Bradycardia

Bradycardia is strictly defined in adults as a pulse rate below 60 beats per minute. However, few individuals are symptomatic unless the heart rate is <50 and a resting bradycardia can be normal, for example in trained athletes. Absolute bradycardia is defined as below 40 beats per minute. Physiologically heart rate can vary in normal adults from 40 beats per minute up to 180 beats per minute. However a relative bradycardia may be greater than 60 beats per minute if that rate is too slow for the haemodynamic requirements of the patient.

Children tend to have a higher resting pulse rate than adults and generally the smaller they are the faster the heart rate. Hence in a neonates bradycardia may be defined as a rate below 100 beats per minute.

It is impossible to give meaningful figures on incidence and prevalence. In most young people bradycardia is physiological and represents athletic training. The incidence of pathological bradycardia rises with age as the underlying causes become more frequent.

History

• Any history of chest pain or collapse?
• Any shortness of breath on exertion? It is important to ask about exercise and tolerance of exercise. An athlete with a resting bradycardia will raise heart rate and cardiac output to meet demand. Anyone who can sustain even moderate exercise without undue distress is most unlikely to have a pathological cause.
• Is the patient aware of heart rate? Is it always slow or just at times? Are there any 'thumps' in the chest, extra or missed beats?
• Is there a history of faintness, dizziness, nausea or chronic fatigue?
• It is important to ask about medication as drugs are an important cause of bradycardia.

Examination

• Does the patient look well or are there signs of inadequate cardiac output, for example cold peripheries, peripheral cyanosis or features of congestive cardiac failure?
• Examination of JVP may reveal:
  • Elevation of the JVP in heart failure.
  • Cannon waves may be seen in complete A-V dissociation. This is an intermittent very high jugular pulse as the atrium contracts against a closed tricuspid valve.
• Careful examination of the pulse and count for at least 30 seconds (the slower the rate the longer the duration). An athlete may show sinus arrhythmia but this is rare beyond 30.
• Is there any shift in the cardiac apex?

Remember that sinus bradycardia may be physiological with a high resting vagal tone, for example in athletes and with the dive reflex in young children.

Sinus bradycardia

The causes of a pathological sinus bradycardia include:

• Drugs (negative chronotropes):
  • Beta blockers
  • Calcium channel blockers
  • Digoxin
  • Amiodarone
  • Clonidine
  • Verapamil
• Hypoxia
• Pain (may also cause tachycardia)
• Hypothyroidism
• Hypothermia
• Cushing reflex
• Bezold-Jarish reflex - parasympathetic stimulation in early inferior MI
• Pericardial tamponade
• Adrenal insufficiency
• Severe jaundice
• Pleural/peritoneal stimulation
• Rarely infection (e.g. Typhoid - relative bradycardia)
• Raised intracranial pressure

Ectopic atrial rhythm or wandering atrial pacemaker

• Ectopic atrial foci, if ≥3 foci = wandering atrial pacemaker
• Different P wave morphologies ± PR duration variations
• Not normally clinically significant

Sinoatrial (SA) block or sinus exit block

• SA node fails to produce an impulse or not conducted to atria
• ECG typically shows absent P waves with escape rhythm
  • Junctional - narrow complexes @ 45-60 bpm
  • Ventricular - wide complexes @ 30-45 bpm
• Usual causes:
  • Ischaemia
  • Hyperkalaemia
  • Excess vagal tone
  • Negative chronotropes
  Treat if symptomatic

Sick sinus syndrome

• Tachy-brady syndrome
• Causes:
  • SA & AV nodal fibrosis.
  • Ischaemia.
  • Congenital heart disease.
• ECG may show SA block, sinus or atrial bradycardia with bursts of atrial tachycardia (usually AF).
• Management:
  • Treat any symptomatic acute arrhythmia.
  • Most require permanent pacemaker for the bradycardia component ± antiarrhythmic (e.g. digoxin or verapamil) to suppress tachycardias.

AV blocks

• First degree
  • Slow AV node conduction
  • ECG: PR interval >200ms
  • All atrial impulses conducted to ventricles
  • Benign
• Second degree
  Some atrial impulses are not conducted to ventricles
  • Mobitz type I (Wenckenbach)
    • AV node conduction defect.
    • ECG: Repeated lengthening of PR until a P is not followed by a QRS complex.
    • Usually asymptomatic and treatment not required.
    • Treat if symptomatic or in context of inferior MI.
  • Mobitz Type II
    • Conduction defect below AV node.
    • Degenerative Lev or Lenegre disease.
    • ECG: constant PR with intermittent QRS absence.
    • Risk of progression to third degree block.
    • Atropine ineffective as block below AV node.
    • Permanent pacing is required if symptomatic.
  • 2:1 block
    • ECG: 2 P waves for every QRS complex.
    • May occur in digoxin toxicity or ischaemia.
    • Needs further electrophysiological tests to determine treatment.
• Third degree
  • AV dissociation.
  • Atrial impulses not conducted to ventricles.
  • ECG: Both P waves and QRS escape complexes may be present, but occur independently.
  • Treat as below - though atropine is unlikely to be effective and a permanent pacemaker will be needed.
  • Myocardial fibrosis is commonest cause.
  • Associations:
    • Inferior AMI.
    • Sick sinus syndrome.
    • Mobitz type II.
    • Second degree block plus new bundle branch or fascicular block.
• With all AV blocks additionally rule out:
  • Lyme disease.
  • Myocarditis/endocarditis.
  • SLE.

Consider:

• A 12 lead ECG will indicate the true nature of the rhythm and possibly show ischaemic changes, myocardial infarction and other conduction defects like bundle branch block.
• If the bradycardia is variable a 24 hour tape may be necessary.
• Ischaemic heart disease may require investigation.
• Electrolytes, glucose, calcium, magnesium, thyroid function tests, and toxicology to exclude causes as above.

• Rule out and treat any underlying causes of sinus bradycardia.
• Treatment indicated if significantly symptomatic (syncope, hypotension, cardiac failure).
• Diagnose and treat myocardial ischaemia.
• If symptomatic (often not until HR <40) treat as below.

• Resuscitation according to latest guidelines and ABC principles.²
• IV access with cannula insertion.
• Bloods:
  • FBC.
  • Urea and electrolytes.
  • Liver function tests including albumin and total protein.
  • Blood glucose.
  • Calcium.
  • Creatinine.
  • Troponin/CK.
  • TFT.
  • Digoxin level if appropriate.
• ECG.
• Treat underlying cause if present (cease negative chronotrope, correct electrolytes, etc.).
• Treat bradycardia only if signs & symptoms:
  • Syncope.
  • Systolic blood pressure <90mmHg.
  • Heart rate <40bpm.
  • Ventricular arrhythmias requiring suppression.
  • Heart failure.
  • Reduced consciousness or cognitive function.
• Drugs:
  • Atropine: 0.5-1.0 mg (0.02 mg/kg, minimum of 0.1 mg in child) repeated up to 2 mg
    Only useful if increase vagal tone i.e. problem above AV node.
  • Isoprenaline (isoproterenol): bolus 20-40 mcg IV, infusion 0.5 mcg/min of 2 mg/100 ml N.Saline
    Caution: As a pure beta agonist can cause beta2 vasodilatation in muscle beds leading to hypotension.
  • Adrenaline: infusion 2-10 mcg/min
    Useful if hypotension an issue. Ideally needs a central line.
  • Others:
    • Dopamine: 5-20 mcg/kg/min through central line.
    • Glucagon (beta blocker/calcium channel OD).
    • Digoxin Fab (digoxin toxicity)
• Pacing:
  • Temporary if drug therapy fails.
    • Transcutaneous.
      • Via fist or defibrillator pacing function.
      • Will normally require analgesia/sedation.
      Temporising measure before:
    • Transvenous wires inserted.
  • Permanent pacemaker.

• With excessive vagal tone it can be corrected either by ceasing the activity that caused excessive vagal tone or by giving a drug such as atropine.²
• Hypothyroidism, hypothermia, raised intracranial pressure, etc need treatment of the underlying condition.
• Infective causes usually recover spontaneously.
• Where heart block or sick sinus is the cause, implantation of pacemaker may be required.

See Resuscitation Council Website for Bradycardia Algorithm.²

Glycopyrrolate (anti-muscarinic agent) is used in anaesthesia to prevent the bradycardia induced by cholinergic drugs such as the anticholinesterases.

Heart-block was commonly known as Adams-Stokes syndrome, but was actually described by 3 observers before Adams:

• Marcus Gerbezius (1658-1718) described it first in the Appendix ad Ephemeridum Acedemiae Caesaro-Leopoldino-Carolinae Naturae Curiosum in Germania published the year after his death in 1719.
• Giovanni Battista Morgagni (1682-1771) in his monumental work, De Sedibus et Caucis Morborum (which founded the science of pathological anatomy), published when he was 80, describes cerebral gummata, mitral disease, aneurysms, acute yellow atrophy of the liver, tuberculosis of the kidneys, and gives the first clear account of heart-block.
• The first British physician to describe heart-block was Thomas Spens (1769-1842) of Edinburgh in 1793.
• Sir William Burnett (1779-1861), also an Edinburgh graduate, who rose from the rank of surgeon's mate to physician general to the navy, physician to the King, and was present at both the battles of the Nile and of Trafalgar, described a case of epilepsy, attended with remarkable slowness of the pulse, in 1824, though it was not published until 1827.
• Robert Adams (1791-1875) classic account appeared in 1827, and that of William Stokes (1804-1878) (who published the first treatise in the English language: "Treatise on the use of the stethoscope" in 1825) in 1846.