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Patient/anamnesis: n/a
ECG interpretation/discussion: This ECG is a printout from a telemetry station, derived from a 5 lead patient monitoring. So, what have we here? The underlying rhythm is sinoatrial, but both PR and RR interval varies. Remember, Wenckebach is not the name of a certain type of block, but rather a type of conduction. This is often misunderstood, as Second Degree AV Block Type 1 or Mobitz 1 is also often labelled Wenckebach block. A more precise term would be Wenckebach periodity, phenomenon, conduction. Wenckebach conduction is usually considered benign and can be recognized by the following criteria:
1) PR interval is progressively prolonged until a P wave is blocked
2) The shortest PR interval is the one immediately following the dropped beat. The longest PR interval is the one immediately before the dropped beat. The incremental change in PR interval is in the beginning of the Wenckebach cycle, thus between the first and second PR interval in a sequence.
3) The RR intervals progressively shorten until a QRS is ‘dropped’ due to the non-conducted atrial/sinoatrial impulse.
Now, looking at this ECG, the two first beats are at the end of a Wenckebach cycle. After the second QRS a non-conducted P wave occurs. The following beat is wide and bizarre and is a ventricular escape beat that occurs due to the long preceding pause. After the escape beat, a new Wenckebach cycle starts. The PR interval lengthens until a P wave is blocked. After this pause, a narrow QRS is preceded by a P wave with a very, very short PR interval. This is a junctional escape beat. Then, the Wenckebach cycle restarts.
When counting P waves and QRS complexes in the cycles, we’ll see that for every three QRS complexes there are four P waves, since one of the QRS complexes gets dropped repeatedly. This gives a 4:3 atrioventricular (AV) ratio, which is also called 4:3 conduction.
What a beauty! Thanks to my colleague and fellow ECG-dork for bringing me this rare gem!
September 6, 2009
The patient is an 80 y/o woman with known sick sinus syndrome, aortic sclerosis, aortic valve insufficiency, mitral valve insufficiency, tricuspidal valve insufficiency and left ventricular hypertrophy.
About the sick sinus syndrome and the tachy-brady syndrome
There are two types of Sick Sinus Syndrome (SSS): one with and one without associated tachyarrhythmias. SSS is due to many mechanisms related to SA-nodal failure, and in many patients with the syndrome more than one of the mechanisms are present. The most common mechanisms for SSS are severe, persistent sinus bradycardia, sinus arrest, both brief and sustained, with or without initiation of escape pacemakers, sometimes resulting in sustained asystole. Both Stokes-Adams attacks and sudden death is seen with SSS. When SSS is associated with tachyarrhytmhias, this is called the tachy-brady syndrome. Tachy-brady syndrome occurs in more than half of the patients with SSS.¹ The tachy-brady syndrome itself is not a specific condition, but more of a mixture of combinations of arrhythmias. I find it confusing that even the most profilic authors on this subject, as both Marriott² and Chou¹, tend to disagree on whether SSS should be considered part of the tachy-brady syndrome or vice versa. However, there seems to be consistency upon the fact that SSS can occur in two forms, with our without the associated tachycardias. Furthermore the tachy-brady syndrome is usually described as the condition where a tachycardia mechanism is directly associated with the mechanism of a bradycardia or the other way around. One author³ also differentiates between a tachy-brady syndrome and a brady-tachy syndrome, depending on what mechanism that initiates the next.
This series of telemetry strips from the patient described above, show the tachy-brady syndrome in action, manifested by a large and complex cascade of arrhythmic events. Note that there is a baseline first degree AV block at approximately 260 ms.
Note that each strip is not an exact continuation of the strip before it, meaning that i.e. strip number 2 can repeat some of the events in strip 1.
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Top strip: After 4 cycles of sinus bradycardia (43 bpm), atrial flutter occurs. The atrial rate is approximately 260 bpm, and 2:1 AV conduction occurs, resulting in a ventricular rate of 130 bpm. There are F waves (flutter waves) superimposed on each T wave.
Middle strip: Note that this strip is not an exact continuation of strip 1. The first 12 beats are the same. It shows however the atrial flutter persisting with the same AV ratio for several seconds.
Bottom strip: After a while, 4:1 conduction occurs for one cycle. The next cycle is interrupted by a PVC triplet, or a short run of ventricular tachycardia (VT). After the ventricular triplet, the AV node alternates with 2:1 and 3:1 conduction.
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Top strip: Atrial flutter still persists, while 2:1, 3:1 and 4:1 AV conduction occurs successively, before a four beat salvo of premature ventricular contractions occur. Such a salvo would also be considered non-sustained ventricular tachycardia. Following the salvo, AV ratio continues to vary and also with higher degrees of block. 2:1, 3:1 4:1 and 5:1 AV block occurs successively towards the end of the strip.
Middle strip: This strip is almost a repetition of the top strip, and can be ignored.
Bottom strip: Here we can see that even higher degree of AV block occurs, with AV ratio as high as 6:1 before progressively decreasing again.
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Top strip: This strip is recorded at 50mm/s, and shows the baseline atrial flutter being conducted with high degrees of AV block, and interrupted by a 5-beat run of ventricular tachycardia at 140 bpm.
Middle strip: Various degrees of AV block are seen throughout the strip. The deep, negative deflection towards the end is due to a loose electrode.
Bottom strip: AV block continues to vary, here mostly between a 2:1 and 3:1 ratio.
¹ Surawicz, Borys, Chou’s electrocardiography in clinical practice. Philadelphia: Saunders Elsevier, 2006:336-343, 6th edition.
² Wagner, Galen S., Marriott’s Practical Electrocardiography. Philadelphia: Lippincott Williams & Wilkins, 396-404, 10th edition
³ Sandøe, Erik and Bjarne Sigurd, Klinisk Elektrokardiografi. Bingen: Publishing Partners Verlag GmbH, 326-331, 1st edition.
June 18, 2009