Many Wide Complex Tachycardias originate in the ventricles but some do not.
The one’s that do not may include aberrant SVT like a bundle branch block, or a ventricular
reentry problem where the ventricles may contract too early after partial repolarization like
that of a preexcited tachycardia or Wolff-Parkinson White syndrome.
A very common V-Tach is called monomorphic ventricular tachycardia.
This means that all of the complexes are the same size, direction and shape.
This is usually caused by an ectopic pacemaker somewhere located in the ventricle.
In this ECG, the rhythm is regular but may also be slightly irregular.
The rate is around 1 to 200 beats per minute and there are rarely any discernable P-waves.
There is no discernable PR interval and QRS complex is greater than .11 seconds and are
characterized as wide and bizarre with no P-wave to QRS ratio.
Now the main problem with this type of fast wide complex tachycardia is that hemodynamics
are unstable.
The heart rate is so fast, that it inhibits the atrium to prefill and preload the ventricles
prior to their next contraction.
In this case, it’s important to know if the patient is stable or unstable.
If stable, learn more about why the patient may be experiencing this arrhythmia, remember,
wide complex ventricular tachycardia can sometimes be caused by heart disease, electrolyte imbalance
especially potassium, and Q-T interval prolongation.
If patient is stable order a 12 lead ECG to see if the rhythm is supraventricular or ventricular
in origin.
If the patient is unstable, immediate treatment is vital.
Now let’s look at Wide complex Polymorphic Ventricular Tachycardia.
Poly, meaning multiple, describes the origin of the electrical foci in the ventricles well.
In fact, Polymorphic tachycardia is caused by multiple ventricular foci with the resultant
QRS complexes varying in axis, amplitude, and duration.
It can also be described as Bidirectional V-Tach, which is another type of polymorphic
ventricular tachycardia, most commonly associated with digoxin toxicity, and this is known commonly
as Torsades de pointes.
Along with digoxin toxicity, we can see polymorphic VT with hypomagnesemia and hypokalemia.
Let’s take a closer look at the ECG for Polymorphic Wide Complex Tachycardia.
The rhythm is irregular with a rate of between 200-250 beats per minute.
There are no discernable P-waves and there is no PR interval.
QRS complexes are variable but greater than .11 seconds and they’re wide and bizarre.
There is no P-wave to QRS ratio.
Now in Torsades, it can sometimes appear that the apex of the V-wave changes from top to
bottom and back again.
Torsade de pointes, or TDP, translates as “twisting of points.”
The most important thing to remember with this type, and monomorphic wide complex V-Tach,
is that both can become pulseless V-Tach or v-fib very quickly.
It’s important to remember that Wide complex Ventricular Tachycardia can present with or
without a pulse.
We can even see pulseless V-Tach in cardiac arrest patients, but in most cases, pulseless
V-Tach quickly deteriorates into Ventricular Fibrillation.
Remember, Pulseless V-Tach is treated the same as Ventricular Fibrillation.
And recognition and immediate treatment is vital to a potential positive outcome.
The ECG interpretation can be the same as pulsed Ventricular Tachycardia, but the difference
is that the patient is unresponsive, not breathing normally and pulseless.