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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
andarerhythm
Cardiac myocytes 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 (1 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:
Its 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
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
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
1 Degree AV block
st

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

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

Lesion to conduction tissues (AVR, MVR, TVR)


2 Degree AV block type 2
nd

Lesion to conduction tissues (AVR, MVR, TVR)

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

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,
disopyramide) AP
Ib (lignocaine) AP Phase 1
Ic (flecainide) AP IV
Class II: -adrenoceptor Phase 2
0 mV
antagonists (atenolol, sotalol)
Class III: prolong action
potential and prolong refractory Phase 0 III
I Phase 3
period (suppress re-entrant
rhythms) (amiodarone, sotalol)
Class IV: Calcium channel
-80mV Phase 4
antagonists. Impair impulse
propagation in nodal and II
damaged areas (verapamil)
Mechanism of anti arrhythmias drug action

Ant arrhythmic drugs can cause arrhythmias


Some arrhythmias should not be treated
Classification of anti arrhythmia drugs
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)
PROPAFENON + + 3 x(150 60 VES
-300) mg 180

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 600 hati, tiroid, paru & mata
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