5 - Cardiac Arrhythmias Flashcards
What is an arrhythmia due to?
- Disturbance in the cardiac cycle where either the pacemaker (SAN) functions incorrectly or there is abnormal contraction/conduction of the heart.
- This causes a change in rate or timing of the heart beat which is insufficient to maintain cardiac outout
- Diagnosed by ECG and may get symptoms like palpitations, feeling dizzy, fainting, SOB
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What are the phases of the ventricular action potential?
Phase 0: depolarisation as movement of Na into cells
Phase 1: small amount of repolarisation
Phase 2: Plateau stage as Ca influx and K efflux are ewual
Phase 3: Repolarisation as efflux of K
Phase 4: Na/K ATPase sets up membrane potential in refractory period
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What is the Vaughan Williams classification of anti-arrhythmic drugs?
Class I have A, B and C
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What effect do Class 1 drugs have on the cardiac action potential?
Na Channel Blockers
- Depolarisation occurs more slowly in ventricles (decrease slope in phase 0)
- Little effect on APD
- SAN cells aren’t dependent on fast Na channels (think SAN A.P) so can still depolarise meaning rate not affected so rhythm controlling drug
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What effect do Class 2 drugs have on the cardiac action potential?
Beta Blockers
- Block sympathetic nervous system so decreased slope of the funny current so less activation of the A.P in SAN
- Rate controlling drug
- Can’t give to asthmatics
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What effect do Class 3 drugs have on the cardiac action potential?
K Channel Blocker
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- Prolongs phase 3 and refractory period so the APD increases. This prevents early afterdepolarisations
- Rhythm controlling drugs
- Can be pro-arrhythmic as QT extended
What effect do Class 4 drugs have on the cardiac action potential?
Calcium Channel Blockers
- Slow down heart rate by preventing Ca influx in the SAN
- Prolong phase 2
- Rate controlling
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What effect do the following drugs have on the SAN action potential?
- Beta blockers
- Ca channel blockers
- Muscarinic agonists
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What is the fast and slow cardiac action potential?
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What is Wolf-Parkinson-White syndrome and how does it lead to an arrhythmia?
- Accessory rentry pathway in the heart called the Bundle of Kent connecting the atria and ventricles
- Leads to pre-excitation and WPW as fibres allowed to travel back up to the atria from the Purkinje fibres
- Tachycardia
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What are reentry loops and how does it lead to an arrhythmia?
- When an impulse is blocked and so it travels in a retrograde way and reexcites the area it came from giving another action potential in quick succession
- Blockage can be from an area of ischaemia that has scarred
- Causes a ventricular tachycardia
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In general, how do the four classes of drugs correct arrhythmias?
- Abnormal generation: Beta and Ca channel blockers
- Abnormal conduction: Na and K channel blockers
Want to act to decrease conduction velocity, change the duration of the ERP and suppress abnormal automaticity
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Apart from re-entry loops and WPW Syndrome, what are some conditions that can cause a tachycardic arrhythmia?
- After-depolarisations:
- Can be early (phase 2 or 3) or late (abnormal depolarisation in phase 4). Can result in long QT or scarring
- Fibrillations (ventricular or atrial)
- Ectopic pacemaker activity following areas being damaged e.g ischaemia
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What is an example of a Class 1A drug, what arrhythmias is it used to treat, what are the side effects and how will it alter the ECG?
Quinidine (oral or IV)
Used for: AF, flutter, tachycardia, Brugada
Side effects: hypotension, increases QT so can cause torsades de pointes (proarrhytmic), GI effects
ECG: wider QRS, increase QT
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What is an example of a Class 1B drug, what arrhythmias is it used to treat, what are the side effects and how will it alter the ECG?
Lidocaine (IV)
Used for: acute ventricular tachycardia typically due to ischaemic heart disease (don’t use in atrial arrhythmia or heart block)
Side effects: dizziness, drowsiness, abdominal upset, less pro-arrhytmic than 1A
ECG: increases width of QRS in fast heart rate as blocks phase 0 conduction in fast rate
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