What Do You Think 58

Dr. Jeremy asked for an opinion on a set of 5 ECGs from a patient in the Royal Melbourne Hospital with an implanted cardioverter defibrillator (ICD) and strange rhythms.

I will show the two ECGs without the arrhythmia first.

Sinus rhythm 68 bpm at rest with a normal QRS duration < 100 ms.

It was interpreted as incomplete right bundle branch block (red highlight).

What do you think?

The presence of a dominant R wave in V1/V2 doesn’t necessarily mean an incomplete right bundle branch block.A normal QRS duration is usually accepted as < 100 ms and a bundle branch block > 120 ms. There is a narrow zone between these two values referred to as an incomplete or partial right bundle branch block. The definition is confusing as there is no generally accepted lower QRS limit. Although most ECG interpreters prefer 100 ms, others accept 110 ms or no lower limit at all. It is a very common ECG finding and occurs at all ages and particularly in the young males and athletes.

It is OK to call a bundle branch block incomplete or partial, but when it is > 120 ms, one should not call it complete. A block of 160ms one day can be 180 ms the next. Is this more complete? Rather, the diagnosis is simply bundle branch block.

The footprints of an incomplete right bundle branch block are:  

• A QRS duration < 120 m sec with an undefined lower limit. Despite this, most ECG reporters prefer to report incomplete right bundle branch block as a QRS duration of 100 to 120 ms.
• An RSR’ pattern in V1 and maybe V2 (red highlight) with combinations of r, r/S or r/R’ waves. In general, R’ is greater in amplitude than r/R.
• The terminal r’/R’ deflection is usually wider than the initial r/R wave.
• S wave> than R wave duration in leads I and V6 or S wave > 40 ms.  
• T wave inversion in V1.

The confusion with the diagnosis of incomplete right bundle branch block can be seen with the following ECG with the auto-interpretive report being an incomplete right bundle branch block (yellow highlight).

The QRS duration is 92 ms (blue highlight). Rs or Rsr’ pattern (red highlight) in V1, which does not fit the criteria, as the initial R wave is dominant.

What then is the significance of anR’ in V1 with a QRS duration <100 ms?      

This is referred to as a crista supraventricularis pattern. The crista supraventricularis is a muscular ridge in the right ventricle between the tricuspid and pulmonary valves at the junction of the anterior free wall and the interventricular septum.

The ridge separates the inflow tract of the right ventricle from the outflow tract and plays important roles in supporting the free wall, guiding blood through the right ventricle, and helping close the tricuspid valve. During ventricular systole, it is one of the last areas of the right ventricle to be depolarized via the Purkinje network.The R’ pattern is believed to result from delayed activation of the crista supraventricularis.

Two 12 lead ECGs with a crista supraventricularis pattern.

They both have R’ > R and narrow R waves in leads I and V6.

The crista supraventricularis pattern is considered benign and may be amplified by placing leads V1 and V2 higher on the precordial wall. However, with a QRS duration < 100 ms, the pattern may mimic several pathological entities including a previous posterior infarct, Brugada pattern, right ventricular hypertrophy, Wolff-Parkinson-White delta wave or arrhythmogenic right ventricular dysplasia. Therefore, it is important not to just dismiss the crista supraventricularis pattern as a normal oddity, but rather check for other pathognomonic ECG features.

Although incomplete right bundle branch block is usually benign, there is evidence of progression to higher degrees of block. Other associated features, such as abnormal P or T waves may indicate underlying cardiac pathology. In these cases, it is postulated that the incomplete right bundle branch block may result from delayed conduction in other areas of the right ventricle. One of these situations is the association between an ostium secundum atrial septal defect and all degrees of a right bundle branch block, whatever the QRS duration. It probably reflects right ventricular overload and may also be present with right axis deviation. In the pre-echocardiograph era, the ECG findings together with fixed splitting of the second heart sound were important in the diagnosis of an atrial septal defect.

In our ECG from the Royal Melbourne Hospital could the R wave be due to right ventricular hypertrophy?  Once again this is controversial because of dominant left ventricular forces making it hard to diagnose right ventricular hypertrophy on the ECG until it is well established.

ECG criteria for right ventricular hypertrophy include:

• QRS duration < 120 ms, but often > 100ms.
• R wave in V1 > S wave or R wave >7 mm(red highlight).
• Prominent S wave in lateral leads, I, aVL andV6 (yellow highlight).
• Right axis deviation (blue highlight).

• T wave inversion V2, V3  (green highlight) and right atrial abnormality (P wave > 2.5 mm), when the right ventricular pressures are significantly elevated.

The ECG features of right ventricular hypertrophy may be found in the normal paediatric ECG and the term, right ventricular preponderance is preferred. In a child with a thin chest wall, tall R waves in V1 together with right axis deviation, mimic right ventricular hypertrophy.

Normal 12-lead ECG with right axis deviation (blue highlight) and an R wave in V1 (red highlight).

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The second ECG from the RoyalMelbourne Hospital had a slower rate of 65 bpm and showed atrial pacing. Rememberthe patient has an ICD which has probably been programmed DDDR.  

Atrial pacing (Ap) with a stimulus artefact (red arrow) and a normal PR interval and QRS (Vs).

What about the arrhythmia?

What do you think?

Let us review the rhythm strip.

Compared to the resting baseline ECG (red highlight), there are varying heights and widths to the QRS complexes.

This is an accelerated idioventricular rhythm (yellow highlight) which commences and terminates as fusion with sinus rhythm (blue highlight).

Why does this occur? The sinus and ventricular rhythm are similar in rate. With sinus slowing, the idioventricular rhythm gradually consumes the sinus QRS complexes and the PR intervals become shorter and are concealed (blue highlight). Note that the sinus generated T waves are upright, and the ventricular beats deeply inverted.As the fusion beats become more ventricular, the inverted T waves become more prominent.

Let us review idioventricular rhythms.

A ventricular arrhythmia has an ectopic pacemaker focus beyond the AV junction. It represents a minefield of descriptive nomenclature, depending on the ECG appearance, ventricular rate, anatomical site, drug toxicity, electrolyte disturbances, underlying cause, arrhythmia mechanism and hereditary cardiac channelopathies. When the ventricular rate is slow and within the bradycardia range, the rhythms are referred to as an idioventricular rhythm. At faster rates in the range of 70 to 100 bpm, they are an accelerated ventricular rhythm, accelerated idioventricular run, a ventricular run, a slow ventricular tachycardia or a ventricular salvo. When the ventricular rate is > 120 bpm, the encompassing term ventricular tachyarrhythmia is used, which includes ventricular tachycardia, ventricular flutter (> 200 bpm), torsade de pointes and ventricular fibrillation. As with supraventricular arrhythmias, there is a transition zone between 100 and 120 bpm, where many ECG reporters prefer for convenience, to extend the term ventricular run, at least for brief episodes. It is not unusual to see an upper limit of 100, 110 and 120 bpm quoted in the literature.  

The mechanisms for generation of ventricular arrhythmias are complex and involve both normal and abnormal automatic foci, triggered activity and re-entry circuits initiated by a myriad of abnormal substrates which initiate, propagate, and maintain the arrhythmia.These substrates include all forms of heart disease as well as hereditary channel opathies.  

The QRS morphology of slow and accelerated ventricular arrhythmias are identical, differing merely in repetition rate. Unlike ventricular tachycardia, these arrhythmias are usually short lived and uncommon during a resting 12-lead ECG, but not infrequent during Holter monitoring. Whereas an idioventricular rhythm is slow and may represent a subsidiary pacemaker, an accelerated idioventricular rhythm may be indicative of ventricular disease.  

The ECG features of Idioventricular rhythm include:

• Sinus rhythm (red arrows) with an escape, regular, slow (often 50 to 70 bpm), broad QRS rhythm (yellow highlight), of at least three beats.
• Usually nocturnal, with the ventricle acting as the subsidiary pacemaker rather than the AV junction.
• There is no sinus P wave synchrony with the ventricular rhythm, unlike rate dependent bundle branch block.
• During the rhythm, sinus P waves do not conduct to the ventricles and may be embedded in the broad QRS (yellow highlight).
• Sinus P waves (red arrows) continue unabated and concealed (red stippled arrows), conducting once again when the idioventricular rhythm either terminates or slows to a rate less than the sinus rate.
• Like all ventricular rhythms, retrograde (VA)conduction (blue arrows) can occur inhibiting sinus rhythm. Once the ventricular rhythm terminates, sinus rhythm is re-established (red arrow) after a pause.

• A prominent feature of idioventricular rhythm are fusion beats.

Sinus rhythm (red highlight)and a short run of idioventricular rhythm (yellow highlight). A ventricular fusion beat (blue highlight) occurs, when a sinus beat is conducted to the ventricle at the same time the idioventricular rhythm commences, resulting in the ventricle being partially depolarized by both foci.

• Fusion beats (blue highlight) are usually seen at the commencement and termination of a run of idioventricular rhythm (yellow highlight).

• Because an accelerated idioventricular rhythm (yellow highlight)  suggests an abnormal ventricular focus, it may commence prematurely, modestly faster than the sinus rhythm (red highlight) and terminating with a pause (green highlight), confirming that the sinus node has been reset.

Such rhythms are seen with an acute coronary occlusion during reperfusion, as a result of thrombolysis or angioplasty.

Now we understand accelerated idioventricular rhythms, let us return to our case history and review another ECG.

There is an abrupt transition from idioventricular rhythm to sinus rhythm without fusion.

Let us review the rhythm strip.

There is most likely sinus rhythm throughout the tracing at 700 ms cycle length and this is sensed by the pacemaker. One sinus QRS, however, is not sensed (purple stippled arrow) as it is lies in the pacemaker refractory period resulting in a paced P wave (blue arrow) at the low rate of 60 bpm (1000 ms) with normal conduction. This allows sinus generated QRS complexes to remerge (blue stippled arrow). The P waves in the ST segment of the ventricular complexes time out with the sinus beats and move within the ST segment and therefore are likely to be sinus and not retrograde conduction which can also occur with idioventricular rhythms.

Finally this ECG.

This ECG demonstrates fusion with rapid reversion to sinus conduction due to sinus tachycardia. Although there appears to be a “nasty” ventricular triplet, the appearance and timing strongly suggest this is artefact (red highlight) within the  accelerated idioventricular rhythm.  

In summary:

• Probable right ventricular hypertrophy.
• Atrial pacing.
• Accelerated idioventricular rhythm.
• Ventricular fusion beats.
• Artefact.

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Harry Mond