ECG Interpretation Review #52 (Wide Tacycardia - Toxins - Hyperkalemia - Ventricular Tachycardia - Sinoventricular Rhythm)

The ECG in Figure 1 was obtained from an acutely ill but alert (and hemodynamically stable) patient.

• Is the rhythm VT (Ventricular Tachycardia)?
• How certain are you of your diagnosis?
• If told that the patient was a 31-year old woman with abnormal renal function who presented in DKA (Diabetic KetoAcidosis) ― Could you come up with an explanation as to why the rhythm in Figure 1 might not be ventricular tachycardia?

Figure 1: WCT rhythm in a 31yo woman with renal disease and DKA. Is this VT? 

INTERPRETATION: The rhythm in Figure 1 is a regular WCT (Wide-Complex Tachycardia) at a rate of ~135/minute. No P waves are seen. The usual differential diagnosis for a monomorphic regular WCT of uncertain etiology is shown in Figure 2:

Figure 2: Common Causes of a Regular WCT when sinus P waves are not seen.

Our reason for listing VT as the first 8 entities in LIST #1 ― is that VT is by far the most common cause of a regular WCT of uncertain etiology – and – that VT should not be missed.

• Assessment of QRS morphology in Figure 1 reveals an exceedingly wide, amorphous QRS complex that does not at all resemble any form of bundle branch block.
• The QRS is entirely negative in lead V6 (deep QS complex) ― and it is entirely positive in lead aVR (monophasic R wave) ― both being features that under normal circumstances identify VT with near-100% specificity.
• There is extreme axis deviation (totally negative QRS in leads I and aVF) ― which also normally conveys near-100% specificity for a diagnosis of VT.

The above said – clinical circumstances in this case differ from the usual setting for VT, and are KEY to recognizing the correct diagnosis. The patient is a 31-year old woman with abnormal renal function and acute DKA. The reason for QRS widening is marked hyperkalemia! (serum K+=9.8 mEq/L at the time Figure 1 was obtained).

• ECG changes of hyperkalemia typically follow a progressive sequence (See ECG Blog #10). Initially ― there is generalized T wave peaking (serum K+ ~5.5-6.5 mEq/L).
• As serum K+ levels approach ~7-8 mEq/L range ― the QRS widens and P wave amplitude decreases.
• Eventually, P waves disappear. Interestingly, the sinus node is still able to transmit the electrical impulse to the ventricles even though no P wave is seen. This is known as a sinoventricular rhythm ― and could be an explanation for how the regular WCT in Figure 1 might reflect sinus rhythm despite the absence of P waves ... 
• Ultimately ― transmission of sinus impulses ceases, and a sinusoidal-widened pattern supervenes. Ventricular fibrillation or cardiac standstill invariably follow.

---------------------------------------------------

BOTTOM LINE: Whether the rhythm in Figure 1 represents VT from marked electrolyte disturbance vs sinoventricular rhythm with QRS widening (and loss of P waves) from hyperkalemia is uncertain. We favor the latter ― because the treating clinician in this case recalled that onset of QRS widening was gradual following an initial ECG in which the QRS was narrow and T waves were peaked. IF the rhythm in Figure 1 had been VT ― we would have expected a much more abrupt onset of the regular WCT rhythm.

• Treatment with emergency K+-lowering treatment (calcium gluconate; glucose plus insulin; acute dialysis) resulted in resolution of QRS widening and return of electrically-evident sinus rhythm.

ADDENDUM: Perhaps List #1 in Figure 2 should be amended by addition of an Item #11 = “Something else” to include entities such as hyperkalemia and/or toxin effect (as might be seen with tricyclic overdose, in which marked QRS widening may be seen despite persistence of sinus mechanism).

----------------------------------------------------

ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.

----------------------------------------------------

• See Section 11.0 on Electrolyte Disturbances (in ECG-2014-ePub) ― with the part on Hyperkalemia beginning in Section 11.3.

-------------------------------------------------------------------------------------