5.1 Antiarrhythmics Flashcards
(29 cards)
where does the fast cardiac action potential happen?
myocardium
where does the calcium come from in fast cardiac AP?
SR
which transporter resets AP to normal?
NAK ATPase
which part of AP is prolonged by class 3 drugs in fast cardiac AP?
refractory period
examples of class 4 CCBs
verapimil
diltiazem
where does the slow cardiac AP occur?
pacemaker cells
effect of CCBs on slow cardiac AP
decrease calcium entry so slope of phase 0
increase refractory period
how do B agonists affect automaticity?
increase rate of automatic function of SA node
how do muscarinic agonists and adenosine affect automaticity?
decrease rate of automatic function of SAN
when would you switch from lidocaine to mexiletine?
when patient stable
how does flecainide help WPW syndrome?
attached to extra circuit
contraindications to flecainide
structural heart disease
ischaemia
B blockers aren’t used in acute HF. which HF can they be used for?
stable
how to give amiodarone. why?
oral/IV, via large central vein due to risk of thrombophelibits
which tests should be done every 6 months when taking amiodarone>
LFT, TFT
which drugs should be reconsidered when taking amiodarone?
warfarin digoxin due to inducing hepatic CYP enzymes
absorption of sotalol
oral
cardiac effects of sotalol
increase AP duration and refractory period
slow phase 4
slow AV conduction
ECG effects of sotalol
increase QT
decrease HR
uses of sotalol
SVT, VT
side effects of sotalol
fatiguem insomnia, arrhythmias
why cant you give verapamil/diltiazem with B blocker?
can if pacemaker
reduce HR too much=asystole
mechanism of adenosine
nucleoside binds A1 receptors, blocks adenylyl cyclase, reducing cAMP, activates K current in AVN+SAN= hyperpolarisition
decrease HR
cardiac effects of adenosine
slows AV conduction, short half life so give for acute e.g. narrow/wide complex tacky
