Arryhthmias Flashcards
(46 cards)
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.
