6th March 2024

Tachycardias

Tachycardia is defined as a ventricular rate of above 100 bpm and can arise from a primary cardiac aetiology or secondary to demand for an increased cardiac output, such as sinus tachycardia in response to hypovolaemia. Patients may complain of feeling tired, palpitations, light-headedness, shortness of breath, chest discomfort, and may arrest in certain tachyarrhythmias where output is significantly compromised e.g., VT or VF. The various tachycardia syndromes can be organised by the width of the QRS complex into narrow (QRS <0.12s) or broad (QRS >0.12s). 

Supraventricular Arrhythmias

Supraventricular tachycardias (arising from above the level of the ventricles) produce narrow QRS complexes. However, in the event of a supraventricular tachycardia in the presence of a bundle branch block or an accessory pathway (aberrancy), the QRS complex will be broad.

Atrial fibrillation (AF) 

AF is characterised by chaotic atrial activity as a result of electrical discharge from multiple foci, predominantly within the pulmonary veins that drain into the left atrium. It is commonly an accompanying feature of hypertension or ischaemic heart disease. It can also be due to structural cardiac changes e.g. valve disease, hypertrophy or dilation, as well as an infiltrative or inflammatory process. More commonly, however, AF is seen as a result of non-cardiac causes, e.g. infection, hyperthyroidism, hyponatraemia, hypokalaemia and PE. Other factors such as caffeine, alcohol and smoking may also contribute to the development of AF. AF is also strongly correlated with obstructive sleep apnoea, obesity and metabolic syndrome. It is::

• Paroxysmal: if it occurs for less than 7 days (typically less than 48 hours)
• Persistent: if it continues beyond 7 days 
• Permanent: arrhythmia is longstanding, where cardioversion has failed and when it is accepted that no further attempts will be made to cardiovert. 

Patients may be asymptomatic or report palpitations, breathlessness, and fatigue. Where there is a rapid ventricular response or underlying coronary artery disease, chest pain may develop. Very rarely, AF may present with syncope. The ECG is characterised by an absence of p waves and irregularly irregular QRS complexes due to the variation in AV node conduction of the chaotic atrial electrical activity. 

Beyond the ECG, blood tests can help to confirm infection, thyroid dysfunction and electrolyte abnormalities including sodium, potassium, calcium and magnesium. An echocardiogram can assess for an underlying structural cause such as valvular pathology (i.e. mitral stenosis or regurgitation) but also look for left atrial dilation, which can inversely correlate with the success of rhythm control / management. 

Management

This focuses on rate and/or rhythm control and anticoagulation to reduce stroke risk. NICE guidance on when rhythm control is more appropriate over rate control includes patients with new-onset AF, those with a reversible cause, AF leading to LV dysfunction, or those with flutter amenable to ablation. Rhythm control is also considered where rate control strategies have failed or symptoms persist despite adequate rate control.

Rate control involves beta blockers or rate limiting calcium channel blockers (preferential in asthmatics) as first line, or digoxin if there are concerns for LV dysfunction. In the event of an accessory pathway (i.e. pre-excited AF) then AV nodal blocking agents should be avoided as they reduce the buffering effect of the AV node and allow the atrial arrhythmia to degenerate into a ventricular arrhythmia. Therefore, in the event of pre-excited AF, class 1a, 1c and 3 antiarrhythmics are utilised, including procainamide, flecainide and amiodarone, respectively. If the onset of AF is <48 hours, rate control should be initiated, and if the rhythm does not return to the sinus within 24 hours, consideration can be made for cardioversion using flecainide if there is no underlying evidence of coronary disease or LV dysfunction. Alternatively, Amiodarone may be used. Most episodes of AF will resolve spontaneously, especially where there is an underlying cause, such as infection. In the event of haemodynamic compromise, returning to sinus rhythm is a priority using direct current cardioversion. Beyond 48 hours of onset or where the timeline is unclear, rate control and anticoagulation for at least 3 weeks with either warfarin or a DOAC is initiated in preparedness for outpatient cardioversion. Amiodarone can be given prior to cardioversion to increase the likelihood of success. 

Anticoagulation is continued for 4 weeks following cardioversion in low-risk patients. The CHA2DS2-VASc score (Table 2) is used to assess the need for long term anticoagulation.  The HAS-BLED score has been superseded by the ORBIT score in assessing bleeding risk. Scoring high encourages caution with oral anticoagulation and a review of bleeding risk factors. Catheter ablation may be used in AF but following a single procedure may return in up to 20-30% of patients.

 Table 2: CHA2DS2-VASc score determines stroke risk in patients with AF. Score of 2 or more warrants anticoagulation. A score of 1 in men warrants consideration.

Atrial Flutter

In contrast to the chaotic atrial activity of AF, flutter is characterised by a more organised arrhythmia, typically with a counter-clockwise macro reentry circuit occurring within the right atrium. This circuit is seen on the ECG as flutter waves, which have a characteristic saw-tooth pattern in V1 and negative flutter waves inferiorly (leads II, III, AVF). These waves occur at a rate of around 300/min, which is dampened by the AV node, which may result in a 2:1, 3:1, or 4:1 block giving a ventricular rate of 150, 100 or 75 bpm, respectively. In the presence of a variable block, the rhythm may be irregular. 

Management is similar to AF and the principles of thromboprophylaxis remain the same for elective cardioversions as outlined for AF. It is useful to calculate the CHA2DS2-VASc score and consider anticoagulation in those with a high score to prevent thromboembolic events, as patients may experience both flutter and fibrillation episodes.

Rate control is typically difficult to attain with atrial flutter, which tends to respond less to digoxin. Initially, a beta blocker or rate limiting calcium channel blocker may be used. Atrial flutter responds well to electrical cardioversion, requiring very low energy levels to restore sinus rhythm; but in view of stroke risk, similar recommendations as in AF are advocated with respect to three-weeks of uninterrupted anticoagulation prior to cardioversion for onset >48 hours. 

Typical atrial flutter is often successfully definitively managed with radio-frequency ablation within a localised area between the tricuspid valve annulus and the inferior vena cava (the cavo-tricuspid isthmus) which is key to the macro reentry circuit. First attempts are often 90% successful at attaining curative intent. 

Focal Atrial Tachycardia

Accelerated atrial activity arising from a focal area within the atria other than the SA node presents with a regular but abnormal p wave morphology with a rate >100/bpm. There may be some level of AV block but 1:1 AV conduction of atrial tachycardias can result in dangerous exacerbations of the ventricular rate.  

A variation of this is multifocal atrial tachycardia, most commonly seen in patients with COPD or congestive heart failure. As above, there is an accelerated atrial rhythm but there are at least three distinct p wave morphologies. The management is similar to AF with rate and rhythm control, but anticoagulation does not play a role here due to relatively organised atrial activity.

Atrioventricular nodal reentry tachycardia (AVNRT)

AVNRT occurs due to two (fast and slow) pathways within the AV node. These pathways have varying refractory periods which allow for a re-entry tachycardia to arise. The ECG will show a regular narrow complex tachycardia with no discernible p waves and pseudo-R’ waves in V1/V2, characteristic of retrograde conducted p waves.

Patients may describe transient episodes of palpitations that are well tolerated. The arrhythmia is managed by creating a temporary block in the AV node to interrupt the re-entry circuit and can be achieved by vagal manoeuvres; adenosine or verapamil if adenosine is contraindicated (e.g., asthmatic patients). Medical prophylaxis includes beta-blockers, verapamil or digoxin and curative treatment involves radiofrequency ablation. In those with refractory AVNRT Amiodarone may be used. 

Atrioventricular reentry tachycardia (AVRT)

This is less common than the AVNRT but is equally a re-entry tachycardia where there is an accessory pathway running between the ventricles and atria, distinct from the AV node. It can be difficult to discern AVNRT from AVRT, with the latter typically conducting at faster rates. Management is with AV nodal blocking agents with preference for those that work on both the AV node and the accessory pathway, such as Flecainide or Sotalol. There is good success with radiofrequency ablation as a curative option.

Wolff-Parkinson-White (WPW) 

The existence of an anterograde pathway between the atria and ventricles called the bundle of Kent, allows conduction to travel faster via the accessory pathway and normal speed through the AV node and normal conductive pathway. This causes a slurred upstroke to the QRS complex known as a delta wave and shortened PR interval. When this conduction abnormality results in tachyarrhythmia, it is termed Wolff-Parkinson-White Syndrome. 

There is a small familial link with WPW, however the condition is also associated with congenital structural cardiomyopathies such as hypertrophic cardiomyopathy or Ebstein’s anomaly (apical displacement of tricuspid valve resulting in tricuspid regurgitation and atrialisation of the basal right ventricle). It is estimated that the majority of patients with WPW pattern ECG are asymptomatic.

Treatment of haemodynamically stable WPW supraventricular tachycardias includes vagal manoeuvres and medications such as Amiodarone or Procainamide. Often, pre-excited AF in the context of WPW is poorly tolerated; however, where there is haemodynamic compromise, DCCV with sedation is appropriate. Radiofrequency ablation of the accessory pathway is the treatment of choice for patients with WPW. AV nodal blocking agents such as verapamil, diltiazem, adenosine, and digoxin should be avoided in WPW as they can increase conduction via the accessory pathway leading to a ventricular arrhythmia. 

Ventricular Arrhythmias 

As a rule, all tachycardias that are ventricular in origin will have broad QRS complexes due to the relatively slower conduction within ventricular myocardial cells. 

Ventricular Tachycardia (VT)

VT is a broad, complex tachycardia originating from the ventricles. It is sustained if it lasts more than 30s or non-sustained if it lasts between 3 beats and 30s. Risk factors for VT include structural heart disease, typically 48 hours after or even many years following acute ischaemic events and previous cardiac surgery. VT in younger patients is likely a consequence of a cardiac genetic syndrome. VT may present with cardiac arrest, syncope, chest pain and breathlessness. 

When QRS complexes are similar in morphology they are monomorphic, or polymorphic if they vary, the latter has an increased risk to progress to ventricular fibrillation. Identifying VT can be challenging and in the event of a cardiac arrest, a broad complex tachycardia should be treated as such. The following ECG features make VT more likely: 

• AV dissociation
• Capture beats 
• Fusion beats
• Very broad complex (>140ms)
• Positive/negative concordance across chest leads and extreme axis deviation. 

An important mantra to remember is that a regular broad complex tachycardia is VT until proven otherwise; if in doubt, treat any broad complex tachycardia as VT.

Management is with drug therapy including intravenous Amiodarone and Lidocaine if the patient is haemodynamically stable. In sustained VT with haemodynamic compromise, urgent DC cardioversion is warranted. Verapamil is contraindicated as it can lead to further clinical deterioration. If there is no obvious precipitating cause, consideration should be made for ICD insertion for secondary prevention. 

Torsade de pointes

This is a polymorphic VT which occurs with a prolonged QT interval (measured from start of Q wave to end of T wave). A long QT may be a result of a congenital genetic abnormality or acquired (see Table 3).  Management includes stopping the precipitating agent which may resolve the episode of torsade. IV Magnesium is administered to stabilise the cardiac membrane and where there is haemodynamic instability DCCV is used. 

 Table 3: Causes of QT prolongation. [Adapted from the Oxford Textbook of Medicine].

Ventricular Fibrillation (VF)

This describes a chaotic irregular ventricular tachyarrhythmia, with no discernibility of any wave formation. It is the most common cause of death within a few hours of a myocardial infarction, as this can precipitate an R on T phenomenon. This describes a ventricular ectopic depolarisation i.e., the R wave being superimposed on the prior repolarisation i.e., the T wave. Other than ischaemia, other causes of VF include:

• Structural disease with impaired ventricular function or severe LV hypertrophy
• Preceding VT can rapidly deteriorate to VF
• AF with aberrancy, especially in the presence AV blocking agents (adenosine, digoxin, verapamil, b-blockers)
• Metabolic states such as hypoxia and acidosis can precipitate VF 
• It is important to note that genetic syndromes can also precipitate VF, such as patients with Brugada and long-QT syndrome, such patients may subsequently receive ICD implantation

VF is not compatible with life and so requires urgent electrical cardioversion.

References

• Chhabra L, Goyal A, Benham MD. Wolff Parkinson White Syndrome. StatPearls. Last updated August 11th 2021. Available at https://www.ncbi.nlm.nih.gov/books/NBK554437/ 
• Atrial Fibrillation. Clinical Knowledge Summaries. National Institute for Health and Care Excellence (UK). Last updated January 2022. Available at https://cks.nice.org.uk/topics/atrial-fibrillation/ 
• Burns E, Buttner R. Focal Atrial Tachycardia (FAT). Life in the Fast Lane. Last updated December 19th 2021. Available at https://litfl.com/atrial-tachycardia-ecg-library/