S3) Cardiac Arrhythmias Flashcards by shreya Arun

What is an arrhythmia?

An arrhythmia is a heart condition arising due to disturbances in pacemaker impulse formation and/or contraction impulse conduction
It results in a rate and/or timing of myocardial contraction that is insufficient to maintain normal CO
occur due to automatic or triggered activity, re-entry due to a scar

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Describe the movement of ions in the fast cardiac action potential

0 → sodium enters the cell via funny channels and causes depolarisation
1 → K leaves the cell causing early depolarisation
2 → ca moves from the sarcoplasmic recticulum inside the cell via t type channels
3 → K starts to move out of the cell causing depolarisation
Na/K ATPase resets it to normal

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Describe the effect of drugs blocking Na⁺ channels on the fast cardiac action potential

Marked slowing conduction in tissue (phase 0)
takes longer to depolarise the cell
Minor effects on action potential duration (APD)
eg: Flecainide and propaferone*

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Describe the effect of beta blockers on the fast cardiac action potential

Diminish phase 4 depolarisation and automaticity

→ heart will beat more slowly, with less force and lower blood pressure

→ block actions of adrenaline

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Describe the effect of drugs blocking K⁺ channels on the fast cardiac action potential

Increased action potential duration (APD)

slows depolarisation

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Describe the effect of calcium channel blockers on the fast cardiac action potential

CCBs decrease inward Ca²⁺ currents resulting in a decrease of phase 4 spontaneous depolarization
Effect plateau phase of action potential
refractory period is increased

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Describe the movement of ions in the slow cardiac action potential

this occurs in the SAN or the AV node
4 → slow Na channels / spontaneous depolarisation
0 → depolarisation
4 → K leaves the cell and causes depolarisation

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Outline the mechanisms of arrhythmogenesis due to abnormal impulse generation

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Outline the mechanisms of arrhythmogenesis due to abnormal conduction

conduction block: impulse is not conducted from the atria to the ventricles

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Describe the two possible actions of anti-arrhythmic drugs in terms of abnormal generation

Decrease the phase 4 slope (in pacemaker cells) → slowed down
Raises the threshold so takes longer to reach and slows heart down

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Describe the two possible actions of anti-arrhythmic drugs in terms of abnormal conduction

Decrease conduction velocity (phase 0) / reduced conduction in tissues
Increase ERP (effective refactory period)

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Why are anti-arrhythmic drugs used?

Anti-arrhythmic drugs are used to:

Decrease conduction velocity
Change the duration of ERP
Suppress abnormal automaticity

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What are the different types of anti-arrhythmic drugs?

Class I: Na⁺ channel blockers
Class II: beta-adrenergic blockers
Class III: K⁺ channel blockers (prolong repolarisation)
Class IV: Ca²⁺ channel blockers

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what does automaticity mean

Pacemaker cells ability to create an action potential and spontaneously depolarise

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Describe the actions of the different types of class I anti-arrhythmic drugs

Class IA – Moderate phase 0
Class IB – No change in phase 0
Class IC – Marked phase 0

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Provide two examples of Class IA anti-arrhythmic agents

Procainamide
Quinidine

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How are Class IA anti-arrhythmic agents administered?

Oral preparation
IV preparation

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Describe the four effects of Class IA anti-arrhythmic agents on cardiac activity

Decrease conduction – ↓ phase 0 of the action potential (Na⁺)
Increase refractory period – ↑ APD (K⁺) and ↑ Na⁺ inactivation
Decrease automaticity – ↓ slope of phase 4, fast potentials
Increase threshold (Na⁺)

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Describe the effects of Class IA anti-arrhythmic drugs on the ECG

↑ QRS
± PR
↑ QT

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Describe the uses of Class IA anti-arrhythmic drugs

Quinidine: maintain sinus rhythms in atrial fibrillation and flutter, prevent recurrence, Brugada syndrome
Procainamide: acute IV treatment of supraventricular and ventricular arrhythmias

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Identify 5 side-effects of Class IA anti-arrhythmic drugs

Hypotension (reduced CO)
Proarrhythmia e. g. Torsades de Points (↑ QT interval)
Dizziness & confusion
Gl effects (common)
Lupus-like syndrome (esp. procainamide)

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Provide two examples of Class IB anti-arrhythmic drugs

Lidocaine
Mexiletine

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How are Class IB anti-arrhythmic agents administered?

Lidocaine: IV preparation
Mexiletine: oral preparation

start out with lodicaine and then once stable move onto mexiletine

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Describe the five effects of Class IB anti-arrhythmic agents on cardiac activity

Fast binding offset kinetics
No change in phase 0 in normal tissue (no tonic block)
APD slightly decreased (normal tissue)
↑ increase threshold (Na⁺)
↓ phase 0 conduction in fast beating or ischaemic tissue

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Describe the effects of Class IB anti-arrhythmic drugs on the ECG

- No effects in normal / fast beating / ischaemic - ↑ QRS

Describe the uses of Class IB anti-arrhythmic drugs

- Acute use in **ventricular tachycardia** (esp. during ischaemia) - Not used in **atrial arrhythmias** or **AV junctional arrhythmias**

Identify 3 side-effects of Class IB anti-arrhythmic drugs

- Less proarrhythmic than Class 1A - CNS effects: dizziness & drowsiness - Abdominal upset

Provide two examples of Class IC anti-arrhythmic drugs

- Flecainide - Propafenone

How are Class IC anti-arrhythmic agents administered?

- Oral preparation - IV preparation

Describe the four effects of Class IC anti-arrhythmic agents on cardiac activity

- Very slow binding offset kinetics (\>10 s) - Substantially ↓ phase 0 (Na⁺) in normal - ↓ automaticity (↑ threshold) - ↑ APD (action potential duration) (K⁺) and ↑ refractory period (esp in rapidly depolarising atrial tissue)

Describe the effects of Class IC anti-arrhythmic drugs on the ECG

- ↑PR - ↑QRS - ↑QT

Describe the uses of Class IC anti-arrhythmic drugs

**Wide spectrum use:** - Supraventricular arrhythmias (fibrillation and flutter) - Premature ventricular contractions (caused problems) - Wolff-Parkinson-White syndrome (congenital condition where the heart suddenly starts beating very fast for a period of time)

Identify 4 side-effects of Class IC anti-arrhythmic drugs

- Proarrhythmia and sudden death (esp chronic use) → need stable ventricles and valves - Increase ventricular response to supraventricular arrhythmias (flutter) - CNS effects - GI effects

Provide two examples of Class II anti-arrythmic agents

- Propranolol - Bisoprolol

How are Class II anti-arrhythmic agents administered?

- **Propranolol**: Oral, IV - **Bisoprolol**: Oral

Describe the two effects of Class II anti-arrhythmic agents on cardiac activity

- ↑ APD and refractory period in AV node to slow AV conduction velocity - ↓ Phase 4 depolarisation (catecholamine dependent)

Describe the effects of Class II anti-arrhythmic drugs on the ECG

- ↑PR - ↓HR

Describe the uses of Class II anti-arrhythmic drugs

- Treating sinus and catecholamine-dependent **tachycardia** - Converting **re-entrant arrhythmias** at AV node - Protecting the ventricles from **high atrial rates** (slow AV conduction)

Identify 2 side-effects of Class II anti-arrhythmic drugs

- Bronchospasm - Hypotension ***Don’t use in partial AV block or heart failure or if there are any major conducting problems***

Provide an example of a Class III anti-arrythmic agents

Amiodarone

How are Class III anti-arrhythmic agents (amiodarone) administered?

- Oral preparation - IV preparation it has a VERY high half life of (3 months)

Describe the four effects of Class III anti-arrhythmic agents on cardiac activity (amiodarone)

- ↑ refractory period and ↑APD (block K⁺) ↓ phase0 and conduction (Na⁺) - ↑ Threshold - ↓ Phase 4 (β block and Ca²⁺ block) - ↓ Speed of AV conduction

Describe the effects of Class III anti-arrhythmic drugs on the ECG (amiodarone)

- ↑ PR - ↑ QRS - ↑ QT → if you prolong too much then you will risk getting torsades de pointes - ↓ HR

Describe the uses of Class III anti-arrhythmic drugs (amiodarone)

Very wide spectrum: effective for most arrhythmias but lots of side effects

Identify 6 side-effects of Class III anti-arrhythmic drugs (amiodarone)

- Pulmonary fibrosis - Hepatic injury - Increase LDL cholesterol - Thyroid disease - Photosensitivity - Optic neuritis (transient blindness)

Provide two examples of Class IV anti-arrythmic agents

- Verapamil - Diltiazem

How are Class IV anti-arrhythmic agents administered?

- **Verapamil**: oral/IV preparation - **Diltiazem**: oral preparation

Describe the three effects of Class IV anti-arrhythmic agents on cardiac activity

- Slow conduction through AV (Ca²⁺) - ↑ Refractory period in AV node - ↑ Slope of phase 4 in SA to slow HR

Describe the effects of Class IV anti-arrhythmic drugs on the ECG

- ↑ PR - ± HR (depending on BP response and baroreflex)

Describe the uses of Class IV anti-arrhythmic drugs

- Control ventricles during supraventricular tachycardia - Convert supraventricular tachycardia (re-entry around AV)

Identify 2 side-effects of Class IV anti-arrhythmic drugs

- Asystole (if β blocker is on board) - Some GI problems ***Caution when partial AV block, hypotension, decreased CO or sick sinus present***

How can adenosine be administered?

Rapid IV

Describe the mechanism in which adenosine functions

- Binds α₁ receptors and activates K⁺ currents in AVN & SAN - ↓ APD, hyperpolarization → ↓HR - ↓ Ca²⁺ currents – ↑ refractory period in AVN

Describe the effect of adenosine on cardiac activity

Slows AV conduction

Describe the uses of adenosine

- Convert re-entrant supraventricular arrhythmias - Hypotension during surgery - Diagnosis of CAD

Describe the mechanism in which digoxin functions

- Enhances vagal activity (↑K⁺ currents, ↓Ca²⁺ currents, ↑refractory period) - Slows AV conduction and slows HR

Describe the use of digoxin

Digoxin is used in treatment to reduce ventricular rates in atrial fibrillation and flutter

where do fast action potentials occur vs slow action potentials?

cardiac tissue vs SA/AV node

what is the re-entry mechanism?

due to a circuit within the myocardium, occurs when a propagating impulse fails to die out after normal activation of the heart and persists as a result of continuous activity around the circuit to re-excite the heart after the refractory period has ended;

what is the Vaughan-williams classification

what is sotalol used for and how does it do this

Class III drug: → Supraventricular and ventricular tachycardia increases APD and refactors period in atrial and ventricular tissue slow phase 4 ( B blocker) slow AV conduction

effects of Sotalol on ECG

increased QT reduced HR

side effects of sotalol

proarrhythmia, fatigue and insomnia

orthodromic vs antidromic tachycardia

orthodromic is when the impulses are being sent in the right direction

Ivabradine

→ very good for treating POTS with the preventing sudden increase in heart beating

Atropine

* anti-arrhythmic drug * selective muscarinic antagonist * blocks vagal activity to speed AV conduction and increase HR * treats bradycardia

efficacy of anti-arrhythmic drugs

but the safety and tolerability reduces as you move up to using amidarone

considering anti-platelet drug dipyridamole, what are some drug interactions with adenosine

dipyridamole inhibits cellular uptake of adenosine so increase adenosine in the AV node this might