Anti-Arrhythmics Flashcards
(34 cards)
Phases of cardiac potential: how many phases? What are they called?
Five phases from 0 - 4
0- rapid depolarisation 1- initial repolarization 2- plateau phase 3- repolarization 4- resting potential
What happens in Phase 0?
Results from rapid influx of Na+
Depolarisation raises resting membrane potential from -85mV to +20mV. At this point threshold potential has been reached and an all or none action potential response occurs.
Rapid influx Na+ raises membrane potential further to 20mV.
What happens in Phase 1?
Initial repolarization:
Voltage gated Na channels close as transmembrane potential becomes sufficiently positive.
Notch caused by transient outward K+ and inward Cl- movement.
What happens in Phase 2?
Inward movement of Ca+ ions through slow L-type Ca channels,
and outward movements of K+.
Cancel out each other, and only slow downward slope to repolarisation.
What happens in Phase 3?
Repolarization as calcium efflux slows/stops and
K+ movement out via concentration gradient via open K+ channels.
Relative refractory period.
What happens phase 3-4?
Resting membrane potential is re-established by 2K+ moving inwards for every 3Na+ outwards
Gives a net outward movement of positive charge.
Mechanisms of Arrhythmia generation (4)?
- Enhanced automaticity
- Abnormal automaticity
- Triggered activity
- Re-entry (circus movement)
what arrhythmias occur with
- enhanced normal automaticity
- Abnormal automaticity
- Triggered activity
- Inappropriate sinus tachycardia, by phase 4 depolarisation.
- Ectopic atrial tachycardia by phase 4 depolarisation
- Torsades de pointes- action potential duration/ early afterdepolarisation
Digixon induced arrhythmia- calcium over load or delayed afterdepolarization.
What are the re-entry arrhythmias?
Atrial flutter type 1- conduction and excitability
Wolf Parkinson White - conduction and excitability
Ventricular fibrillation - refractory period vulnerable
How many phases of cardiac cycle do pacemaker cells have?
3 phases, - 0, 4 and 3
How is resting membrane potential re-established?
- the resting membrane potential is re-established by 2K+ in and 3Na+ out.
What classification does The Vaughan-Williams Classification Scheme?
5 classes with class 1 (a, b, c) 1- Na channel blockers (fast, intermediate, slow) 2- B blockers 3- K channel blockers 4- Ca channel blockers 5- work by unknown mechanism
How do Vaughan-Williams Class I work?
Provide examples of the subclasses, effect on action duration and effective refractory period and clinical uses.
Drugs reduce the phase 0 slope and the peak of the action potential - decrease membrane excitability and conduction velocity.
a - quinidine, procainamide. (increase ADP + ERP) (AF/SVT)
b - lidocaine (reduced ADP + ERP) (Dig Toxicity/ VF)
c - flecainide (no change) (AF/SVT)
Propranolol also has some Class 1 action.
Side effects of Na channel blockers?
CVS side effects - hypotension, bradycardia, arrhythmia
CNS side effects- Two phases: excitatory phase followed by depressive phase with increasingly heavier exposure.
- Nervous, anxiety, tremor, dizziness, hallucinations, seizures, psychosis, euphoria
- Drowsy, lethargic, slurred speech, confusion, LOC, respiratory depression
Contraindications to Na channel blocker?
- Syndromes:
Adam Stokes syndrome
Wolf Parkinsons White - Conduction defects:
2/3 heart block
Serious SA node block without pacemaker - Meds:
Prior use of amiodarone
Use of other Class 1 antiarrhythmics
Flecainide:
Uses
Side effects
Avoided?
Use: pill in the pocket to terminate AF, treatment of supraventricular tachycardias (inc those in WPW)
Side effects: arrhythmias (Torsades de Pointes), prolonged PR, widened QRS, can be negatively ionotropic effect
Avoid- structural heart diseases
Mechanism of B-blocker activity
Decreases sympathetic activity on the heart by acting as antagonists at b-receptors (antagonising catecholamines).
Prolongs Phase 4 ‘diastolic’ depolarization.
reduces intracellular cAMP levels and therefore reduces Ca influx. Produce bradycardia, depress myocardial contractility, prolong AV conduction.
Useful in treating supraventricular tachycardias.
Side effects of B-blockers
Hypotension Bradycardia Heart block Depression Sexual dysfunction Impaired glucose handling
Mechanism of K+ channel blockers
Prolong repolarization by blocking potassium channels, K+ efflux in Phase 3.
- > prolongs action potential duration and effective refractory period
- > bradycardia
Amiodarone:
Uses
Side effects
Contraindications
Uses- treatment of ventricular and supraventricular tachycardias, WPW
Increases APD, ERP
Side effects: interstitial lung disease, thyroid dysfunction (hypo/hyper), abnormal liver enzymes, corneal micro deposits and photosensitivity
Contra- pregnancy, bradycardia,
Mechanism of the Ca channel blocker?
Contra-indications
Side effects
- prevents influx of Ca through slow L-type channels in the AV and SA node, slowing conduction and automaticity.
- This shortens phase 2 - plateau of cardiac potential.
- Reduce contractility of the heart.
Contraindication: Should not be used in WPW- precipitate VT.
Side effects: constipation, dizziness, headache, redness on the face, ankle oedema, bradycardia
Adenosine mechanism action?
What arrhythmias can it be used to differentiate?
AV node block via specific adenosine-A receptors.
Short half life, less than 10 seconds - taken up rapidly by red blood cells.
Can be used to differentiate between VT and SVT. Will only treat SVT.
Adenosine side effects and contraindications.
Side effects: diaphoresis, metallic taste, nausea, sense of impending doom.
Contra-indications: asthma, decompensated heart failure, long QT syndrome.
Digoxin mechanism of action
Commonly used for rate control in AF
Action is to inhibit Na/K ATPase in the myocardium. Raises Na intracellular levels - eventually raises Ca and therefore prolongs phase 4 and phase 0 of the cardiac potential.
Also indirectly increases acetylcholine at cardiac muscarinic receptors. Slows conduction and prolonging the refractory period in the AV node and bundle of His.
Weak ionotrope.
