11 - Cardiac Arrhytmias 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
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
What is the Vaughan Williams classification of anti-arrhythmic drugs?
Class I have A, B and C
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
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
What effect do Class 3 drugs have on the cardiac action potential?
K Channel Blocker
- 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
What effect do the following drugs have on the SAN action potential?
- Beta blockers
- Ca channel blockers
- Muscarinic agonists
What is the fast and slow cardiac action potential?
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
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
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
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
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
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
What is an example of a Class 1C drug, what arrhythmias is it used to treat, what are the side effects and how will it alter the ECG?
Flecainide (oral or IV)
Used for: supraventricular tachycardia (AF and flutter), WPW syndrome as binds to Bundle of Kent, premature ventricular contractions
Side effects: proarrhytmic and can cause sudden death if patient has ischaemic heart disease (e.g angina), CNS and GI effects, can raise heart rate more
ECG: Wider QRS, increased QT, increased PR
When should you not use Flecainide (Class IC drug)?
- Most potent Na channel blocker
- Do not use in ischaemic heart disease as risk of sudden death
- Use with AVN blocker in flutter and fibrillation as this drug can increase ventricular response to supraventricular arrhythmias causing really high heart rate
What is an example of a Class 2 drug, what arrhythmias is it used to treat, what are the side effects and how will it alter the ECG?
Bisoprolol (oral), Propanolol and Metoprolol
Used for: inappropriate sinus tachycardia, protect the ventricles from high atria rates (e.g AF and flutter), converting reentrant arrhytmias
Side effects: bronchospasm, hypotension
ECG: increase QT, decrease heart rate, widen QRS, increase PR
When should you not use bisoprolol to treat a cardiac arrhythmia?
- Asthmatic
- On antihypertensives
- With CCBs as can cause asystole
- Partial AV block or acute heart failure
What is the main Class 3 drug used, what arrhythmias is it used to treat, what are the side effects and how will it alter the ECG?
Amiodarone
Used for: wide spectrum, most arrhythmias
Side effects (with long term): see image. May need to reduce dose of digoxin and monitor warfarin closely when using this drug
ECG: slows HR, prolongs PR and QT, widens QRS
Apart from amiodarone, what is another type of class 3 drug that can also be classed as a class 2 drug?
Sotalol (oral)
- Lower efficacy than amiodarone
- Used wide spectrum
- Increases QT and lowers heart rate
- Can cause fatigue and insomina due to B antagonist effects
- Proarrhythmic
What is an example of a Class 4 drug, what arrhythmias is it used to treat, what are the side effects and how will it alter the ECG?
Diltiazem (oral) and Verapamil (oral or IV)
Used for: convert supraventricular tachycardia and control the venricles
Side effects: hypotension (sick sinus), constipation, AV block and therefore asystole if used with beta blocker
ECG: increased PR and change in HR (up or down dependent of blood pressure)
What is the mechanism of action of Adenosine, what arrhytmias is it used for, what are the side effects and what effects does it have on the ECG?
- Bolus dose given IV to stop heart beating for 20 seconds reducing spontaneous impulses from the SAN. Short half life so wears off
- Binds to A1 receptors and activates K+ channels in AVN and SAN to hyperpolarise, longer APD and lower heart rate. Also decreases Ca currents. All slow AV conduction
- Convert reentrant supraventricular tachycardias and can help diagnose coronary heart disease
- Abdominal discomfort, hot flushes, chest pain, sense of impending doom, proarrhythmic
What is the mechanism of action of Ivabradine, what arrhythmias is it used for and what are the side effects?
Oral
MOA: blocks funny current in SAN to slow the sinus node but not effect blood pressure
Side effects: flashing lights, teratogeicity in pregnancy
Uses: reduce inappropriate sinus tachycardia and reduce heart rate in heart failure and angina as no drop in blood pressure
What is the mechanism of action of Digoxin, what arrhythmias is it used for and what are the side effects?
Cardiac Glycoside
Uses: slow ventricular rates in AF and flutter
MOA: slows AV conduction and heart rate and enhances vagal activity by blocking Na/K ATPase
Side effects: only used in AF when beta blockers and CCBs don’t work, proarrhythmic, GI effects, dizziness
What is the mechanism of action of Atropine, what arrhythmias is it used for and what are the side effects?
Selective muscarinic antagonist
MOA: blocks vagal activity to speed up AV conduction and increase HR
Uses: vagal bradycardia until pacemaker can be used
Side effects: dizziness, photophobia, tachycardia
Which anti-arrhythmic drugs have the highest efficacy?
- Amiodarone - Sotalol/Flecainide/Lignocaine
- Bisoprolol/Metaprolol/Verapamil/Diltiazem
Reciprocal for safety/tolerability. Use car analogy to patient to weigh up efficacy and safety
What antiarrhymic drug should be used in the following scenarios:
- AF/Flutter
- WPW syndrome
- Supraventricular Tachycardia
- AF: first give rate controlling drugs like beta blockers (bisoprolol) and CCBs (verapamil) and then digoxin if not working. then give rhythm controlling drugs for cardioversion like flecainide and amiodarone. Need to give AV nodal blocking drugs with Flecainide to prevent ventricular tachycardia.
Consider giving anticoags like warfarin
- WPW: Flecainide as not a structural or ischaemic disease but long term need ablation
- SVT: Carotid Sinus massage or Adenosine
What antiarrhymic drug should be used in the following scenarios:
- Sinus Tachycardia
- Ectopic Beats
- Reentrant SVT
- ST: Ivabradine as no drop in B.P or bisoprolol/verapamil (b-blockers/CCBs)
- Ectopics: Beta Blockers like bisoprolol
- Reentrant SVT: acutely can use adenosine then verapamil then flecainide IV. Chronically can give bisoprolol and verapamil oral but long term need ablation
What ions are moving in the funny current?
What are the 4 main causes of a supraventricular tachycardia?
- Atrioventricular nodal rentry tachycardia
- Atrial Flutter (rentry in the atria)
- WPW syndrome
- AF
How can you tell the difference between AVNRT and Atrial Flutter on an ECG?
Give the patient adenosine to block AV node by blocking A1 receptors so can just see what is going on in the atria.
Will produce sawtooth appearance on ECG
Adenosine works by causing hyperpolarisation by blocking K+ influx so cannot reach the threshold
When should you not use a calcium channel blocker (non-dihydropyridine) for a heart arrhythmia?
When a patient has heart failure with reduced ejection fraction as these drugs will lower contractility of heart (as well as beta blockers)
What effects does flecainide have on the heart?
- Slows conduction
- Prolongs refractory period
- Reduces automaticity
