PULSELESS VENTRICULAR TACHYCARDIA: A WARNING
There is a danger in thinking that pulseless ventricular tachycardia (VT) is the same a ventricular fibrillation (VF). The electrophysiologic mechanisms of both arrhythmias are different. Although VF always results in pulselessness, VT can have a wide array of effects on perfusion ranging from adequate to no cardiac output. Whenever VT causes inadequate systemic perfusion (is unstable), immediate conversion using electrical counter-shock is indicated.
However, due to the differences in the electrophysiology and myocardial response, termination of fibrillation commonly requires higher therapeutic energy levels, whereas VT is a circuitry issue that most often requires lower therapeutic energy levels to terminate the arrhythmia. Considering that DC counter-shock has been shown to create myocardial damage in some patients, it would seem prudent to be pragmatic about delivered energy and potentially protecting already damaged tissue. If in the case of shockable VT, if a low-energy shock fails, there is always the option to increase joules in a stepwise manner.
The other problem associated with the incorrect concept that “pulseless VT should be treated the same as VF” is refractoriness to shock. This is rarely seen in VT, however commonly seen in VF. Treatment algorithms seem to suggest that if the patient fails to convert with counter-shock in VT, the administration of epinephrine is appropriate. Adding a potent ß1 stimulator in this case could support the anomalous circuitry and hamper further attempts at resuscitation. Additionally, if conversion occurs, the epinephrine could induce a significant tachycardia resulting in further damage to the myocardium. If the goal of the use of epinephrine is enhancement of coronary perfusion pressure, the use of a pure alpha agonist seems more appropriate.
This may be a simple case of trying to “over think” to the point of error. It might serve practitioners well to view VT as “stable” and “unstable”. There is essentially no basic difference in a patient with a heart rate of 180 and a systolic blood pressure of 20mmHg or a patient with a heart rate of 180 and has lost cardiac output. Immediate DC counter-shock is the first step. In cases of incessant reinduction of the VT after a successful conversion, the use of appropriate antiarrhythmic agents make sense.
Not understanding the differences between VT and VF when called upon the treat these critically ill patients could significantly alter a chance of a good outcome.
Unstable ventricular tachycardias occur when an anomalous ventricular circuit is activated, reducing cardiac muscle activity, leading to inadequate cardiac output.
The reduction in cardiac output resulting can cause symptoms ranging from decreased level of consciousness to a total lack of cardiac output, known as a pulseless ventricular tachycardia.
Unstable ventricular tachycardia may present with the following characteristics:
Many tachyarrhythmias with heart rates above 150 BPM cause serious impairment of perfusion, especially in patients with pre-existing cardiac dysfunction. However, a patient with an obstructed coronary artery developing ventricular tachycardia (VT) with adequate perfusion, who develops clinical signs of worsening ischemia (i.e. chest pain, etc.) would also be considered having an unstable event. To allow the tachycardia to worsen ischemia and extend an infarct would not be acceptable.
Both narrow QRS and broad QRS tachycardias can produce hemodynamic instability. Thus, from a basic perspective, either can render perfusion inadequate, requiring immediate treatment.
A deeper understanding of arrhythmia recognition allows a practitioner to possibly differentiate between VT and broad QRS atrial fibrillation (AF). This may provide information which could reduce the range of options for treatment to more appropriate solutions, (i.e. VT tends to respond to lower levels of therapeutic electrical therapy, whereas AF often requires higher levels to convert the arrhythmia).
The behavior of the arrhythmia may dictate the best therapy. If the patient is having short episodes of the arrhythmia, followed by spontaneous conversion out of it and returned stability, pharmacologic therapy may be the best course of action, rather than cardioversion.
Ventricular Tachycardias typically emanate from underlying organic disease (acute or chronic), inherited or congenital channelopathies, electrolyte imbalances, or pharmacologic agents.
Some examples of these include:
A prolonged, sustained episode of Unstable VT can result in a variety of potential complications, including:
When considering the range of possibilities for treating stable VT, the differentiation of the broad QRS tachycardia is important. However, when either supraventricular tachycardia (SVT) or VT produces hemodynamic or cardiovascular instability, a differential diagnosis is not an instant priority.
Either SVT or VT, when producing instability, require emergency termination of the arrhythmia. In most settings, emergency cardioversion is mandatory. Unless you have a strong reason to believe the underlying mechanism is AF, the majority of circuit/bypass tract mechanisms respond to lower levels of therapeutic energy.
Unstable SVT or VT require emergency countershock. Several misunderstandings are common when discussing details of treatment.
* = it is acceptable to use the "synchronized mode" for organized arrhythmias. However, should the patient convert into VF, immediately deliver an NON-SYNCHRONIZED shock (immediate defibrillation)
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