b-BLOCKERS

 

Etiology:

  1. OD, usually accidental, can be 2ry to non-selectives (propranolol, timolol, pindolol), selectives like b 1(metaprolol, atenolol, acebutolol, esmolol) or ,µ b1 &b2 antagonist (labetolol) or those that have ISA properties (pindolol, acebutolol).

S & S:

  1. Usually manifests the toxicity in ½ -2hrs
     
  2. AV blocks, bradycardia, ¯BP, CHF, bronchospasm
     
  3. Change in mental status, seizure

DX:

  1. History
     
  2. EKG
     
  3. SMA may show ¯ glucose and ­ K

Treatment:

  1. GI lavage and AC administration especially beneficial when long acting preparation is ingested.  If insertion of the tube causes to much gagging, avoid since this ­ the vagal  tone and worsens the bradycardia.
     
  2. If pt is asymptomatic - observe on monitored bed for amount of T ½ of  the medication
  3. If symptoms are present, medications that oppose the blockade are used. These are Atropine, Dopamine, Dobutamine, Norepinephrine.
     
  4. The medication considered to be the Antagonist is Glucagone that stimulates cAMP blocked by b-blocker. The dose is 3-10 mg IV bolus followed by 1 mg/h.

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