DO NOT USE FOR CLINICAL PRACTICE
Please use current guidelines available on the UHNM intranet for patient treatment
Please use current guidelines available on the UHNM intranet for patient treatment
RECOGNITION AND ASSESSMENT
- Treat patient first and arrhythmia second.
- Accurate diagnosis is not possible without a 12-lead ECG
Symptoms (in order of increasing severity/urgency)
- Palpitation
- Dyspnoea
- Chest pain
- Dizziness
- Syncope
- Cardiac arrest
Signs
- Heart rate <60 or >100 beats/min
- Hypotension (systolic BP<100 mmHg)
- Hypoperfusion
- Jugular venous pressure (JVP) elevated
- Cannon waves or flutter waves in internal jugular vein
- Variable intensity of first heart sound
- Signs of heart failure
Investigations
- 12-lead ECG unless patient unconscious with no pulse, when resuscitation takes priority - see Cardiopulmonary resuscitation - life support procedure. A single-lead rhythm strip is an inferior alternative, but better than no ECG at all
- Urgent U&E
IMMEDIATE TREATMENT
- Atrial fibrillation - follow Atrial fibrillation guideline
- Continuous ECG recording
- If arrhythmia causing hypotension, cardiac failure, chest pain, shock or requiring pacing, seek urgent advice from cardiology team
Potassium
- Correct any abnormalities of potassium - see Hypokalaemia/Hyperkalaemia guidelines
Is the arrhythmia?
Bradycardias
- Sinus bradycardia may need no treatment - if symptomatic, give atropine 500 microgram IV, and repeat once after 5 min if necessary or consider isoprenaline
- Sinus pauses and sino-atrial block - if episodes prolonged and symptomatic, consider isoprenaline or pacing: contact cardiology team
- Sino-atrial disease manifest as tachycardia-bradycardia - seek urgent advice from cardiology team
- Atrio-ventricular (AV) conduction block
- first degree: no treatment necessary
- second and third degree: consider isoprenaline or pacing and contact on-call cardiology SpR
- Intraventricular conduction block/bundle branch block - contact cardiology team to consider pacing if:
- new appearance of bifascicular block (right bundle branch block and left axis deviation) or alternating left and right bundle branch block
- bifascicular block/trifascicular block with otherwise unexplained syncope
Tachycardias
Clinical significance
- Accurate diagnosis requires 12-lead ECG (paper speed 25 mm/sec, 40 msec = 1 small square)
- Narrow (<120 msec) QRS complexes originate from sinus node, atrium or AV junction
- Broad (>120 msec) QRS complexes should be considered ventricular in origin unless or until proved otherwise
- If diagnosis in doubt, try carotid sinus massage (CSM) first
- recent CVA/TIA, or known established carotid disease are contraindications to CSM
- If CSM unsuccessful, unless there is a history of wheezing, give adenosine 3 mg IV over 2 sec via a large bore cannula into antecubital fossa vein with sodium chloride 0.9% flush
- NB: in patients taking dipyridamole (which decreases adenosine metabolism), initial dose of adenosine should be 1 mg IV and subsequent doses should be halved
- if no response after 1-2 min, give adenosine 6 mg IV over 2 sec. If no response after a further 1-2 min, give 12 mg IV over 2 sec
- NB: in patients taking theophylline (which antagonises the anti-arrhythmic effect of adenosine), higher doses will usually be necessary (CAUTION with adenosine in these patients as adenosine can cause bronchospasm)
- obtain rhythm strip
- following adenosine, atrial tachycardias should be revealed (P waves with AV block) or junctional re-entrant tachycardias terminated; ventricular tachycardias will be unaffected
Initial treatment
- If tachycardia associated with hypotension, shock, or cardiac failure, before giving any anti-arrhythmic drug IV, seek urgent advice from cardiology team to discuss DC cardioversion (or overdrive pacing for selected tachycardias)
- If patient with pathological tachycardia haemodynamically stable with no overt heart failure or impaired ventricular function, an anti-arrhythmic drug may be given by slow IV injection provided full resuscitation facilities are available, preferably on CCU. Seek urgent cardiology team advice
Specific rhythms
Is the tachycardia:
- Sinus tachycardia is usually physiological - identify and treat cause (e.g blood loss, heart failure, thyrotoxicosis, anaemia)
- if no obvious underlying cause, cardiac function adequate, and tachycardia inappropriate and distressing, consider oral atenolol 50 mg daily
- Atrial tachycardia arises from atrial myocardium – seek urgent cardiology team advice about giving beta-blockers or calcium blockers etc.
- Wolff-Parkinson-White can present as AF – QRS complexes will be pre-excited (i.e. wide and bizarre) and ventricular response very fast with a tendency to degenerate to ventricular flutter and fibrillation (VF). NEVER give digoxin/beta-blockers/amiodarone or verapamil but seek urgent advice of cardiology team with a view to restoring sinus rhythm with flecainide if patient stable or DC cardioversion if patient unstable
- Junctional re-entry tachycardia usually involves AV node in re-entry circuit and is likely to be terminated by AV nodal blockade. Unless there is a history of wheezing, give adenosine 3 mg IV over 2 sec via a large bore cannula into antecubital fossa vein with sodium chloride 0.9% flush
- NB: in patients taking dipyridamole (which decreases adenosine metabolism), initial dose of adenosine should be 1 mg IV and subsequent doses should be halved
- if no response after 1-2 min, give 6 mg IV over 2 sec. If no response after a further 1-2 min, give 12 mg IV over 2 sec
- NB: in patients taking theophylline (which antagonises the anti-arrhythmic effect of adenosine), higher doses will usually be necessary
- If not responsive, seek urgent cardiology team advice about giving verapamil 5 mg IV over 2 min (3 min if patient >65 yr), repeated if necessary at 5-10 min intervals to total 10 mg
Do not give verapamil if patient already taking a beta-blocker
- Ventricular tachycardia arises from ventricular myocardium. Haemodynamic consequences are related to ventricular rate and underlying left ventricular function
- seek urgent cardiology team advice, with a view to DC cardioversion if patient unstable or consider IV procainamide or amiodarone if patient stable
- Torsade de pointes (polymorphic VT) usually self-terminating, but often produces haemodynamic collapse - seek urgent cardiology advice
- stop any precipitating drugs (call Medicines Information)
- do not give further anti-arrhythmic drugs
- correct serum K+ to >4.5 mmol/L. Give sodium chloride 0.9%. 500 mL with potassium chloride 20 mmol IV, as commercially prepared pre-mixed bag, over 2 hr, with continuous ECG monitoring
- if not given earlier, give magnesium sulphate 2 g (equivalent to 8 mmol Mg++) made up to 50 mL with sodium chloride 0.9% by IV infusion over 10-15 min
- consider beta-blocker/pacing
- If sustained, leads to cardiac arrest and must be treated by immediate DC cardioversion (when patient unconscious)
- Seek urgent cardiology team advice to consider the following:
- if arrhythmia fails to terminate or recurs, consider and deal with possible trigger factors:
- electrolyte abnormalities (hypokalaemia, hypocalcaemia, hypomagnesaemia)
- anti-arrhythmic or anti-psychotropic drug toxicity
- underlying relative bradycardia (temporary pacing will be necessary)
- acute MI - consider urgent revascularisation by angioplasty - for recurrent episodes, try lidocaine (with ECG monitoring) by IV infusion 4 mg/min for 30 min, then 2 mg/min for 2 hr, then 1 mg/min - reduce concentration further if continued beyond 24 hr
- for electrical storm (e.g. recurrent VF), maintain plasma K+ > 4.5 mmol/L, give sodium chloride 0.9% 500 mL with potassium chloride 20 mmol IV (as commercially prepared pre-mixed bag) over 2 hr, with continuous ECG monitoring
- give IV magnesium sulphate 2 g (equivalent to 8 mmol Mg++) made up to 50 mL with sodium chloride 0.9% by IV infusion over 10-15 min, repeated once if necessary and atenolol 2.5 mg IV at rate of 1 mg/min, repeated at 5 min intervals to a maximum of 10 mg
- in peri-arrest situation, give IV amiodarone 300 mg as bolus injection
- in patients with ventricular tachycardia or VF occurring ≥48 hr after acute MI or with no obvious reversible factors, consider implantable cardioverter defibrillator
- 24-hr tape for patients with impaired LV function and IHD - if non-sustained VT present, refer to electrophysiology service for assessment for ICD implant.
- if arrhythmia fails to terminate or recurs, consider and deal with possible trigger factors:
- If intracardiac electrophysiological studies or ablation therapy contemplated, send formal referral to cardiac electrophysiology department
MANAGEMENT AFTER STABILISATION
- If recurrent arrhythmias, seek urgent advice from cardiology team
General
- After any emergency treatment to revert or stabilise a patient's heart rhythm, further assessment should include:
- accurate identification of arrhythmia - a 12-lead ECG during the arrhythmia will give the diagnosis in most cases, sometimes with the addition of specific manoeuvres, such as carotid sinus massage/adenosine, or by comparison with ECG in sinus rhythm. Electrophysiological testing may be required where there is doubt
- diagnosis of cause - ECGs in sinus rhythm, troponin T, thyroid function tests, chest X-ray
- definition of underlying heart disease - echocardiography, cardiac catheterisation where appropriate
- identification of precipitating/contributing factors - electrolytes (including Ca2+, Mg2+), ECG monitoring
- provocation testing where necessary (e.g. exercise testing, tilt testing, carotid sinus pressure, drug challenge, invasive electrophysiologic testing)
- for most patients with SVT/atrial tachycardia/atrial flutter, radiofrequency ablation - refer to cardiology SpR for out-patient review with electrophysiologists
Do not use amiodarone as a first-line agent for long-term treatment because of the risk of serious adverse effects
DISCHARGE AND FOLLOW-UP
- Refer patients with recurrent arrhythmias requiring prophylactic anti-arrhythmic treatment to a cardiologist
- Make appropriate arrangements with anticoagulation management service for follow-up of patients with AF who are anticoagulated