Atrial fibrilation

  • 2,170 views
Uploaded on

atrial fibrillation, classification, pathophysiology

atrial fibrillation, classification, pathophysiology

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
No Downloads

Views

Total Views
2,170
On Slideshare
0
From Embeds
0
Number of Embeds
3

Actions

Shares
Downloads
311
Comments
0
Likes
1

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. http://cardiologysearch.blogspot.in/ Atrial fibrillation (Classification, Mechanism &Management)
  • 2. http://cardiologysearch.blogspot.in/ Introduction… AF is characterised by wavelets propagating in different directions causing disorganized atrial depolarization without effective atrial contraction Electrical activity of atrium can be detected in ECG as small irregular baseline undulations of variable amplitude & morphology (f waves) at rate of 350 to 600 Ventricular response is irregularly irregular, & in untreated patients with normal AV conduction, is usually between 100 to 160 WPWsyndrome ventricular rate may be rapid >300 due to conduction over accessory pathway( short antegrade refractory periods)
  • 3. http://cardiologysearch.blogspot.in/ Introduction… ventricular rate during AF is altered due to Autonomic tone Property of AV node Effect of drugs on AV conduction
  • 4. http://cardiologysearch.blogspot.in/ Introduction Atrial fibrillation is the most common arrhythmia & the incidence & prevalence increases with the age The incidence <0.5% below 50Yrs 2% in age 60-69 4.6% in age 70-79 8.8% in age 80-89 Men were 1.5 times more likely to develop AF than women Whites were more likely to develop AF than blacks
  • 5. http://cardiologysearch.blogspot.in/ Framingham heart study ---cardiac factor predicting AF• CHF• RHD• HT• Stroke• Left atrial enlargement• Increased LV wall thickness• Decreased LV fractional shortening
  • 6. http://cardiologysearch.blogspot.in/ Relative risk of stroke - 6 fold in non rheumatic AF Relative risk of stroke - 17 fold in rheumatic AF Annual risk of stroke in pt aged 50- 59:1.5% Annual risk of stroke in aged 80-89:23.5%
  • 7. http://cardiologysearch.blogspot.in/ Underlying causes of AF CVS  Tumors Rheumatic heart disease  WPW syndrome ASD  Systemic Cardiac surgery  Alcohol (holiday heart Cardiomyopathy syndrome) Hypertrophic  CVA Idiopathic Infiltrative  COPD Hypertension  Defibrillation CAD (Acute & chronic)  Effort MVPS  Electrocution Non rheumatic mitral or tricuspid valve disease  Electrolyte abnormalities Pericarditis  Fever Tacycardia-bradycardia syndrome  Hypothermia
  • 8. http://cardiologysearch.blogspot.in/ Underlying causes of AF… Pneumonia  Congenital Pulmonary embolism  Multiple sclerosis Sudden emotion  Muscular dystrophy Thyrotoxicosis  Pheochromocytoma Trauma  Right atrial cold injections Rare  Swallowing Acute hypovolemia  Tyramine foods
  • 9. http://cardiologysearch.blogspot.in/Classification of Atrial fibrillation
  • 10. http://cardiologysearch.blogspot.in/ Classification of Atrial fibrillation First detected AF -usually <48hr in AF during diagnosis Paraoxysmal AF - last < 7days (most<24hrs) self-terminating episodes Persistent AF - last >7days requires electrical or pharmacologic cardioversion Permanent AF - sustained >1yr & failed cardioversion
  • 11. http://cardiologysearch.blogspot.in/ Mechanisms It was first thought that irregular contractions of the atria are caused by either single or multiple foci In 1924, Garry had suggested reentry to be the mechanism behind the AF In 1960, Moe suggested the “multiple wavelet hypothesis ” AF is characterized by fragmentation of a wavefront into multiple, independent daughter wavelets that move randomly throughout the atrium, giving rise to new wavelets that collide with each other & mutually annihilate, or that give rise to new wavelets in a perpetual activity that resembles Brownian motion
  • 12. http://cardiologysearch.blogspot.in/ Mechanisms Stability of AF is a function of several factors Non-uniform distribution of refractory periods Specially large tissue area Either a relatively brief refractory period or a relatively slow conduction velocity of the impulse, or both Average no. of the wavelets Allessie et al, estimated the critical no. of wavelets to sustain AF was approximately 4 - 6
  • 13. http://cardiologysearch.blogspot.in/Mechanisms
  • 14. http://cardiologysearch.blogspot.in/ Mechanisms Trigger factor - self-terminating AF Perpetuating factor - AF does not terminate spontaneously Paraoxysmal AF - 95% of Triggering foci are mapped in pulmonary vein Other foci - within SVC ,coronary sinus
  • 15. http://cardiologysearch.blogspot.in/Anatomic distribution of focal trigger in Paraoxysmal AF
  • 16. http://cardiologysearch.blogspot.in/ Mechanisms Waldo et al divided AF into 4 types according atrial electrogram• Type – I --- ECG showed discrete complexes of variable morphology separated by a clear isoelectric baseline• Type – II --- ECG characterized by discrete atrial complexes with variable cycle lengths and morphology, the baseline is not isoelectric• Type – III --- ECGs were highly fragmented, showing no discrete complexes or isoelectric intervals• Type – IV --- Fibrillation was characterized by
  • 17. http://cardiologysearch.blogspot.in/ Mechanisms “ f” waves They do not represent total atrial activity but depict only the larger vectors generated by the multiple wavelets of depolarization that occur at any given time Why ventricular response is irregularly irregular? Large no. of atrial impulses that penetrate the AV node, makes it partially refractory to subsequent impulses These effect of non conducted atrial impulses to influence the response of subsequent atrial impulse is called as “concealed conduction”
  • 18. http://cardiologysearch.blogspot.in/ Mechanisms Electrical remodelling It means long term changes in refractory periods resulting from prolonged changes in atrial rate EPS --- ↓ERP,↓Action potential, ↓ amplitude of AP plateau Mechanisms --- Structural , cellular or ion channels It encompasses diverse structural changes in the myocardium -interstitial fibrosis Alteration in quantity or properties of ion channel proteins in sarcolemma Microscopic changes in cell size , content & extra cellular matrix leads to irreversible macroscopic changes
  • 19. Mechanisms http://cardiologysearch.blogspot.in/ Maladoptations of atrial refractionaries – cause of chronic AF Atrial remodelling Caused by atrial ischemia & stretch leads to AF due to ↑ automaticity & reentry After AF has continued for a long time, atria are not only electrically remodelled, but atrial contractile function is also disturbed Recovery of atrial transport function may depend upon duration of AF After sinus rhythm is restored, it may take several weeks before atrial contractility fully returns
  • 20. http://cardiologysearch.blogspot.in/ Mechanisms Modulating factors The onset & persistence of AF may be modulated by autonomic nervous system Coumel et al distinguished vagal & adrenergic AF (distinction is not clear) Vagally mediated AF Occurs more frequently in men than in women Usually younger age group (30 – 50 years)
  • 21. http://cardiologysearch.blogspot.in/ Mechanisms Predominantly occurs in the absence of structural heart disease Rarely progresses to permanent AF Attacks occur at night, end of the morning Neither emotional stress nor exertion trigger the arrhythmia Rest, postprandial state, & alcohol are other precipitating factors Mechanism may relate to vagally induced shortening of the atrial refractory period
  • 22. http://cardiologysearch.blogspot.in/ Mechanisms Adrenergic AF More frequently associated with structural heart disease (IHD) Occurs during the day time, & it is precipitated by stress, exercise, tea, coffee or alcohol The underlying mechanism is unknown
  • 23. http://cardiologysearch.blogspot.in/ Hemodynamic effect Loss of atrial contraction Rapid ventricular rate - ↓duration of diastole & ventricular filling irregular ventricular rhythm - ↓ CO & coronary blood flow Loss of AV synchrony - ↓LVEDP - ↓SV AF causes hypotension or pulmonary oedema in the setting of restrictive physiology
  • 24. http://cardiologysearch.blogspot.in/ Antiarrhythmic therapy of atrial fibrillation Three antiarrhythmic strategies Acute pharmacologic termination Prevention of recurrence after cardioversion Control of ventricular rate Acute conversion of paroxysmal AF Pharmacologic cardioversion Most effective if initiated within 7 days after onset of AF Restoration of sinus rhythm can be achieved in 70% of the patients First choice : Propafenone & flecainide (po & iv), ibutilide, dofetilide Second choice : Amaiodarone (high dose, iv +oral) & Qunidine (po)
  • 25. http://cardiologysearch.blogspot.in/Antiarrhythmic to maintain sinus rhythm in AF
  • 26. http://cardiologysearch.blogspot.in/ Antiarrhythmic therapy of atrial fibrillation Class IC drugs – Restore sinus rhythm with in a short period of time ( 1 hour) – conversion rate up to 90% (PAFIT-3) Ibutilide It acts twice more effectively for conversion of atrial flutter than atrial fibrillation (63% v 31%) Efficacy decreased significantly with AF of >7 days Studies, enrolled patients with mild to moderate underlying disease, so these results may not be generalizable to patients with markedly depressed LVF
  • 27. http://cardiologysearch.blogspot.in/ Antiarrhythmic therapy of atrial fibrillation Dofetilide DIAMOND-CHF Study of 1518 patients with symptomatic heart failure (EF <35%) Therapy with 1000mic.g was associated with a greater rate of conversion to sinus rhythm (44% v14%) SAFIRE-D Study of 325 patients with persistent AF &/or atrial flutter Cardioversion rates were 6.1%,9.8% & 29.9% for 125, 250 & 500mic.g bid compared with 1.2% of conversion with placebo
  • 28. Antiarrhythmic therapy of atrial http://cardiologysearch.blogspot.in/ fibrillation Amiodarone Produce sinus rhythm in 80% within 24hours (late conversion) Advantages It lowers ventricular rate before conversion (IC drugs increase the rate) Recommended in hemodynamically compromised patients since it is less negatively inotropic Prefered in pts with LVF, LVH, IHD IV amiodarone is moderately effective in converting AF compared with placebo (63% v 44%), with maximum effect at 24hours (74% v 55%) --- 12 meta-analysis Higher than usual dose & combination of IV & oral administration may enhance the cardioversion rate
  • 29. Antiarrhythmic therapy of atrial http://cardiologysearch.blogspot.in/ fibrillation Quinidine Usually administered in conjunction with B-Blocker Cumulative dose of up to 1350mg has shown to cardiovert 50- 77% of patients with recent onset AF Sotalol It is ineffective in acute conversion It is effective for the prevention of AF This discrepancy relates to its property to prolong the refractory period predominantly at lower atrial rates, but not during rapid AF
  • 30. http://cardiologysearch.blogspot.in/ Antiarrhythmic therapy of atrial fibrillation Availability of studies on the efficacy of procainamide & disopyramide is limited, precluding definite conclusions Digitalis, B-Blockers, & CCBs are ineffective for acute conversion of AF DAAF study (Digoxin in acute AF) There was no difference in cardioversion rates at 16 hours between IV digoxin & placebo (51% v 46%) Digoxin can facilitate AF due to its cholinergic effects which may cause a non-uniform reduction in conduction velocity & effective refractory periods of the atria, and to delay the reversal of remodelling after restoration of sinus rhythm
  • 31. http://cardiologysearch.blogspot.in/Conversion of paroxysmal AF(<3days)
  • 32. http://cardiologysearch.blogspot.in/ Antiarrhythmic therapy of atrial fibrillation Prevention of paroxysmal AF No need for prophylactic AAD After first episode of AF which may self terminate or require electrical or pharmacologic cardioversion Patients with infrequent, self limiting & well tolerated paroxysms of AF Prophylactic AAD are recommended if Occurs frequently (1 episode per 3 months) Associated with significant symptoms
  • 33. http://cardiologysearch.blogspot.in/ Antiarrhythmic therapy of atrial fibrillation Prophylactic AAD are recommended if… Worsening of LV function In the presence of left atrial enlargement, LVD, underlying CVS pathology, long duration of AF, advanced age B-blockers Effective in adrenergic dependent AF (class IA & IC are ineffective) It prevents the recurrence of persistent AF after cardioversion
  • 34. http://cardiologysearch.blogspot.in/ Antiarrhythmic therapy of atrial fibrillation Control of ventricular rate during paroxysmal AF Digitalis, B-blockers, CCBs are useful Addition of rate controlling drugs is necessary with class IA & IC drugs (not needed with amiodarone or sotalol) Control of ventricular rate in the setting of SSS may be impossible without implanting pacemaker In WPW syndrome complicated by AF – acute rate control & conversion to SR may be achieved by procainamide or flecainide
  • 35. http://cardiologysearch.blogspot.in/
  • 36. http://cardiologysearch.blogspot.in/ Antithrombotic therapy Whether AF is persistent or intermittent --- Predisposes to stroke Non valvular AF Most common cardiac disease associated with cerebral embolism The risk of stroke is 5-7 times greater when compared to control group Risk factors that predicts stroke Previous stroke or TIA Diabetes mellitus Systemic hypertension Increasing age CAD CHF
  • 37. http://cardiologysearch.blogspot.in/ Antithrombotic therapy LV dysfunction & left atrial size > 2.5cm/sq.m --- associated with thromboembolism Age - 60-65, normal echo, no risk factors --- Extremely low risk for stroke (1% per year) Results from 5 large anticoagulation trails Annual rate of stroke in control group --- 4.5% Annual rate of stroke in warfarin-treated group --- 1.4% (68% risk reduction) Aspirin 325mg/d produced a risk reduction of 44%
  • 38. http://cardiologysearch.blogspot.in/ Antithrombotic therapy Annual rate of major hemorrhage Control group --- 1% Aspirin group --- 1% Warfarin group --- 1.3% No difference was noted in stroke risk, when patients with paroxysmal (intermittent) AF were compared with chronic AF Anticoagulation was 50% more effective than aspirin in preventing ischemic stroke
  • 39. http://cardiologysearch.blogspot.in/ Antithrombotic therapy Risk factors for stroke Prior stroke or TIA Significant valvular heart disease Hypertension Diabetes mellitus Age >65 years Left atrial enlargement CAD Congestive heart failure
  • 40. http://cardiologysearch.blogspot.in/ Antithrombotic therapy Lone AF Age <60years, no risk factors ---No antithrombotic therapy Age - 60-75 years (risk-2%per year) ---Aspirin Age > 75 years --- Anticoagulation (INR – 2.0) Any patients with AF + Risk factors for stroke --- Treated with warfarin anticoagulation (INR – 2 to 3) Patients with contraindication to anticoagulation (or) unreliable individual (or) no risk factors --- Aspirin
  • 41. http://cardiologysearch.blogspot.in/ Antithrombotic therapy Risk of embolism after cardioversion Risk --- 0 -7% Risk is independent of mode of cardioversion High risk patients are Prior embolism, Mechanical valve prosthesis, Mitral stenosis In AF (>2d) --- Warfarin for 3 weeks before cardioversion + 3-4 weeks after reversion to sinus rhythm Alternate strategy --- TEE (to exclude LA thrombus) + heparin before cardioversion + followed by warfarin for 4weeks
  • 42. Antithrombotic therapy http://cardiologysearch.blogspot.in/ Risk of embolism after cardioversion… For emergency cardioversion (TEE cannot be obtained) --- heparin before cardioversion + followed by warfarin for 4weeks Low risk patients Age <65 years without risk factor for stroke in nonvalvular AF Anticoagulation may not be necessary before cardioversion but aspirin is indicated It is important to emphasize that suggestions must be individualized for a given patient Absolute contraindication for anticoagulation - ICH,SDH,GI bleed
  • 43. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Rhythm control strategies Device therapy Single site pacing --- High right atrial & septal In many patients with SSS, atrial pacmaker allows higher dose of AAD since sinus node dysfunction is treated In patients with paroxysmal AF, there is evidence for intraatrial conduction delay Atrial pacing may decrease the frequency of recurrent AF in patients who have SSS
  • 44. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Incidence of AF is lower in patients treated by atrial pacing than ventricular pacing (prospective studies) Multisite pacing --- Biatrial synchronous & Dual site atrial pacing In addition to the high RA lead, another atrial lead is placed just outside the CS ostium for stability & LA synchronization These pacing cause resynchronization of atrial depolarisation & helpful in patients with intra atrial conduction delay
  • 45. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Usually performed in patients with recurrent, symptomatic & drug refractory AF ECG showed biphasic ‘p’ wave in inferior leads with abbreviation of ‘P’ wave duration Implantable atrial defibrillator Automatic atrial defibrillator• It detect AF by means of implanted RA, CS & RV leads
  • 46. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies• It delivers ‘R’ wave synchronization shock of 6J after a minimal preceding R-R interval of 500 ms• Unfortunately this device in its current form is not in use Atrial-ventricular defibrillator/pacemaker• It has dual chamber algorithm-based arrhythmia detection• Pacing & defibrillation therapies for treatment of AF & atrial tachycardias
  • 47. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Ablation therapy --- surgical His bundle ablation (surgical ligation, mechanical, cryothermia) + Pace maker implantation Corridor surgery Creating an isolated strip of muscle to isolate the SA & AV nodes, thus driving ventricular rate via AV node-His bundle complex But, atrial areas outside of narrow RA corridor continued to fibrillate with persistent loss of atrial transport function & persistent risk of thromboembolism
  • 48. http://cardiologysearch.blogspot.in/
  • 49. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Maze procedure The principle is compartmentalize both atria so that AF cannot be maintained Right & left atrial appendages were resected, pulmonary vein ostia are isolated, linear RA & LA lesions are connected to anatomic structures to form an “electrical maze” --- “Maze 3” Appropriately placed atrial incisions not only interrupt the conduction routes of reentrant circuits, but they also direct the sinus impulse from SA to AV along a
  • 50. http://cardiologysearch.blogspot.in/ Indication for maze procedure Symptomatic AF Refractory to AAD Recurrent systemic embolism despite anticoagulation
  • 51. http://cardiologysearch.blogspot.in/ Maze procedure 90% pt cured of AF with operative mortality <1 <10% requires PPI due to sinus node dysfunction Transient fluid retention due to ↓atrial natriuretic peptide must be treated with diuretics The entire atrial myocardium was electrically activated & atrial transport function is preserved
  • 52. http://cardiologysearch.blogspot.in/Non – pharmacologic therapies
  • 53. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Tans catheter ablation therapy Linear atrial ablation (Radiofrequency) It is employed in LA & RA for substrate compartmentalization Trigger ablation (Radiofrequency) Focal pulmonary vein Pulmonary vein isolation - transseptal puncture followed by pulmonary venography to define anatomy Adverse effect Stroke Phrenic nerve injury Pericardial effusion & tamponade Pulmonary vein stenosis
  • 54. http://cardiologysearch.blogspot.in/ Indication for ablation Symptomatic AF Refractory to AAD Without structural heart disease
  • 55. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Rate control strategy Catheter AV junctional modification (radiofrequency) Principle --- Posterior inputs of AV node have shorter ERP, their ablation slows the ventricular response during AF Patient who becomes symptomatic due rapid ventricular response will benefit Currently, AV node modification is usually reserved for patients who require non-pharmacologic control but are opposed to pacemaker implantation
  • 56. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Catheter ablation (DC shock or radiofrequency) + Pacemaker It is performed in patients with unmanageable symptoms related to rapid ventricular response DC current ablation is highly dangerous --- produce electrical arcing & barotrauma ( cardiac perforation, tamponade, acute depression of LV, proarrhythmia & sudden death Radiofrequency ablation ---avoid complications Disadvantages Dependence on pacemaker Atria will continue to fibrillate --- need long term
  • 57. http://cardiologysearch.blogspot.in/ Non – pharmacologic therapies Choice of pace maker type --- determined by the current phase of AF Chronic AF --- VVIR + AV nodal ablation Paroxysmal AF ( usually in sinus rhythm between episodes) --- Dual-chamber pacemaker with mode switching Stroke prevention strategy Percutaneous LA appendage transcatheter occlusion (PLAATO) Involves insertion of an occlusion device by catheter into the LA appendage via trans septal puncture
  • 58. http://cardiologysearch.blogspot.in/A circular mapping catheter is in the ostium of the left lower PV and an ablation catheter with a large-tip electrode is recording a PV potential from the nearby strand.
  • 59. During radiofrequency ablation near Lasso-8 recording http://cardiologysearch.blogspot.in/site, the sharp PVPs are seen in the first two beats but are absent during the last two beats
  • 60. http://cardiologysearch.blogspot.in/
  • 61. http://cardiologysearch.blogspot.in/Thank you
  • 62. http://cardiologysearch.blogspot.in/ http://cardiologysearch.blogspot.in/
  • 63. http://cardiologysearch.blogspot.in/ Kindly send your suggestions to improve this site Visit us regularly for updates Send your articles/ ppt/pdf to publish in this site . http://cardiologysearch.blogspot.in/
  • 64. http://cardiologysearch.blogspot.in/
  • 65. http://cardiologysearch.blogspot.in/
  • 66. http://cardiologysearch.blogspot.in/
  • 67. http://cardiologysearch.blogspot.in/
  • 68. http://cardiologysearch.blogspot.in/ Introduction Paroxysmal AF Short lasting < 1 hour Long lasting >1; < 48 hours AF interspersed with periods of sinus rhythm & usually terminates spontaneously Persistent AF Occur between 2days - weeks Intervention is needed to restore the sinus rythum Chronic or permanent AF Persists for months to years No spontaneous conversion Interventions to restore sinus rythum are either ineffectual or
  • 69. http://cardiologysearch.blogspot.in/
  • 70. http://cardiologysearch.blogspot.in/ Mechanisms Type – I --- Activation consisted of single, broad wavefronts propagating without conduction delay & either only short arcs of conduction block or small areas of slow conduction that did not disrupt the main course of propagation Type – II --- Activation consisted of either the presence of 2 wavelets or of single wave (with either considerable conduction block or slow conduction or both) Type – III --- Activation was characterized by 3 or more wavelets combined with areas of slow conduction & multiple arcs of conduction block As the fibrillation changed from type I to III, AFs frequency & irregularity increased, creating a higher incidence of continuous electrical activity & reentry
  • 71. http://cardiologysearch.blogspot.in/ Mechanisms Familial AF• Genetic predisposition – is a hypothesis• Defect linked to chromosome 10q (21 of 49 members from 3 spanish families presented with AF)• Missense mutation in the lamin A/C gene (In DCM – associated with AF)• Missense mutation Arg663His ( In specific phenotype of HCM – associated with 47% of AF)
  • 72. http://cardiologysearch.blogspot.in/Rate control in atrial fibrillation
  • 73. http://cardiologysearch.blogspot.in/Rate control in atrial fibrillation
  • 74. http://cardiologysearch.blogspot.in/
  • 75. http://cardiologysearch.blogspot.in/Antiarrhythmic therapy of atrial fibrillation
  • 76. http://cardiologysearch.blogspot.in/
  • 77. http://cardiologysearch.blogspot.in/ 30%