As the name suggests, arrhythmias are abnormal heart rhythms. They result from an interruption to the normal electrical signals that coordinate the contraction of the heart muscle. There are several types of arrhythmias each with different causes and management options.
Please read the Resuscitation Guidelines from the Resuscitation Council (UK) and attend their courses prior to treating patients. This section is a summary of these guidelines to improve your knowledge and understanding rather than guide treatment.
Four Cardiac Arrest Rhythms
These are the four possible rhythms that you will see in a pulseless unresponsive patient. They can be categorised into shockable (meaning defibrillation may be effective) and non-shockable (meaning defibrillation will not be effective and should not be used).
- Ventricular tachycardia
- Ventricular fibrillation
- Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
- Asystole (no significant electrical activity)
Tachycardia Treatment Summary
- Consider up to 3 synchronised shocks
- Consider an amiodarone infusion
In a stable patient:
Narrow complex (QRS < 0.12s)
- Atrial fibrillation – rate control with a beta blocker or diltiazem (calcium channel blocker)
- Atrial flutter – control rate with a beta blocker
- Supraventricular tachycardias – treat with vagal manoeuvres and adenosine
Broad complex (QRS > 0.12s)
- Ventricular tachycardia or unclear – amiodarone infusion
- If known SVT with bundle branch block treat as normal SVT
- If irregular may be AF variation – seek expert help
Normally the electrical signal passes through the atria once, simulating a contraction then disappears through the AV node into the ventricles. Atrial flutter is caused by a “re-entrant rhythm” in either atrium. This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway. The signal goes round and round the atrium without interruption. This stimulates atrial contraction at 300 bpm. The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction. It gives a “sawtooth appearance” on ECG with P wave after P wave.
- Ischaemic heart disease
Treatment is similar to atrial fibrillation:
- Rate/rhythm control with beta blockers or cardioversion
- Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
- Radiofrequency ablation of the re-entrant rhythm
- Anticoagulation based on CHA2DS2VASc score
Supraventricular Tachycardias (SVT)
Supraventricular tachycardia (SVT) is caused by the electrical signal re-entering the atria from the ventricles. Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.
Paroxysmal SVT describes a situation where SVT reoccurs and remits in the same patient over time.
There are three main types of SVT based on the source of the electrical signal:
- “Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.
- “Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).
- “Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm.
Acute Management of Stable patients with SVT
When managing SVT take a stepwise approach trying each step to see whether it works before moving on. Make sure they are on continuous ECG monitoring.
- Valsalva manoeuvre. Ask the patient to blow hard against resistance, for example into a plastic syringe.
- Carotid sinus massage. Massage the carotid on one side gently with two fingers.
- Adenosine (see below)
- An alternative to adenosine is verapamil (calcium channel blocker)
- Direct current cardioversion may be required if the above treatment fails
Adenosine 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. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway. It will often cause a brief period of asystole or bradycardia that can be scary for the patient and doctor, however it is quickly metabolised and sinus rhythm should return.
A few key points on administering adenosine:
- Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
- Warn patient about the scary feeling of dying / impending doom when injected
- Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)
- Initially 6mg, then 12mg and further 12mg if no improvement between doses
Long Term Management of patients with paroxysmal SVT
When patients develops recurrent episodes of SVT then measures can be taken to prevent these episodes. The options are:
- Medication (beta blockers, calcium channel blockers or amiodarone)
- Radiofrequency ablation
Wolff-Parkinson White Syndrome
Wolff-Parkinson White Syndrome is 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. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.
The definitive treatment for Wolff-Parkinson White syndrome is radiofrequency ablation of the accessory pathway.
- Short PR interval (< 0.12 seconds)
- Wide QRS complex (> 0.12 seconds)
- “Delta wave” which is a slurred upstroke on the QRS complex
Note: If the person has a combination of atrial fibrillation or atrial flutter and WPW there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia. Most antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine etc) increase the risk of this by reducing conduction through the AV node and therefore promoting conduction through the accessory pathway – therefore they are contraindicated in patients with WPW that develop atrial fibrillation or flutter.
Radiofrequency Ablation (RFA)
Catheter ablation is performed in a electrophysiology laboratory, often called a “cath lab”. It involves local or general anaesthetic, inserting a catheter in to the femoral veins and feeding a wire through the venous system under xray guidance to the heart. Once in the heart it is placed against different areas to test the electrical signals at that point. This way the operator can hopefully find the location of any abnormal electrical pathways. The operator may try to induce the arrhythmia to make the abnormal pathways easier to find. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity. The aim is to remove the source of the arrhythmia.
This can be curative for certain cases of arrhythmia caused by abnormal electrical pathways, including:
- Atrial Fibrillation
- Atrial Flutter
- Supraventricular Tachycardias
- Wolff-Parkinson-White Syndrome
Torsades de pointes
Torsades de pointes is a type of polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”, describing the ECG characteristics. It looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval.
A prolonged QT interval is the ECG finding of prolonged repolarisation of the muscle cells in the heart after a contraction. Depolarisation is the electrical process that leads to the heart contraction. Repolarisation is a period of recovery before the heart muscle cells (myocytes) are ready to depolarise again. Waiting a longer time for repolarisation can result in random spontaneous depolarisation in some areas of heart myocytes. These abnormal spontaneous depolarisations prior to repolarisation are known as “afterdepolarisations”. These depolarisations spread throughout the ventricle, leading to a ventricular contraction prior to proper repolarisation occurring. When this occurs and the ventricles continue to stimulate recurrent contractions without normal repolarisation it is called Torsades de pointes.
When a patient develops Torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress in to ventricular tachycardia. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest.
Causes of Prolonged QT
- 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
- Avoid medications that prolong the QT interval
- Correct electrolyte disturbances
- Beta blockers (not sotalol)
- Pacemaker or implantable defibrillator
Ventricular ectopics are premature ventricular beats caused by random electrical discharges from outside the atria. Patients often present complaining of random, brief palpitations (“an abnormal beat”). They are relatively common at all ages and in healthy patients however they are more common in patients with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure).
They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.
This is where the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.
- 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)
AV Node Blocks (Heart Block)
First degree heart block
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 waves 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
Second-degree heart block is 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 described below:
Wenckebach’s phenomenon (Mobitz Type 1)
This is where the atrial imputes becomes gradually weaker until it does not pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong. This cycle then repeats.
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.
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 with third-degree heart block.
Treatment for Bradycardias / AV Node Blocks
Unstable or risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):
- Atropine 500mcg IV
- Atropine 500mcg IV repeated (up to 6 doses for a total to 3mg)
- Other inotropes (such as noradrenalin)
- Transcutaneous cardiac pacing (using a defibrillator)
In patients with high risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):
- Temporary transvenous cardiac pacing using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
- Permanent implantable pacemaker when available
Note. Atropine is an antimuscarinic medication and works by inhibiting the parasympathetic nervous system. This leads to side effects of pupil dilatation, urinary retention, dry eyes and constipation.
Last updated November 2018