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Many wide complex tachycardias originate in the ventricles but some do not. The ones that do not may include a bare SVT like a bundle branch block, or a ventricular re-entry problem where the ventricles may contract too early after partial repolarization. Like that of a pre-excited 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 one to 200 beats per minute and there aren't really any discernible P waves. There's no discernible P to R 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 why complex ventricular tachycardia can sometimes be caused by heart disease, electrolyte imbalance, especially potassium, and a Q to T interval prolongation. If the 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 why complex polymorphic ventricular tachycardia. Poly, meaning multiple, describes the origin of the electrical foci in the ventricle as well. In fact, polymorphic tachycardia is caused by multiple ventricular foci with the resultant QRS complex is varying in access, amplitude, and duration. It can also be described as bi-directional V-tach, which is another type of polymorphic ventricular tachycardia, most commonly associated with digoxin toxicity. And this is know 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 between 200 to 250 beats per minute. There are no discernible P waves and there is no P to R 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. Torsades 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 pulse ventricular tachycardia. But the difference is that the patient is unresponsive, not breathing normally, and pulseless.
Many wide complex tachycardias originate in the ventricles, but not all. The ones that don't include a bundle branch block, and a ventricular reentry problem, where the ventricles contract too early after a partial repolarization – like a pre-excited tachycardia or Wolff-Parkinson-White (WPW) syndrome.
In this lesson, we'll look at monomorphic ventricular tachycardia (including an ECG), polymorphic ventricular tachycardia, or (thankfully) PVT for short (also including an ECG), and pulseless ventricular tachycardia. And at the end of the lesson, we'll give you a word or two on pulseless electrical activity.
One very common V-tach is called monomorphic ventricular tachycardia, which means that all of the complexes are the same size, direction, and shape. It's usually caused by an ectopic pacemaker located somewhere in the ventricles.
An ECG for a patient with monomorphic V-tach will exhibit the following signs.
*Monomorphic V-tach ECG
The main problem with this type of fast and wide complex tachycardias is that the hemodynamics are unstable. The heart rate is so fast that it inhibits the atrium from prefilling and preloading the ventricles before the next contraction. In these cases, it's important to know whether or not the patient is stable or unstable.
Pro Tip #1: If the patient is stable, try to learn more about why the patient could be experiencing this type of arrythmia. And remember, wide complex V-tach can sometimes be caused by heart disease, electrolyte imbalance (especially potassium) and a Q to T interval prolongation.
If the patient is stable, check to see if their rhythm is supraventricular or ventricular in origin.
Warning: If the patient is unstable, immediate treatment is vital.
Poly simply means multiple and describes the origin of electrical foci in the ventricles. In fact, polymorphic V-tach is caused by multiple ventricular foci with the resulting QRS complexes varying in axis, amplitude, and duration.
Polymorphic V-tach can also be described as bi-directional V-tach, which is another type of polymorphic V-tach that is commonly associated with digoxin toxicity, commonly known as torsades de pointes.
Along with digoxin toxicity, we often see polymorphic V-tach with hypokalemia or hypomagnesemia.
An ECG for a patient with polymorphic V-tach will exhibit the following signs.
*Polymorphic Ventricular Tachycardia ECG
In torsades, it can sometimes appear that the apex of the V-wave changes from top to bottom and back again. And actually, torsades (French in origin) literally translates as a twisting of points.
The most important thing to remember with this type, along with monomorphic wide-complex V-tach, is that both can become pulseless V-tach or VFib pretty quickly.
Pro Tip #2: One important thing to remember is that wide complex V-tach can present with or without a pulse and you may even see pulseless V-tach in a cardiac arrest patient. However, in most cases, pulseless V-tach will quickly deteriorate into VFib.
Also keep in mind that pulseless V-tach is treated the same as VFib and that recognition of the condition and treatment for it will be vital for a potential positive outcome.
Pro Tip #3: An ECG interpretation for pulseless V-tach can be the same for pulsed V-tach. The difference is that the patient is unresponsive, not breathing normally, and has no pulse.
Pulseless electrical activity (PEA), which will be covered in more detail in a subsequent lesson, is not a specific rhythm. Instead it's a term used to describe any organized electrical activity – but not VFib or asystole — on an ECG or cardiac monitor that is associated with no palpable pulses.
Pulsations can be detected by an arterial waveform or Doppler study. However, pulses are not palpable. The rate of electrical activity may be slow (which is most common), normal, or fast. Very slow PEA can also be referred to as agonal.
When a patient is in PEA, the ECG can display normal or wide QRS complexes, as well as other abnormalities, which include:
It's important to remember to assess the patient's monitored rhythm and note the rate and width of the ORS complexes.
PEA can be caused by reversible conditions easily remembered as the H's and T's. We addressed the H's and T's briefly in a prior lesson and will dig a little deeper into them in the lesson on asystole.
Warning: One important takeaway is this: Unless you can quickly identify and treat the cause of PEA, the rhythm will likely deteriorate to asystole.