Arrhythmias Flashcards
What are the 2 main sub-categories of arrhythmias?
Supravenricular and ventricular
What are the 4 conducting pathways spreading from the SA node?
Anterior, middle, posterior intermodal tracts and then Bachmann’s bundle to the LA
In which 2 ways can electrical dysfunction occur?
Defects in impulse formation eg. altered automaticity or defects in impulse conduction eg. re-entrant rhythms
What are the 5 main mechanisms of arrhythmia?
Defects in impulse formation:
- 1) Ectopic beats/Altered automaticity
- 2) Triggered activity
Defect in impulse conduction:
- 3) Re-entry
- 4) Conduction block
- 5) Accessory Tract Pathways
Altered automaticity can be physiological or pathological, what are the physiological examples?
Modulation of SA node activity by the ANS (e.g. sinus tachycardia, sinus arrhythmia) or during respiration when HR increases on inspiration and decreases on expiration
Altered automaticity can be physiological or pathological, what are the pathological examples?
Latent pacemaker subverts the SA node’s function as the normal pacemaker of the heart (overdrive suppression is lost)
Arrhythmia
Abnormality of the heart rate or rhythm
How can pathological altered automaticity occur?
Either SA node is firing pathologically low resulting in an escape beat/rhythm from the latent pacemaker. Or if the latent pacemaker fires at a rate faster than the SA node rate resulting in an ectopic rate/rhythm
Ectopic beats
Beats that occur somewhere in the heart other than the SA node. The ectopic focus may cause single beats or take over and pace the heart, dictating its entire rhythm as a sustain arrhythmias.
What is triggered activity as a cause of arrhythmias?
Afterdepolarisations triggered by a normal action potential (oscillations in the membrane potential which occur during depolarisation). Can be ether early afterdepoalrisation (EAD) or delayed after depolarisation (DAD). Occurs with digoxin toxicity, torsades de pointes or hypokalaemia
What are early afterdepoalrisations (EAD)?
Occur during the exciting action potential (phase 2/3). Associated with prolonged QT interval, such as in QT syndrome
What are delayed afterdepolarisations (DAD)?
Occurs after complete depolarisation and isa associated with raised intracellular Ca2+, such as during sympathetic stimulation
What is re-entry as a cause of arrhythmias?
Self sustaining electrical circuit (anatomically may be two parallel conduction pathways), stimulates an area of myocardium repeatedly/rapidly
**What causes re-entry?
Normally 2 signals go around either side of an area of non-excitable tissue, collide at the other side and go their separate ways. In re-entry, a unidirectional block on one side of the non-excitable tissue caused by trauma/ischaema etc means that there is no signal for the other signal on the other side to collide with, so it continues around as this area is no longer re-fractory like normal. so it creates a are re-entrant circuit
What is conduction block as a cause of arrhythmias?
Any disease which disrupts electrical conduction may reduce conduction velocity or block conduction altogether causing bundle branch block, bradycardia or heart block
What are the 3 types of conduction block?
1) Partial bock - Slowed conduction: tissue conducts all impulses, but more slowly than usual eg. First degree AV block
2) Intermittent - Tissue conducts some impulses, but not others eg. Second degree AV block
3) Complete - No impulses are conducted through the affected area e.g. Third degree AV block
What are accessory tract pathways as a cause of arrhythmias?
Normally the only point of electrical continuity between the atria and the ventricles is the AV node – It is the only thing to pierce the fibrous cardiac skeleton. Some individuals possess electrical pathways that bypass the AV node eg. the Bundle of Kent. Ventricles receive impulses from both the normal and accessory pathways – can set up the condition for a re-entrant loop predisposing to tachyarrhythmias
How to anti-arhythmic drugs generally work?
Generally inhibit specific ion channels with the intention of suppressing abnormal electrical activity e.g. the 3 main conductances
How are anti-arrhythmic drugs classified pharmacologically?
Vaughn Williams classification. The classification defines four classes I, II, III and IV, with class I subdivided into subclasses Ia, Ib and Ic - characterised by their effects on the APs in Purkinje fibres
**Which channels do Class I anti-arrhythmic drugs block and what effect do they therefore have? What differentiates the subtypes?
Block voltage active sodium channels. This slows the rate of rise of AP and prolongs the refractory period. The differences between the subtypes are the rate at which they unbind from the sodium channel
What is a Class IA anti-arrhythmic drug?
Disopyramide
What is a Class IB anti-arrhythmic drug?
Lignocaine
What is a Class IC anti-arrhythmic drug?
Flecainide
**Which channels do Class II anti-arrhythmic drugs block and what effect do they therefore have?
Act as beta –agonists by decreases the rate of depolarisation and rate of conductance through the AV node
What is a Class II anti-arrhythmic drug?
Metoprolol, atenolol, propanolol, sotalol
**Which channels do Class III anti-arrhythmic drugs block and what effect do they therefore have?
Block voltage activated potassium channel, so they prolong the AP and therefore the refractory period
What is a Class III anti-arrhythmic drug?
Amiodarone, stool
**Which channels do Class IV anti-arrhythmic drugs block and what effect do they therefore have?
Act on the calcium channels so affect the muscular AP plateau, and the upstroke in the nodal AP
What is a Class IV anti-arrhythmic drug?
Verapamil
Which state of the Na+ channel do Class I anti-arrhythmic drugs block?
The open state (as opposed to closed or inactive state). state. During high frequency firing (e.g. tachyarrhythmias) relatively more time is spent in the open and inactivated states than normal. This means there is more time for Class I agents to block the open state, and stabilise the inactive state. They spare the normal cardiac rhythm and target these areas of high-frequency firing
Anti-Arrhythmic drugs can also be classed based on the site of the arrhythmia. Which class of drugs would you use for atrial arrhythmias?
Class IC and III - both as rate controllers of SVT
Which drugs would you use for AV node arrhythmias?
Adenosine, digoxin and classes II and IV - rhythm control of SVT
Which drugs would you use for ventricular arrhythmias?
Classes IA, IB and II
What is the main aim of treatment of supra ventricular tachycardia?
To stop the spread of electrical activity from the atria to the ventricles. Can do this by blocking the AV node
What drugs would you use to treat supra ventricular arrhythmias?
1) Adenosine (IV bolus) - Hyperpolarizes the AV node briefly, suppressing impulse conduction 2) Digoxin (IV infusion or oral) - Stimulates vagal activity and slows conduction and prolongs refractory period in AV node and bundle of His (esp. in AF) 3) Verapamil - class IV agent (oral) - Blocks L-type voltage-activated Ca2+ channel. Slows conduction and prolongs refractory period in AV node and bundle of His esp atrial flutter/fibrillation
What drugs would you use to treat ventricular arrhythmias?
1) Lignocaine (Class IB) - Rapid block of voltage-activated Na+ channels. Used mainly (IV) in the treatment of ventricular arrhythmias following a myocardial infarction.
What drugs would you use to treat atrial and ventricular arrhythmias?
Classes IA and IC, II and III:
1) Disopyramide and procainamide (Type Ia agents)
2) Flecainide (Type Ic agent) - mainly prophylaxis of paroxysmal AF
3) Propranolol and atenolol (Type II agents, β-blockers) - control SVT by suppressing AV conduction
4) Amiodarone and sotolol (Type Ill agents) - increase action potential duration and the effective refractory period - Supress re-entry
What determines whether arrhymthias are symptomatic or not?
Whether they affect the cardiac output
Wolf Parkinson White Syndrome
Presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles: Bundle of Kent. Electrical signals traveling down this abnormal pathway may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular re-entrant tachycardia.