Giant R-waves. What are they?

This case was sent to me by my frequent co-author, Brooks Walsh, with some editing by me:

An elderly patient was brought in by EMS from a nursing home, after having been intubated for hypoxic respiratory failure. Transport was notable for an episode of VF that responded to CPR and defibrillation. In the ED, the patient was persistently hypoxic, with significant hemodynamic instability in the ED and several episodes of PEA, hypotension, and 2 defibrillations for VF/VT.

Here is the initial 12-lead ECG:

What do you think?

The team was concerned for hyperkalemia, given the apparently wide QRS.  Thus, Calcium, sodium bicarb, insulin, and dextrose were given.

However, the QRS did not change after this therapy.

What is this?

Why did we mistake the initial ECG for hyperkalemia? A full discussion of diagnostic/cognitive biases is best left to others with more insight, but there are, I think, a few specific issues.

Probable answer: the dramatic combination of “spikey complexes” an apparently wide QRS, and a sine wave appearance.

A wide QRS absolutely should prompt consideration of hyperkalemia, and empiric treatment is warranted if there are signs of hyperkalemia on the ECG.  

However: The QRS isn’t nearly as wide as it appears.  There is a right bundle branch block (RBBB) and left anterior fascicular block (LAFB), but what appears to be make it an even wider QRS is actually ST segment.   

How wide is the QRS?  Whenever there is RBBB, one should find the lead where you can see the end of the QRS.  Then you can measure the QRS duration, and see the end of the QRS in every lead.  Here, the end can easily be seen in leads V1 and II.  

Before we do that, what is the rhythm?  There do not appear to be P-waves.  Thus, this is either junctional rhythm with RBBB and LAFB, or it is a left posterior fascicular escape.

Now let's look at the QRS and ST segments: See this annotated ECG below:

The red line represents the end of the QRS in V1 and II.  We can find the same point on lead II across the bottom, then draw the lines up so that we find the end of the QRS in every lead.  Now you can see that the complex beyond the end of the QRS is ST Segment, hugely elevated.

At this point, STEMI was considered.  A bedside echo was obtained (and repeated when the interventionalist arrived). The images were limited to poor windows, but did not clearly demonstrate large regional wall motion abnormalities. Nonetheless, cardiology immediately agreed to cath lab activation.

Before leaving the ED, the patient had runs of wide-complex tachycardia.  This 12-lead was recorded, which showed one short run of VT, resolution of ST elevation, and one other interesting finding: 

What is the interesting finding?  It may be better seen in the next ECG.

Here is the next ECG:  

What is it?

This is accelerated idioventricular rhythm (AIVR), which is a common reperfusion arrhythmia.  It is a very good sign.  It can be mistaken for VT, but VT is fast and AIVR is not.  (There are inverted P-waves in front of the QRS which I find difficult to explain.  Are they isorhythmic low atrial P-waves? 

If there were persistent STEMI superimposed on this AIVR, it would look like LBBB with STEMI (concordance or proportionally excessive discordance).  There is none here, which also indicates spontaneous reperfusion.  In other words the ST elevation has resolved and this indicates that the artery is now open.

Angiography demonstrated a 95% thrombotic lesion in the proximal LAD. The patient did well after PCI. The potassium level was 5.4.

Comment

--Hyperkalemia, of course, causes narrow, spiked upright T-waves (although not invariably). The T-waves in this ECG, however, are wide, and either inverted (V1-V5), or blunted.

--There is indeed a sine-wave type of pattern here, but it is arguably “backwards” from the typical hyperkalemia pattern. In hyperkalemia, a wide, blunt, inverted QRS is often followed by a sharp, narrow, upright T-wave (example from a prior post). By contrast, our ECG showed a sharp, upright QRS, followed by a blunt, inverted T-wave.

A dramatic and unusual “shark-fin” morphology of the anterior QRS complexes distracts us from the other leads.

The anterior QRS/T complexes tower over those in the lateral leads (I, aVL, V6), distracting us from those more typical findings of STEMI. A diagnostic pattern of STEMI is seen, but mostly in the perennially under-appreciated lateral leads.

The dramatic and unusual anterior T-wave inversions also distracts us.

Most T-waves in anterior STEMI without any reperfusion are upright.

So what accounts for the unusual QRS/T morphology?  It is extreme ST elevation, and has been referred to as "Giant R-waves."

The towering “shark-fin” anterior STEMI is unusual, but not rare. A few cases can be seen on the internet (from Jason Winter’s ECG blog, from a British paramedic blog, and from the Wave-Maven site. ) Dr. Wang has a very similar example from his recently published book.

I've reproduced it here:

Giant R-waves

This QRS/T morphology is also known as the “giant R-wave” pattern of STEMI. For example, Madias reported on an elderly male who presented with chest pain, and an ECG strikingly similar to our patient.¹ This pattern was transient, and resolved within 30 minutes. Catheterization was not performed, but anterior MI was diagnosed based on enzymes and development of anterior Q-waves.

Madias also reported a series of 3 similar cases, including this patient:² 

He noted that this pattern was usually found very soon after onset of ischemic symptoms or defibrillation, and rapidly evolved to more “typical” ischemic patterns soon after.

Experimental work, involving ligation of coronary arteries in animals, has suggested that this pattern may be more the rule than an exception. For example, one study found giant R-waves and T wave inversion within 10 minutes after tying off the coronary arteries of dogs.³ An example: 

Another study, reproduced in Madias, shows a similar hyperacute pattern developing within 3 minutes:²

The anterior T-wave inversion – spontaneous reperfusion?

It is worth noting that inverted T waves are not a universally reported feature of giant R-waves. In our case, the inverted T wave may have indicated that our patient was spontaneously reperfusing.

Our interventionalist found a subtotal occlusion, with fresh distal embolic debris, suggesting partial spontaneous recanalization. Also, as indicated, the ECG performed just before leaving the ED shows not only the resolution of ST-segment elevation, but also AIVR, a rhythm often seen in the context of reperfusion of a STEMI.  

1. Madias JE. The “giant R waves” ECG pattern of hyperacute phase of myocardial infarction: A case report. J Electrocardiol. 1993;26(1):77-82. doi:10.1016/0022-0736(93)90068-O.

2. Madias JE, Krikelis EN. Transient giant R waves in the early phase of acute myocardial infarction: Association with ventricular fibrillation. Clin Cardiol. 1981;4(6):339-349. doi:10.1002/clc.4960040606.


3. Ekmekci A, Toyoshima H, Kwoczynski JK, Nagaya T, Prinzmetal M. Angina pectoris: V. Giant R and receding S wave in myocardial ischemia and certain nonischemic conditions. Am J Cardiol. 1961;7(4):521-532. doi:10.1016/0002-9149(61)90510-0.