ST Elevation and a Wide QRS. EMS activates the Cath Lab.

A middle aged male with nausea, abdominal discomfort, and weakness called 911.  The medics recorded this ECG:

There are prolonged pauses, then the rate picks up.  There is a wide QRS, and ST elevation in leads V1 and V2. 

Another ECG was recorded 8 minutes later:

Bradycardia with escape. Possibilities include: 
1. Junctional rhythm with RBBB + LAFB
2. Ventricular escape from the Left Posterior Fascicle
3. Other?
There is some ST elevation in V2 and aVL

The patient arrived in the ED and had this ECG recorded:

6 minutes later, 14 min after the first

Again, junctional with RBBB and LAFB, or a left posterior fascicle escape.  
The QRS duration is 206 ms.
This ECG is nearly pathognomonic.  What is the diagnosis? 

The diagnosis is hyperkalemia until proven otherwise.  The emergency physicians immediately recognized it, and gave 6 g (6 doses, or "amps") of calcium gluconate.

The patient had a dialysis graft in his arm.  The K returned at 8.0 mEq/L.

The QRS duration on the monitor narrowed.  They recorded another 12-lead 18 minutes later, 32 minutes after the first:

There is now sinus bradycardia with first degree AV block.  The RBBB is gone.  The LAFB remains.  
The QRS duration is now 153 ms.  
ST elevation in V1-V3 remains, but is not due to ischemia.

6 more grams of Ca gluconate were given and the K was "shifted" with standard therapy.  He went for emergent dialysis.

Learning Points

1. Hyperkalemia frequently mimics STEMI:

----Case 1 of pseudo-inferior-posterior STEMI
----Here is the 2nd case of Pseudo-inferior-posterior-STEMI due to hyperkalemia.
----More cases of Pseudo- Anteroseptal STEMI due to hyperK

****Think about hyperK as an etiology of ST elevation
****Be skeptical of STEMI when a patient has no chest discomfort

2. The P-wave and sinus node activity in hyperkalemia

That the LAFB remains suggests that the initial ECGs were supraventricular, junctional, or sinus.

Hyperkalemia may obscure the sinus beat even though the sinus node is operative and transmitting the impulse.  A P-wave is due to the propagation of the electrical wavefront in the atrium, not due to sinus activity.  Hyperkalemia eliminates this atrial wavefront even though the sinus node is functional and transmitting the impulse to the AV node.

The first ED ECG probably had a sinus origin (but without a P-wave it is not certain and cannot be called "sinus rhythm with an "invisible" P-wave and RBBB + LAFB".   It may indeed have been junctional.

Here is from Chou's electrocardiography (6th edition, Surawicz, 2008):

"A regular rhythm in the absence of P-waves has been attributed to sinoventricular conduction via atrionodal tracts in the presence of sinoatrial SA block.  This concept is suported by the observations that when the P wave disappeared during hyperkalemia in dogs, the electrical activity was recoreded from the SA node, crista terminalis, and antrionodal tracts, and each QRS complex was preceded by a His bundle electrogram.  A regular rhythm in the absence of P waves can be caused by displacement of the pacemaker into the atrioventricular junction or the Purkinje fibers, but precise localization of the pacemaker in patients with absent P waves is usually not possible."

References for this statement:

1. Hariman RJ et al.  Effects of hyperkalemia on sinus nodal function in dog: sino-ventricular conduction.  Cardiovasc Res 17:509; 1983  http://cardiovascres.oxfordjournals.org/content/17/9/509.short

2. Racker KD.  Sinoventricular transission in 10 mM K+ by canine atrioventricular nodal inputs.  Circulation 83:1738, 1991.  Full text link:  http://circ.ahajournals.org/content/83/5/1738.full.pdf