Management
Management of patients presenting with any tachyarrhythmia should be preceded by an immediate ABCDE assessment and then follow the resus council guidelines for adult tachycardia. The primary treatment for any tachycardia is to identify and treat reversible causes e.g. electrolyte abnormalities, hypovolaemia etc.
Life-threatening features
If a patient presenting with an atrial tachycardia has been adequately resuscitated medical and has ongoing evidence of haemodynamic compromise, syncope, myocardial ischaemia or severe heart failure then proceed as below:
- Deliver up to 3 synchronised DC shocks (sedate patient if conscious)
- If unsuccessful – give amiodarone 300mg over 10-20 minutes
- Reattempt synchronised DC cardioversion
Regular narrow-complex tachycardias
For patients who are haemodynamically stable and have a regular narrow-complex tachycardia, follow the steps below:
- Attempt vagal manoeuvres. This can be sufficient to cardiovert the patient back to sinus rhythm.
- If unsuccessful and there is no evidence of a pre-excitation syndrome (e.g. WPW), give adenosine under direct ECG monitoring. The doses are 6mg rapid IV bolus, then 12mg if unsuccessful, then 18mg if unsuccessful.
- If unsuccessful, give verapamil or beta-blocker (metoprolol is the drug of choice in acute situations due to its fast onset of action)
- If ineffective, attempt DC cardioversion as above (note atrial flutter is unlikely to chemically cardiovert and will often need DC cardioversion if treatment of underlying causes is unsuccessful).
Patients with a pre-excitation syndrome such as Wolff-Parkinson-White should not be given digoxin or verapamil, as these can provoke fatal arrhythmias through blockade of the SA node, encouraging conduction down the aberrant pathway.. If cardioversion is unsuccessful, patients should be referred for consideration of radio-frequency ablation of their aberrant conduction pathway.
| Class | Mechanism |
|---|---|
| Class 1 | Inhibits fast Na+ channels during depolarisation, reducing depolarisation and conduction velocity. Membrane stabilisers |
| Class 1a
e.g. quinidine, procainamide |
Prolonged action potential duration by reducing the excitability of non-nodal regions of the heart during phase 0 depolarisation |
| Class 1b
e.g. lignocaine, phenytoin |
Reduce action potential duration by decreasing the rate of spontaneous phase 4 in myocardial cells (reduces automaticity) |
| Class 1c
e.g. flecainide, encainide |
Potent Na+ channel blockers – little effect on duration of action potential in ventricular myocardium, shortens action potential in Purkinje fibres. Decreases speed of conduction of cardiac impulses. |
| Class 2 (beta-blockers)
e.g. metoprolol, esmolol |
Decrease rate of depolarisation and increase effective refractory period of AV node & decreased automaticity, decreased QT duration. Decreases heart rate and oxygen consumption. |
| Class 3
e.g. amiodarone, sotalol |
Inhibit K+ channels to prolong the refractory period, cardiac depolarisation and action potential duration. Effectively decreases the amount of time cardiac cells are excitable.
Note amiodarone has some class 1, 2, 3 and 4 effects. |
| Class 4 (calcium-channel block)
e.g. verapamil, diltiazem, nifedipine |
Inhibit slow Ca2+ channels – slow calcium ion currents may contribute towards development of VT. Block L-type Ca2+ channels to impair SA node pacemaker activity. Decrease duration of action potential but no effect on automaticity. |
Table 4: Vaughan-Williams classification of anti-arrhythmic drugs.
Irregular narrow-complex tachycardias (i.e. atrial fibrillation)
Atrial fibrillation is the most common tachyarrhythmia in the UK. In the acute setting the priority should be on rapid pharmacological rate control of the stable patient, and then subsequent decision regarding rate vs rhythm control. There is no evidence to suggest mortality is any worse following a rate control rather than a rhythm control strategy for patients, if high-risk patients are anticoagulated. However, patients in sinus rhythm may report a better quality of life than those in AF. The mainstay of treatment in AF therefore is rate control and prevention of thromboembolic events.
Atrial fibrillation can be classified as paroxysmal (less than 7 days, then terminating), persistent (greater than 7 days, would last indefinitely unless cardioverted) and permanent (greater than 7 days, sinus rhythm not possible).
- Rate control
- Usually with a standard beta-blocker (e.g. bisoprolol) or rate-limiting calcium-channel blocker (diltiazem or verapamil)
- Consider digoxin if above contra-indicated
- Amiodarone should not be used for long-term rate control
- Anticoagulation
- Use CHA2DS2VASc and ORBIT scores to assess patient for suitability of anticoagulation
- First-line anticoagulation for AF is a direct oral anticoagulant (DOAC) such as apixaban, dabigatran, edoxaban or rivaroxaban
- Vitamin K antagonists such as warfarin can be used if DOACs are contraindicated
| CHA₂DS₂VASc stroke risk score | Points |
|---|---|
| Congestive cardiac failure
Reduced ejection fraction or requiring hospitalisation regardless of EF |
1 |
| Hypertension
Systolic BP >140 mmHg and/or Diastolic BP >90 mmHg On at least 2 occasions, or on antihypertensive medication |
1 |
| Age greater than 75 years | 2 |
| Diabetes mellitus
Fasting plasma glucose >7.0 mmol/l or treatment with oral hypoglycaemic drugs +/- insulin |
1 |
| Stroke/TIA | 2 |
| Vascular disease
Previous MI, peripheral arterial disease, or aortic plaque |
1 |
| Age 65-74 years | 1 |
| Sex – female | 1 |
Table 5: CHA2DS2VASc scoring system for stroke risk in AF. Consider anticoagulation in any patient scoring 2 or more.
| ORBIT bleeding risk score | Points |
| Hb < 130 in males
Hb < 120 in females |
2 |
| History of bleeding (GI or intracranial) | 2 |
| Age > 74 years | 1 |
| eGFR < 60ml/min/1.73m² | 1 |
| Concurrent antiplatelet therapy | 1 |
Table 6: ORBIT scoring system to assess bleeding risk when considering a patient for anticoagulation. A score of 1-2 is deemed low risk, 3 is medium risk and 4-7 high risk for a significant bleed if started on anticoagulation.
- Cardioversion
- DCCV may be appropriate for patients presenting with fast AF if onset is within 48 hours of presentation.
- If the history is suggestive of symptoms beginning earlier than this, or the patient is asymptomatic with no clear time of onset, cardioversion is contraindicated due to the risk of stroke from atrial thrombus formation.
- It is important to note that chemical cardioversion with flecainide or amiodarone carries the same risk, and therefore in patients presenting longer than 48 hours after development of AF, the management strategy should focus on rate or rhythm control, as detailed above.
Take your subscriptions with you
Our mobile app allows you to access your interview and exam question banks wherever you are.