1. Junctional Dysrhythmias13
Junctional Dysrhythmias
Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program

2. Junctional Dysrhythmias
Originate in AV junction (area around AV node and bundle of His)
Can result from suppression or blockage of the SA node, increased automaticity of the AV junction or a reentry mechanism

3. Junctional Dysrhythmias
Key characteristics
P’ waves may be inverted with a short P’R interval, absent (as they are buried by the QRS complex), or follow QRS complexes
QRS complexes usually normal unless there is an intraventricular conduction defect, aberrancy or preexcitation
Instructional points:
Because the AV junction is located in the middle of the heart the impulse travels upward and causes backward or retrograde depolarization of the atria. This results in an inverted P’ wave (when they would otherwise be upright) with a short P’R interval (less than 0.12 second in duration). At the same time the impulse travels down to the ventricles and depolarizes them.
Junctional dysrhythmias will only have clinical consequences to the patient if cardiac output is adversely affected. I

4. Effect of Junctional Dysrhythmias
If the atria are depolarized concurrently or after the ventricles, the atria are forced to pump against the contracting ventricles, which contract with much greater force
Results in a loss in atrial kick, decreased stroke volume, and, ultimately, decreased cardiac output
Decreased cardiac output can also occur with slow or fast junctional dysrhythmias

5. Premature Junctional Complex (PJC)
Single early electrical impulse that arises from the AV junction
Disrupt regularity of underlying rhythm
Question to ask the students: “How will the premature beat affect the P-P and R-R intervals?”
Answer: With a premature beat the P-P and R-R interval is shorter between the beat that the premature beat follows and the premature beat.
Instructional point:
PJCs can also occur in bigeminal, trigeminal or quadrigeminal patterns. Q I

6. Causes of PJCs Typically result from increased automaticity
Other causes include:

7. Effects of PJCs
In the healthy heart, isolated PJCs are of little clinical significance
Patient may be asymptomatic or may experience palpitations
Frequent PJCs (more than 4 to 6 per minute) warn of more serious conditions and may cause hypotension due to a transient decrease in cardiac output
Instructional points:
PJCs rarely cause any concern but could indicate increased sympathetic tone which should be investigated and corrected if possible. However, frequent PJCs can result in decreased stroke volume and lead to compromised cardiac output.
PJCs are not usually followed by a compensatory pause. I

8. Treatment of PJCs Generally do not require treatment
PJCs caused by the use of caffeine, tobacco, or alcohol, or with anxiety, fatigue, or fever can be controlled by eliminating the underlying cause

9. Junctional Escape Rhythm
Arises from AV junction at rate of 40 to 60 BPM
Instructional point:
Junctional Escape is potentially lethal because it indicates that the patient’s primary pacemaker is not functioning. These patients may require the placement of a pacemaker. Furthermore, the slow rate may adversely affect cardiac output. I

10. Causes of Junctional Escape Rhythm
Junctional escape rhythm is brought about by AV heart block or conditions that interfere with SA node function
Other causes include:
Question to ask the students “What is the key difference between junctional escape rhythm, accelerated junctional rhythm and junctional tachycardia?”
Answer: The heart rate. Q

11. Effects of Junctional Escape Rhythm
Rates of greater than 50 beats per minute are usually well tolerated
Slower rates can cause decreased cardiac output and may lead to symptoms (chest pain or pressure, syncope, altered level of consciousness, hypotension)

12. Accelerated Junctional Rhythm
Arises from AV junction at rate of 60 to 100 BPM
Instructional point:
Accelerated Junctional rhythm is a common rhythm seen following cardiac arrest resuscitation until the SA node awakens and takes control of the rate. The rate is increased because of either high sympathetic tone or the effects of the adrenergic agents such as epinephrine used during resuscitation. I

13. Causes of Accelerated Junctional Rhythm
Due to increased automaticity or irritability of the AV junction

14. Effects of Accelerated Junctional Rhythm
Usually well tolerated
However, it may predispose patients with myocardial ischemia to more serious dysrhythmias
Also, because the atria are depolarized by way of retrograde conduction and may actually follow ventricular depolarization, atrial kick may be prevented resulting in decreased cardiac output

15. Treatment of Accelerated Junctional Rhythm
Given the heart rate seen with accelerated junctional rhythm, the patient is typically asymptomatic
Treatment is directed at identifying and correcting the underlying cause
Patient should be continually observed for signs of decreased cardiac output
Temporary pacing may be indicated if the patient is symptomatic

16. Junctional Tachycardia
Fast ectopic rhythm that arises from bundle of His at rate of 100 to 180 BPM
Instructional point:
Junctional Tachycardia is relatively rare but when present may serious drop cardiac output because of the very fast rate. I

17. Causes of Junctional Tachycardia
Due to enhanced automaticity and commonly the result of digitalis toxicity

18. Effects of Junctional Tachycardia
Short bursts of junctional tachycardia are well tolerated in otherwise healthy people
Palpitations, nervousness, anxiety, vertigo, lightheadedness, and syncope are frequently seen
Sustained rapid ventricular rates and retrograde depolarization of the atria results in incomplete ventricular filling during diastole leading to compromised cardiac output in patients with underlying heart disease
Loss of atrial kick may cause up to a 30% reduction in cardiac output

19. Effects of Junctional Tachycardia
Increases in cardiac oxygen requirements may increase myocardial ischemia and frequency and severity of the patient’s chest pain
Can extend the size of MI; cause congestive heart failure, hypotension, and cardiogenic shock; and possibly predispose the patient to ventricular dysrhythmias

20. Atrioventricular Nodal Reentrant Tachycardia
Some people have an abnormal extra anatomical pathway (congenital in nature) within or just next to the AV node

21. Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
Early beats can trigger AVNRT
Most common regular supra-ventricular tachycardia
Occurs more often in women than men

22. Preexcitation
Some people have accessory conduction pathways that provide a direct connection between the atria and ventricles, thereby bypassing the AV node and bundle of His
These accessory pathways allow atrial impulses to depolarize the ventricles earlier than usual
This condition is called preexcitation

23. Preexcitation
One type of preexcitation is Wolff-Parkinson-White (WPW) Syndrome
Here, the bundle of Kent, an accessory pathway, connects the atria to the ventricles, bypassing the AV node
Key ECG features include:
QRS complexes that are widened with slurring of the initial portion (delta wave)
PR interval is usually shortened (less than 0.12 seconds)

24. Preexcitation
Another type of preexcitation is Lown-Ganong-Levine (LGL) Syndrome
In LGL syndrome, the accessory pathway, referred to as the James fibers, is within the AV node
This accessory pathway bypasses the normal delay within the AV node but ventricular conduction occurs through the usual ventricular conduction pathways

25. Preexcitation
Because ventricular depolarization occurs through the normal ventricular conductive pathway the only indication of LGL on the ECG is shortening of the PR interval as a result of the accessory pathway bypassing the delay within the AV node

26. Preexcitation
Unless tachycardia is present, WPW and LGL are usually of no clinical significance
However, preexcitation (specifically WPW) can predispose the patient to various tachydysrhythmias
The most common tachydysrhythmia is atrioventricular reentrant tachycardia (AVRT), followed by atrial fibrillation and atrial flutter
Atrial fibrillation and atrial flutter seen with WPW are extremely dangerous

27. Atrioventricular Reentrant Tachycardia
AVRT, also known as circus movement tachycardia (CMT), results from a reentry circuit that includes the AV node and an accessory pathway from the atria to the ventricle such as the bundle of Kent
This reentry circuit is physically much larger than the one associated with AVNRT

28. Atrioventricular Reentrant Tachycardia
Reentry through an accessory pathway can take one of two directions, orthodromic conduction or antedromic conduction

29. Atrioventricular Reentrant Tachycardia
Orthodromic AVRT
Because of the normal conduction to the ventricles, regular, narrow QRS complexes are seen
Antedromic AVRT
Because the accessory pathway initiates conduction in the ventricles outside of the bundle of His, the QRS complex is often wider than usual, with a delta wave

30. Supraventricular Tachycardia
Collectively, the three types of tachycardia discussed in this chapter and the tachycardias referred to in the previous two chapters are referred to as supraventricular tachycardia as they originate from above the ventricles

31. Treatment of Supraventricular Tachycardia
Determine whether tachycardia is the primary cause of the presenting symptoms or secondary to an underlying condition that is causing both the presenting symptoms and the faster heart rate

32. Treatment of Supraventricular Tachycardia
Maintain patent airway and assist breathing as necessary
If oxygenation is inadequate or the patient shows signs of increased breathing effort, provide supplementary oxygen
Attach an ECG monitor to the patient, evaluate blood pressure and oximetry, and establish IV access
If available, obtain a 12-lead ECG to better define the rhythm, but do not delay immediate cardioversion if the patient is unstable

33. Treatment of Supraventricular Tachycardia
Symptomatic patients who are experiencing rate-related decreased cardiac output should receive immediate synchronized cardioversion
If the patient is conscious, consider establishing IV access before cardioversion and administering sedation
However, avoid any delay in cardioversion if the patient is extremely unstable
If not hypotensive, the patient with a regular narrow-complex SVT may be treated with adenosine while preparations are made for synchronized cardioversion
Stable patients may await expert consultation because treatment has the potential for harm

34. Treatment of Supraventricular Tachycardia
If adenosine or vagal maneuvers fail to convert SVT, if it recurs after such treatment, or if these treatments reveal a different form of SVT such as atrial fibrillation or flutter,  consider the use of longer-acting AV nodal blocking agents, such as the nondihydropyridine calcium channel blockers (verapamil and diltiazem) or beta-blockers
Frequent attacks may require radiofrequency ablation
In the clinical setting, patients who have had a recent MI or heart surgery may need a temporary pacemaker to reset the heart’s rhythm

35. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 50 BPM, Ventricular rate 50 BPM, regular rhythm, inverted P′ wave preceding each QRS complex, normal QRS complexes at 0.10 seconds, PRI seconds, QT seconds. Junctional escape rhythm. I

36. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 188 BPM, Ventricular rate 188 BPM, regular rhythm, inverted P′ wave preceding each QRS complex, normal QRS complexes at 0.12 seconds, PRI seconds, QT seconds. Junctional tachycardia. I

37. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 79 BPM, Ventricular rate 79 BPM, occasionally irregular, upright and normal P waves in the underlying rhythm, P′ waves associated with premature beats are absent, QRS complexes are 0.10 seconds, PRI seconds in underlying rhythm and immeasurable in the premature beats, QT seconds. Normal sinus rhythm with 2 junctional complexes (PJCs) (6th and 8th complexes), this could be progressing into a junctional bigeminy. I

38. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 56 BPM, Ventricular rate 56 BPM, regular rhythm, P′ waves are absent, normal QRS complexes at 0.10 seconds, PRI is immeasurable, QT 0.40 seconds. Junctional escape rhythm. I

39. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 80 BPM, Ventricular rate 80 BPM, patterned irregularity, upright and normal P waves in the underlying rhythm, P′ waves associated with premature beats are absent, normal QRS complexes at 0.10 seconds, PRI seconds in underlying rhythm and immeasurable in the premature beats, QT seconds.Normal sinus rhythm with bigeminal premature junctional complexes (PJCs) (2nd, 4th, 6th and 8th complexes). I

40. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 120 BPM, Ventricular rate 120 BPM, regular rhythm, inverted P′ wave follows each QRS complex, normal QRS complexes at 0.08 seconds, P′RI seconds, QT seconds. Junctional tachycardia. I

41. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 65 BPM, Ventricular rate 65 BPM, irregular rhythm, P waves normal in underlying rhythm, absent with the PJC, narrow RS complexes at 0.10 seconds, PRI is 0.12 in underlying rhythm, immeasurable with the PJC, QT 0.52 seconds. Sinus rhythm with one PJC (3rd beat) I

42. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 92 BPM, Ventricular rate 92 BPM, regular rhythm, P′ waves are absent, normal QRS complexes at 0.08 seconds, PRI is immeasurable, QT 0.36 seconds. Accelerated junctional rhythm. I

43. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 30 BPM, Ventricular rate 30 BPM, regular rhythm, inverted P′ wave follows each QRS complex, normal QRS complexes at 0.08 seconds, P′RI 0.18 seconds, QT seconds. Slow junctional escape rhythm. I

44. Practice Makes Perfect
Determine the type of dysrhythmia
Answer: Atrial rate 82 BPM, Ventricular rate 82 BPM, regular rhythm, P′ waves are absent, normal QRS complexes at 0.10 seconds, P′RI is immeasurable, QT 0.34 seconds. Accelerated junctional rhythm. I

45. Summary Junctional rhythms originate in the AV junction
Impulses originating in the AV junction travel upward and cause backward or retrograde depolarization of the atria resulting in inverted P’ waves in lead II with a short P’R interval, absent P waves or P waves that follow the QRS complexes
With junctional dysrhythmias the QRS complexes are usually normal unless there is an intraventricular conduction defect, aberrancy or preexcitation

46. Summary
A premature junctional complex (PJC) is a single early electrical impulse that arises from the AV junction
Junctional escape rhythm arises from the AV junction at a rate of 40 to 60 beats per minute
Accelerated junctional rhythm arises from the AV junction at a rate of 60 to 100 beats per minute
Junctional tachycardia is a fast ectopic rhythm that arises from the bundle of His at a rate of between 100 and 180 beats per minute

47. Summary
In AVNRT, fast and slow pathways are located within the right atrium in close proximity to or within the AV node
These pathways can allow for development of SVT
Preexcitation syndromes occur when accessory conduction pathways exist between the atria and ventricles that bypass the AV node and bundle of His and allow the atria to depolarize the ventricles earlier than usual
Preexcitation is diagnosed by looking for a short PR interval

48. Summary
In WPW syndrome, the bundle of Kent, an accessory pathway, connects the atria to the ventricles, bypassing the AV node
Criteria for WPW include a PR interval less than 0.12 seconds, wide QRS complexes due to a delta wave (seen in some leads)
Patients with WPW are vulnerable to PSVT
In LGL, there is an intranodal accessory pathway that bypasses the normal delay within the AV node.
Criteria for LGL include a PR interval less than 0.12 seconds and a normal QRS complex

49. Summary
AVRT results from a reentry circuit that includes the AV node and an accessory pathway from the atria to the ventricle such as the bundle of Kent
This reentry circuit is physically much larger than the one associated with AVNRT
Reentry through an accessory pathway can take one of two directions, orthodromic conduction or antedromic conduction