Case 4 – Answer

First of all thanks to those of you who interpreted this EKG.  It’s a difficult one to begin with and to do it without a history is even harder.

So lets fill in some of the blanks about this patient’s history.  This was a 69 y/o woman w/ PMH of HTN, HLD and CHF presenting with exertional SOB.  Her vitals were:  160/84     155     40     97.8    100% on RA

Her initial EKG is shown above.  As with any EKG, a methodical approach to interpretation is best to prevent overlooking important details.

Rate: 132 BPM based on 22 QRS’s in the rhythm strip.  If you look at the individual distance between each QRS you may get a rate above 150

Rhythm:  Is there a P before each QRS… This is probably the hardest question to answer for this EKG.  If there are P-waves, they are difficult to find… but we’ll come back to this…

Axis:  The QRS is predominantly negative in I.  This suggests a right axis deviation.  The positive aVF means that the axis is somewhere between 90 and 180 degrees.  If we look at the relative size of the QRS aVF is about 12 boxes high while I is about 6-7 boxes in the negative.  This means that the true axis of the heart is closer to aVF (90) than it is to the opposite of lead I (180).  The EKG machine calculated the axis to be 103 which fits with our guess.

Intervals:  Since we can’t find P waves, its difficult to determine the PR interval, but the QRS interval is about 4 small boxes (160ms).  The QT interval is also difficult to assess but if you look at the rhythm strip you can get an idea that it is long.  Measuring from the beginning of the QRS to the end of the T, in some places it looks like its reaching 400ms (2 large boxes).  However, we always have to correct the QT because it can be falsely shortened or lengthened based on the heart rate.  At a rate of 150 the RR interval is going to be 400ms so the QTC = QT/square root (RR) = 632.  If you use other formulas you may get an answer ranging from 492 but in any case, this is prolonged.

ST segments:  This is also fairly difficult to assess given  the variable baseline of the EKG but you can clearly see T-wave inversions in the inferior leads (II, III, aVF).  In the precordial leads, the T waves are discordant with the QRS.

So… at the end of all of that do we have a diagnosis… the QRS is long and we don’t see clear P waves so at the onset we have to think this is a wide complex tachycardia.  Our differential for wide complex tachycardia’s is in Table 1.

The article this table comes from a is a great reference for how to approach wide complex tachycardia.  It is in the June 2008 issue of EM Practice.

Some pearls to note breifly:

• Monomorphic VT usually results from the presence of a scar in the myocardium
• In pre-excitation tachycardia since the impulse does not travel through the His-Purkinje system their management is similar to that of VT
• Toxic causes like anti-arrhythmic overdose, TCA overdose and hyperkalemia often are unresponsive to standard treatments for wide complex tachycardia
• Hx of MI, CHF or recent unstable angina increases the likelihood of having VT

So how do we determine which broad category our patient falls into?  The article referenced goes through a step by step method to determine the cause of the wide complex tachycardia.

1. Obtain an 12 lead EKG to rule out pacemaker related WCT or artifacts
2. Obtain a prior EKG.  If the wide complexes in the current EKG are similar in morphology and axis in all leads to the prior sinus EKG then it is less likely to be VT and more likely to be be SVT
   
3. Determine if the rhythm is irregular or regular.
   1. Irregular WCT is usually either polymorphic VT, AF with aberrant conduction or AF with WPW.  Polymorphic VT should have significant variations in QRS amplitude while AF with aberrant conduction and AF with WPW do not.  A rate of > 200 also prefers VT  or AF with WPW rather than AF with aberrant conduction.  
   2. Regular WCT could be monomorphic VT, SVT with aberrant conduction, SVT with WPW or pacemaker related tachycardia.
4. Apply Griffith EKG Morphology / Axis Criteria
   
   1. REGULAR WCT – If the EKG has a classic RBBB and the axis is not NW it is less likely to be VT.  If the EKG has a classic LBBB pattern and the axis is not 90-270 (RAD or NW) then it is less likely to be VT.
   2. IRREGULAR WCT – Look for classic RBBB or LBBB pattern.  If this is not present, its more likely to be VT.
5. Look for signs of AV dissociation (REGULAR WCT)
   1. P waves that “march” through the WCT.  Best visualized in V1 or inferior leads
   2. If P waves conduct they can create a FUSION BEAT (combination of supraventricular impulse with ventricular impulse) or CAPTURE BEAT (supraventricular impulse that is conducted through the normal pathways – narrow QRS).  The image below shows VT followed by a fusion and two capture beats.
6. Entirely positive or negative concordance in precordial leads

 

Going back to our EKG, the rhythm looks irregular.  This is especially clear if you look at lead II.  The RR interval is clearly not uniform.    Applying the Griffith Morphology Criteria our EKG meets the criteria for LBBB.  In addition, the rate is <200 and the QRS amplitude is only minimally variable.  All of these points suggest that our underlying rhythm is Afib with pre-excitation or aberrancy.  However, Afib with pre-excitation rarely has a QRS that matches LBBB pattern, so it is more likely to be Afib with aberrancy.

In our case, the astute physicians at the bedside noted that the patient’s rate was variable, ranging from 113-150s while at rest.  They performed a vagal maneuver which slowed the rate and narrowed the complexes.  A repeat EKG confirmed the irregular rate.  After a dose of cardizem, the following EKG was obtained.

The repeat EKG clearly shows P waves that have a flutter/fib pattern.  Going back to our original EKG, although it’s difficult you can see P waves specifically in lead V1 between the 3rd and 4th complexes and the same corresponding P waves in the rhythm strip.  The presence of P waves in an EKG that otherwise looks like a wide complex tachycardia narrows our differential to tachycardia of supraventricular origin.

 

 References:

EM Practice June 2008, Vol 10, No. 6. “Wide Complex Tachycardia: Diagnosis and Management in the Emergency Department”

Lifeinthefastlane.com – “VT Versus SVT with Aberrancy” – http://lifeinthefastlane.com/2010/12/vt-versus-svt-with-aberrancy/