Atrial fibrillation -latest

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ATRIAL FIBRILLATION THE GRANDFATHER OF ALL ARRYHTHMIAS

Atrial fibrillation -latest

  1. 1. ATRIAL FIBRILLATION<br />…..Grand father of arrhythmias<br />
  2. 2. <ul><li>The most essential part of a student's instruction is obtained...not in the lecture-room, but at the bedside. Nothing seen there is lost; the rhythms of disease are learned by frequent repetition; its unforeseen occurences stamp themselves indelibly in the memory.
  3. 3. - Oliver Wendell Holmes, M.D.</li></li></ul><li>Professor: define seminar<br />Student :seminar is defined as process in which one spoils his sleep for one night in an effort to make others sleep.<br />
  4. 4. ARRYHTHMIAS <br />For an arryhthmia to occur,to be sustained.<br />Either of three properties to be present.<br /><ul><li>1.TRIGGERING ACTIVITY OF FOCUS
  5. 5. 2.AUTOMATICITY
  6. 6. 3.REENTRY
  7. 7. In AF all three play a role
  8. 8. In AFL – reentry circuit.
  9. 9. WAVELETS
  10. 10. SPIRAL WAVE </li></li></ul><li>What is triggering?<br />Triggering is a phenomenon due to cellular afterdepolarization.<br />1.at end of AP during phase 3 –early AD<br />2.after AP –phase 4 –late AD<br />Increases in intracellular Ca<br />VPC –TDP early after DP<br />Late after DP- atrial,ventricluar ,faciculardysarrhythmias due to digoxin toxicity.<br />Catecholamine response VT --- late AD<br />Provoked by pacing<br />
  11. 11. Action potential<br />
  12. 12. Foci of excitation in AF<br />
  13. 13. What is automaticity?<br /><ul><li>Due to increase in the slope of phase 4 depolarization.
  14. 14. Decreased threshold for AP depolarization in myocardium other than sinus node.
  15. 15. Most of APCs
  16. 16. VPCs
  17. 17. AT
  18. 18. Cannot be provoked by pacing</li></li></ul><li>
  19. 19.
  20. 20. What is reentry?<br />Inhomogenous in myocardial conduction and recovery.<br />Unidirectional block with slow conduction<br /><ul><li>WPW.</li></ul>Fibrosis ---SVTs,VTs<br />FIXED– cristaterminalis,vertical crest on the inferior wall of right atrium.<br />Functional dynamic --- unstable-<br /><ul><li>VF –acute MI
  21. 21. Polymorphic VT</li></li></ul><li>REENTRY<br />
  22. 22. AVNRT<br />
  23. 23. Wavelets in AF <br />
  24. 24. SPIRAL WAVE <br />Functional rentrant circuit.<br />The centre of reentry is excitable but not activated.<br />Latest model of AF<br />Still not clearly understood<br />
  25. 25. What is pacing?<br />DELIVERING THE PULSES<br />Treatment in case of SSS<br />And also to suppress the tachyarryhthmias<br />
  26. 26. What is overdrive suppression?<br />OVERDRIVE SUPPRESSION is the phenomenon in which the rate of the pacemaker decides the ryhthm over the underlying other cells..<br />One which is at a faster rate will be the pacemaker..<br />Others will not give impulses of their own and are suppressed –overdriven by the pulse of other one..<br />Normally all other pacemaker cells are overdriven by siuns node.<br />Sometimes SA node may be overdrive n by ectopic foci—tachycardia.<br />
  27. 27. ATRIAL FIBRILLATION<br />…..Grand father of arrhythmias<br />
  28. 28. History<br /><ul><li>Earliest record of AF –yellow emperor ‘s classic of internal medicine in 17 th century.
  29. 29. WILLIAM HARVEY---auricular fibrillation in animals in 1628.
  30. 30. Pulse tracing of a patient with AF---Chauveau and Marey
  31. 31. First clinical case of AF after surgery of ovarian tumor –Arthur Cushy in london,1907.
  32. 32. Rebellious palpitation ---Jean BaptisteSenae
  33. 33. Absence of p waves---Lewis
  34. 34. Irregular pulse of AF---</li></ul> “intermssion of pulsation of heart”--Laennec<br /> ‘Ataxia of pulse’– Bouilland<br /> ‘Delirium cordis’—Nothnagil<br /> ‘PulsusIrregularisPerpetius’--- Hering<br />
  35. 35. MichealHaissaguerre<br /><ul><li>Showed that AF can be initiated by ectopic beats originating in the pulmonary veins and that ablation of these sites are curative </li></li></ul><li>CLASSIFICATION OF A F <br /><ul><li>Temporal classification clinically.
  36. 36. Why?---management strategy changes.
  37. 37. Individualised –h/o, compliance ,other disorders.
  38. 38. ACC/AHA/ESC 2006 GUIDELINES
  39. 39. ETIOLOGICALLY—
  40. 40. NON VALVULAR AF—abs of RHD,MVR,prosthetic valve
  41. 41. VALVULAR AF--- presence
  42. 42. LONE AF.
  43. 43. CLINICALLY
  44. 44. FIRST EPISODE
  45. 45. TRANSIENT AF/REVERSIBLE AF
  46. 46. RECURRENT AF
  47. 47. PAROXYSMAL AF
  48. 48. PERSISTENT AF
  49. 49. PERMANENT AF</li></li></ul><li>LONE AF<br />To be categorised as lone AF ,it is after exclusion of other factors.<br /><ul><li>1.age <60 yrs
  50. 50. 2.absence of heart disease or pulmonary disease
  51. 51. 3.non hypertensive
  52. 52. 4.no clinical or echocardiographic evidence
  53. 53. 20-25% of persistent AF
  54. 54. Why imp?
  55. 55. Low risk of thromboembolism
  56. 56. Can be kept on plain aspirin 81-325 mg daily.
  57. 57. Trials--- paris prospective study RR of CV mortality ---4.22 %total mortality --- 1.97 %</li></li></ul><li><ul><li>FIRST EPISODE AF—symptomatic or asymptomatic revert to SR spontaneously in most patients.
  58. 58. RECURRENT AF--- 2 or more episodes occurred.> 30 sec
  59. 59. PAROXYSMAL AF– recurrent AF that ends spontaneously</li></ul><48 hrs – 7 days .<br /><ul><li>PERSISTENT AF --- > 7 days .</li></ul>Requires pharmacotherapy or cardioversion for termiantion<br /><ul><li>PERMANENT AF ---</li></ul>Cannot be reverted.<br /><ul><li>REVERSIBLE/TRANSIENT AF----ac URTI, AMI,pericarditis,thyrotoxicosis,pulmonaryembolism,afterCABG,holiday heart syndrome.</li></li></ul><li>EPIDEMIOLOGY<br /><ul><li>Incidence in age >22 yrs –2% --- FRAMINGHAM study.
  60. 60. M>W
  61. 61. 0.5% prevalence 50-59 yrs,,8.8%--80-89 yrs
  62. 62. Increases with age.
  63. 63. SAFE STUDY–MEN—7.8% overall,elderly -10.8%
  64. 64. West briminghamAF project—HTN—37%,IHD—29%
  65. 65. Lifetime risk @ 4o yrs –26% in men ,23% in women—FRAMINGHAM STUDY.
  66. 66. Relative risk for death –1.5 in men ,1.9 in women—no age influence.
  67. 67. PAROXYSMAL- >>>>>>>PERMANENT---8% per yr</li></li></ul><li>ETIOLOGY<br />CARDIAC<br /><ul><li>1.HYPERTENSION
  68. 68. 2.VALVULAR HEART DISEASE
  69. 69. 3.CORONARY HEART DISEASE
  70. 70. 4.CARDIOMYOPATHY
  71. 71. 5.CONGENITAL HEART DISEASE
  72. 72. 6. CARDIAC SURGERY
  73. 73. 7.ELECTRICAL DISEASE—SINUS NODE DYSFUNCTION,TACHY INDUCED,FAMILIAL
  74. 74. 8.PERICARDIAL DISEASES
  75. 75. 9.GENETIC</li></li></ul><li>NON CARDIAC<br /><ul><li>ENDOCRINE--THYROID DISEASE
  76. 76. TOXIC SUBSTANCE—ALCOHOL
  77. 77. AUTONOMICALLY MEDIATED
  78. 78. PULMONARY DISEASE
  79. 79. NEUROLOGICAL
  80. 80. IDIOPATHIC</li></li></ul><li>PATHOPHYSIOLOGY<br /><ul><li>still a clear picture of pathophysiology is not known.
  81. 81. Several mechanisms were put forward based on etiology.
  82. 82. What actually initiates is not known..
  83. 83. What makes an ectopic to trigger?</li></ul>For an AF to occur<br /><ul><li>1.diseased atria
  84. 84. 2.susceptible substrate
  85. 85. 3.triggering foci
  86. 86. 4.sustained activity of that trigger
  87. 87. 5.reentry circuits electrically
  88. 88. 6.structural remodelling
  89. 89. 7.wavelets formation</li></li></ul><li><ul><li>Sympatho vagal discharges--- Ca release from SR in diastole---early .delayed after depolarisation----- ectopic activity--- presence of susceptible substrate– AF
  90. 90. REENTRY depends on balance between cellular refractoriness and conduction speed.
  91. 91. refractory period decreased,slow conduction---continuous conduction in a potentially reentry zone electrically---LEADING CIRCLE THEORY..
  92. 92. Around central core--- rapidly circulating roto with a wave front .size of wave depends on tissue excitability and refractoriness--- SPIRAL WAVE THEORY.. </li></li></ul><li>CONTINUED…AF BEGETS AF<br />TRIGGER --- AF ----increased atrial rate --- decreased AP duration ----- decreased effective refractory period --- cycle of reentry continues --- atria gets habituated electrically ---- ---- electrical remodelling – increased sustained reentry--- AF <br /><ul><li>AF BEGETS AF </li></ul>This explains all the categoristion of AF <br /><ul><li>Paroxysmal -- trigger present , not sustained
  93. 93. Persistent --- electrical remodelling occurred.
  94. 94. Permanent ---- cellular remodelling occurred.</li></ul>dobrev.d HERZ 2006 : 31: 108-12<br />duytschaever--- drugs action after remodelling,cardiac res. 2005 ;67-69<br />burstein –atrial fibrosis –JACC 2008<br />
  95. 95. Pressure overload,volume overload ---- atrial enlargement --due to stretch activated channels intracellular acidosis---AF.<br />Where is the trigger coming from/<br /><ul><li>Sleeves of atrial myocardium extending into pulmonary veins.
  96. 96. SVC
  97. 97. Vein of marshall
  98. 98. Coronary sinus</li></ul>haissaguerre m NEJM 1998<br /><ul><li>REENTRANT ARRHYTHMIA----- JACC 2004</li></li></ul><li>electrophysiology<br />A.multiple wavelet reentry-<br /><ul><li>Sweep through atrium in random fashion
  99. 99. >5 to 6
  100. 100. Enough atrial tissue to be present for propagation.</li></ul>B.1 rentrant circuits or rotors-<br /><ul><li>Constant forming and disappearing
  101. 101. Cycle length too short</li></ul>C.musculature of pulmvein,posterior left atrial wall<br /><ul><li>Reentrant excitation</li></li></ul><li>ATRIAL REMODELLING<br />
  102. 102. Abnormal conduction<br />
  103. 103. AF IN HYPERTENSION<br /><ul><li>MC cause in developed countries.
  104. 104. 50 % cases.
  105. 105. HTN– reduced LV compliance ---- LA dilation ---- AF
  106. 106. HTN ---- CAD ---- AF -- THROMBO EMBOLISM
  107. 107. “ increasing pulse pressure is a strong predictor of subsequent AF”------------------------------ -Crawford
  108. 108. More risk of stroke .
  109. 109. Given a score of 1.
  110. 110. In CAD – Infrequent
  111. 111. In Ac MI --- early phase 10- 15 % cases.
  112. 112. a marker of poor prognosis earlier ….
  113. 113. Self limited</li></li></ul><li>AF IN ALCOHOLICS<br /><ul><li>Acute and chronic alcohol ingestion.
  114. 114. 60% of binge drinkers regardless of presence of alcoholic cardiomyopathy.
  115. 115. Episode of AF after heavy alcohol ingestion ---holiday heart syndrome.
  116. 116. Chronic alcohol---- htn,cardiomyopathy---- HF ---- AF</li></li></ul><li>AF IN THYROID DISORDERS<br /><ul><li>20-25 % of older patients.
  117. 117. Uncommon in < 30 yrs
  118. 118. Serum free thyroxine concentration ---independently assosciated with AF.
  119. 119. Digoxin alone cannot control the heart rate.
  120. 120. B blockers are drug of choice
  121. 121. Usually transient.
  122. 122. Cardioversion not to be attempted until normo thyroid..</li></li></ul><li>AF IN CARDIOMYOPATHY<br /><ul><li>28% of HOCM
  123. 123. Reversible after cardioversion ,ventricular rate control .
  124. 124. 20 % of DCM
  125. 125. Mild to moderate --- no change in mortality.
  126. 126. Advanced HF – SCD</li></ul>Genetic causes<br /><ul><li>4 genes --- k channel subunits
  127. 127. Shortening of AP
  128. 128. Decreased atrial effective refractory period
  129. 129. DNA polymorphisms</li></li></ul><li>AF post operative <br />20- 40 % of CABG 2-8 th postoperative days<br />Who are at risk<br /><ul><li>Elderly
  130. 130. Prev h/o of AF
  131. 131. RCA stenosis
  132. 132. B blockers discontinued preoperatively.
  133. 133. Left atrial volume --- strong ,independent predictor of post op AF. CRAWFORD</li></li></ul><li>AF IN RHD<br /><ul><li>MS --- 29%
  134. 134. MR 16 %
  135. 135. TR
  136. 136. MS with MR --- 52 %
  137. 137. In AS with HF
  138. 138. If a patient in MS had AF ---- risk of stroke is 3-7 times than that of in NSR .
  139. 139. All patients to be anticooagulated.</li></li></ul><li>Clinical features<br />Asymptomatic<br />Triggers—fever ,chest infection , HTN , HF<br />
  140. 140. WHEN SYNCOPE OCCURS,SUSPECT?<br /><ul><li>Pre excitation
  141. 141. Increased AV CONDUCTION
  142. 142. Sinus node disease---sinus arrest
  143. 143. HOCM
  144. 144. AS
  145. 145. Apex pulse deficit
  146. 146. BP average of three
  147. 147. Hypotension or normal or hypertensive</li></li></ul><li>Diagnosis<br /><ul><li>ECG
  148. 148. 2D ECHO
  149. 149. HOLTER MONITORING—PAROXYSMAL
  150. 150. EXERCISE STRESS TEST- IHD
  151. 151. CATHETERISATION –BEFORE ABLATION
  152. 152. THYROID FUNCTION TESTS IN ALL.
  153. 153. Chest x ray
  154. 154. Fasting lipid profile</li></li></ul><li>ECG of AF<br />
  155. 155. Evaluation of AF based on ECG<br /><ul><li>Very irregular ,disorganisedatrial activity– fibrillatory waves.
  156. 156. F waves– several independent re entrant wavelets within atria.
  157. 157. Fine or coarse
  158. 158. May be flat line between R-R complexes
  159. 159. AR . 350 -500 bpm
  160. 160. VR --- irregularly irregular , conduction of AV NODE.
  161. 161. How are QRS complexes/
  162. 162. Narrow/broad
  163. 163. Broad--- BBB, aberrant conduction ,pre excitation
  164. 164. HR calculation– 6 second time lines—6*10</li></li></ul><li>How do you differentiate?<br />In case of FVR to differentiate from SVT<br /><ul><li>Carotid sinus pressure
  165. 165. The R-R interval increases ---undualting base line.
  166. 166. From MAT ---- coarse waves of AF taken as P waves .
  167. 167. P waves do change in MAT ..not so in AF.
  168. 168. Regular R-R intervals in AF –
  169. 169. implanted ventricular pacemakers.
  170. 170. Complete AV dissosciation ---- 60 bpm
  171. 171. Complete AV Block ---- 40 bpm
  172. 172. Digitalis toxicity
  173. 173. From PVC s</li></li></ul><li>ASHMANN PHENOMENON<br /><ul><li>Long R- R interval is followed by short R- R intervals.
  174. 174. Atrial impulse may find the RBBB still refractory..
  175. 175. Wide QRS complexes.
  176. 176. Complex with a short cycle following long cycle is called ashmann phenomenon.
  177. 177. How you diff--- lack of compensatory pause. </li></li></ul><li>AF with WPW <br /><ul><li>Shorter refractory period in specialised cells of abnormal pathway..
  178. 178. They don’t have refractory period of 0.35 seconds as in AV NODE.
  179. 179. So there will be a fast ventricular rate.
  180. 180. What is the imp?
  181. 181. AV NODAL blocking drugs are contraindicated.
  182. 182. SCD </li></li></ul><li>
  183. 183. 2d echo<br /><ul><li>see for left atrial size..
  184. 184. Normal is less than 4 cm in adults.
  185. 185. Early marker of uncontrolled hypertension.
  186. 186. Check for valvular lesions
  187. 187. Check for left ventricular end diastolic volumes.
  188. 188. Cardiac catheterisation ---- pacemaker implantation
  189. 189. Holter monitoring ---- paroxysmal events..
  190. 190. stress testing in case of IHD.
  191. 191. Stress testing for CVR.</li></li></ul><li>DIFFERENTIAL DIAGNOSIS<br /><ul><li>1.AFL
  192. 192. 2.MULTIFOCAL ATRIAL TACHYCARDIA.
  193. 193. 3.ATRIAL PREMATURE COMPLEXES
  194. 194. 4.SINUS TACHYCARDIA
  195. 195. 5.VENTRICULAR TACHYCARDIA
  196. 196. 6.VENTRICULAR FIBRILLATION</li></li></ul><li>THANK YOU<br />

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