- Beta-Blockers.
- Most will cause both bradycardia and hypotension. Keep in mind that some BBs with intrinsic sympathetic activity (ISA ) can cause transient tachycardia or hypertension (ex: pindolol).
- Propanolol can cause widened QRS (due to sodium channel blockade) and coma/seizures (lipophilic; crosses into brain easily). Atenolol is renally cleared and can be dialyzed in overdose.
- Treatment of B toxicity: Glucagon. Use higher doses than typical: 5-10 mg and begin a drip if needed (use the dose required to improve BP/HR per hour).
- If glucagon fails, use pressors (epinephrine) or intraaortic balloon pump. Pacers may improve HR but not BP.
- Use sodium bicarbonate for wide QRS due to propanolol.
- Use whole-bowel irrigation for extended release products.
- Calcium channel blockers
- Similar to BB in that patients usually develop bradycardia and hypotension. CCBs tend to cause less sedation, more hyperglycemia (pancreatic ca channel blockade of insulin release).
- Some CCBs are more dangerous than others; peripherally acting cmpds (dihydropyridines e.g. nifedipine) are less cardiotoxic and cardiac output is maintained so these are less fatal than phenylalkylamines (verapamil) which is more centrally toxic.
- Sustained release products: Start whole bowel irrigation.
- Treatment: Glucagon should be tried but it may not work.
- Calcium is considered first line—use calcium chloride in a central line if available (about 12 mEq per amp); otherwise calcium gluconate (3.5 mEq per amp) in a peripheral line. Goal is to keep calcium level at or above 15.
- Pressors and IV fluids are also important supportive measures.
- New therapeutic approach: Insulin. This improves carbohydrate metabolism by the myocardium. (remember, CCBs block insulin release from the pancreas). Use high doses (1 unit/kg loading dose then 0.5-1 units/kg/hour) and maintain normoglycemia with D5 or D10 drips.
- Pacers, atropine, intraortic balloon pumps may also used adjunctively.
- Clonidine and Related Compounds
- Imidazolines and Tetrahydrazolines. (Ex: oxymetazoline aka afrin)
- Mechanism: These agents act as both imidazoline receptor agonists and central alpha-2 agonists. Imidazoline receptors have a complex interaction with opioid and catecholamine pathways centrally, which may explain the symptoms overlapping with classic "opioid" overdoses (see d and e below).
- Initial hypertension, very brief! May need nipride in some rare cases to combat hypotension, but expect to have late and prolonged hypotension.
- A longer period of hypotension, bradycardia, sedation, small pupils, hypothermia.
- Resemble opioid overdose, and in some cases naloxone can reverse effects.
- Supportive care with fluids. Pressors rarely required, but if needed use direct alpha agonist.
- ACE-inhibitors. Generally benign in isolated overdoses; treat symptoms with fluids, pressors. Narcan (naloxone) is sometimes cited as a possible antidote but lacks any credible evidence (not to mention pharmacologic explanation) supporting its use as a standard treatment. Check and correct any potassium/magnesium abnormalities; patients on chronic ACE-inhibitor therapy are prone to multifactorial renal dysfunction. Although angioedema is an incompletely understood but well-known adverse effect of ACE-inhibitor therapy, acute overdose does not confer a higher risk of developing angioedema.
Tuesday, January 27, 2009
antihypertensive overdoses: how to TURN AROUND a total eclipse of the heart (click on this)
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