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




ACLS : Transcutaneous Pacing

6 02 2021

Pacing 101.

  1. Sedation and analgesia.
    My personal preference is a combination of fentanyl and midazolam. If your patient is awake – briefly explain the procedure to them and get their consent if possible.
  2. Use the pads.
    The paddles are going to be harder to hold. Make sure that the pads and the 3 leads are via the same machine. If your bay/bed has a monitor + defibrillator and you separate the monitoring and pacing – it won’t work. Also prep the chest for appropriate contact – clip excess hair (avoid shaving), wipe off excess fluids, move jewelry aside, keep medical devices away and remove any drug patches. Anterior Posterior position is preferred.
  3. Switch to pacing mode and choose fixed.
    I cannot find any sources mentioning which mode is superior. Demand mode is useful if the patient has an intermittent perfusing rhythm, in the ED we often just use fixed mode. The pacing mode is also sensitive to good sensing eg if there’s artifacts because of poor contact with the pads, this might go haywire.
  4. Set a rate.
    I like to use 60-80bpm.
  5. Set an output.
    The sicker your patient, the higher you want to start, you can do 70-80 mA and adjust accordingly. Aim to be 10-20 mA above the minimum to maintain that pacing (eg if the patient moves and there’s poor contact etc)
  6. Check for capture.
    This should be both electrical (a pacing spike is consistently followed by a waveform) as well as mechanical (a consistent pulse is felt – preferably distally to avoid the confusion from the muscle twitch, as well as an improvement in the hemodynamics)
  7. Call your friendly cardiologist.
    The patient may need to be on transvenous pacing, an urgent angiography / angioplasty or even a permanent pacemaker. Most of these patients need to be in a cardio High Dependency or Intensive Care Unit anyway.

Further Reading :

Physio-Control Manual on Non-invasive Pacing

Internet Book of Critical Care – Bradycardia