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Antidotes for cardiovascular drug poisoning

Antidotes for cardiovascular drug poisoning. David H. Jang Assistant Professor Masters of Science Degree in Clinical Investigation (K30) Clinical and Translational Science Institute (CTSI). New York University Department of Emergency Medicine/Medical Toxicology.

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Antidotes for cardiovascular drug poisoning

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  1. Antidotes for cardiovascular drug poisoning David H. Jang Assistant Professor Masters of Science Degree in Clinical Investigation (K30) Clinical and Translational Science Institute (CTSI) New York University Department of Emergency Medicine/Medical Toxicology *Funded by the American Academy of Clinical Toxicology Junior Investigator Research Grant and also supported in part by grant 1UL1RR029893 from the National Center for Research Resources, National Institutes of Health.

  2. Case • 44 year-old man presents with a “overdose” after an argument with his mother • Patient obtained these medications from his mother who he still lives with in her basement

  3. Case • Vitals on presentation: • Blood pressure: 140/90 mmHG • Heart rate: 90 BPM • Respiratory rate: 12 • Temperature: 98.6 • Oxygen saturation: 100% RA

  4. Case 6 hours later…

  5. Case • Repeat Vitals: • Blood pressure: 85/40 mmHG • Heart rate: 40 BPM • Respiratory rate: 20 • Temperature: 98.6 • Oxygen saturation: 100% RA

  6. Intubated Hemodynamic support On norepinephrine On dopamine On epinephrine Still hypotensive… Case

  7. Options?

  8. Antidotes for cardiovascular drug poisoning

  9. Cardiovascular drug class • Antihypertensives • Imidazolines • Beta-blockers • Calcium channel blockers • ACE-Is and ARBs • Cardioactive steroids • Digoxin • Antidysrhythmics • Flecainide

  10. Cardiovascular drug class • Antihypertensives • Imidazolines • Beta-blockers • Calcium channel blockers • ACE-Is and ARBs • Cardioactive steroids • Digoxin • Antidysrhythmics • Flecainide

  11. Not all things are created equal…

  12. Beta-blockers • Non-selective • Carvedilol • B1-selective • Atenolol • Esmolol • Intrinsic sympathomimetic • Pindolol

  13. Beta-blockers • Potassium channel blockers • Sotalol • Membrane-stabilizing • Propanolol

  14. Calcium channel blockers • Phenylalkylamine • Verapamil • Benzothiazepine • Diltiazem • Dihydropyridines • Nifedipine • Amlodipine • Nicardipine

  15. Epidemiology

  16. Epidemiology

  17. Epidemiology

  18. Epidemiology

  19. Beta and calcium channel blocker poisoning • Clinical Features • Bradycardia • Hypotension • Management • Isotonic fluids • Glucagon • Inotropes/Pressors • High-insulin • Lipid emulsion

  20. Beta and calcium channel blocker poisoning • Clinical Features • Bradycardia • Hypotension • Management • Isotonic fluids • Glucagon • Inotropes/Pressors • High-insulin • Lipid emulsion

  21. Beta and calcium channel blocker poisoning • Clinical Features • Bradycardia • Hypotension • Management • Isotonic fluids • Glucagon • Inotropes/Pressors • High-insulin • Lipid emulsion

  22. High insulin-euglycemic therapy (HIE)

  23. Historical use • Glucose-insulin-potassium (GIK) • Acute myocardial infarction • Heart failure Myocardium

  24. Background • Hallmark of BB and CCB poisoning • Bradycardia • Vasodilation • Decreased contractility

  25. Background • Altered myocardial physiology • Hyperglycemia (pancreas/liver) • Altered myocardial substrate use • Inhibition of lactate oxidation

  26. Mechanism of action • Alters ions homeostasis (potassium/calcium/sodium) • Metabolic support • Increase lactate uptake • Epi and glucagon promote FFA use (increase energy)

  27. Experimental evidence

  28. Experimental evidence Groups 1. Control: (0/6) 2. Epi: (4/6)(2/4) 3. HIE: (6/6)(6/6) 4. Glucagon: (3/6)(0/3)

  29. Experimental evidence Groups 1. Control: (0/6) 2. Epi: (4/6)(2/4) 3. HIE: (6/6)(6/6) 4. Glucagon: (3/6)(0/3)

  30. Clinical experience

  31. Clinical experience

  32. Adverse events • Hypoglycemia • Hypokalemia

  33. Treatment guidelines

  34. Intralipid

  35. Background • Triglycerides and phospholipids • Primary triglycerides composed of linoleic, linolenic, and stearic acid • pH 8, isotonic, various concentrations availiable (20% is primarily used)

  36. Mechanism of action 1. Modulation of intracellular metabolism 2. Lipid sink 3. Activation of ion channels

  37. Experimental evidence

  38. Experimental evidence

  39. Clinical experience

  40. Adverse events

  41. Adverse events

  42. Treatment guidelines www.lipidrescue.org

  43. Treatment guidelines

  44. Consider HIE early for suspected CCB poisoning Consider lipid emulsion when a patient is perimortem with suspected lipid-soluble medication Summary

  45. Methylene blue (MB)

  46. Methylene blue • Sentinel node detection • Acquired methemoglobinemia • Vasodilatory shock • Anaphylaxis • Sepsis

  47. Nitric oxide synthase

  48. Physiology of vascular tone

  49. The evidence for MB

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