Tuesday, January 27, 2009

antihypertensive overdoses: how to TURN AROUND a total eclipse of the heart (click on this)



Uploaded by hushhush112



  1. Beta-Blockers.
    1. 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).
    2. 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.
    3. 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).
    4. If glucagon fails, use pressors (epinephrine) or intraaortic balloon pump. Pacers may improve HR but not BP.
    5. Use sodium bicarbonate for wide QRS due to propanolol.
    6. Use whole-bowel irrigation for extended release products.
  2. Calcium channel blockers
    1. 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).
    2. 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.
    3. Sustained release products: Start whole bowel irrigation.
    4. Treatment: Glucagon should be tried but it may not work.
    5. 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.
    6. Pressors and IV fluids are also important supportive measures.
    7. 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.
    8. Pacers, atropine, intraortic balloon pumps may also used adjunctively.
  3. Clonidine and Related Compounds
    1. Imidazolines and Tetrahydrazolines. (Ex: oxymetazoline aka afrin)
    2. 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). 
    3. Initial hypertension, very brief! May need nipride in some rare cases to combat hypotension, but expect to have late and prolonged hypotension.
    4. A longer period of hypotension, bradycardia, sedation, small pupils, hypothermia.
    5. Resemble opioid overdose, and in some cases naloxone can reverse effects.
    6. Supportive care with fluids. Pressors rarely required, but if needed use direct alpha agonist.
  4. 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.     

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