VTac versus VFib

In reality, we don't stand around and debate whether it is polymorphic VT, or VF. They are both chaotic pulseless electrical rhythms that are fatal without converting the rhythm. PVT is considered a more convertible rhythm due to the fact it follows a more organized pattern through the ventricles. Due to the different foci in polymorphic VT on the ventricles the patient can actually maintain (however brief) a pulse. Although life threatening, because it is more organized in the ventricles it can be easier to convert then VF. The haphazard undulating nerve fibers that encompasses VF make it difficult to reset the heart into more organized rhythm.

http://circ.ahajournals.org/content/82/6/2035.full.pdf

Ventricular tachycardia (VT) refers to any rhythm faster than 100 (or 120) beats per minute arising distal to the bundle of His. The rhythm may arise from working ventricular myocardium and/or from the distal conduction system

Polymorphic ventricular tachycardia

When the QRS complex varies from beat to beat, the rhythm is described as polymorphic VT and suggests a variable electrical activation sequence. The most notorious, and probably the most common, form of polymorphic VT is torsade de pointes. The disorder’s name is a French term that suggests a "twisting of the points" of the QRS complexes over time

Torsade de pointes has unusual shifting-axis QRS complexes that appear (on ECGs) as if the heart is rotating upon an axis. It typically occurs during sinus rhythm and in the presence of drugs or conditions that prolong the QT interval (eg, type 1A antiarrhythmics, hypomagnesemia, droperidol). The dysrhythmia may occur either in the presence or in the absence of myocardial ischemia or infarction

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Ventricular Fibrillation

Ventricular fibrillation (VF) is the most commonly identified arrhythmia in cardiac arrest patients. This arrhythmia is a severe derangement of the heartbeat that usually ends in death within minutes unless corrective measures are promptly taken.

Ventricular fibrillation (VF) begins as a quasi periodic reentrant pattern of excitation in the ventricles with resulting poorly synchronized and inadequate myocardial contractions. The heart consequently immediately loses its ability to function as a pump. As the initial reentrant pattern of excitation breaks up into multiple smaller wavelets, the level of disorganization increases. Sudden loss of cardiac output with subsequent tissue hypoperfusion creates global tissue ischemia; brain and myocardium are most susceptible. VF is the primary cause of sudden cardiac death (SCD).

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I hope this helps.

correct.