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Junctional Dysrhythmias

Junctional Dysrhythmias

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Junctional Dysrhythmias

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  1. 13 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 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 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 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 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: 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 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 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 ReentrantTachycardia • Some people have an abnormal extra anatomical pathway (congenital in nature) within or just next to the AV node

  21. Atrioventricular Nodal ReentrantTachycardia (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 orvagal maneuvers fail to convert SVT, if itrecurs after such treatment, or if these treatments reveal adifferent 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 (verapamiland 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 I

  36. Practice Makes Perfect • Determine the type of dysrhythmia I

  37. Practice Makes Perfect • Determine the type of dysrhythmia I

  38. Practice Makes Perfect • Determine the type of dysrhythmia I

  39. Practice Makes Perfect • Determine the type of dysrhythmia I

  40. Practice Makes Perfect • Determine the type of dysrhythmia I

  41. Practice Makes Perfect • Determine the type of dysrhythmia I

  42. Practice Makes Perfect • Determine the type of dysrhythmia I

  43. Practice Makes Perfect • Determine the type of dysrhythmia I

  44. Practice Makes Perfect • Determine the type of dysrhythmia 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 antedromicconduction