Ectopic Arrhythmias and Triggered Activity




Day 6: Ectopic Arrhythmias and Triggered Activity



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  1. Ectopy—a disorder of impulse formation




    1. Mechanisms of ectopic arrhythmias




      1. Ectopic arrhythmias require:




        1. Default—slowing of the normal dominant sinus pacemaker which allows a slower focus to take control, or



        2. Usurpation—an acceleration of a lower pacemaker which takes control by virtue of being faster than the sinus rate



      2. Disorders of the sinus node, such as SA arrest, SA exit block, or excessive vagal tone may allow a lower focus to take control by default



      3. A variety of factors, including digitalis toxicity, hypoxia, electrolyte disturbances, ischemia, or chronic lung disease may stimulate an ectopic focus to accelerate and usurp control from the SA node



    2. Properties of ectopic arrhythmias




      1. Ectopic arrhythmias usually start and stop gradually (non-paroxysmally)



      2. They are not usually initiated by a premature beat



      3. They may be somewhat irregular



      4. They are not terminated by vagal maneuvers, although AV block may be increased



      5. AV block of varying degrees is frequently present (particularly if digitalis toxicity is the cause)



      6. These arrhythmias are usually quite resistant to treatment with standard class I or III agents



      7. Catheter ablation may be effective if a causative agent cannot be identified or treated



  2. The major ectopic arrhythmias




    1. Wandering atrial pacemaker




      1. Mechanisms and causes




        1. There are three or more ectopic atrial pacemakers



        2. This arrhythmia is typically seen in young healthy persons, particularly athletes



        3. The etiology is uncertain



      2. Heart rate—the heart rate is 60–100 and is usually irregular



      3. ECG morphology (Day 6-01)




        1. There are at least three P wave morphologies with varying PR intervals



        2. There is usually moderate variation in the heart rate



    2. Multifocal atrial tachycardia




      1. Mechanisms and causes




        1. Caused by multiple ectopic atrial foci



        2. Chronic lung disease is typically the underlying clinical abnormality, although it can also occur in the setting of hypoxia, electrolyte abnormalities, acid-base disturbances, and ischemia (i.e., frequently in the intensive care setting)



      2. ECG morphology (Day 6-02)




        1. There are at least three P wave morphologies with varying PR intervals



        2. The rate is 100–140



        3. There is typically 1:1 AV conduction



        4. This arrhythmia is frequently confused with atrial fibrillation; the distinction is an important one since management is usually very different



    3. Ectopic atrial rhythms




      1. Mechanisms and causes




        1. A single ectopic atrial focus accelerates and usurps control from the sinus node, or the sinus node slows down and allows an ectopic focus to appear



        2. Digitalis toxicity, electrolyte abnormalities, ischemia, hypoxia, and chronic lung disease are typical causes



      2. ECG morphology (Day 6-03) (Day 6-04)




        1. The P waves are of the same morphology but have an abnormal axis, indicating their ectopic origin



        2. The atrial rate may be slightly irregular



        3. AV block of varying degrees is sometimes present (particularly if digitalis toxicity is the cause)



        4. Atrial tachycardia with AV block should be considered a manifestation of digitalis toxicity until proven otherwise (Day 6-05)



        5. The atrial rate in atrial tachycardia is usually 140–200



        6. Atrial tachycardia may be confused with atrial flutter, but the latter is usually faster and has the typical saw tooth pattern



    4. Ectopic junctional rhythms




      1. Mechanisms and causes




        1. A single focus near the AV node accelerates and usurps control from the sinus node



        2. Digitalis toxicity, electrolyte abnormalities, ischemia, hypoxia, and chronic lung disease are typical causes



      2. ECG morphology (Day 6-06)


         


        DAY 6-01



         


        DAY 6-02



         


        DAY 6-03



         


        DAY 6-04



         


        DAY 6-05



         


        DAY 6-06



         




        1. If P waves are visible, they demonstrate an abnormal axis and appear slightly before or after the QRS complex



        2. Junctional tachycardia (rate >60), or accelerated junctional rhythm, should be considered a manifestation of digitalis toxicity until proven otherwise (Day 6-07) (Day 6-08)



        3. Junctional tachycardia may be confused with atrial tachycardia, but the latter has a normal PR interval (>120 msec)



    5. Ectopic ventricular rhythms




      1. Mechanisms and causes




        1. A single focus in the right or left ventricle, usually near the His-Purkinje fibers, accelerates and usurps control from the sinus node



        2. Ischemia, a scar from a previous MI, electrolyte abnormalities, and dilated cardiomyopathy are typical causes



        3. VT can also be associated with right ventricular dysplasia, a congenital condition effecting the right ventricular free wall and/or RV outflow tract (this abnormality may also produce reentrant VT)



      2. ECG morphology




        1. The ECG demonstrates a wide QRS tachycardia



        2. There may be AV dissociation



        3. In RV dysplasia, the ECG shows LBBB, right axis deviation, and T wave inversion over the right precordium



        4. Summary of ectopic arrhythmias


     



     



     


    DAY 6-07



     


    DAY 6-08



     



  3. Triggered activity




    1. Mechanisms of triggered activity




      1. Triggered activity is initiated in conducting tissue by afterdepolarizations



      2. Afterdepolarizations are oscillations of membrane voltage induced by one or more preceding action potentials



      3. If the afterdepolarization voltage reaches the membrane threshold potential, a sustained arrhythmia may result



      4. Patients with the congenital long QT syndromes or those treated with class I or class III antiarrhythmic agents (e.g. quinidine, procainamide, sotalol), erythromycin, or other drugs some are at increased risk for triggered activity arrhythmias



      5. Triggered activity arrhythmias are exacerbated by hypokalemia or hypomagnesemia



    2. Properties of triggered activity arrhythmias




      1. Sustained, rapid ventricular tachycardia may be caused by triggered activity



      2. Another from of VT, torsade de pointes, is a subset of polymorphic ventricular tachycardia, and is characterized by a rapid, irregular ventricular rate and a cyclically changing morphology



      3. The treatment of these arrhythmias usually involves treatment of the underlying cardiac disease, correction of an electrolyte abnormality, or cessation of an offending drug



      4. Some of these arrhythmias respond to verapamil, ventricular pacing, or beta agonists




Sample Tracings



ECG 1



ECG 2



ECG 3



ECG 4



ECG 5



ECG 6



ECG 7



ECG 8



ECG 9



ECG 10



ECG 11



ECG 12



ECG 13



ECG 14



ECG 15



ECG 16



ECG 17



ECG 18



ECG 19



ECG 20



Ectopic Arrhythmias and Triggered Activity




Interpretations of Sample Tracings



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ECG 1



Atrial rate: 135



Ventricular rate: 60



Rhythm: Sinus tachycardia with variable AV block



P wave: Normal



PR interval:



QRS complex:



 Axis: -60°



 Duration: 100 msec



 Voltage: Low voltage



 Morphology: Q waves in III, aVF, and V1 to V3



ST segment: Nonspecific changes



T wave: Nonspecific changes



QT interval: 460 msec



U wave:



Diagnosis: Sinus tachycardia with variable AV block, left axis deviation, low voltage, old inferior MI, and probable old anteroseptal MI. It is possible that this rhythm represents ectopic atrial tachycardia.



ECG 2



Atrial rate: 200



Ventricular rate: 48



Rhythm: Atrial tachycardia with variable AV block



P wave:



PR interval:



QRS complex:



 Axis: 0°



 Duration: 80 msec



 Voltage: Normal



 Morphology: Only very small R waves are present in the precordial leads



ST segment: Nonspecific changes



T wave: Nonspecific changes



QT interval: 480 msec



U wave:



Diagnosis: Ectopic atrial tachycardia with variable AV block, and lack of R waves in the precordial leads suggesting an old anterior MI. This arrhythmia is suggestive of digoxin toxicity.



ECG 3



Atrial rate: 120



Ventricular rate: 120



Rhythm: Ectopic atrial tachycardia



P wave: Inverted in II, III, and aVF and upright in aVR



PR interval: 140 msec



QRS complex:



 Axis: 45°



 Duration: 80 msec



 Voltage: Normal



 Morphology: Normal



ST segment: Normal

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Related posts:

  1. The Differential Diagnosis of Wide-QRS Tachycardias
  2. SA and AV Nodal Conduction Abnormalities
  3. Electronic Pacemakers
  4. Chamber Abnormalities and Intraventricular Conduction Defects

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Jan 13, 2019 | Posted by in CARDIOLOGY | Comments Off on Ectopic Arrhythmias and Triggered Activity

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