Week 4: Cardiology (5) (antiarrhythmic) Flashcards
(44 cards)
1
Q
rationale for antiarrhythmics
A
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
2
Q
classification system of antiarrhythmics
A
vaughan williams classification
1B
1C
II
III
IV
V
3
Q
class IB
A
action: sodium channel blockers (no change in phase 0)
e. g. lidocaine
]
4
Q
class IC
A
action: sodium channel blockers (marked phase 0)
e. g. flecainade and propafenone
5
Q
class II
A
action: B blocker
e. g. bisoprolol, metoprolol, propranolol
6
Q
class III
A
action: potassium channel blockers- prologed repolarisation
e. g. amiodarone, sotalol
7
Q
class IV
A
action: calcium channel blcoker
e. g. verapamil, dilitiazem
8
Q
class V
A
action: variable
e. g. adenosine, digoxin, atropin, ivabradine
9
Q
most efficacious drug
A
- Amiodarone is the best
10
Q
most tolerable drug
A
B blockers most tolerable, amiodarone least (e.g. sunburn and breathlessness)
11
Q
when are class 1B agents used e.g. lidocaine
A
- Ventricular tachycardia (in relation to a scar in the heart- ischaemia)
- Not used in atrial arrhythmias or AV junctional arrhythmias
12
Q
ventricular tachycardia and class 1B agents e.g. lidocaine
A
- 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
13
Q
adverse drug repsonse clas 1B agents
A
- Less proarrhythmic than Class 1A (less QT effect)
- CNS effect: dizziness, drowsiness
- Abdominal upsets
14
Q
when are class 1C agents used e.g. flecainide
A
- Wide spectrum
- Supraventricular arrhythmias
- Atrial fibrillation
- Atrial flutter
- Premature ventricular contractions
- Wolff- Parkinson-White syndrome (ectopic beats)
- Supraventricular arrhythmias
15
Q
MOA of class 1C agents e.g. flecainide
A
- 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
16
Q
ADR class 1C e.g. flecainide
A
- 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
17
Q
contraindication of class 1C
A
- Coronary heart disease
- Structural heart disease e.g. previous MI
18
Q
when are class 2 agents used e.g. B blockers
A
- 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
19
Q
MOA of class 2 agents e..g b blockers
A
- 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
20
Q
ADR of class 2 agents
A
- Bronchospasm
- Hypotension
21
Q
contraindication of class 2 agents e.g. propanolol
A
- Don’t use if partial AV block or acute heart failure
- Asthma
22
Q
uses of class 3 agents e.g. amiodarone
A
- Very wide spectrum- effective for most arrhythmias
23
Q
MOA of class 3 agents e.g. amiodarone
A
- 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
24
Q
ADR for class 3 agents
A
- Pulmonary fibrosis
- Hepatic injury
- Thyroid disease
- Photosensitivity (factor 50)
- Optic neuritis (transient blindness)
25
contraindication of type 3 agents
may need to reduce dose of digoxin and monitor warfarin
26
sotalol (oral) is used for
* Wide spectrum: Supraventricular and ventricular tachycardia
27
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
28
adr sotalol
* Proarrhythmic
* Fatigue
* insomnia
29
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)
30
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)
31
ADR class 4 agents e.g. verapamil
GI problems (constipation)
32
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
33
NEVER give …… with……
* Don’t give B blockers and CBB together
34
example of class 5 antiarrhythmis agents
ivabradine
digoxin
atropine
35
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
36
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
37
atropine
**Uses**
* Vagal Bradycardia
**Mode of actions**
* Selective muscarinic antagonist
* Blocks vagal activity to speed AV conduction and increase HR
38
**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)
39
**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
40
**Best drug for WPW?**
* Flecainide or amiodarone
* Avoid AV nodal blocking drugs (B blockers) due to risk of pre-excited AF and therefore VF
41
drug used in re-entrant SVT in the acute setting
adenosine
verapamil
flecainide
42
drug used in re-entrant SVT in the chronic setting
bisoprolol, verapamil
sotalol
flecainide
amiodarone
43
1. **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
44
which drugs for sinus tachycardia
ivabradine if not drop in BO
bisorpolol, verapamil
