101014 mechanisms of arrhythmia Flashcards
supraventricular tachycardia
abnormal tachy which requires participation of either atrial or AV nodal tissue
when chaotic, it’s referred to as atrial fib and not SVT
ventricular tachycardia
abnormal tachy originating in ventricle or His-PUrkinje system
by def, doesn’t require involvement of either atrium or Av NODE
when chaotic-referred to as ventricular fib
mechanism of overdrive suppression
in spontaneously active pacemaker cells, hyperpolarizing current of NaK-ATPase is offset by pacemaker current If. however, in passively activated slower pacemaker cells, If is much smaller leading to net hyperpolarization. hyperpolarization leads to slow recovery after overdrive of pacemaker cells by faster foci.
how does sympathetics affect automaticity?
beta stimulation leads to increasing the open probability of pacemaker current If
also makes threshold potential more negative
mechanisms of cellular tachycardia
enhanced automaticity
abnormal automaticity-abnormal impulse formation in tissue not normally capable of pacemaker activity
triggered activity (due to oscillations in membrane potential). can be triggered by preceding tachy or brady
what is early afterdepolarization promoted by
conditions that prolong the AP (QT prolongation on ECG)
delayed afterdepolarization is promoted by
conditions which lead to HIGH INTRACELLULAR CALCIUM
promoted by catecholamines
inhibited by calcium ch blockers
mechanism of idiopathic VT
mechanism of digitalis toxicity
conduction block
occurs when a propagating wavefront encounters tissue which is unexcitable
permanent or fixed-all impulses fail
intermittent-ability to conduct is variable and changes with time
functional-block may be present only at critical rates which are faster than tissue refractory period will accomodate
block in the AV node or His bundle can result in interruption of AV conduction–what are the different degrees?
1st degree-delay w/o failure of conduction
2nd degree-some but not all beats fail to conduct
3rd deg-no propagation from atrium to ventricle (also known as complete heart block)
how is reentry different from automatic and triggered tachycardias?
automatic and triggered tachycardias are cellular phenomena, but reentry occurs in myocardial tissue composed of many myocytes working in sequence
how does reentry occur?
with presence of abnormal conduction (conduction block and slowed conduction)
requirements for reentry
two distinct paths for propagation
slowed conduction in at least one path
unidirectional block (tissue capable of conduction in one but not the opposite direction)
ex of reentry
paroxysmal SVT (in normal pts) WPW ventricular fibrillation (in ischemic heart tissue, there's scars)
all arrhytmias arise from
altered impulse formation or impulse conduction