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CDHB

Cardiac Arrhythmias

Note: Inappropriate treatment of arrhythmias can be rapidly fatal. Whenever possible, seek expert advice.

Classification

• Ectopic activity (atrial and ventricular).
• Heart block.
• Bradyarrhythmias.
• Supraventricular tachycardias.
• Ventricular tachycardias.

Aetiology

• Common in the presence of structural cardiac disease, especially after acute myocardial infarction.
• Electrolyte imbalances (especially hypokalaemia) and acid/base imbalance may initiate and/or perpetuate the arrhythmia and these should be corrected.
• Drugs including tricyclics, phenothiazines, theophylline, digoxin and some anti-arrhythmics.
• Hyperthyroidism.

Clinical features

• Check pulse at apex and wrist, blood pressure, tissue perfusion.
• If there is evidence of hypotension or heart failure due to arrhythmia, urgent treatment is required.

Investigations

• ECG - 12 lead and rhythm strip with the best P wave. If bizarre/wide QRS complexes then check speed of paper.

  Note: Artefact may mimic some arrhythmias.

• Check for abnormalities of potassium, magnesium, calcium; acidosis and hypoxia. Metabolic factors may contribute to the initiation/perpetuation of the arrhythmia.
• Thyroid function tests. Subclinical or overt hyperthyroidism increases the risk of heart failure.

Management

Ectopic Activity

• Atrial ectopics - often normal, benign. Look for atrial beat (may deform preceding T wave) when diagnosing "extrasystole". Does not require treatment.
• Ventricular ectopics - common, usually benign. May be confused with aberrant atrial ectopics. Treatment usually not required.

Heart Block

• Prolonged PR Interval:
  • 1^st degree block does not require treatment. Monitor closely in anterior infarcts. Doses of beta-blockers, calcium antagonists and digoxin should be reviewed.
  • 2^nd degree block:
    • Type I, a progressive increase in PR interval until beat is dropped. May be observed in inferior infarcts but is more serious in anterior infarcts.
    • Type II, PR interval normal or increased but beats lost in unpredictable fashion. Indicates disease in or below the bundle of His. This may progress to complete heart block and a very slow ventricular escape rhythm; consider pacing.
• Bifascicular block (bundle branch block + hemi block) - stable asymptomatic bifascicular block does not require pacing. However, following anterior myocardial infarction it may progress to complete heart block.
• Complete heart block requires monitoring. If stable with regular ventricular escape rhythm and satisfactory blood pressure, may be observed overnight. Be prepared to use isoprenaline (isoprenaline dosing instructions below) to maintain rate if atropine alone is not effective. Discuss with Cardiologist. A temporary pacemaker may be required if there is recurrent syncope, nonsustained ventricular tachycardia, severe bradycardia (<30/min) or cardiovascular compromise.
• Symptomatic A-V block not associated with infarction usually merits placement of a permanent rather than temporary pacemaker.

Bradyarrhythmias

• Sinus Bradycardia - check for excessive beta-blockade. Common after myocardial infarction. Treat with atropine 0.6 mg IV if symptomatic or hypotensive. Smaller additional doses of 0.3 mg may be required. Total dose of 2 mg before atropine side effects occur. Isoprenaline may also be used. Place 2 mg in 500 mL 5% glucose (= 4 microgram/mL) and start at 1 mL (4 microgram) per minute but then run as slowly as possible (0.5-10 microgram/min) to keep heart rate >60.
• Sinus Arrest - common in inferior infarction and usually benign, as nodal escape rhythm maintains adequate heart rate. It may require treatment with atropine or isoprenaline but rarely needs pacing. When sinus arrest is not associated with infarction, it is usually due to the sick sinus syndrome and requires permanent pacing if symptomatic. Temporary pacing rarely required.

Note: Sinus arrest is common in vasovagal syncope. These patients only have bradycardia at the time of symptoms. They can usually be managed medically and pacing is only infrequently required.

Note: Inferior infarcts are associated with a wide range of rhythms which rarely have much adverse effect on myocardial performance. A-V block is common. These arrhythmias are generally not treated vigorously apart from ventricular tachycardia and fibrillation. If they are persistent and cardiac function is impaired, treatment is indicated.

Supraventricular Tachycardia

• Always perform a 12 lead ECG.
• Sinus - slow onset, rate usually below 150/min, slows gradually with carotid sinus massage. Does not require treatment itself but requires an explanation as to its cause (e.g., LVF, anxiety, pain, hyperthyroidism, infection, hypoxia).
• Paroxysmal tachycardia - sudden onset, rate usually >150/minute. Carotid sinus massage causes either no response or reversion to normal or increased AV block. Atrial flutter usually gives a ventricular rate of approximately 150/min (2:1 block) and may be misdiagnosed as another SVT. If not distressed and not in failure and history of short-lived attacks either:
  • Do nothing, or
  • Valsalva manoeuvre (supine)
  • Dive reflex - face into iced water

  Monitor the effect of these manoeuvres with ECG, as they may induce 2:1 block.

• Adenosine given as a rapid bolus IV into a large vein, in increasing doses 6 mg, then 12 mg, then 18 mg, in stepwise fashion at 2 minute intervals. Flush rapidly with 10 to 20 mL saline. Effective for AV nodal re-entrant tachycardia but will not revert atrial flutter. Contraindicated with severe asthma.
• If unsuccessful and not on beta-blockers:
  • Verapamil 5 mg IV by slow bolus (5 minutes) followed by 1 mg/min to a total of 15 mg. ECG monitoring required, measuring BP and with resuscitation equipment nearby as asystole may result.

    Note: Verapamil should never be used for a broad complex tachycardia as this may be ventricular tachycardia. It has considerable negative inotropic effects and should not be used in the presence of ventricular dysfunction or hypotension.

• If on beta-blockers and no structural cardiac disease present give flecainide 2 mg/kg (max 150 mg) diluted in 20 mL 5% glucose over 10 minutes IV (telemetry required) or consider further beta-blockade (make sure patient is not asthmatic).
• If unsuccessful or if the patient is hypotensive, proceed to cardioversion. The patient should be managed in the resuscitation room of the Emergency Department, CCU or ICU. An experienced doctor with anaesthetic skills should be present.

  When anaesthetized, start with 100 joules, then 200 joules, then 360 joules. Do not shock more than twice with 360 joules - consult with Cardiologist.

• Atrial Flutter - This rhythm is often mislabelled as paroxysmal atrial tachycardia because carotid sinus massage or adenosine therapy has not been performed to increase AV block, decrease ventricular rate and demonstrate flutter waves. If compromised, cardiovert as for paroxysmal tachycardia. If not compromised, control rate with digoxin (see below) or beta-blocker or calcium channel blocker using oral protocol given below. If spontaneous reversion to sinus rhythm does not occur within 24 hours, the patient should be considered for cardioversion.
• Atrial Fibrillation - New onset atrial fibrillation with rapid ventricular rate:
  • CBC + diff, creatinine, Na, K, Mg, thyroid function tests.
  • Control rate with either digoxin, calcium channel blocker, beta-blocker.
  • Digoxin - loading dose:
    • Give 0.5 mg digoxin initially (IV if in heart failure or nauseated).
    • Give further 0.25 mg increments every 4 hours to complete a loading dose of 1 mg. Elderly and renally impaired patients are prone to toxicity and may only require a total loading dose of 0.75 mg. Some younger patients may require a further two 0.25 mg increments to give a total loading dose of 1.5 mg. Assess clinically before giving each increment. Do not give a loading dose if recently on digoxin.
  • Other options include:
    • Intravenous beta-blocker (not if already on a calcium antagonist).
    • Oral beta-blocker (e.g., metoprolol; start with 47.5 mg daily, maximum dose 190 mg/day).
    • Oral calcium antagonist (diltiazem 60 mg TDS, verapamil 80 mg TDS).
    • Most patients with recent onset atrial fibrillation will revert to sinus rhythm within 24 hours. Chemical cardioversion may be attempted in patients with structurally normal hearts (not in patients >70 years). Discuss with Cardiologist.
  • Heparin:
    • All patients with atrial fibrillation or flutter should be treated with LMWH, initial dose of enoxaparin is 1 mg/kg subcut q12h. The usual duration of enoxaparin treatment is 48 hours. The dosage of LMWH will need to be reduced if there is significant renal impairment (CrCl <60 mL/min) or for extremes of weight. See the VTE section.
    • Anti-Xa monitoring is recommended if the duration of LMWH therapy is >48 hours. Treatment for longer than 48 hours is associated with an increased risk of haemorrhagic complications and would normally only be considered in patients with ongoing unstable ischaemic symptoms, following discussion with the Consultant, and with intensified monitoring for haemorrhagic complications.
    • Oral anticoagulants may not be required if heparin started within 12 to 24 hours of onset of atrial fibrillation and sinus rhythm achieved within 48 hours and there is no left atrial enlargement or major mitral valve abnormality. Heparin may be stopped at 48 hours under these circumstances. Otherwise start warfarin or dabigatran. Seek advice.
  • Emergency electrical cardioversion:
    • Indicated if there is cardiac compromise with hypotension, angina or persistent atrial fibrillation. Consult Cardiologist.
• Chronic atrial fibrillation on digoxin with rapid ventricular rate:
  • Exclude aggravating causes (ischaemia, heart failure, volume depletion, infection, alcohol).
  • Check digoxin concentration.
  • Add oral beta-blocker or calcium antagonist as above.
  • Add aspirin if heart structurally normal on echocardiogram.
  • Consider warfarin or dabigatran if left atrium dilated or mitral valve abnormal, or age >65 years, previous embolic event, heart failure, hypertension.

Ventricular Arrhythmias

• Idioventricular (rate <100/min) - this is common after myocardial infarction and no treatment is required.
• Ventricular Tachycardia (VT) - may be confused with SVT when aberrant AV conduction causes broad QRS complexes. Cannon waves and a variable first sound are suggestive of ventricular tachycardia. ECG diagnosis depends on P waves, and these are best seen in II, V1, or V2. P waves independent of ventricular rate or fusion beats are diagnostic. Remember VT may be prolonged and not associated with collapse. Treatment is by cardioversion. Unless an emergency, this should be undertaken in CCU or ICU. In an emergency situation proceed to 200-360 joule shock. If in doubt assume that all regular, broad complex tachycardias are VT. Treatment of choice is cardioversion.
• QT prolongation and torsades de pointes VT
  • Acquired long QT: Generally, QT prolongation is acquired and is associated with bradycardias, myocardial ischaemia, metabolic disturbances or drugs. Causes of acquired QT prolongation include:

    Drug causes include:

    • Antihistamines.
    • Antiarrhythmics (Class 1: quinidine, flecainide, disopyramide and Class 3: amiodarone, sotalol).
    • Psychoactive drugs (lithium, tricyclics, haloperidol, phenothiazines).

      Note: Drug Interactions: The following may increase the concentration of the above drugs. Fluconazole, grapefruit juice, metronidazole, macrolides, SSRIs, diltiazem and many others.

    Other factors:

    • Myocardial ischaemia.
    • Bradycardia.
    • Low potassium.
    • Low magnesium.

    Check for possible causes and withhold any drugs that may be potentially responsible. Correct all metabolic disturbances and treat ischaemia.

  • Congenital long QT - Usually presents in patients younger than 40 years with syncope.
    • Withhold all QT lengthening drugs.
    • Check and correct any metabolic disturbances.
    • Beta-blockers may help suppress recurrent episodes.
    • Refer to Cardiologist for long term management.

      Note: Refer to the CDHB Clinical Pharmacology bulletin on Drug-Induced QT Interval Prolongation.

• Torsades de pointes - This polymorphic ventricular tachycardia is due to QT prolongation, either congenital or acquired. It may revert spontaneously, otherwise it may require immediate cardioversion. See also Investigations for Poisoning/Drug Overdose.

  If recurrent, IV magnesium may be tried, but consult Cardiologist. Temporary pacing at 90 beats/minute may suppress this arrhythmia.

• Ventricular Fibrillation (VF) - D.C. shock.
• Amiodarone - Intravenous amiodarone is useful though slow acting in the treatment of atrial and ventricular arrhythmias. However, potentially important side effects may occur with long term therapy.

  Amiodarone has less effect on myocardial contractility than other anti-arrhythmics. Therefore, intravenous amiodarone may be the treatment of choice for arrhythmias if there is known severe left ventricular impairment or concurrent left ventricular failure. Give 5 mg/kg (or 150 mg to 300 mg) dissolved in 250 mL of 5% glucose over 30 to 60 minutes intravenously. Continue with 10 mg/kg over 24 hours as two successive 12 hour infusions as amiodarone is unstable in solution. Can give up to 1200 mg in 24 hours.

  Because of risk of chemical thrombophlebitis, amiodarone should be given into a proximal arm vein. Consider a PICC central venous line if planning to give more than 24 hours intravenous infusion.

  Patients receiving intravenous amiodarone should be on continuous ECG monitoring.

• Recurrent Ventricular Tachycardia/Fibrillation in a patient with implantable defibrillator ("arrhythmic storm").
  • This is a medical emergency.
  • The patients are often distressed by multiple shocks and will benefit from sedation.
  • If the shocks are inappropriate, the implantable defibrillator can have the shocks disabled by placing a magnet over the device.
  • Consult Cardiology immediately and arrange early transfer to CCU.
  • Look for exacerbating causes for arrhythmias, and correct if present.

Topic Code: 1329