This pair of ECGs feature one of our recurring themes: wide-complex tachycardia (WCT). It is a fascinating topic, as tachycardia has many causes and many mechanisms, and wide QRS also has many causes, with the mechanism being slow conduction through the ventricles.
Sometimes, it is not possible to diagnose the true origin of a WCT from one ECG, or even serial ECGs. Is the tachycardia due to increased sympathetic activity (fear, dehydration, exercise, hypoxia, hypovolemia, etc.)? Or is the fast rate due to reentry, where one impulse gets “caught” in a loop, repeating itself rapidly, and depolarizing the myocardium with each pass? What is the location of the pacemaker that is responsible for the rhythm? Is it a supraventricular rhythm that has suffered an intraventricular conduction delay, widening the QRS? Or is the rhythm originating in a ventricular pacemaker, without the ability to travel on the fast highway that is the intraventricular conduction system?
If you or your students work in an acute care setting, such as pre-hospital or emergency department, you may not be with the patient long enough or be able to conduct enough tests to determine without a doubt the answers to the above questions. Some WCTs cause such severe symptoms that they must be dealt with quickly, to avoid rapid deterioration to ventricular fibrillation. For that reason, there is a widely-accepted rule for WTC treatment:
TREAT ALL WIDE-COMPLEX TACHYCARDIA AS IF IT IS V TACH UNTIL PROVEN OTHERWISE.
The Patient: These two tracings were taken from an elderly man who complained of feeling sick. He was found by paramedics to be alert, diaphoretic, tachypneic, and complaining of palpitations. His initial vital signs were: BP 80/60, Pulse 167 and regular, respirations 30/min. Pulse oximetry 96%.
ECG No. 1 at 18:18:44 The rhythm is regular at 167/min. The QRS width is about .12 seconds (120 ms). It is difficult to measure the QRS width with precision due to artifact and slurred terminal portions of most of the QRS complexes. No clear P waves are seen, possibly due to the rate causing P-on-T. Several features of the QRS morphology suggest VENTRICULAR TACHYCARDIA, including the extreme axis (almost vertical), and the negative deflection in Lead V6. When V tach has this pattern: a minimally-wide QRS with a right bundle branch block pattern, it is usually “fascicular ventricular tachycardia”.
Initial Treatment: Because of the patient’s hemodynamic instability and symptoms, the EMS crew elected to follow the above rule and treat this rhythm as VENTRICULAR TACHYCARDIA. He was administered Amiodarone 150 mg IV while the crew prepared to cardiovert him under light sedation. As soon as they were able, he was cardioverted with 120 j. The new rhythm is shown in ECG #2.
ECG No. 2 at 18:31:55 The patient’s rhythm remains regular at about 130 / min. Respiratory rate 20/min. and unlabored. BP 92/58. Pulse ox: 97% on nasal O2.
The most interesting finding is the QRS morphology has not changed. The width is still .12 sec., and the axis and other features of the QRS complexes are the same as they were in the faster rhythm. In addition, in spite of the artifact, I feel that P waves are present. A cleaner ECG might prove it, but I am confident of the P waves in Leads II, III and V3. I will readily admit that a clear, artifact-free ECG might prove me wrong. If this is SINUS TACHYCARDIA, the first ECG was most certainly not V Tach, because the QRS complexes haven’t changed. If we accept that there are P waves, the first rhythm was paroxysmal supraventricular tachycardia. The wide complexes would be due to right bundle branch block and anterior superior fascicular block (also called hemiblock). The RBBB causes rSR’ pattern in V1 and wide S waves in I and V6, and explains the slightly widened QRS.
The fascicular block causes the extreme left axis shift.
If you don’t see P waves, then we would have to explain how the cardioversion changed the rhythm from a “fast V Tach” to a “slow V Tach.”
Patient Outcome: The crew, by treating this WCT as V tach, obtained a quick improvement in the rate, which helped with the symptoms. Amiodarone and cardioversion are both appropriate treatments for V tach and PSVT.
The patient was diagnosed at the hospital with “arrhythmia due to an infection, combined with effects of a weight-loss medication”. He had a cardiac catheterization which was negative for significant coronary artery disease. We have no information on the diagnosis of the arrhythmia, or what his ECG looked like on discharge, one week later.
As always, we welcome your comments and opinions on this case.
Many thanks to Lt. Curtis Jepsen for donating these tracings.
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