Arrythmia-I.pptx
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This document provides information on supraventricular tachycardia (SVT), including: - The anatomy and conduction system of the heart that is relevant to SVT. - The mechanisms that can cause cardiac arrhythmias, including disorders of impulse formation, conduction, and combinations of the two. - Characteristics used to classify different types of arrhythmias based on rate, rhythm, site of origin, and QRS morphology. - Specific types of SVT like atrial fibrillation, AV nodal reentry tachycardia, and accessory pathway mediated tachycardias. - Methods for diagnosing and treating SVT such as electrophysiology studies, catheter ablation
![Mechanism of arrythmia
Disorder Experimental Examples Clinical examples
Disorders of Impulse Formation
Automaticity
Normal automaticity Normal in vivo or in vitro in SA nodal, AV nodal, and Purkinje cells Sinus tachycardia or bradycardia inappropriate for the clinical situation; possibly
ventricular parasystole
Abnormal automaticity Depolarization-induced automaticity in Purkinje myocytes Accelerated ventricular rhythms after myocardial infarction
Triggered Activity
EADs Drugs (sotalol, N -acetylprocainamide, terfenadine, erythromycin), cesium, barium, low
[K + ] o
Acquired LQTS and associated ventricular arrhythmias
DADs Gain-of-function mutations in the gene encoding RyR2 Catecholaminergic polymorphic ventricular tachycardia; atrial ectopic beats
Disorders of Impulse Conduction
Block and Reentry
Bidirectional or unidirectional without reentry SA, AV, bundle branch, Purkinje muscle Sinoatrial, AV, bundle branch block
Unidirectional block with reentry AV node, Purkinje-muscle junction, infarcted myocardium Reciprocating tachycardia in Wolff-Parkinson-White syndrome, AV nodal reentry
tachycardia, ventricular tachycardia caused by bundle branch reentry
Combined Disorders
Interactions between automatic foci Depolarizing or hyperpolarizing subthreshold stimuli speed or slow the automatic discharge
rate
Modulated parasystole
Interactions between automaticity and conduction Deceleration-dependent block, overdrive suppression of conduction, entrance and exit block Similar to experimental](https://image.slidesharecdn.com/arrythmia-i-220721065328-dbe152a0/85/Arrythmia-I-pptx-10-320.jpg)
Arrythmia-I.pptx
- 4. CONDUCTIION SYSTEM OF THE HEART
- 5. Currents and channels involved in generating resting membrane and action potentials
- 6. Transmembrane Potentials in Heart Cells Property Sa Nodal Cell Atrial Myocyte Av Nodal Cell His Purkinje Cell Ventricular Myocyte Resting potential (mV) −50 to −60 −80 to −90 −60 to −70 −90 to −95 −80 to −90 Action Potential Features Amplitude (mV) 60–70 110–120 70–80 120 110–120 Overshoot (mV) 0–10 30 5–15 30 30 Duration (msec) 100–300 100–300 100–300 300–500 200–300 V ̇max (V/sec) 1–10 100–200 5–15 500–700 100–200 Propagation velocity (m/sec) <0.05 0.3–0.4 0.1 2–3 0.3–0.4 Fiber diameter (μm) 5–10 10–15 1–10 100 10–15
- 7. Funny current in the SA node
- 8. Action potentials in the heart
- 9. CARDIAC CHANNELS AND ACTION POTENTIAL
- 10. Mechanism of arrythmia Disorder Experimental Examples Clinical examples Disorders of Impulse Formation Automaticity Normal automaticity Normal in vivo or in vitro in SA nodal, AV nodal, and Purkinje cells Sinus tachycardia or bradycardia inappropriate for the clinical situation; possibly ventricular parasystole Abnormal automaticity Depolarization-induced automaticity in Purkinje myocytes Accelerated ventricular rhythms after myocardial infarction Triggered Activity EADs Drugs (sotalol, N -acetylprocainamide, terfenadine, erythromycin), cesium, barium, low [K + ] o Acquired LQTS and associated ventricular arrhythmias DADs Gain-of-function mutations in the gene encoding RyR2 Catecholaminergic polymorphic ventricular tachycardia; atrial ectopic beats Disorders of Impulse Conduction Block and Reentry Bidirectional or unidirectional without reentry SA, AV, bundle branch, Purkinje muscle Sinoatrial, AV, bundle branch block Unidirectional block with reentry AV node, Purkinje-muscle junction, infarcted myocardium Reciprocating tachycardia in Wolff-Parkinson-White syndrome, AV nodal reentry tachycardia, ventricular tachycardia caused by bundle branch reentry Combined Disorders Interactions between automatic foci Depolarizing or hyperpolarizing subthreshold stimuli speed or slow the automatic discharge rate Modulated parasystole Interactions between automaticity and conduction Deceleration-dependent block, overdrive suppression of conduction, entrance and exit block Similar to experimental
- 11. RHYTHM
- 12. Arrythmia • Abnormal rate/minute :Tachycardia or Bradycardia with or without • Abnormal morphology of P or QRS
- 13. Classification cardiac arrythmia Description Effect RATE TACHY OR BRADY RHYTHM REGULAR OR IRREGULAR SITE SUPRAVENTRICULAR OR VENTRICULAR MORPHOLOGY OF QRS NARROW OR WIDE
- 15. Why does arrythmia occurs • Impulse formation disorder • Automaticity • Trigger Activity • Impulse conduction disorder • Combined Impulse formation and conduction disorder
- 17. When QRS is wide or narrow during tachy • Narrow :QRS width < 120 milli sec • Wide :QRS width >120 milli sec • When the depolarization current propagates directly through the ventricular muscle ,it is wide because of the slow conduction • RBBB: RV is activated direct propagation of current through RV muscle • LBBB : LV is activated direct propagation of current through LV muscle
- 18. SUPRAVENTRICULAR TACHYCRDIA • HR > 100/bpm • Atrial and/or ventricular • The mechanism of which involves tissue from the His bundle or above
- 19. Supraventricular Arrhythmia Types • Atrial Premature Complexes or Ectopic Beats • Sinus tachycardias • Physiological • Inappropriate • Postural orthostatic (POTS) • SA node re-entrant tachy (SNRT) • Atrial Tachycardias :Focal and multifocal • Atrial flutter (Clock and counter clock) • Atrial Fibrillation • AV junctional tachycardia • AVNRT (Typical and Atypical) • Accessory pathway mediated tachy (Ortho and concealed )
- 20. Narrow vs wide QRS tachy Narrow • Most of the SVT except some fascicular VT Wide Ventricular tachycardia SVT with bundle branch aberrancy o Rate-related/Pre-existing/Antiarrhythmic induced (e.g., flecainide)/Metabolic derangement (e.g., hyperkalaemia) Accessory pathway related o Antidromic tachycardia/Preexcited tachycardia (atrial tachycardia or AVNRT with bystander accessory pathway) Rapid ventricular pacing
- 21. Regular narrow complex tachycardia
- 22. Favor Supraventricular Tachycardia Favor Ventricular Tachycardia Initiation with a premature P wave Initiation with a premature QRS complex Tachycardia complexes identical to those in resting rhythm Tachycardia beats identical to PVCs during sinus rhythm “Long-short” sequence preceding initiation “Short-long” sequence preceding initiation Changes in the P-P interval preceding changes in the R-R interval Changes in the R-R interval preceding changes in the P-P interval QRS contours consistent with aberrant conduction (V 1 , V 6 ) QRS contours inconsistent with aberrant conduction (V 1 , V 6 ) Slowing or termination with vagal maneuvers AV dissociation or other non-1:1 AV relationship Onset of the QRS to its peak (positive or negative) <50 msec Onset of the QRS to its peak (positive or negative) ≥50 msec Fusion beats, capture beats QRS duration ≤0.14 sec QRS duration >0.14 sec Normal QRS axis (0–+90 degrees) Left-axis deviation (especially −90–180 degrees) Concordant R-wave progression pattern Contralateral bundle branch block pattern from the resting rhythm Initial R, q, or r >40 msec or notched Q in aVR Absence of an “rS” complex in any precordial lead
- 23. Atrial Fibrillation • Supraventricular arrhythmia • Electrocardiographically by low- amplitude baseline oscillations (fibrillatory or f waves from the fibrillating atria) • Irregularly irregular ventricular rhythm • The f waves, 300 to 600 beats/min, are variable in amplitude, shape, and timing • Atrial flutter waves have a rate of 250 to 350 beats/min and are constant in timing and morphology
- 24. INVESTIGATION TO DIAGNOSE SVT • HISTORY • CLINICAL PRESENTATION • ECG • HOLTER • ELECTROPHYSIOLOGY STUDY • ELECTRO ANATOMICAL MAPPING
- 25. ELECTRO ANATOMICAL MAPPING • A color-coded time scale of activation • Red :earliest • Purple: latest
- 26. TREATMENT OF SVT • COUNSELLING • SYMPATHETIC OR PARASYMPATHETIC MODULATION • PHYSICAL MANEUVER • MEDICATIONS • ANTI ARRYTHMIC MEDICATION • CARDIOVERSION • RADIO FREQUENCY ABALATION/CRYO ABLATION • Preventing or reducing complications • ORAL ANTI-COAGULATION • LAA APPENDAGE CLOSURE
- 28. CRYOABLATION
- 29. LAA DEVICE CLSOURE VS SURGICAL LIGATION
- 30. LAA closure without surgery