Bradycardia


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If the heart rate is <60 beats/min, the patient, by definition, has a bradycardia (an arbitrary definition). Bradycardia may be transient, chronic or intermittent. A slow pulse can be physiological (in trained athletes) but may also be indicative of potentially serious cardiac disease.

Bradycardia may result from

  •  Increased vagal tone.
  •  Decreased sympathetic drive.
  •  Cardiac drug therapy is a prominent cause, e.g.
    • – -adrenergic blockers (Note: -blocker eye drops (used in treatment of glaucoma) may be systemically absorbed causing bradycardia).
    • – Digoxin (AV block).
    • – Diltiazem.
    • – Verapamil.
    • – Amiodarone (Note: may also cause iatrogenic hypothyroidism).
    • iInjudicous combinations of these drugs may lead to serious bradycardia or heart block. Consider self-accidental or deliberate self-poisoning (includes opiates).
  • Other causes
    • During normal phases of sleep.
    • After fever (typhoid).
    •  As a reflex response in hypertension (nephritis/phaeochromocytoma).
    • Complicating acute inferior myocardial infarction (usually transient).
    •  Transient—vasovagal, sick sinus syndrome.
    •  Hypothyroidism (sinus bradycardia).
    •  Increased intracranial pressure, e.g. cerebral tumour.
    •  Hypothermia (Note: myxoedema coma).
    •  Obstructive jaundice.
    •  Hyperkalaemia (severe).
    •  Phaeochromocytoma—with hypertension ( -adrenergic effect; rare—tachycardia more common).
    •  Anorexia nervosa.

A thorough history and examination is mandatory (e.g. dizzy spells, blackouts; preceding or intercurrent chest pain; headache and other causes include 4 intracranial pressure 4 ICP); cardiac amyloid, myocarditis, diphtheria, Chagas’ disease
Investigations

  •  12-lead ECG—look for junctional rhythm or heart block (1st degree,2nd degree or complete); atrial fibrillation with slow ventricular response (may be difficult to distinguish clinically from sinus bradycardia).


If there is a history of chest pain check cardiac enzymes

  •  Serum creatine kinase (if >6h of onset of MI).
  •  Serum troponin I (if >8h of onset of symptoms).
  •  Continuous monitoring of cardiac rhythm on CCU.

Further investigations will be determined by ECG and clinical features

  •  Check core temperature with low-reading thermometer (?hypothermia).
  •  J waves on ECG.
  •  U&E.
  •  TFTs (?hypothyroid).
  •  LFTs (if cholestatic jaundice).
  •  24h ECG, e.g. in suspected sick sinus syndrome.
  •  Cranial CT if 4 ICP strongly suspected, e.g. if papilloedema.

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