Ventricular Tachycardias: 

Definitions: 
- NSVT : >3 beats & <30 seconds
- MMVT : monomorphic VT: All QRS complexes have the same morphology
- PMVT: polymorphic VT: variable QRS morphology
- Torsades: PMVT with long QT
- V-fib: disorganized rapid ventricular activity, typically > 200 bpm

VT in structural heart disease- ischemia
- Usually re-entry around a scar
- Someone comes in in MMVT - less likely "this guy is having an MI right now" - more likely the VT is involving scar from an old MI - triggered by volume overload, electrolyte abnormalities, or ischemia
- re-entry around ventricular tissue - vtach
- re-entry in bundles - will look like BBB (goes down R bundle looks like LBBB)

ARVC/D
- Arrhythmogenic RV cardiomyopathy/dysplasia
- fibrofatty replacement of cardiac tissue
- microaneurysms (tissue in RV bulges out)
- Dx - diagnosis based on Echo, MRI, fam hx, biopsy, EKG criteria
- EKG: t-wave should be upright in V1-V3, but T-waves will be inverted in those leads in ARVC (without RBBB) ; Epsilon waves - you'll get a little ditzel at end of QRS complex (slow conduction of electricity through fibrofatty tissue)

Ventricular arrhythmia in structurally normal hearts
- Outflow tract tachycardia (RVOT,  LVOT)
- Idopathic LV tach - belhassen, verapamil sensitive, fasciular
- VT/VF with brugada
- VT/VF with long QT syndrome
- Catecholaminergic PMVT

RVOT/LVOT PVCs
- 20-40 y/o, F>M
- NSVT
- Sudden death rare if LV/RV normal
- EKG: LBBB type, inferior axis (depolarizing from outflow tract - pulmonic or aortic valve - straight down - super tall QRS complexes in II, III, aVF leads)
- Likely benign

Fascicular VT - aka belhassen, aka verapamil sensitive, aka ILVT
- using one limb of fascile to go down
- if it exits from left posterior fascicle - looks like RBBB with LAFB (beat comes down LP fascicle - re-enters up the RB and LAF - "blocks" so the signal can't come down those channels)
- cured with ablation of L posterior fascicle

Brugada
- AD Na channel dysfunction (loss of function mutation) - reduces inflow of Na - differing parts of the heart have differing sensitivity to this, and thus voltage gradients appear between different parts of the heart tissue
- Can look like incomplete RBBB and ST elevation in anterior precordial leads (check V2)
- Can cause syncope and sudden cardiac death - must be managed with ICD
- Picture from medscape:

Long QT syndrome
- Type I (KCNQ1 - K channel mutation) - triggered by exercise - esp swimming - ask about a family hx of drowning
- Type II (HERG - K channel mutation) - triggered by loud noise or emotional stress - alarm or phone ring
- Type III (Na channel mutation - same channel as Brugada, but gain of fxn instead of loss of fxn) - triggered by rest - people die in sleep
- type 4-15: rare
- Prolonged QT - can lead to torsades
- Triggers: abx, psych meds, Methadone!!

Wide complex tachycardia: Differentiating VT vs SVT+aberrancy (i.e. BBB or pre-excitation)
- Wellens criteria - favors VT
- Brugada criteria - algorithm
- R-S distance: if is a sharp upslope you're probably using the conduction system (SVT c aberrancy), otherwise you're not (VT)
- AV disassociation tells you you're in VT -- in SVT with aberrancy, A and V are still associated
- Capture beats: ie in AV disassociation, the ventricle is going on alone, occasionally a well timed atrial beat will actually conduct down and "capture" the ventricle
- Fusion beats: not timed well enough to capture, partially captures
- Capture and fusion beats imply AV disassociation - implies VT - absence of these beats doesn't imply NOT VT - if your ventricular beats go up through AV node and conduct to atria, that signal can't come down to cause a capture/fusion beat
- Waves that look like they are using the conduction system - SVT  - not using conduction system - VT

Adenosine cannot be used to definitively differentiate VT and SVT with aberrancy! 
- The traditional teaching is that SVT uses the AV node and VT doesn't, so SVT will break with adenosine, but this is not true!
- Not all SVT uses AV node - there may be an accessory pathway
- Some VT does use the AV node (outflow tract VT)

Bidirectional VT
- Hallmark of Dig toxicity
- Catecholaminergic polymorphic VT

Afib with accessory pathways
- on every boards
- don't give any drugs that block the AV node (adenosine, CCB, B-blockers)
- Tx with procainamide - blocks accessory pathways - might convert A-fib

VT storm
- 3 or more episodes of VT in 24 hr period
- Causes: ischemia, ischemia, ischemia, CHF, metabolic (low K/Mg, thyroid storm - can precipitate thryoid storm in hypothyroid person with dye load), pro-arrhythmic drugs