ACLS : Bradycardia Differentials

5 04 2021

Differentials for Bradycardia

I am a little biased towards figuring out if the patient had a STEMI or if they are hyperkalemic because those are likely to be immediately life threatening and have drastically different management. Trying to manage Hyperkalemia induced bradycardia with ACLS drugs is not so effective. Hence my most high yield bedside investigations are an Electrocardiogram and point of care potassium (draw carefully to avoid hemolysis)

  1. Cardiac – Sinus node or AV node dysfunction from various etiologies (including STEMI, myocarditis, post-surgery)
  2. Hyperkalemia – most often in ESRF with missed dialysis, but also in acutely ill patients (eg severe dehydration, shock with Acute Kidney Injury)
  3. Drugs – multitude of drugs especially cardiac ones such as beta blockers, Calcium channel blockers, Digoxin, Opioids, Sodium channel blockers. Consider illict drugs and poisonings such as Organophosphate
  4. Neurological causes – raised intracranial pressure (evolving towards a Cushing’s Triad), Neurogenic Shock (taking out the sympathetic drive)
  5. Others – Hypothyroidism, Hypothermia, Hypoxia
  6. Infectious diseases – typhoid etc (not common in Singapore) especially if disproportionate to fever
  7. Periarrest – any critically ill patient can decompensate and become suddenly bradycardic.

Some other causes to consider

  1. Conditioning – athletes with high vagal tone, many know their resting heart rates
  2. Vagal response – to pain, emotional distress – recovers within minutes

Always consider and investigate the most critical causes first before suggesting a benign cause.

References

  1. emDOCS – An Approach to Bradycardia in the Emergency Department
  2. Circulation – Part 7.3: Management of Symptomatic Bradycardia and Tachycardia