Fairly niche but important area of interest.

Receptor binding cannot be reversed acutely in either beta blocker or calcium channel blocker overdose the acute myocardial depression reversal relies on myocytes accessing fuel sources.

In drug induced shock states – cardiac myocytes switch energy source preferentially frmo fatty acid to carbohydrate.

Metabolic starvation is exacerbated in Ca channel overdose due to calcium channel mediated insulin release suppression.

Supranormal levels of glucagon and insulin can provide an energy source to allow optimal contractility.

Glucagon mediates a positive inotropic effect at cellular level by increasing cytosolic levels of adenylate cyclase. True efficacy of this is not clearly proven in modern studies as initial reports used bovine glucagon which may have also contained insulin.

Insulin may be the main positive inotropic agent of choice.

Use of vasoactive agents may have limited efficacy – receptor blockade may mean primarily achieving vasoconstriction without inotropy which will further impact cardiac output.

Consider:

  • Activated charcoal early.
  • Haemodialysis.
  • Intravenous fat emulsion infusion.
  • Glucagon/insulin and dextrose infusion.

If contractility impaired:

  • Fluid optimisation.
  • Positive inotropic support.

Heart rate impaired:

  • Positive chronotropic agents.
  • Pacing.

No improvement:

  • Consider mechanical support.

Echo features will often demonstrate – non dilated, severely impaired left ventricule with dilated, impaired right ventricle. Signs of venous congestion.

Serial echos will be important to assess response to treatment.