Arrhythmias Flashcards
(38 cards)
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).
Shockable rhythms:
- Ventricular tachycardia
- Ventricular fibrillation
Non-shockable rhythms:
- Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
- Asystole (no significant electrical activity)
Tachycardia management in the unstable patient:
Consider up to 3 synchronised shocks
Consider an amiodarone infusion
Tachycardia management in a stable patient with a narrow QRS complex?
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
Tachycardia management in a stable patient with a broad QRS complex?
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
What is atrial flutter?
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.
Associated Conditions of atrial flutter?
Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis
Treatment of atrial flutter?
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
What are 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
- 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 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.
ECG Changes in Wolf-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
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.
What is 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.
Radiofrequency ablation (RFA) 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 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.
Torsades de pointes pathophysiology?
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
