraventricular tachycardia

• Abnormal rhythm after weaning from CPB

• May be poorly tolerated
• Amiodarone

http://www.emedu.org
 Supraventricular
tachycardia

• Abnormal rhythm after weaning from CPB

• May be poorly tolerated
• Amiodarone, adenosine
http://www.emedu.org
Supraventricular tachycardia

http://www.emedu.org
Supraventricular tachycardia

http://www.emedu.org
 Junctional tachycardia

• Valve surgery (+++)

http://www.emedu.org
 Ectopic atrial tachycardia

• Valve surgery (+++)

http://www.emedu.org
 Multifocal Atrial tachycardia

• Valve surgery (+++): Mitral, tricuspid

• COPD and advanced Pulmonary hypertension
http://www.emedu.org
http://www.emedu.org
Rhythm abnormalities
Ventricular level
 Ventricular fibrillation

• Mechanical arrest
• Great O2 consumption +++
• Before CPB: critical ischemia (Left main, severe CAD)
• During CPB: poor myocardial protection
• On weaning from CPB: Reperfusion
• After CPB: Myocardial ischemia, electrolyte disturbances
 PVC (ESV)

• Bigeminism
 PVC (ESV)

• paired
 PVC (ESV)

• Polymorphic
 PVC (ESV)

• Triplet
 PVC (ESV)

• Ischemic
• Ventricle irritation
http://www.emedu.org
PVC (ESV)

http://www.emedu.org
Ventricular tachycardia
 Ventricular tachycardia

• Mechanical arrest or severe hypotension

• Great O2 consumption +++
• Before CPB: critical ischemia (Left main, severe
CAD)
• After CPB: Myocardial ischemia, electrolyte
disturbances
• electroshock
http://www.emedu.org
 Conduction
abnormalities
 Sinus bradycardia

• Beta-blockers
• Calcium Channel blockers Katrina Kardos, MD
PGY-3
Albany Medical Center
 LBBB

• Preoperative: HTA, LVH, CHF, Ischemia

• New LBBB
– MI
Risk of complete
– poor myocardial protection
heart bloc with
– incomplete revascularization
Swan Ganz KT
– Technical problem with graft (Kink, Twist)
– Air embolism
– Lesion to conduction tissues (AVR, MVR) http://www.emedu.org
 Conduction System

His Bundle

L Bundle

R Bundle

Katrina Kardos, MD
PGY-3
Albany Medical Center
 RBBB

• Preoperative: Normal (10%), RVH

• New RBBB
– poor RV myocardial protection (imperfect retrograde
cardioplegia)
– incomplete revascularization to RCA
– Technical problem with graft (Kink, Twist) to RCA
– Air embolism in the RCA ostium (+++ valve surgery)
– Lesion to conduction tissues (tricuspid) http://www.emedu.org
 1st Degree AV block

• Beta blockers
• Frequent in elderly
• AV node (valve surgery, MI) http://www.emedu.org
 1st Degree AV block

• Beta blockers
• Frequent in elderly
• AV node (valve surgery, MI)
http://www.emedu.org
 2nd Degree AV block type 1

– Lesion to conduction tissues (AVR, MVR, TVR)

 2nd Degree AV block type 2

– Lesion to conduction tissues (AVR, MVR, TVR)

http://www.emedu.org
 3rd Degree AV block

– Lesion to conduction tissues (AVR, MVR, TVR)

http://www.emedu.org
Junctional Escape Rhythm

http://www.emedu.org
 CARDIAC ARRHYTHMIAS
 CLINICAL MANIFESTATIONS:

• ASYMPTOMATIC

• PALPITATIONS

• EMBOLISM

• LOW CARDIAC OUTPUT

 Hypotension
 Syncope

• HEART FAILURE
 Acute pulmonary edema
 Muscle weakness, fatigue

• MYOCARDIAL INFARCTION

• SUDDEN DEATH
Anti Arrhytmic drugs
Vaughan Williams classification
of antiarrhythmic drugs
 Class I: block sodium
channels
• Ia (quinidine,
procainamide, Phase 1
disopyramide) AP IV
Phase 2
• Ib (lignocaine) AP 0 mV
• Ic (flecainide) AP
 Class II: ß-adrenoceptor Phase 0 III
I Phase 3
antagonists (atenolol,
sotalol)
 Class III: prolong action -80mV Phase 4
potential and prolong II
refractory period (suppress
re-entrant rhythms)
(amiodarone, sotalol)
 Class IV: Calcium channel
antagonists. Impair impulse
propagation in nodal and
Mechanism of anti arrhythmias drug action
Decreased phase 4 slope
• β blocker

Increased threshold
•Na+ channel blocker
•Ca++ channel blocker

Increased max – diastolic potential

•Adenosine
•Acetylcholine

Increased action potential duration

•K+ channel blocker

Ant arrhythmic drugs can cause arrhythmias

Some arrhythmias should not be treated
 Classification of anti arrhythmia drugs
Sodium channel blocker
• Sodium channel (++)
• Diisopyramide, Quinidine, Procainamide
• Blocks K+ Efflux (+)
• Lidocaine, Mexiletine, Tocainide
• Sodium channel (+++)
• Flecainide, Encainide, Propafenone

Anti adrenergic
• β blocker

K+ channel Efflux blockers also Na+ blockers

• Amiodarone
• Sotalol

Ca++ channel blockers

• Verapamil & Diltiazem

Autonomic Effects
• Vagus stimulation
• Digoxin
• Adenosine receptor activation
• Adenosine
Farmakokinetik
O P Dosis Kadar Meta Eks Indikasi Efek samping
puncak b
KINIDIN + + 3 X 200 60 – 90’ H G/H AF, SVT
mg
PROKAINAMI + + 3X 45 – 70’ H G VES, SVT Lupus like
D (250000 – syndrome,
500) mg leukopeni
DIISOPIRAMI + - 3X 100 mg 60 – H G VES, SVT Mulut kering,
D 120’ konstipasi,
penglihatan
kabur
LIDOKAIN - + 1 MG/ KG H VT (pasca hipotensi
bb =1mg/ miokard
jam infark)
Hipotensi / Sinkop
PROPAFENON + + 3 x(150
Kardiovaskular - 60 – VES
300) mg 180’ •SA block
•QRS – Interval •AV block
•Long QT •Torsades de Poentes
• ↑ ventrikuler rate (efek
anti kolinergik)

Cinchonism

•Demam
•Tinitus
•Penglihatn kabur
•Diplopia
•Sakit kepala
•Delirium
•Prikosis
•Gangguan GIT
 Amiodaron
Farmakokinetik indikasi Efek samping
O P T1/2 Dosis VT, AF Pro aritmik,
Hipotensi, gangguan fungsi:
+ + 25 – 60 jam Loading hati, tiroid, paru & mata
600 s/d 800
mg/ hari
Maintenanc
e 300mg/
hari

Sotalol
Farmakokinetik indikasi Efek samping
O P T1/2 Dosis SVT, VT Gagal jantung
+ - 11 jam 800 s/d 320
mg/hari
 Bradicardy
Sinus Bradicardy
1. Ephedrine
2. Aminophyline
3. Atropine (I.V.)

Heart Block
1. Atropine (I.V.)
2. Temporary Pacemaker
3. Permanent Pacemaker
Permanent Pacemaker