Arrhythmia Flashcards
(37 cards)
what is overdrive suppression
SAN pacemaking being dominant over latent pacemakers such as AVN and purkinje fibres
how does SAN maintain overdrive suppression
discharge of AP faster than other heart structures
if san is low, what may a latent pacemaker due
create an escape beat
if latent pacemaker fires faster than SAN it creates a
ectopic rhythm
other cardiac myocytes may have the ability to take over pacemaking if there is?
tissue damage
what conditions cause latent pacemakers to discharge APs fast
ischaemia, hypokalaemia, fibre stretch, increased sympathetic activity
what is an EAD and what may trigger it
early afterdepolarisaton which occur during AP
prolongation of AP and drugs prolonging QT interval
bradycardia
What channels mediate EADs, where are they most frequent and what can it lead to
calcium channel in phase 2 and sodium in phase 3
purkinje fibres
may lead to torsades de pointes
what are DADs
delayed afterdepolarisations occurring after repolarisation
excessive CICR release from SR and sodium influx
where are DADs likely to occur and what may they be triggered by
tachycardia, increased and decreased by prolongation and shortening of AP
may be triggered by drugs increasing calcium influx or detention, catecholamines or digoxin
what is re-entry
self sustaining electrical circuit repeatedly stimulating myocardium due to lack of opposition AP to negate it
what is conduction block
slowing or failure of conduction through AVN
what is first degree AV block
slowed conduction to AVN, prolonged PR
what is Type 1 2nd degree AV block
PR increases until AV node fails and misses ventricular beat
what is type 2 2nd degree AV block
PR interval constant but every Nth ventricular depolarisation missing
what is 3rd degree AV block
independent beating of atria and ventricles
ventricular beating controlled by purkinje fibres so bradycardic
what is the bundle of kent
accessory tract that is parallel to AVN and conducts faster. may form reentry loop with ventricles
what is the vaughn williams classification
pharmacological classification of drug effects on cardiac AP
what do class IA drugs do
act on Na channel to slow AP rise and prolong refractory period
what do class IB drugs do
act on Na channel to prevent premature beats
what do class IC drugs do
act on Na channel to depress conduction
what do class II drugs do
beta antagonists
decrease depolarisation rate in SAN and AVN
what do class III drugs do
K channels - prolong AP duration so increase refractory period
what do class IV drugs do
Ca channels - slow AVN conduction and SAN conduction to decrease cardiac conduction force
