Download Physiologic Basis and Mechanism of Cardiac Arrhythmias by Dr

MECHANISMS OF CARDIAC
ARRHYTHMIAS.
DR AMNA TAHIR
PHYSIOLOGY DEPARTMENT.
KEMU.
CRITERIA FOR NORMAL
CARDIAC RHYTHM
Heart Rate between 60-100 beats per minute
Every heart beat originate from SA node
All cardiac impulses should pass through normal
conduction pathway.
It should pass through normal pathway with
normal velocity.
TERMINOLOGIES
Brady arrhythmias
Tachy arrhythmias---100-150 simple
tachyarrhythmia
If 150-250 HR --paroxysmal tachy arrhythmia
If HR 250-350---flutters atrial or ventricular
If HR above350---fibrillation atrial or
ventricular(medical emergency)
If HR 40-60mild brady
If HR 20-40moderate
If HR <20severe
CLASSIFICATION ACCORDING TO
SITE OF ORIGIN OF ABNORMAL
RHYTHM.
From SA node—Sinus arrhythmias
From atrial muscle—atrial arrhythmias
From AV node—junctional or nodal arrhythmias
From ventricles---ventricular arrhythmias
First three are known as SVT or supraventricular tachy
arrhythmias.
MECHNISMS OF CARDIAC
ARRHYTHMIAS
1-Increased automaticity in any part of cardiac tissue
2-Triggered automaticity
3-Re-entry or Circus movement.
MECHANISMS OF ARRHYTHMIAS
1.
Abnormal impulse generation (abnormal
automaticity)
a. increased automaticity of normally automatic cells (SA, AV,
His)
b. generation of impulses in normally non-automatic cells
- development of phase 4 depolarization in normally
non-automatic cells
- ‘triggered activity’ due to afterdepolarizations
- early afterdepolarization
2.Abnormal impulse conduction (more common
mechanism)
a. AV block – ventricle free to start own pacemaker rhythm
b. Re-entry: re-excitation around a conducting loop, which
produces tachycardia
- unidirectional conduction block
- establishment of new loop of excitation
- conduction time that outlasts refractory period
INCREASED
AUTOMATICITY.
SA node under goes depolarization spontaneously. Why?
Under effect of sympathetic stimulation and sinus
tachycardia.
Early after depolarization or late after depolarization--triggered automaticity.injury or catecholamines—produce
cationic load leading to triggering.
ANS AND SINUS NODE FUNCTION
Early after depolarization or late
after depolarization---triggered
automaticity. Injury to myocardium
or catecholamine's or caffeine —
produce cationic load leading to
triggering.
MECHANISM OF TRIGGERED
ARRHYTHMIAS
MECHANISM OF TRIGGERED
ARRHYTHMIAS
RE-ENTRY.
If cardiac impulse moves around an electrically dead area
and on one side of this area impulse is blocked.The other
side impulse reaches the previously blocked area and finds it
excitable and enters into it .then it starts moving in circles
increasing the heart rate.
REENTRY
ARRHYTHMIAS
TYPICAL ATRIOVENTRICULAR
NODAL REENTRY TACHYCARDIA (
AVNRT)
SINO-ATRIAL NODE
Sinus arrhythmias
Sinus tachycardia
SINUS TACHYCARDIA.
SINUS BRADYCARDIA.
Athletes have increased vagal tone
Hypothyroidism
Hypothermia
Cholestasis jaundice –bile salts accumulate and slow down
SA node.
Sick sinus syndrome—is tachy- brady syndrome due to
variations in SA node firing.
ATRIAL
ARRHYTHMIAS.
Atrial tachycardia increased automaticity by sympathetic
stimulation
Atrial flutter re-entry F waves
Atrial fibrillation multiple ectopic foci f waves
ATRIAL FLUTTER.
AV NODE OR
JUNCTIONAL
ARRHYTHMIAS.
Av node specialized electrical connection between
atria and ventricles.
AV node is specialized in slow conduction.AVnodal delay.
Juntional tachy and brady arrhythmias.
RMP is -60 mv.fast Na channels are closed.
If something slow down AV node PR segment
prolonged.
Caffine increases AN node conduction and
shortening of PR segment.
AV NODAL OR
JUNCTIONAL BRADY
CARDIAS
Heart blocks.
WPW SYNDROME.
Re-entrent tachy cardia through bundle of Kent
Avoid coffee, smoking ,stress,anxiety.this can produce an
ectopic and start re-entry through the bundle of Kent.
The slurring of QRS and short PR-interval.PJ interval is
normal however.
VENTRICULAR ARRHYTHMIAS.
Irritable foci –extra systole.
Ischemia or injury—less oxygen supply—less ATP produced
–decreased Na-K pumping—cationic load in side vent
muscle cell—RMP fluctuate and when touches threshold
level it fires—giving rise to VPCs and V-Tach
Caffiene –inhibit phosphodiesterase and increase cAMP—
protein kinse A—phosphorylation of Ca Channels—cationic
load—Fluctuating RMP—late after depolarizations.
Ventricular Tachycardia.
Ventricular flutter
Ventricular fibrillation
CARDIAC BRADYARRHYTHMIA-RX
Treatment strategy
Factors
Short term Rx
Type of bradyarrhythmia
Treat reversible /
underlying causes
Severity of symptoms
Medication to increase
heart rate
Temporary pacemaker
Severity of underlying cardiac
pathology
Long term Rx
Permanent pacemaker
Severity of co-morbid
diseases
CARDIAC TACHYARRHYTHMIA - RX
STRATEGIES
Short term treatment
Electrical Therapy in unstable patients
Cardioversion, Defibrillation
Control ventricular rate
Ventricular rate control
Rhythm control: Medical / Electrical
Identify and treat reversible causes
Long term treatment
RF ablation
Medication
Anticoagulation
Devices (pacemaker, AICD)
Surgery
Considering factors
Type of tachyarrhythmia
Mechanism of tachyarrhythmia
Underlying Cardiovascular pathology
Local expertise
Patient factors
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