Arrthymia: therapies, Drugs for irregular heart rhythms Flashcards
1
Q
What is an arrhythmia?
A
- A deviation from the “normal” rhythm of the heart.
- (Sinus arrhythmia)
- Tachycardias: supraventricular arrhythmia, Ventricular arrhythmia
- (Bradycardias(Heart block))
2
Q
Features of the resting membrane potential
A
- Inside the cell is a net negative charge relative to the outside:
- Due to uneven distribution of ions across the cell membrane.
- Dependant on the sodium-potassium ATPase pump (needs energy)
3
Q
Vaughan-Williams classification drugs of antiarrhythmics
A
- IA: Quinidine, Procainamide, Dispyramide
- IB: Lidocaine, mexiletine, tocainide
- IC: Flecainide, propafenone
- II: Atenolol
- III: Amidarone, bretylium, sotalol
- IV: Diltiazem, verapamil
- V: Digoxin
4
Q
Vaughan-Williams class I features
A
- Membrane-stabilising agents: decrease the amplitude (size of action potential)
- Reduces velocity of conduction/excitability
- Act on “Fast” sodium channel responsible for phase 0: present in “Non-nodal” cells
- Divided into Ia, Ib and Ic agents.
- Show use dependence (i.e. More effective at higher HR)
5
Q
What is the agent mainly used in class I antiarrhythmics?
A
Flecainide
- Strong Na+ channel blockade
- prolongs ERP (effective refractory period)
6
Q
Vaughan-Williams class II features
A
Beta blockers: atenolol, bisoprolol, propanolol
- Acts via Beta1 receptors to block sympathetic stimulation of the heart: prolongs phase 4 depolarisation, shortens phase 2
- Now first line for atrial fibrillation (Bisoprolol)
7
Q
Vaughan-Williams class III features
A
Amiodarone, bretylium, sotalol
- Increase action potential duration
- Prolong repolarisation in phase 3
- Prolongs ERP
- Used for dysrhythmias that are difficult to treat
- Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter: resistant to other drugs
- Sustained ventricular tachycardia
8
Q
Features of Amidarone
A
- Used for VT (ventricular tachycardia) and occasionally in supraventricular tachycardia
- Many interactions with other drugs: particularly digoxin
- Because of tissue effects has striking side effect profile: thyroid, pulmonary fibrosis, Slate-grey pigmentation, corneal deposits, LFT abnormalities
9
Q
Vaughan-Williams class IV features
A
Verapamil, Diltiazem
- Calcium channel blockers: bind to Lcard type voltage gated Ca channels
- Depress phase 4 depolarisation in SA and AV nodes: slows the heart rate
- Shorten phase 2 plateau phase (reduce contractility)
- Show use dependence
- Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter.
10
Q
Vaughan-Williams class V features
A
Other antiarrhythmics
- Digoxin, adenosine
- Have properties of several classes and are not placed into one particular class.
11
Q
Features of Digoxin
A
- Cardiac glycoside
- Inhibits the sodium-potassium ATPase pump
- Increases vagal tone through: slows SA/AV node conduction
- Complex effect on the cardiac action potential: reduces the refractory period in myocardium
- Increases Ca2+ concentration intracellular: positive inotropic effect
12
Q
What are indications for Digoxin?
A
Atrial dysrhythmias
- AF
- Atrial flutter
- (SVT)
Heart failure
13
Q
Features of Digoxin toxicity
A
- Nausea and vomiting
- Xanthopsia!
- Bradycardia
- Tachycardia
- Arrhythmias: VT and VF
14
Q
Signs of digoxin toxicity
A
- ‘Reverse tick’ appearance of ST segment in lateral leads
- Confusion
- Irregular pulse
15
Q
What is Digoxin toxicity treatment?
A
- Stop digoxin: but long half life
- If levels very high and risk of significant arrhythmia: give Digiband
- Digoxin toxicity is more serious if potassium levels are low
