Anti Arrhythmic Drugs Flashcards
What’s the QT duration in ECG?
refractory phase of non-nodal AP
Define arrhythmia
abnormalities in heart rhythm
Symptoms of arrhythmia?
palpitations, dizzy, faint, fatigue, unconscious, cardiac arrest, blood coagulation (stroke, MI)
Causes of arrhythmia?
cardiac ischemia (MI, angina), heart failure, hypertension, coronary vasospasm, heart block, excess sympathetic stimulation
Origin of arrhythmia?
supraventricular (above ventricles SAN, atria, AVN) or ventricular
Effect of arrhythmia on heart rate?
Tachycardia (>100 bpm) or Bradycardia (<60 bpm)
How does arrhythmia affect CO?
lead to incorrect filling + ejection –>incorrect CO
What are common arrhythmias?
atrial fibrillation (AF), supraventricular tachycardia (SVT), heart block, ventricular tachycardia (VT), ventricular fibrillation (VF)
What’s atrial fibrillation (AF)?
Quivering atria activity (no P wave)
Irregular ventricular contraction
‘Clot-producing’ – risk of stroke
What’s supraventricular tachycardia (SVT)?
P wave buried in T wave
Fast ventricular contractions
What’s heart block?
Failure of conduction system (SA, AV, or bundle of his)
Uncoordinated atria/ventricular contractions
What’s ventricular tachycardia (VT)?
Fast, regular
What’s ventricular fibrillation (VF)?
Fast, irregular
Why’s there no P waves in atrial fibrillation (AF)?
atria depolarising + repolarising all the time
How does atrial fibrillation (AF) cause stroke?
blood not ejected from atria so clot,can move to L ventricle -> aorta -> brain ->
Mechanisms of arrhythmogenesis?
Abnormal Impulse Generation
Abnormal Conduction
Causes of abnormal impulse generation?
Automatic rhythms -↑ SAN activity, ectopic activity
Triggered rhythms -Early after depolarisations (EADs), delayed-after depolarisations (DADs)
Causes of abnormal conduction?
Re-entry electrical circuits
Conduction block
What’s ectopic pacemaker activity
other heart areas have pacemaker activity to safeguard against SAN damage SAN= 60-70/s AVN= 40-60 /s Bundle of His= 30-40/s Purkinje fibres= 15-25/s
How’s ectopic pacemaker activity increased?
sympathetic nerve activity by increasing: HR, AVN conduction, excitability of ventricular tissue
How does ectopic pacemaker increased activity cause arrhythmia?
continuous/enhanced sympathetic stimulation –> stress, heart failure –> arrhythmia
How does early after depolarisations (EADs) + delayed-after depolarisations (DADs) cause arrhythmia?
Abnormal levels of Ca2+ in SR Ca2+ leaks into cytosol - diastolic leak Stimulate Na/Ca exchanger (NCX) 1 Ca2+ out and 3 Na+ in – depolarisation Altered ion channel activity - no refractory period
How are re-entry pathways produced?
damaged myocardium so some heart areas more conductive
Why do AP stop conducting?
surrounding tissue refractory
How is heart block produced?
fibrosis / ischaemic damage of conducting pathway-AVN issue
What’s 1st degree heart block?
PR interval > 0.2 s
What’s 2nd degree heart block?
> 1 atria impulses fail to stimulate ventricles
What’s 3rd degree heart block?
complete block, atria + ventricles beat independently of one another
Why do the ventricles contract at slow rate?
SAN pacemaker potential generating activity in atrium but disconnected to ventricles so bundle of his + purkinje fibres generate own electrical activity (ectopic)
Why can heart block cause?
unconsciousness, Adams-Stokes attacks – syncope
Goals of arrhythmia treatment?
- Restore sinus rhythm + normal conduction
- Prevent more serious + fatal arrhythmia occurring
What can anti-arrhythmia drugs do?
Reduce conduction velocity
Alter refractory period
Reduce automaticity (decrease EADs, DADs, ectopics)
What’s the anti-arrhythmia drugs classification based on?
Vaughan Williams classification system
What’s class I anti-arrhythmia drug?
Na+ channel blockers (non-nodal tissue)
-reduces upstroke
What’s class II anti-arrhythmia drug?
β blockers (nodal and non-nodal tissue)
-reduces sympathetic on heart so affects both AP
What’s class III anti-arrhythmia drug?
K+ channel blockers (non-nodal tissue)
-not repolarising quickly, increasing AP length increases refractory period
What’s class IV anti-arrhythmia drug?
Ca2+ channel blockers (nodal and non-nodal tissue)
-affects upstroke in nodal + plateau in non-nodal
Features of class I anti-arrhythmia drugs?
Block Na+ channels in non-nodal tissue (atria/ventricles)
Has use-dependence : only block Na+ channels in high frequency firing tissue cause in INACTIVATED state
Describe how class I anti-arrhythmia drugs work on high frequency firing tissue
- binds to inactivated Na+ channel
- fast dissociating drug (off channels in <0.5 s)
- still bound to inactivate site when next impulse arrives
- inhibits high frequencies
Describe how class I anti-arrhythmia drugs work on normal frequency firing tissue
- binds to inactivated Na+ channel
- fast dissociating drug (off channels in <0.5 s)
- drugs comes off inactivate site for next impulse
- no effect on normal firing
What’s Lidocaine?
class I anti-arrhythmia drug for fast arrhythmia (VT + VF)
Describe how class II anti-arrhythmia drugs work
Blocks β1 in heart so reducing sympathetic :
decrease in SAN + AVN firing rate
decrease [Ca2+] so reduce ventricular excitability
What’s Atenolol?
class II anti-arrhythmia drug reduce VT after myocardial infarctions + slow conduction via AVN to reduce ventricular firing rate in SVT
Describe how class III anti-arrhythmia drugs work
- inhibit K+ channels responsible for repolarisation in atria/ventricles
- increases QT duration so slower repolarisation
- maintains depolarisation
- Na+ channels inactivated so can’t fire more AP
What’s Amiodaron?
class III anti-arrhythmia drugs for SVT + VT
What’s Sotalol?
class III anti-arrhythmia drugs + combined class II actions for SVT + VT
Describe how class IV anti-arrhythmia drugs work
Block L-type vgcc:
affects phase 0 firing of SAN + AVN
affects phase 2 of atria/ventricle
affects vascular smooth muscle so vasodilation of blood vessels + reduce BP
What’s Verapamil?
class IV anti-arrhythmia drug cardiac specific - control ventricular response rate in SVT
What’s Diltiazem?
class IV anti-arrhythmia drug cardiac + vascular smooth muscle - control ventricular response rate in SVT
What’s Adenosine?
non-classified
decreases activity in SAN + AVN
used for SVT
What’s Atropine?
non-classified
Mus antagonist
reduce para activity
used to treat sinus bradycardia after MI
What’s Digoxin?
non-classified
central effects, increases vagus activity, decrease HR + conduction
used for AF
How can anti-arrhythmic drugs be pro-arrhythmic?
- Class III drugs increases QT duration, long QT syndrome –> EADs + DADs - arrhythmia
- Classes I, II, IV increase refractory period (less SA, AV, atria/ventricular firing) + reduce conduction time
- Class IV reduce contractility
What’s torsades de pointes?
ventricular tachycardia
Goal of sinus tachycardia + treatment?
Slow down SAN
Class II, III
Goal of AF + treatment?
Reduce atria activity, return of atria output, prevent clot formation
II, III, IV, digoxin + anticoagulants
Goal of SVT + treatment?
Reduce ventricular response rate
Class II, III, IV
Goal of heart block + treatment?
Coordinate atria/ventricular contractions
pacemaker
Goal of VT + VF + treatment?
Reduce ventricular activity, return ventricular output
Class I, II, III
