Antiarrhythmics Flashcards
Electrical activity of the heart
- SA node discharges AP
- spread through atria
- AV node discharge
- propagation through purkinje fibers
cardiac muscle cells contract by a process called…
excitation-contraction coupling
contraction graph symbols
P = contraction of atria
R = contraction of ventricle
T = repolarization
membrane potential is maintained by which ions on either side of the cell membrane
- Na+, Ca2+, K+
- at rest intracellular Na+ concentration is low - maintained by ATPase
action potemtial phases and distribution of ions
- Rapid depolarization: Na+ influc through rapidly opening Na+ channels
1-2. Plateau phase: Ca2+ influx through slower opening Ca2+ channels - Repolarization: closure of Ca2+ channels, K+ efflux through K+ channels
excitation-contraction coupling in cardiac contraction
- action potential causes increase of Ca2+
- Ca2+ binds troponin C and uncovers myosin binding site on actin
- actin and myosin cross-linkages form - cause contraction
how does a cardiac action potential lead to tension
cardiac AP - Ca+ enters cell during plateau - Ca+ induced calcium release from the SR - Ca+ binds to troponin C - cross-bridge cycling - tension
route of AP to cause contraction in the heart
- SA node fires
- signal spreads to atria
- coordinated contraction
- AV node
- propagates through bundle of His
- signal spreads via purkinje fibers
- synchronized contraction
what are arrhythmias
electrical alterations - abnormalities in heart rhythm
stypes of arrhythmias
bradycardia = slow rate
tachycardia = fast rate
automaticity = SA node, altered rate, altered site
reentrant: irregular electrical wave propagation
what is reentrant
- different parts of the heart are propagating at different rates
- due to change in how signal is initiated or propagated
- occurs in damaged/ischemic tissue
types of atrial arrhythmias
atrial flutters
atrial fibrillation
atrial flutters
- 200-350 bpm
- SA node might still fire regularly
- parts of atria out of sync
atrial fibrillation
- 300-500 bpm
- 2 or 3 parts contracting out of sync with atria sinus rhythm
- irregular and dissorganized
- sometimes have no symptoms when resting but seen when active
characteristics of atrial arrhythmias
- do not always lead to ventricular arrhythmias (so might not affect CO)
- can lead to more serious rhythm disturbances, stroke
- treat if they cause symptoms or at risk for complications
types of ventricular arrhythmias
ventricular tachycardia
ventricular fibrillation
ventricular tachycardia
- ventricles contract faster
- occasional premature ventricular contractions dont require treatment
- steady/prolonged - prompt treatment required
ventricular fibrillation
- irregular and rapid contraction of ventricles
- cannot pump blood properly
- if not treated immediatly can be fatal
what is the purpose of defibrillators
temporarily stop all electrical activity to allow normal rhythm to resume
characteristics of antiarrhythmic agents (drugs)
- aimed at normalizing cardiac rhythm
- all antiarrythmic drugs directly or indirectly alter ion flow across membrane
- have a narrow therapeutic index and can also lead to arrhythmias
- need to elevate risks and benefits
when is treatment wirh antiarrythmic drugs required
reduced CO
risk of thrombus
risk of conversion to serious arrhythmia
classes of antiarrhythmic agents
Class I: Na+ channel blockers
Class II: Beta-blockers
Class III: K+ channel blockers
Class IV: Ca2+ channel blockers
Class I antiarrhythmic agents: Na+ channel blockers
- targets the open channel to decrease Na+ entering the cell
- reduce excitation
- quinidine and lidocaine
Class II antiarrhythmic agents: Beta-blockers
- propanolol and metoprolol
- inhibit SNS effects and slow heart rate
- most useful of the antiarrhythmics
Class III antiarrhythmic agents: K+ channel blockers
- amiodarone
- prolong action potential duration
- amiodarone also effects B1 receptors and Na+/Ca2+ channels
Class IV antiarrhymic agents: Ca2+ channel blockers
- verapamil
- decreases cardiac contractility
- can lead to vasodilation
Na+ channel blockers vs K+ channels blockers to treat arrhythmias
- Na+ blockers reduce the recovery of Na+ channels - decrease conduction and excitation
- K+ blockers prolong the action potential and therefore the refractory period
Quinidine: a class IA antiarrhythmic agent - Na+ channel blocker
- prototypical drug in this category
- side effects include vomitting, headache, dizziness, enhance digoxin toxicity, anti-cholenergic effects
Lidocaine: a class IB antiarrhythmic agent - Na+ blocker
- used in emergency
- most commonly ised IV antiarrhythmic (ventrivular tachycardia/fibrillation)
- IV route treats arrhythmias, local rout is an anesthetic
class IC antiarrhythmic agents - Na+ channel blockers
- also effects K+ channels
- only used for severe ventricular arrhythmias
how does blocking Na+ channels block depolarization
- in cells discharging at high frequencies Na+ blockers (quinodine and lidocane) enter the open channel to prevent Na+ from getting through
- keep inactive fir long period of time
when to use each class of antiarrhythmic drugs
Class IA: if you dont want to change AP profile
Class IB: treat ventricular tachycardia/fibrillation
Class II: slow down SA node activity
Class III: change AP profile via slowing the sodium efflux
Class IV: slow contraction by slowing influx of Ca2+
