MECHANISMS OF CARDIAC ARRHYTHMIAS. DR AMNA TAHIR PHYSIOLOGY DEPARTMENT. KEMU.
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Transcript of MECHANISMS OF CARDIAC ARRHYTHMIAS. DR AMNA TAHIR PHYSIOLOGY DEPARTMENT. KEMU.
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.
TERMINOLOGIESBrady 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 afterdepolarization2.Abnormal impulse conduction (more common
mechanism)a. AV block – ventricle free to start own pacemaker rhythmb. 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.AV-nodal 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-RXTreatment strategy
Short term Rx
Treat reversible / underlying causes
Medication to increase heart rate
Temporary pacemaker
Long term Rx
Permanent pacemaker
Factors
Type of bradyarrhythmia
Severity of symptoms
Severity of underlying cardiac pathology
Severity of co-morbid diseases
CARDIAC TACHYARRHYTHMIA - RX STRATEGIES
Long term treatmentRF ablationMedicationAnticoagulationDevices (pacemaker, AICD)Surgery
Short term treatmentElectrical Therapy in unstable patients
Cardioversion, Defibrillation Control ventricular rate
Ventricular rate controlRhythm control: Medical / Electrical
Identify and treat reversible causes
Considering factorsType of tachyarrhythmiaMechanism of tachyarrhythmiaUnderlying Cardiovascular pathologyLocal expertisePatient factors
THANK YOU FOR YOUR ATTENTION