Antiarrhythmics Flashcards
Phase 0
Rapid Depolarization (ventricular contraction)
- increased NA conductance (channels open) through FAST channels (-70 mV)
- end w/ Na channels “inactive” @ +65 mV
Phase 1
Early Rapid Repolarization
- Na channels closed, inactivated
- K channels open, begin transient efflux of K to “reset” voltage. (rapidly inactivated)
Phase 2
- Plateau
- via calcium influx through SLOW channels (L & T type channels)
- K channels still open, maintain plateau through K+ efflux
- voltage = +10 to -20 mV
Phase 3
Rapid Repolarization
- lots of K movement
- No significant movement of Ca or Na
Phase 4
Spontaneous Depolarization
- slow depol. characteristic of all pacemaker cells
- interaction of outward Ca and inward K during diastole
- ATP dependent pumps move ions to regain balance
Slow channels, calcium mediated
- responsible for phase 0 in SA and AV noes (slow conduction velocity
- contribute to phase 2 in ventricular contractile cells (prolongs refractory period)
- affects phase 4 spont. depol
- facilitates catecholamines (cAMP)
Fast channels, Na mediated
- phase 0 (rapid, sharp upstroke in His-Purkinje and atrial and ventricular muscle
- rapid conduction velocity
Automaticity
impulse generation
T/F: Cells that undergo spontaneous phase 4 depol are automantic anc capable of impulse generation
True,
Factors that reduce automaticity at the higher pacemaker sites will passively favor movement of pacemaker to lower site
Ectopic Foci result from…
- enhanced automaticity at a site outside the SA node
- SNS influences, hypercarbia, hypoxia, dig tox
- ex.) A.Fib - little cells just firing on their own, increased clot risk
Re-Entry
-circles around pacemaker sites to generate new paths
Na Channel impulse generation…
Atria
Ventricles
Ca Channel impulses generate…
SA node
AV node
Amiodarone and anticoags
increase bleed risk, increased INR
Amiodarone and meds that prolong QT interval
Torsades de Pointes
Amiodarone and Digoxin
increased dig toxicity
Amiodarone and lidocaine
increased lidocaine toxicity
amiodarone and statins
increase myalgias
amiodarone and midazolam
prolonged sedation, increased risk of resp depression
amiodarone and suggamedex
increased risk of bradycardia, additive effect
amiodarone and AV nodal blockers
increased risk of bradycardias, sinus arrest, AV block
Prodysrhythmic Effects
brady or rachy that represent new cardiac dyrrhythmias associated w/ chronic antidysrhythmic tx
ex. torsades, increased ventric tachy’s, wide complex vent. rhythm
Torsades de Pointes
K channel blockade may prolong QT interval and induce triggered activity in ventricle –> polymorphic VT or VF
-occurs in 1-8% of pts recieving QT prolonging drugs
will develop torsades
Which class blocks potassium channels and prolongs QTc interval
Class 1A and Class 3