Sinus rhythm with a new wide complex QRS

This is another case written by Pendell Meyers, a G2 at Stony Brook.  As I mentioned before, Pendell will be helping to edit and write the blog.

Case

A middle aged female with type 2 diabetes presented to her endocrinologist for a regularly scheduled follow up appointment for diabetes management. Her history included ischemic cardiomyopathy (CM) with placement of an AICD, CAD s/p CABG, and recent elective LAD stent complicated by ischemic colitis requiring hemicolectomy and colostomy.

During the appointment she complained of several days of off and on dizziness and bilateral leg weakness, and she also told the endocrinologist that she felt as though "life is not worth living anymore" due to multiple concurrent psychosocial stressors as well as her medical issues. Her endocrinologist sent her immediately to the ED for psychiatric evaluation. On the way to the ED she experienced several episodes of left sided chest and abdominal pain described as brief stabbing pains.

On initial exam in the ED she complained of sharp intermittent chest and abdominal pains, increased weakness from baseline, and continued anxiety and tearfulness concerning her overall quality of life given her recent illnesses.

Here is her initial ECG:

What is your interpretation?

There is sinus rhythm at approximately 75 bpm with prolonged PR interval. The QRS complex is wide, approximately 160ms. There are ST deviations which appear appropriate and proportional to the abnormal QRS.

To some long-time readers, the diagnosis will be obvious. I will delay giving away the diagnosis to give learners the best opportunity for reasoning it out.


How to Evaluate a Wide Complex QRS:

When one encounters a wide complex QRS, there should be both an immediate, type 1 thinking, instant-recognition version of evaluation, as well as a more deliberate, logical, double-checking version:

Type 1:
An experienced electrocardiogapher looking at a wide complex may immediately sort it into the most common categories that have earned instant recognition status: LBBB morphology, RBBB morphology (+/- LAFB or LPFB), ventricular paced rhythm (based on pacer spikes and appropriately wide QRS immediately following), or something that doesn't easily fit into any of those categories.

Type 2:
In order to provide a logical approach to the wide QRS that doesn't fit into an obvious category, we must know how a QRS complex becomes wide. A wide QRS complex can only be created by a limited number of ways:

1) Ventricular Origin: The action potential originated in the ventricles, outside of the proximal intrinsic conduction system, or (in the case of WPW) reached the ventricles without using the conduction system:
Examples: Ventricular paced rhythm, ventricular tachycardia, WPW, AIVR, fascicular VTs

2) Supraventricular Origin with Conduction Abnormality: The action potential originated above the ventricles, entered the conduction system correctly, then at least one of the following must have happened:

        2a) Abnormal conduction system: Normal speed of conduction, but structural blockade somewhere within the conduction system
Examples: LBBB, RBBB, nonspecific intraventricular conduction delay, cardiomyopathy

        2b) Abnormal conduction speed: Normal conduction system, but slowed speed of conduction
Examples: Hyperkalemia, Na channel blockade (medication, toxin), severe acidosis

Every wide complex QRS must be a combination of the above causes.

Let's apply this method to our current ECG:

The QRS morphology in some leads (V2-V4) could be mistaken at first glance for LBBB, however the lateral leads in LBBB should show a predominant or mostly monomorphic R wave, which is not the case here, therefore this is not LBBB. There are no pacer spikes. It is something that doesn't fit into a prescribed category.

P-waves before each QRS complex suggest (but do not prove) that the origin of the QRS complex is supraventricular. It does not satisfy the criteria or morphology of RBBB or LBBB, therefore we are left with Non specific intraventricular conduction delay (IVCD) or abnormal conduction speed.

The next obvious step is to look for the patient's prior baseline ECG. Here it is:

Baseline ECG from 1 month prior. How does this ECG affect your reasoning of the presentation ECG?

Here is the presentation EKG again, for easy visual comparison:

The baseline ECG shows SR with normal PR interval and narrow QRS complex. Take a close look at the morphology and QRS components ("up, then down," "small R, then big S") in each lead in the baseline ECG compared to the presentation ECG. What do you notice?

The components are almost exactly the same. The only difference in the QRS complexes between the two ECGs is the width. This suggests that the action potential followed exactly the same pathway down the conduction system, but was SLOWER than before. This patient has a derangement of action potential propagation that is slowing down the speed of conduction and widening the QRS complex.

Of the conditions that cause slowing of action potential speed and wide QRS complexes, there is one condition that is more common, more dangerous, more recognizable, more rapidly life threatening, and more readily treatable than all the others: hyperkalemia.

Now that all readers are on the same page, please notice the corroborating features of hyperkalemia on the presentation ECG: first degree AV block, widened P-waves seen in V4-V6, and peaked T waves in V3-V5.

The possibility of hyperkalemia was not noticed initially by the providers. Initial labs were drawn and sent, and the providers had planned for a broad evaluation including chest pain and abdominal pain workups given her recent colostomy and abdominal pain.

45 minutes after arrival, with no labs back yet, she was suddenly noted to have intermittent periods of obtundation alternating with respiratory distress and worsening pain. Before being rushed to the resuscitation bay, a repeat ECG was performed:

Extremely wide QRS which is difficult to delineate from the ST segment and T wave. This is approaching a sine-wave pattern, and indicates end-stage hyperkalemia which usually precedes an unstable tachy- or bradyarrhythmic cardiac arrest. Even in the absence of electromechanical dissociation which is present in severe hyperkalemia, this disorganized and morbidly wide QRS complex is likely not providing a reasonable cardiac output. 

Hyperkalemia was not suspected immediately after this ECG. Given that the patient had chest pain on arrival, and hyperkalemia had not been suspected on the initial ECG, in a patient with acute worsening, one can understand why acute STEMI +/- intermittent VT/VF may have seemed more likely to explain her acute change. A STEMI alert was called based on perceived ST elevations in the anterior leads V2-V4.

On the way to the resuscitation bay, the patient became unconscious and lost pulses. CPR was initiated. The monitor showed VFib, and she was shocked twice without conversion. On review of the initial ECGs, hyperkalemia was suspected at this point, and the patient received IV calcium and bicarb with ROSC achieved 1-2 minutes later.


Initial labs (~1hour prior to arrest) finally returned showing:
K = 8.1
BUN = 99
Cr = 6.84
Troponin = undetectable


A post-ROSC ECG was obtained just as a change in rhythm occurred:

The first 3-4 QRS complexes are very wide with bizarre morphology of QRS and ST-T-wave. The rhythm then changes to regular and tachycardic, with probable P-waves, (~120 bpm) for the remainder of the ECG.   

The patient's blood pressure on the arterial line dropped acutely:

This shows sustained polymorphic wide complex tachycardia. It is somewhere on the spectrum between polymorphic VT (PMVT) and VFib. The exact point on that spectrum is irrelevant, as the spectrum is more of a vortex ending in VFib arrest. The treatment for either is immediate, unsynchronized defibrillation.

Defibrillation was attempted several times, each with temporary improvement to a more organized wide complex tachycardia, then returning to PMVT/VFib:

Similar to prior

More calcium chloride and bicarb were administered. The exact amount is not available. Within minutes the patient achieved ROSC:

Sinus rhythm with much narrower (but still wide) QRS complex. There is perhaps a short QT and QTc interval here which may be caused by the calcium (a well described finding in hypercalcemia) which appears to have saved this patient's life. 

A dialysis catheter was placed, and the patient underwent immediate CVVHD. No further arrests or deterioration in rhythm occurred. The patient recovered for 1 week in the ICU, then signed out AMA only to return 4 days later with shortness of breath. She had another prolonged admission in which she gradually recovered kidney function, and has not yet required long-term dialysis.



Learning Points:

1) Hyperkalemia is one of the most important causes of a wide QRS complex. Hyperkalemia is immediately life threatening, immediately recognizable on ECG, and immediately treatable.

2) You must become facile with recognizing RBBB, LBBB, and paced rhythms in order to correctly diagnose wide QRS complexes.

3) The initial treatment for life-threatening hyperkalemia is IV calcium. There is no limit to the amount of calcium given if the patient is unstable. Titrate to normalized QRS complex. The serum calcium level is irrelevant.