Week 4: Cardiology (5) (antiarrhythmic) Flashcards
rationale for antiarrhythmics
prevent dangerous and restore normal sinus rhythm and conduction
o Decrease conduction velocity
o Change duration of the effective refractory period (ERP)
o Supress abnormal automaticity
classification system of antiarrhythmics
vaughan williams classification
1B
1C
II
III
IV
V
class IB
action: sodium channel blockers (no change in phase 0)
e. g. lidocaine
]
class IC
action: sodium channel blockers (marked phase 0)
e. g. flecainade and propafenone
class II
action: B blocker
e. g. bisoprolol, metoprolol, propranolol
class III
action: potassium channel blockers- prologed repolarisation
e. g. amiodarone, sotalol
class IV
action: calcium channel blcoker
e. g. verapamil, dilitiazem
class V
action: variable
e. g. adenosine, digoxin, atropin, ivabradine
most efficacious drug
- Amiodarone is the best
most tolerable drug
B blockers most tolerable, amiodarone least (e.g. sunburn and breathlessness)
when are class 1B agents used e.g. lidocaine
- Ventricular tachycardia (in relation to a scar in the heart- ischaemia)
- Not used in atrial arrhythmias or AV junctional arrhythmias
ventricular tachycardia and class 1B agents e.g. lidocaine
- Damaged areas of myocardium may be depolarised and fire automatically
- More Na+ channels are open in depolarised tissue
- Lidocaine blocks these sodium channels
- Preventing automatic firing of depolarised ventricular tissue
- Effect on cardiac activity
- Fast binding offset kinetics
- In normal tissue
- No change in phase 0 (no tonic block)
- ADP slightly decreased
- Fast beating or Ischaemic tissue
- Increase threshold for Na
- Decrease phase 0 conduction
- Effect on ECG
- None in normal
- In fast beating or ischaemic = increase QRS
adverse drug repsonse clas 1B agents
- Less proarrhythmic than Class 1A (less QT effect)
- CNS effect: dizziness, drowsiness
- Abdominal upsets
when are class 1C agents used e.g. flecainide
- Wide spectrum
- Supraventricular arrhythmias
- Atrial fibrillation
- Atrial flutter
- Premature ventricular contractions
- Wolff- Parkinson-White syndrome (ectopic beats)
- Supraventricular arrhythmias
MOA of class 1C agents e.g. flecainide
- Na+ channel blocker
- Effect on cardiac activity
- Very slow binding offset kinetics (>10s)
- In normal tissue
- Decreased phase 0 (Na+)
- Decreased automaticity
- In rapidly depolarising atrial tissue
- Increased APD (K+) and increased refractory period
- Effect on ECG (beware of Torsades de Pointe)
- Increase PR
- Increase QRS
- Increase refractory
ADR class 1C e.g. flecainide
- Pro-arrhythmia and sudden death especially with chronic use and ins structural hear disease
- Increase ventricular response to supraventricular arrhythmias (flutter)
- CNS and GI effects like other local anaesthetics
contraindication of class 1C
- Coronary heart disease
- Structural heart disease e.g. previous MI
when are class 2 agents used e.g. B blockers
- Treating sinus and catecholamine dependent tachycardia e
- Converting repentant arrythmias at AV node
- Protecting the ventricles from high atrial rates (slow AV conduction) in atrial flutter or atria fibrillation
MOA of class 2 agents e..g b blockers
- Inhibition of sympathetic influences on cardiac electrical activity i.e. B1 antagonists- blocking NA binding (also reduce sympathetic stimulation of aberrant pacemaker activity- ectopic foci)
- Reduction in influx of calcium
- Effect on cardiac activity
- Increase Action Potential Duration and refractory period
- Decrease phase 4 depolarisation (catecholamine dependent)
- Blocking arrhythmias caused by re-entry
- Effect on ECG
- Increase PR
- Decrease HR
ADR of class 2 agents
- Bronchospasm
- Hypotension
contraindication of class 2 agents e.g. propanolol
- Don’t use if partial AV block or acute heart failure
- Asthma
uses of class 3 agents e.g. amiodarone
- Very wide spectrum- effective for most arrhythmias
MOA of class 3 agents e.g. amiodarone
- Block potassium channels
- Class effects of 1,2,3 and 4
- Reduction in influx of calcium
- Effect on cardiac activity
- Increase APD and refractory period and increase APD (K+)
- Decrease phase 0 and conduction (Na)
- Increase threshold for AP
- Decrease phase 4 depolarisation (B block and Ca2+ block)
- Decrease speed of AV conduction
- Effect on ECG
- Increase PR
- Increase QRS
- Increase QT
- Decrease HR
ADR for class 3 agents
- Pulmonary fibrosis
- Hepatic injury
- Thyroid disease
- Photosensitivity (factor 50)
- Optic neuritis (transient blindness)
contraindication of type 3 agents
may need to reduce dose of digoxin and monitor warfarin
sotalol (oral) is used for
- Wide spectrum: Supraventricular and ventricular tachycardia
MOA of sotalol
- Block potassium channels
- Class effects of 1,2,3 and 4
- Effect on cardiac activity
- Increase APD and refractory period in atrial and ventricular tissue
- Slow phase 4 (B blockers)
- Slow AV conduction
-
Effect on ECG
- Increase QT
- Decrease HR
adr sotalol
- Proarrhythmic
- Fatigue
- insomnia
class 4 agents uses e.g. verapamil and diltiazem
- Control ventricles during supraventricular tachycardia
- Convert supraventricular tachycardia (re-entry around AV)
- Used with people who have asthma (cant use B blockers)
MOA of class 4 agents
- Calcium channel blockers
- Effect on cardiac activity
- Slow conduction through Av (Ca2+)
- Increase refractory period in AV node
- Increase slope of phase 4 in SA to slow HR
- Effect on ECG
- Increase PR
- Decrease HR (or increase depending on baroreceptor reflex)
ADR class 4 agents e.g. verapamil
GI problems (constipation)
contraindication of class 4 agents e.g. verapamil
- AV block- can get asystole if B blocker is on board
- Don’t give B blockers and CBB together
- Hypotension
NEVER give …… with……
- Don’t give B blockers and CBB together
example of class 5 antiarrhythmis agents
ivabradine
digoxin
atropine
ivabradine
Drug name: Ivabradine
- Oral
Uses
- Reduce inappropriate sinus tachycardia
- Reduce heart rate in heart failure and angina (avoiding blood pressure drops)
Mode of actions
- Blocks If ion current highly expressed in sinus node
- Cardiac effect
- Slows sinus node but does not affect blood pressure
Adverse drug reaction
- Flashing lights
- Teratogenicity not known (avoid in pregnancy)
Contraindication
- Pregnancy
digoxin (cardiac glycoside)
Uses
- Treatment to reduce ventricular rates in AF and flutter
Mode of actions
- Enhances vagal activity (increases k+ current, decreases calcium current and increases refractory period)
- Slows AV conduction, slowing HR
atropine
Uses
- Vagal Bradycardia
Mode of actions
- Selective muscarinic antagonist
- Blocks vagal activity to speed AV conduction and increase HR
Which IV drug would you use first for VT
Depends on which drugs that are already on
- Intravenous metoprolol/bisoprolol
- If BP low- cardiovert electrically
- If BP okay just metoprolol
- If already on B blocker
- IV lignocaine or oral mexiletine
- Or Amiodarone (IV central line)
Should flecainide be used alone for atrial flutter?
No- give AV nodal blocking drugs to reduce ventricular rates in atrial flutter
- Can be used alone in atrial fibrillation
Best drug for WPW?
- Flecainide or amiodarone
- Avoid AV nodal blocking drugs (B blockers) due to risk of pre-excited AF and therefore VF
drug used in re-entrant SVT in the acute setting
adenosine
verapamil
flecainide
drug used in re-entrant SVT in the chronic setting
bisoprolol, verapamil
sotalol
flecainide
amiodarone
- Which drugs would be used for ectopic atrial tachycardia?
- First line- bisoprolol (safest
- Next line- CCB
- Lastly: Flecainide, sotalol, amiodarone
- First line- bisoprolol (safest
- Next line- CCB
- Lastly: Flecainide, sotalol, amiodarone
which drugs for sinus tachycardia
ivabradine if not drop in BO
bisorpolol, verapamil
