Arryhthmias Flashcards
Shockable rhythms
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Ventricular tachycardia
> Ventricular fibrillation
Non-shockable rhythms
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Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse) Asystole (no significant electrical activity)
Acute management of Supraventricular Tachycardias (SVT)
o vagal manoeuvres: e.g. Valsalva manoeuvre, carotid sinus massage
o intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option
o electrical cardioversion
Management of Atrial Flutter
Treatment is similar to atrial fibrillation:
- Rate/rhythm control - beta blockers/cardioversion
- Treat the reversible underlying condition
- Radiofrequency ablation of the re-entrant rhythm
- Anticoagulation based on CHA2DS2VASc score
ECG changes seen for Atrial Flutter
Saw tooth u waves on ECG
Adenosine adverse effects
o chest pain
o bronchospasm
o transient flushing
o can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
Adenosine contraindications
It should be avoided in asthmatics due to possible bronchospasm.
Adenosine mechanism of action
Works by slowing cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm.
Adenosine method of delivery
Adenosine should ideally be infused via a large-calibre cannula due to its short half-life,
Wolff-Parkinson White Syndrome
Caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node.
What is the name of the extra pathway that is present in Wolff-Parkinson White Syndrome?
Bundle of Kent
Treatment of Wolff-Parkinson White Syndrome
Radiofrequency ablation of the accessory pathway.
ECG changes for Wolff-Parkinson White Syndrome
- Short PR interval (< 0.12 seconds)
- Wide QRS complex (> 0.12 seconds)
- “Delta wave” which is a slurred upstroke on the QRS complex
Torsades de pointes
A type of polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”, describing the ECG characteristics.
When a patient develops Torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress into ventricular tachycardia. Usually they are self-limiting but if they progress to VT it can lead to a cardiac arrest.
What arrhythmia is a patient at risk of developing with prolonged QT intervals?
Torsades de pointes
Causes of Long QT intervals
- Long QT Syndrome (inherited)
- Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
- Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
Acute Management of Torsades de pointes
- Correct the cause (electrolyte disturbances or medications)
- Magnesium infusion (even if they have a normal serum magnesium)
- Defibrillation if VT occurs
Long Term Management of Prolonged QT Syndrome
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Avoid medications that prolong the QT interval Correct electrolyte disturbances Beta blockers (not sotalol) Pacemaker or implantable defibrillator
Ventricular ectopics
Premature ventricular beats caused by random electrical discharges from outside the atria.
Patients often present complaining of random, brief palpitations (“an abnormal beat”).
ECG characteristics for Ventricular ectopic beats
They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.
Management of Ventricular ectopics
- Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
- Reassurance and no treatment in otherwise healthy people
- Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)
First-degree heart block
Occurs where there is delayed atrioventricular conduction through the AV node.
Despite this, every atrial impulse leads to a ventricular contraction, meaning every p wave results in a QRS complex.
On an ECG this presents as a PR interval greater than 0.20 seconds (5 small or 1 big square).
Second-degree heart block
Where some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes. There are several patterns of second-degree heart block; Mobitz type 1 & 2, 2:1 block etc.
Wenckebach’s phenomenon (Mobitz Type 1)
On an ECG this will show up as an increasing PR interval until the P wave no longer conducts to ventricles. This culminates in absent QRS complex after a P wave. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle repeats itself.
Mobitz Type 2
This is where there is intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes, for example 3 P waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal. There is a risk of asystole with Mobitz Type 2.
What is the risk associated with Mobitz Type 2 heart block?
There is a risk of asystole with Mobitz Type 2.
2:1 Block
This is where there are 2 P waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex. It can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which.
Third-degree heart block
This is referred to as complete heart block. This is no observable relationship between P waves and QRS complexes. There is a significant risk of asystole.
What is the risk associated with third degree heart block?
There is a significant risk of asystole with third-degree heart block.
Treatment for Bradycardias / AV Node Blocks
Stable: Observe
Unstable or risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):
First line: Atropine 500mcg IV
What conditions have a high risk of asystole?
i.e. Mobitz Type 2, complete heart block or previous asystole
Atropine mechanism of action
Antimuscarinic medication and works by inhibiting the parasympathetic nervous system. This leads to side effects of pupil dilatation, urinary retention, dry eyes and constipation.
Ventricular tachycardia (VT)
Broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.
What are the two sub-types of VT?
- monomorphic VT: most commonly caused by myocardial infarction
- polymorphic VT: A subtype of polymorphic VT is Torsades de pointes which is precipitated by prolongation of the QT interval.
What condition is associated with monomorphic VT?
myocardial infarction
What condition is associated with poymorphic VT?
Torsades de pointes which is precipitated by prolongation of the QT interval.
Congenital causes of prolonged QT interval
Jerrell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)
What drugs cause prolonged QT intervals?
> amiodarone, sotalol, class 1a antiarrhythmic drugs > tricyclic antidepressants, fluoxetine > chloroquine > terfenadine > erythromycin
Management of VT
If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure) then immediate cardioversion is indicated.
In the absence of such signs antiarrhythmics may be used. If these fail, then electrical cardioversion may be needed with synchronised DC shocks
Examples of Class 1 anti-arrhythmic drugs
Class IA drugs: Quinidine, Amiodarone, Procainamide, Disopyramide.
Class IB drugs: Lidocaine, Mexiletine, Tocainide. …
Class IC drugs: Flecainide, Propafenone, Encainide, Moricizine
Examples of Class II anti-arrhythmic drugs
Beta blockers: Metoprolol, Carvedilol, Atenolol, Propranolol, Bisoprolol.
Examples of Class III anti-arrhythmic drugs
amiodarone, dronedarone, sotalol, ibutilide, dofetilide, and bretylium.
Class III anti-arrhythmic drugs - mechanism of action
As a generalization, class III antiarrhythmics prolong cardiac action potentials, resulting in an increase in the effective refractory period. With the exception of ibutilide, which slows outward Na+ currents during repolarization, the class III drugs block potassium channels.
Class I anti-arrhythmic drugs - mechanism of action
These drugs bind to and block the fast sodium channels that are responsible for the rapid depolarization (phase 0) of fast-response cardiac action potentials.
Class IV anti-arrhythmic drugs - mechanism of action
Slow non-dihydropyridine calcium channel blockers. They decrease conduction through the AV node, and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure.
Examples of Class IV anti-arrhythmic drugs
Verapamil, Diltiazem
