Sympatholytic toxidrome

AGENTS

  • beta-blocker (BB)
  • ca2+ blocker (CCB)
  • clonidine
  • digoxin
  • true sympatholytic agents (e.g. alpha-blockers like phentolamine, and vasodilatory agents such as GTN, SNP, etc)

CLINICAL FEATURES

CCBs and BBs

  • CVS: bradycardia, hypotension, AV block, heart failure
  • CNS: lethargy, confusion, seizures, coma (generally secondary to the CVS effects)

Digoxin is also characterised by increased automaticity (e.g. PVCs, PACs and other dysrhythmias)

Propanolol causes sodium channel blockade as well as B-blocker effects

True sympatholytic agents present with vasodilation, hypotension, reflex tachycardia +/- evidence of poor perfusion

INVESTIGATIONS

– ECG: bradycardia, PR, QRS, QT prolongation, heart blocks, asystole.

SPECIFIC MANAGEMENT AND TRIGGERS FOR INTERVENTION

Decontamination

  • decontamination with activated charcoal and whole bowel irrigation (if risk assessment is for severe toxicity from a sustained release agent  before toxicity is apparent)
  • charcoal haemoperfusion in verapamil OD?

Ca2+ channel blockers and beta-blockers

  • Ca2+ chloride 1-3g -> 2-6g/hr (maintain ionized Ca2+ between 2-3mmol/L)
  • glucagon 5-10mg bolus -> 2-5mg/hr (traditional treatment, but not as useful as HIET)
  • atropine
  • vasopressors and inotropes:
    – isoprenaline 2mcg/min
    – adrenaline 0.1-1mcg/kg/min
    – noradrenaline 0.1-1mcg/kg/min
    – milrinone
    – levosimendan
  • pacing to achieve ventricular capture @ 50-80/min (often ineffective)
  • high-dose insulin euglycaemic therapy (MAINSTAY of modern therapy, start early)
  • lipid emulsion: may bind calcium channel blockers in plasma and prevent myocardial penetration
  • extracorporeal support – intra-aortic balloon pump, VA ECMO or cardiopulmonary bypass

Digoxin

  • digi-bind

Clonidine

  • supportive care (especially respiratory support)
  • IV fluids
  • rarely are vasopressors required
  • trial naloxone (controlversial: may need high doses and has inconsistent effects)

Propanolol

  • NaHCO3

True sympatholytics

  • supportive care
  • IV fluids
  • vasopressors if hypoperfusion: noradrenaline
  • correct Ca
  • treat CN toxicity from SNP

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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