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AV Nodal Blocks

  1. 1. Dr. S. Aswini Kumar. MD Professor of Medicine Medical College Hospital Thiruvananthapuram A V N o d e BLOCK
  2. 2. Sino-Atrial Node <ul><li>Anatomy </li></ul><ul><li>Natural Pacemaker </li></ul><ul><li>Location </li></ul><ul><ul><ul><li>Upper Right Atrium </li></ul></ul></ul><ul><ul><ul><li>Close to SVC, RAA </li></ul></ul></ul><ul><ul><ul><li>epicardial in location </li></ul></ul></ul><ul><li>1.5 cm long 2-3mm wide </li></ul><ul><li>Neuromyocardial cells </li></ul><ul><li>Blood supply </li></ul><ul><ul><li>RCA 60% </li></ul></ul><ul><ul><li>LCX 40% </li></ul></ul><ul><li>Physiology </li></ul><ul><li>IDR - 80 bpm </li></ul><ul><li>sympathetic & parasympathetic </li></ul><ul><li>Sympathetic -  HR </li></ul><ul><li>Parasympathetic  HR </li></ul>2007-06-11
  3. 3. Atrial Depolarisation <ul><li>Anatomy </li></ul><ul><li>? Tracts – </li></ul><ul><ul><li>Bachman, </li></ul></ul><ul><ul><li>Thorel </li></ul></ul><ul><ul><li>Wenkebach </li></ul></ul><ul><li>Muscular ridges </li></ul><ul><li>From SA node across myocardial cells </li></ul><ul><li>Physiology </li></ul><ul><li>Propagated action potential results in myocardial contraction </li></ul><ul><li>Represented on the ECG as P wave </li></ul><ul><li>Passes to AV node in the floor of the RA </li></ul>2007-06-11
  4. 4. AV Node <ul><li>Anatomy </li></ul><ul><li>Tadpole shaped </li></ul><ul><li>2 X 5 mm </li></ul><ul><li>Endocardial, </li></ul><ul><li>IA Septum at the junction of atria and ventricles </li></ul><ul><li>Blood Supply: </li></ul><ul><ul><li>RCA - 95 % </li></ul></ul><ul><ul><li>LCX - 5 % </li></ul></ul><ul><ul><li>occasionally from both </li></ul></ul><ul><li>Physiology </li></ul><ul><li>Spread of depolarisation - from atrial myocardium </li></ul><ul><li>IDR - 60 bpm </li></ul><ul><li>Delay 0.15 seconds </li></ul><ul><ul><li>time atria to expel blood </li></ul></ul><ul><ul><li>time for ventricular filling </li></ul></ul><ul><ul><li>protection to ventricles re; atrial arrhythmias </li></ul></ul>2007-06-11
  5. 5. AV Node <ul><li>Physiology (contd) </li></ul><ul><li>Autonomic nervous control - not as pronounced as SA Node </li></ul><ul><li>Sympathetic stimulation -  IDR &  AV nodal conduction time </li></ul><ul><li>Parasympathetic stimulation - opposite </li></ul><ul><li>Electrocardiogram </li></ul><ul><li>AV nodal conduction is represented on the ECG as the PR segment </li></ul>2007-06-11
  6. 6. The Bundle Of His <ul><li>Anatomy </li></ul><ul><li>Directly continuous with the AV node </li></ul><ul><li>20 mm long </li></ul><ul><li>Endocardial </li></ul><ul><li>Within the IV septum </li></ul><ul><li>Bundle of discreet fibres - crosses AV ring </li></ul><ul><li>No dedicated blood supply </li></ul><ul><li>Physiology </li></ul><ul><li>Only normal pathway Atria  Ventricles </li></ul><ul><li>IDR - 50 bpm </li></ul><ul><li>Nervous stimulation - minor effect </li></ul><ul><li>Depolarisation of the Bundle is not seen on the surface ECG </li></ul>2007-06-11
  7. 7. The Bundle Branches & Purkinje Fibers <ul><li>Bundle branches </li></ul><ul><li>Bundle of His separates into 2 main branches, </li></ul><ul><ul><li>Left bundle </li></ul></ul><ul><ul><li>Right bundle </li></ul></ul><ul><li>Left bundle – </li></ul><ul><ul><li>Antero-Superior division </li></ul></ul><ul><ul><li>Postero-Inferior division </li></ul></ul><ul><li>No dedicated blood supply </li></ul><ul><li>IDR - 40 bpm </li></ul><ul><li>Purkinje Fibers </li></ul><ul><li>Bundle Branches divide further </li></ul><ul><ul><li>Small, dense network conducting tissue </li></ul></ul><ul><li>Endocardial  Epicardial </li></ul><ul><li>No dedicated blood supply </li></ul><ul><li>Entire musculature depolarizes quickly </li></ul><ul><li>IDR - 20 bpm </li></ul><ul><li>Nervous stimulation </li></ul><ul><ul><ul><li>- minor effect only </li></ul></ul></ul>2007-06-11
  8. 8. Ventricular De & Repolarization <ul><li>Depolarization </li></ul><ul><li>Bundle Branch & purkinje fibre depolarisation constitutes ventricular depolarisation </li></ul><ul><li>Represented on the ECG as the QRS </li></ul><ul><li>Repolarization </li></ul><ul><li>Repolarisation is smaller in amplitude & slower than depolarisation </li></ul><ul><li>Atrial repolarisation occurs within the QRS is masked </li></ul><ul><li>Ventricular repolarisation is represented on the ECG as a T </li></ul>2007-06-11
  9. 9. The Conducting System - Summary 2007-06-11
  10. 10. The AV Nodal Conduction <ul><li>AV nodal conduction time is represented on the ECG as the PR segment. </li></ul><ul><li>But - we always measure the PR interval. </li></ul>PR Segment PR Interval 2007-06-11
  11. 11. AV Nodal Blocks (Heart Blocks) <ul><li>Disturbances of the conduction through the heart, occurring at the AV Node </li></ul><ul><li>AV Node – damaged or diseased </li></ul><ul><li>Delay or total block of impulses at the AV Node </li></ul><ul><li>This conduction defect can be seen on the ECG </li></ul>2007-06-11
  12. 12. Causes <ul><li>Increased vagal tone </li></ul><ul><li>Highly trained athletes </li></ul><ul><li>Myocardial Infarction </li></ul><ul><li>Coronary spasm </li></ul><ul><li>Digitalis intoxication </li></ul><ul><li>Beta blockers </li></ul><ul><li>Viral Myocarditis </li></ul><ul><li>Degeneration (Age) </li></ul><ul><li>Sclerosis (Aortic) </li></ul><ul><li>Cardiac surgery (Trauma) </li></ul>2007-06-11
  13. 13. Degenerative diseases <ul><li>Lev’s Disease: </li></ul><ul><ul><ul><li>Calcification and sclerosis of fibrous cardiac cytoskeleton </li></ul></ul></ul><ul><ul><ul><li>Also involving aortic/mitral valves </li></ul></ul></ul><ul><li>Lenegre’s Disease </li></ul><ul><ul><ul><li>Primary sclero-degenerative disease of conducting system </li></ul></ul></ul><ul><ul><ul><li>No involvement of fibrous skeleton of heart </li></ul></ul></ul>2007-06-11
  14. 14. First Degree Heart Block (1 º HB) <ul><li>SA Node – normal </li></ul><ul><ul><ul><li>Normal P wave </li></ul></ul></ul><ul><li>AV Node conducts more slowly than normal </li></ul><ul><ul><ul><li>Prolonged PR Interval </li></ul></ul></ul><ul><li>Rest of conduction is normal </li></ul><ul><ul><ul><li>Normal QRS </li></ul></ul></ul><ul><li>PR Interval > 0.2 seconds (>5 small sq) but constant </li></ul>2007-06-11
  15. 15. First Degree Heart Block (1 º HB) 2007-06-11
  16. 16. First Degree Heart Block (1 º HB) <ul><li>More appropriately called as </li></ul><ul><ul><ul><li>Prolonged AV Conduction </li></ul></ul></ul><ul><li>PR interval is determined by </li></ul><ul><ul><ul><li>Atrial, AV nodal and His purkinje activation </li></ul></ul></ul><ul><li>Site of involvement </li></ul><ul><ul><ul><li>Could be any of these </li></ul></ul></ul><ul><ul><ul><li>Narrow QRS – AV nodal origin </li></ul></ul></ul><ul><li>Clinical significance </li></ul><ul><ul><ul><li>None, Prognosis good </li></ul></ul></ul><ul><li>Treatment </li></ul><ul><ul><ul><li>None </li></ul></ul></ul>2007-06-11
  17. 17. Second Degree Heart Block (2 º HB) (Intermittent Heart Block) <ul><li>Second degree AV block is said to be present when some atrial impulses fail to conduct to the ventricles </li></ul><ul><li>Mobitz Type I (Wenkebach) </li></ul><ul><li>Mobitz Type II </li></ul><ul><li>2 : 1 Fixed Heart Block </li></ul>Karel Frederik Wenckebach 2007-06-11
  18. 18. Second Degree Heart Block (2 ºHB) Mobitz Type I (Wenkebach) <ul><li>Conduction through the AV Node – progressively delayed until a drop beat is seen </li></ul>PR PR PR DROPPED BEAT 2007-06-11
  19. 19. Second Degree Heart Block (2 ºHB) Mobitz Type I (Wenkebach) 2007-06-11
  20. 20. Second Degree Heart Block (2 ºHB) Mobitz Type I (Wenkebach) <ul><li>The PR Interval is NOT constant </li></ul><ul><li>PR Interval prolongs with each beat until a beat is dropped </li></ul><ul><li>The pause that follows is less than full compensatory </li></ul><ul><li>Difference between longest and shortest PR >100msec </li></ul><ul><li>After each dropped beat, the PR interval becomes normal </li></ul><ul><li>Clinical Significance </li></ul><ul><ul><ul><li>Slight symptoms: Lethargy, Confusion </li></ul></ul></ul><ul><li>Treatment </li></ul><ul><ul><ul><li>Pacemaker if during day &/or symptoms </li></ul></ul></ul><ul><ul><ul><li>this can progress to 3 º Heart Block </li></ul></ul></ul>2007-06-11
  21. 21. Second Degree Heart Block (2 ºHB) Mobitz Type II <ul><li>Conduction through the AV node is constant but dropped beats are seen </li></ul>PR PR DROPPED BEAT PR 2007-06-11
  22. 22. Second Degree Heart Block (2 ºHB) Mobitz Type II <ul><li>Occasionally a dropped beat is seen </li></ul><ul><ul><ul><li>Conduction fails suddenly and un expectedly without a preceding change in the PR intervals </li></ul></ul></ul>2007-06-11
  23. 23. Second Degree Heart Block (2 ºHB) Mobitz Type II <ul><li>It is a regularly irregular grouped rhythm </li></ul><ul><ul><ul><li>with dropped QRS complexes that shows no variation in the PR interval whatsoever between the dropped beats. </li></ul></ul></ul><ul><li>PR prolongation </li></ul><ul><ul><ul><li>is a major diagnostic clue that helps to differentiate between these two types. PR Interval normal & constant </li></ul></ul></ul><ul><li>Clinical significance – </li></ul><ul><ul><ul><li>More significant disease due to disease of His Purkinje </li></ul></ul></ul><ul><li>Treatment </li></ul><ul><ul><ul><li>Pacemaker </li></ul></ul></ul><ul><ul><ul><li>This can progress to 3 º Heart Block </li></ul></ul></ul>2007-06-11
  24. 24. Second Degree Heart Block (2 ºHB) 2 : 1 HB <ul><li>Unable to strictly classify as Mobitz Type I or II </li></ul><ul><li>Particular type of second degree Heart Block </li></ul><ul><li>Ratio 2 P waves : 1 QRS </li></ul>DROPPED BEAT DROPPED BEAT 2007-06-11
  25. 25. Second Degree Heart Block (2 º) 2 : 1 2007-06-11
  26. 26. Second Degree Heart Block (2 º) 2 : 1 HB <ul><li>Clinical significance:- </li></ul><ul><ul><ul><li>Unable to classify as Mobitz type I or II </li></ul></ul></ul><ul><ul><ul><li>Difficult to diagnose the level of lesion </li></ul></ul></ul><ul><ul><ul><li>Normal QRS and long PR interval indicate AV nodal </li></ul></ul></ul><ul><ul><ul><li>Associate BBB suggests level below AV node </li></ul></ul></ul><ul><ul><ul><li>This can deteriorate to 3 º Heart Block </li></ul></ul></ul><ul><ul><ul><li>Will be associated with symptoms Dizziness, lethargy etc. </li></ul></ul></ul><ul><li>Treatment :- </li></ul><ul><ul><ul><li>Temporary Trans-cutaneous pacing in low risk </li></ul></ul></ul><ul><ul><ul><li>Temporary Trans-venous pacing </li></ul></ul></ul><ul><ul><ul><li>Permanent Pacemaker Implantation </li></ul></ul></ul><ul><ul><ul><li>Withdraw any offending drugs </li></ul></ul></ul><ul><ul><ul><li>Correction of any electrolyte abnormality </li></ul></ul></ul>2007-06-11
  27. 27. Third Degree Heart Block (3 º HB) (Complete Heart Block) <ul><li>Pathophysiology: </li></ul><ul><ul><li>Complete failure of AV Node to conduct impulses from SA Node </li></ul></ul><ul><ul><li>No impulses from Sinus Node will pass through to the ventricles </li></ul></ul><ul><ul><li>Some part of conducting system will take over as pacemaker </li></ul></ul><ul><ul><li>The escape pacemaker can be in the AV node </li></ul></ul><ul><ul><li>Or it can be in the His bundle or even distal to it </li></ul></ul><ul><ul><li>Even a myocardial cell have an automaticity at a rate of 10-15 bpm </li></ul></ul><ul><li>Symptoms: </li></ul><ul><ul><li>Dizzy spells, near syncope, frank syncope, easy fatiguability </li></ul></ul><ul><li>Level of block </li></ul><ul><ul><li>At AV nodal – Junctional rhythm with narrow QRS complex </li></ul></ul><ul><ul><li>At His-Purkinje level - Ventricular escape rhythm with wide QRS </li></ul></ul>2007-06-11
  28. 28. Third Degree Heart Block (3 ºHB) (Complete Heart Block) <ul><li>P wave rate – normal </li></ul><ul><li>Ventricular rate – slow </li></ul><ul><li>Ventricular complex may be broad </li></ul><ul><ul><ul><li>Idioventricular rhythm </li></ul></ul></ul><ul><li>Complete dissociation between P waves & QRS </li></ul>P P P P P QRS QRS 2007-06-11
  29. 29. Third Degree Heart Block (3 º) (Complete Heart Block) 2007-06-11
  30. 30. Differences between CHBs <ul><li>Congenital CHB </li></ul><ul><li>Present from birth </li></ul><ul><li>Isolated finding </li></ul><ul><li>Connective tissue disorders </li></ul><ul><li>Hereditary form – SCN5A gene </li></ul><ul><li>QRS occurs at 40-50 bpm </li></ul><ul><li>QRS duration normal </li></ul><ul><li>Increases with atropine </li></ul><ul><li>Site of block is AV node </li></ul><ul><li>That is a proximal block </li></ul><ul><li>Pacemaker not mandatory </li></ul><ul><li>Acquires CHB </li></ul><ul><li>Occurs later in life </li></ul><ul><li>Inferior wall infarction - AVB </li></ul><ul><li>Anterior wall infarction – TFB </li></ul><ul><li>Leve’s or Lenegre’sdisease </li></ul><ul><li>QRS occurs at 20-30 bpm </li></ul><ul><li>QRS duration prolonged </li></ul><ul><li>Does not  with atropine </li></ul><ul><li>Site of block distal to AV node </li></ul><ul><li>That is a distal block </li></ul><ul><li>Mandates a pacemaker </li></ul>2007-06-11
  31. 31. Third Degree Heart Block (3 º) (Complete Heart Block) <ul><li>Clinical significance </li></ul><ul><ul><ul><li>Symptoms LOC, Confusion, Dizziness, Low BP </li></ul></ul></ul><ul><ul><ul><li>This can deteriorate to Cardiac Asystole </li></ul></ul></ul><ul><ul><ul><li>This can precipitate VT/VF </li></ul></ul></ul><ul><li>Treatment – medical </li></ul><ul><ul><ul><li>Atropine if block at AV nodal level </li></ul></ul></ul><ul><ul><ul><li>Isoproterenol – IV infusion </li></ul></ul></ul><ul><ul><ul><li>Caution in Acute MI </li></ul></ul></ul><ul><li>Treatment - Pacing </li></ul><ul><ul><ul><li>Temporary trans-cutaneous pacing </li></ul></ul></ul><ul><ul><ul><li>Temporary Trans-venous pacing </li></ul></ul></ul><ul><ul><ul><li>Permanent Pacemaker Implantation </li></ul></ul></ul>2007-06-11
  32. 32. Third Degree Heart Block (3 º HB) (Complete AV Dissociation) <ul><li>P wave rate – normal </li></ul><ul><li>Ventricular rate – slow </li></ul><ul><li>Ventricular complex may be broad or normal </li></ul><ul><li>Occasional Capture Beats </li></ul><ul><li>Complete dissociation between P waves & QRS </li></ul>P P P P P QRS QRS CAPTURED 2007-06-11
  33. 33. Two types of AV Dissociation <ul><li>Isorhythmic Dissociation </li></ul><ul><li>Severe Sinus Bradycardia </li></ul><ul><li>Junctional Escape Rhythm </li></ul><ul><li>Sinus rate = Junctional rate </li></ul><ul><li>They compete against each </li></ul><ul><li>P waves before in or after QRS </li></ul><ul><li>Causes </li></ul><ul><ul><ul><li>Digoxin toxicity </li></ul></ul></ul><ul><ul><ul><li>Poisonings </li></ul></ul></ul><ul><li>Treatment </li></ul><ul><ul><ul><li>Remove cause of bradycardia </li></ul></ul></ul><ul><ul><ul><li>Discontinue digitalis </li></ul></ul></ul><ul><ul><ul><li>Stop verapamil or beta blocker </li></ul></ul></ul><ul><ul><ul><li>Increase sinus nodal rate </li></ul></ul></ul><ul><li>Interference Dissociation </li></ul><ul><li>Lower level pacemaker </li></ul><ul><li>Junctional or ventricular </li></ul><ul><li>Faster intrinsic rate </li></ul><ul><li>Compete with sinus node </li></ul><ul><li>Ventricular Tachycardia </li></ul><ul><li>Causes </li></ul><ul><ul><ul><li>Myocardial Ischemia </li></ul></ul></ul><ul><ul><ul><li>Irritation of cardiac surgery </li></ul></ul></ul><ul><li>Treatment </li></ul><ul><ul><ul><li>Antiarrhythmic drugs </li></ul></ul></ul><ul><ul><ul><li>Correction of ischemia </li></ul></ul></ul><ul><ul><ul><li>Accelerated ideoventricular rhythm </li></ul></ul></ul><ul><ul><ul><li>Treatment of metabolic abnormality </li></ul></ul></ul>2007-06-11
  34. 34. Summary <ul><li>1 º </li></ul><ul><ul><ul><li>Prolongation of PR Interval </li></ul></ul></ul><ul><li>2º </li></ul><ul><ul><ul><li>Mobitz I – Increasing PR Interval until dropped beat is seen </li></ul></ul></ul><ul><ul><ul><li>Mobitz II – Constant PR Interval with more P waves to QRS </li></ul></ul></ul><ul><ul><ul><li>2 : 1 – Constant PR Interval with more P waves to QRS </li></ul></ul></ul><ul><li>3º </li></ul><ul><ul><ul><li>Complete pathological block at the AV node </li></ul></ul></ul><ul><ul><ul><li>Complete dissociation between P waves & QRS </li></ul></ul></ul>2007-06-11
  35. 35. 2007-06-11

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