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Mechanism of arrhythmogenesis

Mechanism of arrhythmogenesis. Abnormal automaticity Triggered activity and afterdepolarization Reentrant mechanism. Automaticity: Alterations in impulse initiation. Abnormal Automaticity. Causes

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Mechanism of arrhythmogenesis

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  1. Mechanism of arrhythmogenesis • Abnormal automaticity • Triggered activity and afterdepolarization • Reentrant mechanism

  2. Automaticity: Alterations in impulse initiation

  3. Abnormal Automaticity Causes • Parasympathetic nervous system activation slows the rate of rise of phase 4 depolarization and vice versa • Ischemia, infarction, hypokalemia, beta agonists enhance phase 4 depolarization Significance • Atrial tachycardia, accelerated idioventricular rhythms, ventricular tachycardia

  4. Afterdepolarizations and Triggered activity

  5. Afterdepolarizations and Triggered activity EAD (Early AD) • Due to increase in cytosolic Ca2+ • Causes - hypokalemia, hypomagnesemia, hypoxia, acidosis, bradycardia, class IA and III antiarrhythmics, antihistaminics, phenothiazines • Significance - torsades de pointes DAD (Delayed AD) • Due to increased Ca2+ • Causes- catecholamines, quinidine, caffiene • Significance - idioventricular rhythms, digitalis toxicity

  6. Reentrant Mechanism → → →

  7. Reentrant arrhythmias • Circulation of an activation wave around an inexcitable obstacle • Most common arrhythmia mechanism • Property of a network of myocytes • Presence of excitable gap • In the absence of excitable gap wavefront propagates through partially refractory tissue with no anatomic obstacle- leading to circle re-entry( functional re entry)

  8. Classification of arrhythmias By heart rate • Bradyarrhythmias • Tachyarrhythmias • Conduction blocks By anatomic origin • Supraventricular • Junctional • Ventricular By type of disorder • Disorders of impulse formation • Disorders of impulse conduction

  9. Disorders of impulse formation Sinus rhythms • Sinus bradycardia • Sinus tachycardia • Sinus arrhythmia Atrial rhythms • Premature atrial complexes • Atrial flutter • Atrial fibrillation • PSVT Junctional rhythms Ventricular rhythms • Ventricular premature beats • Ventricular tachycardia • Ventricular fibrillation

  10. Disorders of impulse conduction Conduction blocks • Sino atrial blocks Atrioventricular blocks • First degree AV block • Mobitz type I block • Mobitz type II block • Third degree AV block Intraventricular blocks • Hemiblocks • LBBB • RBBB

  11. Sinus Bradycardia Heart rate <50 bpm with chronic β–blocker therapy

  12. Sinus Bradycardia (contd.) • Causes: Vagal stimulation, increased intracranial pressure, hyperkalemia, digoxin, beta blocker, hypothyroidism, sedation, obstructive jaundice, glaucoma. • Normal phenomenon in athletes and during sleep

  13. Sinus Bradycardia: Management Atropine: • First drug of choice for symptomatic bradycardia • Dose - 0.5 mg IV bolus repeated every 3-5 min up to a total dose of 0.04 mg/kg or 3mg Other drugs: • Dopamine: 2-10 μg/kg/min infusion • Epinephrine:2-10 μg/min infusion • Ephedrine: 5-25 mg IV bolus • Isoproterenol: 2-10 μg/min infusion Transcutaneous/transvenous pacing: Symptomatic bradycardia with signs of poor perfusion

  14. SinusTachycardia QRS complex- normal May be associated with ST segment depression

  15. Sinus Tachycardia (contd.) Causes • Pain, inadequate anaesthesia, hypovolemia, fever, hypoxia, hypercapnia, cardiac failure, anaemia, thyrotoxicosis, drug effects Significance • Prolonged tachycardia – increased myocardial work, decreased myocardial O2 supply →can ppt MI or CHF in patients with heart disease Treatment • Treat the underlying cause • Beta blockers and calcium channel blockers

  16. Sinus Arrhythmia • Alternate periods of slower and faster rates • Rate increases with inspiration and decreases with expiration • Common in children and young adults • Accentuated by vagotonic procedures and abolished by vagolytic procedures • No treatment required

  17. Atrial Premature Complexes Rhythm- irregular with incomplete compensatory pause QRS complex- usually normal unless ventricular aberration present

  18. Atrial Premature Complexes PACs are of 3 types: • Premature P wave with normal QRS Ectopic focus with different morphology from sinus P wave • Premature P wave with no QRS P waves occur very early AV node in refractory period • Premature P wave with aberrant ventricular conduction Impulse reaches the bundle branch when only one has fully recovered

  19. Atrial Premature Complexes • Increased incidence with age • More common in patients with chronic rheumatic valvular disease, coronary artery disease, CHF, hyperthyroidism • Little clinical significance • Frequent APCs may trigger more serious supraventriculr arrhythmias e.g. atrial fibrillation, flutter, PSVT • Treatment – rarely necessary

  20. Atrial Flutter • Heart rate - atrial rate 250 to 350 bpm, ventricular rate 150 bpm • Rhythm - atrial rhythm regular • P wave- saw toothed appearance (F waves), • F waves best seen in leads II, V1 and oesophageal leads • P/QRS- usually 2:1 (may vary between 2:1 and 8:1) • QRS complex- normal, T waves - lost in f waves

  21. Atrial Flutter (contd.) • Mechanism Re entrant atrial activity (most common) Focal discharge • Significance Can be seen in patients with CAD, mitral valve disease, pulmonary embolism, hyperthyroidism, cardiac trauma, cancer of heart, myocarditis

  22. Atrial Flutter - Management Initial treatment - Control of ventricular response rate • β-blockers - esmolol 1 mg/kg • Calcium channel blockers - verapamil 5-10 mg or diltiazem Excessively rapid ventricular response/ haemodynamic instability/ both • DC cardioversion starting at 100J and increasing to 360J • Ibutilide – 1 mg in 10 ml saline/5% D over 10 min – 4-8 hrs monitoring after treatment • Procainamide – 5-10 mg/kg, no faster than 0.5 mg/kg/min • Amiodarone – 150 mg over 10 min → 1 mg/min for 6 h → 0.5 mg/min for 18 hrs

  23. Atrial Fibrillation • Heart rate- atrial rate 350 to 500 bpm. Ventricular rate 60 to 170 bpm • Rhythm - irregularly irregular • P wave - absent, f waves or no obvious atrial activity • P/QRS- no p waves • QRS complex- normal

  24. Atrial Fibrillation (contd.) • Most common postoperative arrhythmia with significant consequences on patients health • Associated with: old age, thyrotoxicosis, HTN, CAD, CHF, RHD, congenital heart disease • Best seen in leads V1-2 and inferior leads • Caused by numerous wavefronts of depolarization spreading throughout the atria simultaneously leading to absence of coordinated atrial contraction

  25. Atrial Fibrillation (contd.) Hemodynamic effects • Loss of mechanical AV synchrony→ impairs ventricular filling→ decreases cardiac output Thromboembolism • After 24-48 hrs • Atrial thrombi usually arising from left atrial appendage • Increased incidence of stroke(most feared consequence)

  26. Atrial Fibrillation (contd.) Risk Factors for development of thromboembolism

  27. Atrial Fibrillation: Management Control of ventricular rate

  28. Atrial Fibrillation: Management Antithrombotic therapy

  29. Atrial Fibrillation: Management Cardioversion

  30. Atrial Fibrillation: Management Post operative atrial fibrillation • Routine use of beta blockers throughout the periop period • Anticoagulation Maintenance of sinus rhythm • In the absence of structural heart disease- flecainide, propafenone • In the presence of significant structural heart disease- sotalol, amiodarone

  31. Paroxysmal Supraventricular Tachycardia

  32. Paroxysmal Supraventricular Tachycardia Rapid regular rhythm with narrow QRS complex and lacking the normal p wave ECG characteristics • Rate 130-270/min • Rhythm regular • P/QRS 1 : 1 (p wave may be hidden in QRS complex or T wave) • QRS complex generally normal

  33. PSVT - Significance • Seen in 5% normal young adults • Accounts for 2.5% of arrhythmias in anaesthetized patients • Not a/w intrinsic heart disease or systemic illness • Precipitated under anaesthesia by changes in autonomic nervous system tone, drug effects, intravascular volume shifts • Can produce severe hemodynamic deterioration

  34. PSVT: Management • Vagal maneouvres applied only to one side • DOC-iv Adenosine 6mg rapid bolus, 2nd & 3rd doses of 12 and 18 mg if no response • Verapamil 2.5-10 mg iv - terminates AVNRT successfully, provides long term relief • Amiodarone 150 mg infusion over 10 min - recent addition • Esmolol 1 mg/kg bolus → 50-200 mg/kg/min • Phenylephrine 100 μg- if associated hypotension

  35. PSVT: Management (Contd.) • Edrophonium or neostigmine iv • Intravenous digitalization – ouabain 0.25-0.5 mg iv or digoxin 0.5 -1.0 mg iv • Rapid overdrive pacing • Synchronized cardioversion • Electrode catheter ablation with radiofrequency energy

  36. Junctional Rhythm • AV node and sites above and below it act as pacemaker • Heart rate- variable, 40 to 180 bpm • Rhythm- regular • P/QRS- 1:1 • QRS complex- usually normal

  37. Junctional Rhythm (contd.) Types • High nodal rhythm- impulse reaches atrium before ventricles, P precedes QRS, short PR interval • Mid nodal rhythm- impulse reaches atrium and ventricle at the same time, P lost in QRS • Low nodal rhythm- impulse reaches ventricles before atrium, P follows QRS Common in patients under anaesthesia(20%) especially with halogenated anaesthetic agents

  38. Junctional Rhythm (contd.) Treatment • Usually reverts spontaneously, no treatment required • If associated with hypotension & poor perfusion – t/t with atropine/ ephedrine/ isoproterenol • Dual chamber electrical pacing

  39. Ventricular Premature Beats • VPB s arise from ectopic pacemaker activity arising in the ventricles • Heart rate – variable, Rhythm irregular, Compensatory pause seen • P/QRS- no P wave associated with VPB • QRS complex- Wide, bizarre, >0.12 s • QRS and T wave point in opposite direction

  40. VPB - Types • Early in the cycle - R on T phenomenon, dangerous in acute ischaemic situation because ventricles are prone to VT and VF • After T wave • Late in the cycle fusing with next QRS - fusion beats

  41. VPB (contd.) • Unifocal, multifocal • Causes: hypoxia, electrolyte imbalance, blood gas abnormality, digitalis toxicity, CHF, MI • Common during anaesthesia(15%) especially in patients with pre existing cardiac disease

  42. VPB - Significance May progress to VT or VF in following situations • Coronary artery insufficiency, MI • Digitalis toxicity with hypokalemia • Hypoxemia • Multiple, multifocal or bigeminal VPB • R on T phenomenon

  43. VPB: Management • Maintain adequate depth of anaesthesia • Oxygenation and ventilation are the initial treatment for all kinds of ectopics • Correct underlying abnormalities • Treat if hemodynamic impairment or harbinger of worse arrhythmias • Lidocaine(TOC) 1.5 mg/kg initial bolus f/b infusion@1-4 mg/min • Other drugs: beta blockers, procainamide , calcium channel blockers, atropine, disopyramide, quinidine

  44. Ventricular Tachycardia Definition • 3 or more VPB s in a row Types(depending on morphology) • Monomorphic- all QRS complexes have same morphology • Polymorphic- more than 1 morphology • Torsades de pointes – Polymorphic VT with long QTc Types(depending on duration) • Non sustained- upto 30s • Sustained- >30s

  45. Ventricular Tachycardia • Heart rate -100 to 200 bpm • P/QRS- no fixed relationship due to AV dissociation • QRS complex- wide and bizarre, >0.12 s, similar to VPB

  46. Ventricular Tachycardia (contd.) • Causes: MI, hypoxia, electrolyte imbalance, myocardial trauma, digitalis toxicity • Mechanism: usually caused by re entry and most commonly seen in patients following MI • Complications: decreases cardiac output, decreases cardiac perfusion, increases cardiac workload, can deteriorate into VF

  47. VT: Management • Acute onset is life threatening and requires immediate treatment • Treat the precipitating metabolic or toxic causes

  48. Torsades de pointes

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