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A tachycardia is defined as a heart rate greater than 100 beats per minute (bpm). In narrow complex tachycardias the QRS complex is shorter than 120 ms (three small squares on the ECG). Narrow complex tachycardia is common.
To have a narrow complex, the electrical signal must pass forward through the atrioventricular (AV) node - ie contrast with a broad QRS complex means that either the conducting system is not working (bundle branch block) or the electrical circuit is not involving the AV node correctly.
- Sinus tachycardia:
- This is an accelerated sinus rate that is a physiological response - eg, to fever, anxiety, pain, exercise, hyperthyroidism.
- Heart rate is more than 100 bpm and rhythm is usually regular.
- P waves are similar to sinus rhythm.
- Inappropriate sinus tachycardia:
- This has an accelerated baseline sinus rate in the absence of a physiological stress.
- Most often seen in young women without structural heart disease. The underlying mechanism may be abnormality within the sinus node or its autonomic input, or hypersensitivity of the sinus node to autonomic input.
- ECG findings are similar to sinus tachycardia, with P waves similar to sinus rhythm.
- Sinus nodal re-entrant tachycardia:
- Is due to a re-entry circuit, either in or near the sinus node.
- The heart rate is usually 100-150 bpm, and ECG tracings usually demonstrate normal P-wave waves.
- Atrial tachycardias:
- Atrial tachycardia is usually a narrow complex tachyarrhythmia accounting for 10% of supraventricular tachycardias (SVTs).
- It can occur at any age, but there is an increased likelihood if the atria are diseased (hypertension, pulmonary disease, previous cardiac surgery, etc).
- The causes of atrial tachycardia include digoxin toxicity, ischaemic heart disease, cardiomyopathy, rheumatic heart disease and sick sinus syndrome.
- Either focal automatic activity (mainly) or due to re-entrant mechanism. Can have multiple foci of automatic activity.
- Multifocal atrial tachycardia:
- Composed of three or more P-wave morphologies.
- It is fairly uncommon and is usually seen in elderly patients with pulmonary disease.
- The heart rate is greater than 100 bpm, and ECG findings typically include an irregular rhythm, which may look similar to atrial fibrillation.
- Treatment involves correcting the underlying disease process. Magnesium and verapamil may be effective.
- Abnormal-looking P waves; may have different types of P waves on the same ECG.
- Heart rate very variable from 140-240 bpm.
- At higher rates there may be variable AV block.
- Useful drugs: beta-blockers; verapamil or diltiazem; type 1c agents (flecainide), amiodarone.
- Atrial fibrillation
- Atrial flutter.
- AV nodal re-entrant tachycardia (AVNRT):
- Also known as AV nodal tachycardia (AVNT), or AV junctional re-entrant tachycardia (AVJRT).
- The most common type of narrow QRS.
- It typically starts in the later teens and 20s.
- The basis of this arrhythmia is that the AV node can have two pathways as part of it. These paths allow a circuit to be set up at the AV node itself, giving rise to the arrhythmia.
- Narrow QRS tachycardia of about 180 bpm with P waves often absent: they are hidden in the QRS, as atrial and ventricular depolarisation occur at the same time.
- There may be changes in the QRS complex due to simultaneous P-wave activation. This is a small positive deflection before the onset of the T wave.
- Useful drugs:
- Drugs which affect the AV node (digoxin, diltiazem, and verapamil), beta-blockers; type 1c agents (propafenone or flecainide).
- Adenosine can acutely stop the tachycardia as it transiently blocks the AV node (as can vagal manoeuvres).
- Atrioventricular re-entrant tachycardia (AVRT) and Wolff-Parkinson-White (WPW) syndrome:
- Can occur from infancy onwards.
- In infants it may be associated with congenital heart defects.
- One to three people in every 1,000 have an obvious extra pathway on the resting ECG - that is, WPW syndrome.
- The re-entry mechanism is due to a congenital addition of a small piece of atrial tissue which crosses the isolating fibrous ring separating the atria and ventricles. This gives a large circuit with the heartbeat passing down through the AV node, around the ventricle, back up the pathway, and across the atrium back to the AV node. This illustrates why SVT is not such a good name for these arrhythmias: most of this tachycardia's circuit lies in the ventricle.
- The resting ECG can be normal but it can show evidence of the pathway's existence if the path allows some of the atrial depolarisation to pass quickly to the ventricle before it gets though the AV node (WPW syndrome).
- The early depolarisation of part of the ventricle leads to a shortened PR interval and a slurred start to the QRS (delta wave).
- The QRS is narrow; the message via the AV node eventually predominates because it uses the rapid conducting system to depolarise most of the ventricle.
- The tachycardia ECG may be unremarkable, with P waves absent (hidden in the QRS). If the circuit is long or slow enough, the P wave may occur at the end of the QRS and can be visible as a distortion in the T wave (this is best seen in lead V1).
- Drug treatment:
- Beta-blockers; adenosine can acutely stop the tachycardia as it transiently blocks the AV node (as can vagal manoeuvres); type 1c agents (eg, flecainide); type 1a agents (eg, procainamide).
- Atrial fibrillation with accessory pathways:
- Atrial fibrillation has an atrial rate of 300-600 bpm. Fortunately, the AV node protects the ventricle from experiencing such a heart rate.
- In patients with accessory paths there is a mechanism for this very fast heart rate to bypass the AV node and cause atrial fibrillation with a dangerously fast ventricular response.
- Treating this with drugs such as digoxin, verapamil, or diltiazem would further block the AV node but not prevent the atrial fibrillation from passing down the accessory path. The situation would be made a lot worse in this case. This is why the drugs are stated as being contra-indicated in atrial fibrillation in the presence of an accessory pathway.
May present with:
- Many arrhythmias require no treatment.
- Indications for treatment include relief of symptoms and prevention of complications - eg, myocardial infarction, heart failure, embolism.
- Need to correct precipitating factors - eg, myocardial ischaemia, infection, thyrotoxicosis, alcohol, electrolyte disturbance or drug toxicity.
- For acute arrhythmias causing hypotension, heart failure or myocardial ischaemia, perform direct current (DC) cardioversion.
- Give oxygen and establish IV access.
- If pulseless, follow.
- If adverse signs (systolic blood pressure <90 mm Hg, chest pain, heart failure, heart rate >200 bpm):
- Synchronised DC shock under sedation/general anaesthesia; 100 J : 200 J : 360 J; or equivalent biphasic energy.
- If necessary, amiodarone 150 mg IV over 10 minutes, then 300 mg over one hour and repeat shock.
- If the rhythm is irregular, probably atrial fibrillation: control rate with beta-blocker IV or digoxin IV. If the onset is within the previous 48 hours, consider amiodarone 300 mg IV 20-60 minutes; then 900 mg over 24 hours.
- If the rhythm is regular:
- Vagal manoeuvres (caution if there is possible digitalis toxicity, acute ischaemia, or presence of carotid bruit for carotid sinus massage).
- Adenosine 6 mg by rapid bolus injection; if unsuccessful, follow, if necessary, with up to three doses each of 12 mg every 1-2 minutes. Monitor ECG continuously. Theophylline and related compounds block the effect of adenosine. Patients on dipyridamole, carbamazepine, or with denervated hearts have a markedly exaggerated effect which may be hazardous. A starting dose of 6 mg adenosine is currently outside the UK licence for this agent.
- If normal sinus rhythm is not restored, possible atrial flutter: seek expert help and control rate (eg, with a beta-blocker).
- If normal sinus rhythm is restored, probable re-entrant paroxysmal supraventricular tachycardia (PSVT):
- Record 12-lead ECG in sinus rhythm. If it recurs, give adenosine again and consider choice of anti-arrhythmic prophylaxis.
- If there are no adverse signs (systolic blood pressure <90 mm Hg, chest pain, heart failure, heart rate >200 bpm), choose from:
- Esmolol: 40 mg over one minute + infusion 4 mg/min (IV injection can be repeated and infusion increased incrementally to 12 mg/min); or
- Verapamil 5-10 mg IV (not to be used in patients receiving beta-blockers); or
- Amiodarone: 300 mg IV over one hour - may be repeated once if necessary; or
- Digoxin: maximum of two doses of 500 micrograms IV over 30 minutes.
- Paroxysmal supraventricular tachycardia (PSVT): verapamil, beta-blockers and disopyramide are effective in preventing further episodes.
- AV nodal re-entrant tachycardia (AVNRT):
- Drug prophylaxis of AVNRT is achieved with beta-blockers, a combined beta-blocker and a class III agent such as sotalol, or with AV nodal blocking drugs such as verapamil or digoxin.
- Curative treatment is readily achieved by radiofrequency ablation and is indicated if patients are refractory to drugs, intolerant of side-effects or unwilling to take long-term medication.
- Drug prophylaxis is used to reduce the risk of recurrent orthodromic re-entrant tachycardia or atrial fibrillation. Agents acting on both the AV node and the accessory pathway, such as flecainide and sotalol, are preferred.
- Radiofrequency ablation is indicated in patients with tachycardias due to concealed accessory pathways if they are not well controlled on drugs, intolerant of side-effects, or unwilling to take long-term medication.
- Symptomatic WPW syndrome:
- Radiofrequency ablation is increasingly considered as first-line therapy. It abolishes the risk of pre-excited atrial fibrillation as well as preventing further attacks of AVRT.
- The success rate of ablation varies according to the location of the pathway, but is usually over 90%.
Further reading and references
; European Society of Cardiology (2013)
; Targeting tachycardia: diagnostic tips and tools. J Fam Pract. 2012 May61(5):258-63.
; Resuscitation Council UK, 2010
; Resuscitation Council UK Guideline, 2010
; Narrow complex (supraventricular) tachycardias. Postgrad Med J. 2009 Oct85(1008):546-51. doi: 10.1136/pgmj.2009.080101.
Greetings to all you Afibbers out there. I am 84, have had paroxysmal Afib for 15 years, and as it was getting worse (every10 days for24 hours). I tried Amiodarone which I stood for 1 month, and...mohoog
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