Rate-dependent aberration and its restitution

  As the heart rate increases, the refractory period of the His-Purkinje system shortens.

  This helps to preserve normal conduction.

  Failure of the action potential of the bundle branches to shorten results in

      acceleration dependent bundle branch block.

  Paradoxical lengthening of the action potential in response to heart rate increase may also result in

      acceleration dependent bundle branch block.

  Conversely, the refractory period increases as the heart rate decreases.

  When heart rate further increases, the acceleration dependent aberration may sometimes disappear

      (
restitution).

      This may be due to greater shortening of the effective refractory period of the bundle branches than

      that of the AV node.




References

  Josephson ME: Intraventricular conduction disturbances.

      In Josephson ME, editor: Clinical cardiac electrophysiology, ed 4, Philadelphia, 2008,

      Lippincott Williams & Wilkins, pp 114-144.

  Fisch C, Knoebel S: Wolff-Parkinson-White syndrome.

      In Fisch C, Knoebel S, editors: Electrocardiography of clinical arrhythmias,

      Armonk, NY, 2000, Futura, pp 293-314.

  Clinical Arrhythmology and Electrophysiology.

      A Companion to Braunwald’s Heart Disease. SECOND EDITION.

      2012 Elsevier Saunders. pp 194-211.





ECG 7a. The ECG above belongs to a middle-aged woman. She was diagnosed as normal coronary arteries and dilated
cardiomyopathy. The basic rhythm is
sinus rhythm with aberrant conduction as left bundle branch block (LBBB) .
The
Ventricular Premature Systole (VPS) is followed by compensatory pause. As the instantaneous heart rate during the
compensatory pause was slow enough,
aberration disappeared and the sinus beat was conducted normally to the ventricles as
a narrow QRS complex
.

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ECG 7b. The ECG was recorded again.
VPS was observed among sinus beats conducted with LBBB type aberration .
When heart rate was slow enough during the compensatory pause,
the aberration disappeared and the sinus beat was normally
conducted to the ventricles as a narrow QRS complex
.

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ECG 7c. The 3-lead Holter recording of the same patient showed
VPS and normal conduction of the sinus beat following the
compensatory pause.
This Holter recording showed that the normal conduction (without aberration) was related to the
instantaneous heart rate . When the instantaneous heart rate was 69/minute or below the aberration disappeared and
the sinus beat was
conducted normally to the ventricles.

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ECG 7d. Another instance from the 3-lead Holter recording of the same patient shows how important the instantaneous
heart rate is for aberration.
When instantaneous heart rate is 69/minute or below the sinus beat following the compensatory
pause of the
VPS is conducted normally (without aberration) . When instantaneous heart rate is above 69/minute aberration
reappears.

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ECG 7e.
The aberrant conduction persists when the instantaneous heart rate of the compensatory pause of the VPS
is above 69/minute

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ECG 7f.
LBBB type aberrant conduction occurs when the instantaneous heart rate is above >69/minute or below 104/minute.

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ECG 7g.
When the instantaneous heart rate is 104/minute or above the aberration disappears and conduction normalizes
(RESTITUTION)
. When heart rate comes below 104/minute aberration reappears again.

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ECG 8a. The ECG above belongs to a 48 year-old man. It was recorded 3 weeks after his Bentall surgery.
ECHOcardiography showed left ventricular hypertrophy.
The above ECG shows frequent
VPCs with acceleration dependent aberration.
If
compensatory pause following the VPC is not long enough, then acceleration dependent aberration developes and
QRS complex widens
. If compensatory pause following the VPC is long enough, then
acceleration dependent aberration does not develope and QRS complex following the VPC does not widen.

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ECG 8b. The ECG above belongs to the same man. It was recorded 70 minutes before the ECG 8a.
This ECG also shows frequent
VPCs.
However, if
compensatory pause following the VPC is not long enough, then
acceleration dependent aberration developes and QRS complex widens.

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ECG 9. The ECG above belongs to a 57 years-old obese man.
He is under Amlodipin therapy for chronic systemic arterial hypertension.
ECHOcardiography showed normal left ventricular systolic function with normal cardiac dimensions.
Basic rhythm is sinus with right bundle branch block (RBBB) morphology.
There are frequent atrial premature beats deforming the preceding T waves.
The atrial premature beats are conducted to the ventricles with aberration resulting in bizarre QRS complexes.

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ECG 10. During atrial fibrillation, a wide QRS complex may not be due to aberrancy or a VPC.
The ECG above belongs to a 74 years-old woman and the basic rhythm is atrial fibrillation.
She also has a VVI-pacemaker.
The pacemaker spike is not easy to notice, at first glance.
The QRS complex is widened not due to aberrancy or a VPC but due to stimulation from ventricular pacemaker.

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ECG 11.
Aberration during supraventricular tachycardia is seen above.
This ECG belongs to a 25 years-old woman.
10 mg intravenous Adenosine converted her rhythm to sinus.

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ECG 12. The above ECG belongs to a 13 years-old boy with frequent
atrial premature beats.
Atrial premature beats deform the preceding T waves.
Some atrial premature beats are conducted with
aberration resulting in wide QRS complexes.
These wide QRS complexes are not ventricular premature contractions.
There are two reasons for this: T waves preceding
the wide QRS complexes are different
(due to the deforming effect of the atrial premature beat); also there is no compensatory pause.
The seemingly
sinus arrest is in fact due to a blocked atrial premature beat.
There is no sinus arrest.

Arm electrodes were inadvertently reversed in this ECG

Prof. Dr. Nazlıhan Günal has donated the above ECG to our website.

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