AV junctional Rhythm disturbances.pptx

AV junctional rhythm disturbances, causes, differential diagnosis, treatment

1. AV junctional Rhythm disturbances Samir M. Rafla, FACC, FESC Prof. of Cardiology Alexandria University 01001495577 [email protected] WhatsApp Samir Rafla

2. If retrograde activation of the  atria  occurs, a constant relation exists between the  P wave  and the  QRS complex . If retrograde conduction is impaired, the atria remain under control of the sinus impulse, resulting in  AV dissociation . The ventricular rate is generally faster than the atrial rate except when an accelerated junctional rhythm develops in the presence of atrial tachycardia, atrial fibrillation, or  atrial flutter . An accelerated junctional rhythm is seen predominantly in patients with heart disease. Common causes include  digitalis  intoxication,  acute myocardial infarction  (MI),  intracardiac surgery , or  myocarditis . Digitalis was responsible for more than half of the cases. MI and intracardiac surgery are probably the more common causes in recent years. The arrhythmia was reported in up to 10 percent of patients with acute MI. It is more commonly associated with inferior than  anterior MI . it is a poor prognostic sign.

3. Occasionally there is an anterograde exit block of the junctional impulse, and the ventricular rate becomes slow. On the ECG, type I exit block can be suspected in the presence of “group beating” (suggestive of Wenckebach periodicity), and type II exit block can be suspected in the presence of a long cycle that is a multiple of the basic interectopic interval (Figure). If the QRS complex is wide, an accelerated junctional rhythm resembles an accelerated ventricular rhythm. The rate of the ectopic ventricular rhythm is usually 70 to 110 beats/min. The ventricular origin of the rhythm can be recognized if capture complexes with narrow QRS or fusion complexes are present.

4. Etiology- Causes of junctional rhythm include the following: Sick sinus syndrome  (including drug-induced) Digoxin toxicity Ischemia of the AVN, especially with acute inferior infarction involving the posterior descending artery, the origin of the AV nodal artery branch. Acutely after cardiac surgery, especially in children within 4 days after surgery for congenital cardiac defects; a literature review indicated that in patients undergoing surgery for congenital heart disease, the risk of junctional ectopic tachycardia is increased by surgery near the AV node, cardiopulmonary bypass operative time of over 90 minutes, young age, the use of inotropic drugs, and hypomagnesemia   Acute inflammatory processes (eg,  acute rheumatic fever ,  lyme disease ), which may involve the conduction system Diphtheria Other drugs (eg, beta-blockers, calcium blockers, most antiarrhythmic agents) that cause sinus bradycardia Metabolic states with increased adrenergic tone- Isoproterenol infusion

5. Epidemiology Junctional rhythms are common in patients with sick sinus syndrome or in patients who have significant bradycardia that allows the AV nodal region to determine the heart rate. Sex-related demographics Junctional escape rhythms, which are common in younger and/or athletic individuals during periods of increased vagal tone (eg, sleep), occur equally in males and females. Age-related demographics This rhythm may occur in persons of any age. Junctional rhythms during sleep are common in children and in athletic adults.

6. Prognosis- No evidence suggests increased mortality. Prognosis is good. Morbidity/mortality - The heart rate during a junctional rhythm often determines whether the patient has symptoms. Presence of AV dissociation can lead to symptoms in patients because of atrial conduction and subsequent contraction when the tricuspid valve is closed (ie, canon  a  waves). Periods of junctional rhythm are not necessarily associated with an increase in mortality. If an obvious cause is present, such as  complete heart block  or  sick sinus syndrome , then the morbidity or mortality is directly related to that and not to the junctional rhythm mechanism, Complications- Complications of junctional rhythm are usually limited to symptoms such as dizziness, dyspnea, or presyncope. Accidental injury may result from syncope if the arrhythmia is not tolerated well. Exacerbation of cardiac comorbidities, such as congestive heart failure and rate-related cardiac ischemia, may occur. Prognosis- No evidence suggests increased mortality. Prognosis is good. Morbidity/mortality- The heart rate during a junctional rhythm often determines whether the patient has symptoms. Presence of AV dissociation can lead to symptoms in patients because of atrial conduction and subsequent contraction when the tricuspid valve is closed (ie, canon  a  waves). If an obvious cause is present, such as  complete heart block  or  sick sinus syndrome , then the morbidity or mortality is directly related to that and not to the junctional rhythm mechanism, which is serving as a "backup rhythm" during the periods of bradycardia. Accelerated junctional rhythms may be a sign of digitalis toxicity. Complications- Complications of junctional rhythm are usually limited to symptoms such as dizziness, dyspnea, or presyncope. Accidental injury may result from syncope if the arrhythmia is not tolerated well. Exacerbation of cardiac comorbidities, such as congestive heart failure and rate-related ischemia, may occur.

7. The strip below shows a junctional rhythm with retrograde P waves seen just before the QRS complex. The second rhythm strip shows retrograde P waves just after the QRS complex.

8. Three examples of paroxysmal junctional tachycardia demonstrating varying relationships of P and QRS. (A) Retrograde P wave preceding the QRS ("upper nodal"). (B) P and QRS simultaneous ("midnodal"). (C) Retrograde P wave following QRS ("lower nodal").

9. Variation of retrograde conduction with NPJT. (A) NPJT with intact retrograde conduction. Note retrograde P wave following every QRS. (B) NPJT with retrograde Wenckebach periods. The R-P interval gradually increases from 0.16 to 0.20 sec during the first five QRS complexes. Retrograde block occurs after the sixth QRS, which is then followed by a sinus escape and ventricular capture (C). The eighth QRS is followed by a fusion P wave (f), with fusion occurring between sinus escape and retrograde P. (C) NPJT with type II retrograde block. The first two QRS complexes are followed by P waves with a fixed R-P interval. There is retrograde block after the third QRS, which then allows the sinus to escape with an antegrade P wave and ventricular capture with sinus escape and ventricular captures.

10. Nonparoxysmal junctional tachycardia (NPJT) with and without A-V dissociation. (A) NPJT with intact retrograde conduction. Note that as the A-V junctional pacemaker overtakes the sinus pacemaker, retrograde P waves become apparent (last three complexes). A-V dissociation is present only for the two beats between the three sinus captures and the three retrograde captures. (B) NPJT with incomplete A-V dissociation. The sinus rate is 100 beats/min and the ventricular rate is 116 beats/min. Atria and ventricles are dissociated except for the eighth P wave which occurs at a time when A-V junction is not refractory capturing the ventricles (C). (C) NPJT with incomplete A-V dissociation and sinus bradycardia. The atrial rate is 50/min while the ventricular rate is 72/min. The third and fifth P wave captures the ventricles. (D) Double tachycardia with NPJT at a rate of 84 beats/min, and PAT with an atrial rate of 150 beats/min. Complete A-V dissociation is noted. QRS widening is due to preexistent conduction defect.

11. PJT spontaneous and induced. Shown are leads I, II, III, V1, and HBE. Atrial electrograms are labeled A and His bundle electrograms H. (A) There are two sinus beats followed by two atrial premature beats (APC). The second APC is conducted with a long A-H and is followed by an atrial echo and a run of PJT. (B) PJT induced by atrial pacing. Atrial pacing spikes are labeled with arrows. Shown are four paced beats followed by a timed extra stimulus (EX) which is conducted with a long A-H and is followed by a run of PJT. Atrial echoes are present but masked in the ventricular electrogram. These were subsequently demonstrated with intraatrial recording.

12. Junctional Bradycardia (Example)

13. Junctional bradycardia due to profound sinus node dysfunction. No atrial activity is apparent.

14. Note the retrograde P waves that precede each QRS complex.

15. Accelerated junctional rhythm is present. Note the inverted P waves that precede each QRS complex, with a rate of 115 bpm.

16. ECG showing junctional tachycardia. Narrow complex QRS. No P waves. Heart rate fast. Treatment Amiodarone to control the rhythm, electrical cardioversion is not used.

17. Junctional tachycardia (rate about 115/min) dissociated from a slightly slower  sinus tachycardia  (rate about 107/min) producing one form of double tachycardia; pairs of ventricular capture (C) beats (5th, 6th, 19th, and 20th beats);

18. Figure 1A: Baseline postoperative electrocardiogram showing sinus rhythm with right bundle branch block.  B: Electrocardiogram showing junctional ectopic tachycardia at a rate of 205 beats/min with the underlying right bundle branch block and ventriculoatrial dissociation. Intravenous sotalol for the management of postoperative junctional ectopic tachycardia

19. Figure 1Electrocardiogram on initial presentation. Junctional ectopic tachycardia (JET) with aberrant intraventricular conduction vs independent fascicular tachycardia. The shortest cycle length during tachycardia was 160 msec. QRS morphology during JET was similar to that observed during sinus rhythm after resolution of tachyarrhythmia. Junctional ectopic tachycardia secondary to myocarditis associated with sudden cardiac arrest

20. Atrial Overdrive Pacing to Differentiate Junctional Tachycardia (JT) from Atrioventricular Nodal Reentrant Tachycardia (AVNRT) Left side,  Ladder diagrams illustrating response to atrial overdrive pacing.  Top,  During JT, the earliest return signal is an H followed by an A, resulting in an AHHA response.  Bottom,  During AVNRT, the earliest return signal is an A, resulting in an AHA response.  Star  represents atrial pace.  Solid arrows  represent conduction through the atrium, fast AV nodal pathway, and His.  Interrupted arrows  represent conduction through the slow AV nodal pathway.  A,  Atrium;  AVN,  atrioventricular node;  H,  His.  Right side,  Intracardiac electrograms.  Top,  During JT, tachycardia cycle length is 468 ms. Atrial overdrive pacing is performed at 448 ms. After cessation of pacing, an AHHA response is observed.  Solid arrows  represent conduction down the fast AV nodal pathway.  Bottom,  During AVNRT, tachycardia cycle length is 320 ms. Atrial overdrive pacing is performed at 300 ms. After cessation of pacing, an AHA response is observed.  Interrupted arrows  represent slow pathway conduction.  Ap,  Atrial pace;  CS,  coronary sinus;  HRA,  high right atrium;  Reva,  right ventricular apex. (From : Novel use of atrial overdrive pacing to rapidly differentiate junctional tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm 8:840-844, 2011.)

21. Atrial fibrillation with 3rd degree AV block and a junctional escape rhythm (“regularized AF”)

22. Coarse atrial fibrillation (irregular baseline with atrial complexes at rate > 400 bpm) Regular narrow complex rhythm at 60 bpm The combination of atrial fibrillation with a regular rhythm (“ regularised AF”) indicates that none of the atrial impulses are conducted to the ventricles, i.e. complete heart block is present The narrow complex rhythm is therefore a junctional escape rhythm Regularized AF is characteristically seen as a consequence of  digoxin toxicity

23. Rhythm strip in AJR:  Narrow complex rhythm; inverted retrograde P waves seen before the QRS complex

24. Re-entrant Junctional Rhythm (AVNR T )

25. Junctional Tachycardia Narrow complex tachycardia at 115 bpm Retrograde P waves — inverted in II, III and aVF ; upright in V1 and aVR Short PR interval (< 120 ms) indicates a junctional rather than atrial focus

26. Atrioventricular Junctional Rhythms   ACCELERATED AV JUNCTIONAL RHYTHM (NONPAROXYSMAL JUNCTIONAL TACHYCARDIA) Nonparoxysmal junctional  tachycardia is now called  accelerated AV  junctional rhythm  and is believed to be automatic with the following characteristics: 1- The rate of junctional discharge is only moderately increased, being about 70 to 130 beats/min (see Figure). 2-The ectopic rhythm lacks the sudden onset and termination that are characteristic of the paroxysmal type of  AV node  reentrant tachycardia. 3- The relation between the  sinus rhythm  and the accelerated AV junctional rhythm depends on the state of anterograde and retrograde conduction at the  AVJ  and on the atrial and ventricular rates.

27. A 76-year-old woman with a history of paroxysmal atrial fibrillation is admitted to the hospital for elective surgery. Her antiarrhythmic medication is 80 mg of sotalol twice daily. Before the operation, she has a sudden syncopal attack, and an electrocardiogram (ECG) shows a wide QRS self-terminating tachycardia. The diagnosis of drug-induced long QT syndrome

28. AV junctional Rhythm disturbances Samir M. Rafla, FACC, FESC Prof. of Cardiology Alexandria University 01001495577 [email protected] WhatsApp Samir Rafla