Friday, October 26, 2012

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.