Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Overview - Causes of Tachyarrhythmia
- Ishcaemic heart disease
- Valvular heart disease
- Heart failure
- Congenital heart disease
- Stimulants e.g. caffeine
- Metabolic e.g. hyperkalaemia
- Signs and Symptoms of Tachyarrhythmias
- Shortness of breath
- Chest pain (due to rate related ischaemia)
- Syncope or pre-syncope
- Fast pulse
- Irregular pulse
- Low blood pressure
- Signs of acute heart failure including: tachypnoea, desaturation, respiratory crackles on auscultation, raised JVP, peripheral oedema
- Classification of Tachyarrhythmias
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
- Broad vs. Narrow QRS complexes
- Classification of Tachyarrhythmias
Broad Complex Tachyarrhythmias
- Ventricular Tachycardia
- Torsades de Pointes
- Ventricular Fibrillation
Narrow Complex Tachyarrhythmias (Supraventricular Tachycardias)
- Sinus Tachycardia
- Atrial Tachycardia
- Reentrant Tachycardias (AVNRT and AVRT)
- Atrial Fibrillation
- Atrial Flutter
>>>Narrow<<< Complex Tachyarrhythmias
This is a rate of more than 100bpm with a normal ECG morphology. Whilst not strictly an arrhythmia (the rhythm is normal in sinus tachycardia), this is the commonest cause of tachycardia in hospital. As such it is an important differential for the other tachyarrhythmias. A fast heart rate can be appropriate or inappropriate in different circumstances (see below).
Management: If the tachycardia is appropriate then it is serving to maintain cardiac output, so only inappropriate tachycardias can be treated with rate control drugs. In the case of hyperthyroid or anxiety induced tachycardia B-Blockers are commonly used to slow the rate.
Differential Diagnosis: At very high heart rates the ECG for sinus tachycardia can easily be confused with AVNRT, AVRT and Atrial Tachycardia.
Sinus Tachycardia - Causes
This is a rare arrhythmia which is usually regular and narrow complex on the ECG. Because impulses are spread from an ectopic atrial focus, instead of the SA node, the p waves tend to look abnormal. The ectopic rate can be as fast as 250bpm, but the AV node will be electrically refractive to some of these impulses. Thus, the ventricular rate is often lower than the atrial rate and sometimes irregular.
Atrial tachycardia is often paroxysmal in nature and is classically seen in the context of digitoxicity and congential heart disease.
There are many subtypes of atrial tachycardia, but a discussion of these is well beyond the scope of medical finals.
Management: Manage by rate control with a B-blocker or a cardioselective Calcium Channel Blocker e.g. Verapamil. Consider cardioversion if the arrhythmia is persistent and of recent onset.
Differential Diagnosis: AVNRT, AVRT, Atrial fibrillation, Atrial flutter.
Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
AVNRT is the commonest junctional arrhythmia. It occurs due the presence of a second conduction pathway in (or near) the AV node. One pathway conducts quickly and repolarises slowly, whilst the other conducts slowly and repolarises quickly.
This situation can give rise to a normal ECG appearance and a normal heart rate. This is because normal sino-atrial nodal impulses are only conducted through the fast conducting pathway and the ventricles are depolarised as usual.
However, the situation can rise to a short circuit in the context of an ectopic (early) atrial beat. The ectopic beat is forced to use the slower conducting pathway because the fast one is still repolarising. The impulse reenters the AV node, in the opposite direction, through the fast conducting pathway which has by this time recovered. This cycling continues as, essentially, a short circuit loop has been established within the AV node.
This short circuit sends out normal ventricular depolarisations and retrograde atrial depolarisations. This results in a regular, narrow complex tachycardia with a rate of 140-240bpm. Because the atrial and ventricular depolarisations occur virtually simultaneously the p waves are often buried within the QRS complexes on the ECG. Where they are visible they will be inverted due to retrograde depolarisation.
Fortunately AVNRT is often paroxysmal and self terminating, but can require treatment.
Management: Acute managment of AVNRT is as below (adapted from resus council's guidelines).
First line prophylaxis for frequent and symptomatic events are B-blockers, Calcium channel blockers and digoxin. Ablation therapy can be used as second line.
Differential Diagnosis: AVRT, Atrial tachycardia, Sinus tachycardia
AVRT (Wolff-Parkinson White Syndrome)
Atrioventricular reentrant tachycardia (AVRT) is the 2nd commonest junctional tachycardia. It occurs as the result of an additonal pathway through the AV junction called the Bundle of Kent. Normal sino-atrial impulses are preferentially conducted through this pathway, rather than the AV node because it conducts faster. This state is known as pre-excitation and has a characteristic ECG appearance. Pre-excitation predisposes to a short-circuit being established.
AVRT - Pre-excitation
A short circuit is established by an ectopic (early) atrial beat. This impulse is forced to travel through the SA node, because the Bundle of Kent is still repolarising. After depolariing the ventricles, the impulse travels retrogradely through the Bundle of Kent, which has this time repolarised. This cycling continues and results in a narrow complex tachycardia of 140-240bpm.
The atria depolarise very soon after the ventricles, resulting in a short R-P interval on the ECG or the p waves being completely buried in the QRS complex.
This tachycardia state is usually paroxysmal and self-terminating.
Management: Those found to have pre-excitation should have electrophysiology studies to determine the risk of their abberent pathway. The first line treatment for symptomatic patients is pathway ablation. However, if these patients present with a tachyarrhythmia then the (above) resus council guidelines should be followed, as with AVNRT.
Differential Diagnosis: AVNRT, Atrial Tachycardia and Sinus Tachycardia
Atrial Fibrillation (AF)
In atrial fibrillation, the atria chaotically fibrillate instead of contracting in a synchonised manner. The fibrillation rate is between 350 and 600bpm. This results in variable amounts of impulse conduction through the AV node, giving rise to an irregularly irregular ventricular rhythm; characteristic of AF. Ventricular rates vary widely, and clinicians often refer to 'slow AF' and 'fast AF'.
AF is the most common arrhythmia. It's present in 10% of the population over the age of 80. It causes significant morbidity due to the thromboembolic disease associated with it; Unmanaged AF caries a 5% yearly stroke risk.
The fibrillating atria are unable to fully empty their blood load into the ventricles. This leads to blood stasis and thrombus formation within the atria. Emboli can break off, travel through the systemic circulation and block end vessels, leading to cerebral infarction, bowel ischaemia and limb ischaemia.
This section covers the following aspects of AF:
- Classification (what are the different types of AF?)
- Initial Management (an approach to acute AF)
- Cardioversion (electrical and pharmacological)
- Longterm Management of AF
- Anticoagulation (longterm thromboprophylaxis)
AF - Classification
NICE Guidelines classify AF into paroxysmal, persistent and permanent to aid management. However textbooks often make reference to lone AF and acute AF.
AF - Initial Management
The initial management of AF is complex, but it is particularly important to be aware of how to recognise and manage the emergency situations which can arise. These can be broadly divided into those who are unstable and those who require acute rate control measures (see algorithm below).
It is important to exclude or treat reversible causes of AF e.g. infection, blood loss, MI, thyrotoxicosis. If no cause is apparent or AF persists despite treating the cause, then cardioversion can be considered.
NB: Venous thromboembolism risk stratification and treatment should be considered as part of the acute manage of AF (see anticoaguation section below).
AF - Cardioversion
Cardioversion (both electrical and pharmacological) doesn't come without significant risks, and should be undertaken cautiously in stable patients. Given that most AF is paroxysmal and 2/3rds of those self-terminate within 24 hours, it is prudent to wait and see (in stable patients) if it resolves on its own initially. In cases that persist, cardioversion can, for some, permanently restore sinus rhythm.
It is useful to know the exact time of onset because many methods of pharmacological cardioversion have only shown to be beneficial within 48 hours of onset. Pharmacological options include Flecainide and Amiodarone. There is a lower rate of successful cardioversion compared with electrical cardioversion, but it may be preferable because patients don't require conscious sedation or anaesthesia.
Electrical cardioversion can be attempted up to 12 months after onset.
Cardioversion requires prior anticoagulation as the procedure increases the risk of thromboembolism. The longer the atria have been fibrillating the greater the risk of thromboembolism, hence:
- 4 weeks of oral anticoagulation (INR >2.0) required in those presenting >48 hours of onset (or uncertain timing).
- Stat dose of heparin required in those presenting <48 hours since onset.
- All patients must remain anticoagulated for 4 weeks following cardioversion therapy.
Consider also that cardioversion will be contraindicated in many patient with AF because:
- They have been in AF for over 1 year and/or
- Their AF is likely to recur e.g. due to underlying structural heart disease or extra cardiac precipitants like thyrotoxicosis and/or
- Cardioversion has previously failed a number of times and/or
- Anticoagulation is contraindicated.
AF - Management based on sub-type
AF - Longterm Management
Rate Versus Rhythm Control
Longterm, AF can be managed using rate or rhythm control drugs, or a combination of both. The (above) NICE algorithm demonstrates the more recent the onset of AF, the more likely rhythm control will be considered.
Beta-Blockers and rate limiting calcium channel blockers (Verapamil and Diltiazem) are first line choices to lower the ventricular rate in AF. These are used first line in those with permanent AF, those over 65, those with ischaemic heart disease and those who can't tolerate antiarrhythmic drugs. They are used with caution in congestive heart failure, as they can make it worse. Digoxin is preferable in this situation, due to it's concomitant inotropic action on the heart.
Sotalol is commonly used first line as a rhythm control agent. Amiodarone and flecainide are also commonly used. Rhythm control is often the preferred option to treat paroxysmal AF, AF in younger patients, symptomatic AF, if there is no reason for the patient to be in AF (lone AF) or the precipitant has been treated and the AF persists. Rhythm control is sometimes preferred for those in congestive heart failure due to the dangers of slowing the ventricular rate with rate control drugs.
Those with infrequent, symptomatic episodes of paroxysmal AF, can self-administer a single dose of anti-arrhythmic treatment at the onset of their AF symptoms. This is known as the 'pill in the pocket approach'.
Catheter Ablation and Pacing
Ablation of the AV node may be indicated in patients whose AF is unresponsive to pharmacological methods, to slow the ventricular response rate. A permanent pacemaker may be indicated for those who undergo ablation, but have significant left ventricular dysfunction. Pacemakers also have some benefit in terminating paroxysmal AF.
AF - Anticoagulation
Most patients with AF require oral anticoagulation to prevent thromboembolic disease. The decision is made based on their stroke risk stratification, using the following NICE algorithm or a scoring system like the cha2ds2-vasc score.
A narrow complex, regular tachycardia with a baseline of saw-tooth flutter waves. The flutter waves typically have a rate of 300 bpm and the ventricular rate is commonly 150 bpm or 100 bpm, due to an AV node block ratio of 2:1 or 3:1, respectively.
The flutter waves result from an ectopic atrial beat that causes a reentrant circuit to be set up with the atria. The impulse can indefinately circle through the atria at a rate of approximately 300 times per minute. It is usually the right atrium which is involved with an anticlockwise circuit.
As with AF, atrial flutter commonly occurs in the context of ischaemic heart disease and flutter can easily degenerate into AF.
Management: As with AF, atrial flutter may require immediate rate control or a DC shock (see narrow complex, regular tachycardia resus algorithm). In addition external pacing can be consider in the acute setting for those who have well tolerated flutter.
In 60% of patients, flutter has occured due to another disease process e.g. pulmonary or cardiac disease, so reversal of the arrhythmia may occur when the disease process resolves. Therefore no treatment may be indicated in stable patients wth a reversible process.
Electrical and pharmacological cardioversion are both options in flutter. Atrial flutter is more sensitive to electrical cardioversion than AF, requiring lower energies. Flutter is less reponsive to pharmacological cardioversion than AF. As with AF, those with flutter for >48 hours need to be anticoagulated prior to any method of cardioversion and for 4 weeks after.
Long term management options for flutter are rhythm control agents and catheter ablation. Ablation involves making lesions to interrupt the reentrant circuit within the atrium. Ablation is far more successful than the pharmacological methods. With success rates of 80-90% compared with 30-40%, respectively.
Differential Diagnosis: AF, other SVTs.
<<< Broad >>> Complex Tachyarrhythmias
Monomorphic Ventricular Tachycardia (VT)
A broad complex regular tachycardia of a rate >120bpm. Requires 3 or more succesive ventricular (broad complex) beats for diagnosis. VT arises due to mini electrical circuits around edges of infarcted myocardium. VT may arise as an escape rhythm due to bradycardia.
Management: If the patient is pulseless then follow advanced life support algorithms (ie. start CPR aand call for help!). If the patient is clinically unstable i.e. syncopal, shocked or in acute heart failure, then follow the algorithm below. If the patient is stable, there is still a risk of developing ventricular fibrillation, so give amiodarone and get a cardiology opinion. The patient may need an implantable defibrillator or pacing if the rhythm is related to a bradycardia. The arrhythmic focus can be ablated in the electrophysiology lab.
Differential Diagnosis: SVT with a bundle branch block, torsade de pointes.
Polymorphic VT (Torsade de Pointes)
Torsade de Pointes (a ballet term meaning twisting of the points) is a variant of VT with a characteristic undulating baseline around which the broad complexes arise. The rhythm is less regular than monomorphic VT. It is associated with long QT syndrome and sudden cardiac death. Long QT syndrome can be congenital or acquired. Risk factors for QT prolongation include:
- (some) antihistamines
- antibiotics (especially macrolides and fluoroquniolones)
- hypokalaemia and hypomagnesaemia
- female sex
- structural heart disease
Management: Follow the above algorithm if the patient is unstable. Get expert help immediately. IV Magnesium and temporary pacing can help by shortening the QT interval.
Differential Diagnosis: VF, Monomorphic VT
Ventricular Fibrillation (VF)
A chaotic broad complex tachycardia which often occurs as a result of ischaemia and is immediately life threatening.
Management: Sustained VF will always compromise a patient, so treat as per Advanced life support algorithm. If the patient is not unstable then consider a different diagnosis. Having survived VF the patient may need an implantable defibrillator, though if VF occurs within 48 hours of an MI no treatment for the arrhythmia is necessary.
Differential Diagnosis: AF with bundle branch block, polymorphic VT.
- Making Sense of the ECG: A Hands on Guide. 3rd Ed.
- The Cardiovascular System: At a Glance. 2003
- NICE: Atrial Fibrillation: The Management of Atrial Fibrillation. 2006
- ESC Guidelines: Atrial Fibrillation (management of)
- ESC Guidelines: Supraventricular Arrhythmias
For Additional Images/ECGs