Workshop #1 (HRS) Flashcards
BBR VT
HV interval equal to or longer than in sinus
His to onset of QRS complex - first ventricular activation anywhere, including surface
Bellhausen idiopathic LV tachycardia
RBBB
Left axis
Usually from L posterior fascicle
tx: CCB
Mappable
Distinguishing feature - Fascicular spike preceding
Cardiac memory
Seen after:
Termination of arrhythmia
Pacing
Ablation
Presumably caused by change in cardiac ion channels due to aberrant mech of pacing. As timeframe to recover is timeframe of making new channels.
Bidirectional VT
remember: ABCD
Andersen Tawil Syndrome (LQT7)
Bidirectional VT
CPVT
Digoxin toxicity.
CPVT:
Leaky RyR2 receptor
LQT7 - Andersen Tawil Sx
- periodic paralysis with K abn
- dystrophic changes
- prominent U waves
- Nasty PMVT, lots of PVC, Bidirectional VT
responds to flecainide: ATS, CPVT
Flecainide may plug leaky ryanodine receptors (also Coreg)
Jeeves Lange Neilsen
Homozygous mutation if LQT1
Homozygous mutation of KCNQ1 channel or KCNE1 channel
Will get really really really long QT interval
Exercise testing with LQTS (1,2,3)
LQT1: increase HR, QT will not shorten, paradoxically lengthening of QT.
(I Ks is makes AP shorter with adrenergic stimulation, however with mutation of I Ks makes AP longer with adrenergic stim - ?)
LQT2: exaggerated/funny looking Bifid T waves
LQT3: QT gets better because extra inward current (shorter AP - ?)
Negative HV interval
Seen with LV re-entry (myocardial re-entry)
Also with Fascicular VT (RBBB, LAD, Tx:CCB)