What Do You Think 56

Dr Les from the Austin hospital sent me these two ECGs for an opinion. They were taken one day apart in an elderly female with severe dyspnoea at rest.

No significant bradyarrhythmias were documented.  

What do you think?

Let us review the first rhythm strip.

Narrow QRS complex tachycardia(100 bpm) with no visible P waves.

The second rhythm strip is more helpful.

Same heart rate, but non-conducted P waves embedded in the QRS (red stippled arrows). There is a marked first degree AV block (≥ 600 ms) and sinus tachycardia with 3:2 and 2:1 Wenckebach AV block (red arrows).

By extrapolation, the first rhythm strip also has very marked first degree AV block with the sinus P waves buried in the preceding QRS.

Let us review the pathophysiology of marked first degree AV block.

The PR interval on the ECG is the time taken from the beginning of the inscription of the P wave to the commencement of the QRS complex. It is a dynamic measurement, which lengthens with age and in recent years, to recognise this as a physiologic change, the upper limit of the PR interval in the adult has been adjusted from 200 ms to 220 ms, although both values are still used, including 210 ms. Normal physiologic and anatomic variants, apart from age, will also prolong the PR interval, including the autonomic nervous system and diurnal variations.

A PR interval > 220 ms is referred to as first degree AV block.

Because the PR interval increases with age, first degree AV block is common in the elderly. Large long-term follow-up studies suggest that as this prolongation lengthens with time, a small number will progress to higher degrees of AV block requiring cardiac pacing. There is also a greater incidence of atrial fibrillation, although this may reflect concomitant progressive atrial disease.

The PR interval increases physiologically overnight due to vagal influences. As a result, PR prolongation frequently exceeds 220 ms. The question remains whether this should be called first degree AV block, particularly in the young and the athlete. It is best to label this physiologicPR prolongation.

When the PR interval is excessively long, the P wave may lie close to or at the end of the previous T wave.

Two ECG examples where the sinus P wave is close to the preceding T wave even at rest with a sinus rate 58 and 70 bpm.

As the sinus rate increases with exertion, the P wave becomes engulfed in the T wave, even if the resting PR prolongation is modest.

The P wave may be concealed in the T wave and only visible with the slowing of sinus arrhythmia.

Sinus rhythm 90 bpm, with marked PR prolongation (400 ms) with the P wave concealed by the previous T wave, except with sinus slowing during sinus arrhythmia.

As the P wave becomes engulfed by the preceding T wave, atrial contraction occurs towards the end of ventricular systole with closed AV valves.Not only is the benefit of ventricular filling negated by the length of the PR interval, but now atrial systole may abruptly result in retrograde venous flow with cannon waves in the jugular veins, pulsatile headaches and pulsatile retrograde pulmonary venous flow with dyspnoea. During exercise, this may result in abrupt onset of symptoms often described as “hitting a brick wall”. When the retrograde pulmonary flow is at rest, marked dyspnoea may also occur.  

In the case presentation, the pathophysiologic effect of the concealed sinus P waves due to marked first degree AV block was the cause of the dyspnoea and were not identified until Wenckebach AV block occurred.

As well, sinus tachycardia was a physiologic reflex response in order to improve the reduced left ventricular output, which in turn probably made it worse.

Despite the absence of a bradyarrhythmia, the most appropriate treatment is dual chamber pacing in order to physiologically shorten the AV delay.Permanent cardiac pacing is rarely required for first degree or even intermittent Wenckebach AV block. Depending on left ventricular function, an immediate appropriate clinical response is anticipated, particularly at rest and this would be also seen with sinus slowing.  

A similar clinical scenario is seen with single chamber ventricular pacing (VVI) and retrograde conduction.

Ventricular pacing with a variable bipolar stimulus artefact due to dipole changes in the ECG leads with respiration. In the ST segment there is a retrograde P wave (purple arrow). When symptomatic, this is “pacemaker syndrome” and is corrected by upgrade to dual chamber pacing with atrial pacing preceding ventricular pacing.

With dual chamber pacing, an inappropriate long, programmed AV delay may also result in atrial pacing during closed AV valves. Such AV delays are used to avoid ventricular pacing, which may be unsuccessful with AV block.

Dual chamber pacing (DDDR, Ap Vp), 70 bpm with a 360 ms AV delay. With atrial pacing at 90 bpm, the atrial stimulus artefact will lie in the middle of the T wave (red stippled line) and atrial contraction will occur against closedAV valves.  

A very long AV delay (PR interval) can occur with atrial pacing or with inappropriate dual chamber pacing, where an attempt is made to inhibit ventricular pacing by prolonging the AV delay.

Although this markedly prolonged AV delay can occur with single chamber atrial pacing and no ventricular pacing backup, it seems impossible to program an AV delay beyond 560 ms with dual chamber pacing. However, inappropriate prolonged ventricular sensing can be achieved by a number of proprietary ventricular pacing minimization algorithms, that effectively pace AAI(R), but in the event of failed AV conduction will convert to dual chamber-ventricular pacing. Although these algorithms are designed with good intentions, a lack of understanding of the pathophysiology of a prolonged AV delay will result in inappropriate programming and poorly recognised clinical symptoms.  

Harry Mond