AV junctional rhythm disturbances, causes, differential diagnosis, treatment

1. AV junctional Rhythm disturbances
Samir M. Rafla, FACC, FESC
Prof. of Cardiology
Alexandria University
01001495577
smrafla@yahoo.com
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

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.

11. 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.

13. 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.

15. Junctional Bradycardia (Example)

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

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

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

22. ECG showing
junctional tachycardia.
Narrow complex QRS.
No P waves. Heart rate
fast.
Treatment Amiodaro
ne to
control
the
rhythm,
electrical
cardiovers
ion is not
used.

23. 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);

24. 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

25. 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

28. 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.)

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

32. •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

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

36. Re-entrant Junctional Rhythm (AVNRT)

37. 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

43. 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.

47. 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

48. AV junctional Rhythm disturbances
Samir M. Rafla, FACC, FESC
Prof. of Cardiology
Alexandria University
01001495577
smrafla@yahoo.com
WhatsApp Samir Rafla