Understanding Arrythmias Flashcards
What are cardiovascular drugs used to treat?
Cardiovascular drugs are used to treat – Arrhythmias – Heart failure – Angina – Hypertension – Risk of thrombus formation
What are some disturbances of cardiac rhythm?
Abnormality of heart rate or rhythm – Bradycardia – Atrial flutter – Atrial fibrillation – Tachycardia • ventricular tachycardia • supraventricular tachycardias – ventricular fibrillation - extreme
What are causes of tachycardia?
Tachycardia
• Ectopic pacemaker activity - driving at faster rate than SAN
– damaged area of myocardium becomes depolarised and spontaneously active
– latent pacemaker region activated due to ischaemia
• dominates over SA node
• Afterdepolarisations
– abnormal depolarisations following the action potential (triggered activity)
• Atrial flutter / atrial fibrillation
• Re-entry loop
– conduction delay
– accessory pathway
What are the causes of bradycardia?
• Sinus bradycardia - SAN depolarising slowly
– Sick sinus syndrome (Intrinsic SA node dysfunction)
– Extrinsic factors such as drugs (beta blockers, some Ca2+ channel blockers)
• Conduction block
– Problems at AV node or bundle of His
– Slow conduction or blockingconductuin at AV node due to extrinsic factors ((beta blockers, some Ca2+ channel blockers) - ventricles going at slower rate
What are delayed after-delpolarisations?
• Delayed after-depolarisation
• More likely to happen if intracellular Ca2+ high
If lots happening - AP when they shouldnt - irregular
What are early after-depolarisations?
• Early after-depolarisations
• Can lead to oscillations
• More likely to happen if AP prolonged
• Longer AP – longer QT- more likely to get early after-depolarisation
Ossicialtios - can lead to prolonged ventricular tachycardia which is always changeing shape
What is the re-entrant mechanism for generating arrhythmia?
Normal spread will split into 2 at some point - when impulses meet they Weill cancel out - sodium channels inactive so wont fire again
Bc of damage eg old MI - block in conduction to damaged area
Problem occurs if incomplete conduction damage
Incomplete conduction damage (unidirectional block) - excitation can take a long route to spread the wrong way through the damaged area, setting up a circus of excitation
Slow enough for coming back to area -long enough time for cells to have recovered from refractory. -circuit of excitation
What can cause atrial fibrilation?
Multiple re-entrant circuits in the atria
Stretching of atria
Chaotic re entry
Give 2 examplesof re entry loops
Fast and slow pathways in the AV node create a re-entry loop
An accessory pathway between atria and ventricles creates a re-entry loop such as in Wolff-Parkinson-White syndrome
Loop occurring - cells recovered from refractory
What are the 4 basic classes of anti arrhythmic drugs?
There are 4 basic classes of anti-arrhythmic drugs.
I. Drugs that block voltage-sensitive sodium channels II. Antagonists of β-adrenoreceptors
III. Drugs that block potassium channels
IV. Drugs that block calcium channels
Don’t need to know the classification – just understand the way some types of anti-arrhythmic drugs work
How do class i drugs work?
- Typical example is the local anaesthetic lidocaine (class Ib)
- Use-dependent block. Only blocks voltage gated Na+ channels in open or inactive state – therefore preferentially blocks damaged depolarised tissue
- Little effect in normal cardiac tissue because it dissociates rapidly
- Blocks during depolarisation but dissociates in time for next AP
Block but dissociate rapidly
Prevents any premature action potentials taking place from depolarised tissue
But dissociates in time so that next AP can happen when it should
What is lidocaine?
• Sometimes used following MI
– only if patient shows signs of ventricular tachycardia
– given intravenously
• (given to suppress) Damaged areas of myocardium may be depolarised and fire automatically
• More Na+ channels are open in depolarised tissue
– lidocaine blocks these Na+ channels (use-dependent)
– prevents automatic firing of depolarised ventricular tissue
• Not used prophylactically following MI
– Even in patients showing VT generally use other drugs (see later)
- been superseded by other drugs
What are class II drugs?
Beta adrenoceptor agonists
• Examples: propranolol, atenolol (Beta blockers)
• Block sympathetic (adrenaline, NA) action
– act at β1 -adrenoreceptors in the heart
• Decrease slope of pacemaker potential in SA and slows conduction at AV node - slow the pacemaker potential at SAN/AVN
- slow upstroke by inhibiting L type calcium channels
- blocking CAMP
What are beta blockers used for?
• Can prevent supraventricular tachycardia
– β-blockers slow conduction in AV node
– Slows ventricular rate in patients with AF
- If you can slow impulses getting through to ventricles, reduces rate but doesnt fix rhythm
• Used following myocardial infarction
– MI often causes increased sympathetic activity
– Arrhythmias may be partly due to increased sympathetic activity
– β-blockers prevent ventricular arrhythmias
• Also reduces O2
– Reduces myocardial ischaemia
– Beneficial following MI
What are class III drugs?
Drugs that block K+ channels
• Class III anti-arrhythmics
• Prolong the action potential
– mainly by blocking K+ channels - Block depolarisation phase
• This lengthens the absolute refractory period
• In theory would prevent another AP occurring too soon
- BUT
– In reality can be pro-arrhythmic
- most of these not good as anti arrhythmic agents
What are the uses of class III drugs?
• Prolong the action potential
• Not generally used because they can be also be pro-arrhythmic
• One exception – amiodarone
• Included as a type III anti-arrhythmic, but has other actions in
addition to blocking K+ channels
• Used to treat tachycardia associated with Wolff-Parkinson-White
syndrome (re-entry loop due to an extra conduction pathway)
• Effective for supressing ventricular arrhythmias post MI
