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* myocardial infarction
 #132848  
  saonew - 10/27/06 11:06
 
  Following a myocardial infarction, a 52-year-old man develops a life-threatening ventricular arrhythmia and is treated with IV lidocaine. The patient is then switched to an oral agent with a mechanism of action similar to that of lidocaine. Which of the following agents was most likely prescribed? A. Esmolol
B. Diltiazem
C. Disopyramide
D. Mexiletine
E. Procainamide
 
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* Re:myocardial infarction
#530851
  step1_ca - 10/27/06 11:08
 
  dd  
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* Re:myocardial infarction
#530855
  cd45 - 10/27/06 11:09
 
  d??  
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* Re:myocardial infarction
#530857
  vl2ss - 10/27/06 11:09
 
  EE  
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* Re:myocardial infarction
#530860
  vl2ss - 10/27/06 11:10
 
  sorry DD  
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* Re:myocardial infarction
#530862
  saonew - 10/27/06 11:11
 
  The correct answer is D. This classic drug response, called epinephrine reversal, is a favorite on the USMLE and in pharmacology classes. Epinephrine, a nonselective alpha and beta adrenergic agonist, increases blood pressure. The unknown drug is an alpha adrenergic antagonist, such as phentolamine, which blocks epinephrine's vasoconstrictive action on arterioles. Subsequent administration of epinephrine produces only beta receptor stimulation, causing vasodilation in skeletal muscle, leading to a decrease in blood pressure. Epinephrine, for all practical purposes, now acts like the nonspecific beta agonist, isoproterenol. This effect is called epinephrine reversal because of the fact that epinephrine originally increases BP and then produces the opposite effect after phentolamine administration.
An acetylcholinesterase inhibitor (choice A) should not affect the subsequent administration of epinephrine.

A nicotinic ganglionic blocker (choice B) may prevent a potential decrease in heart rate due to baroreceptor reflexes, but epinephrine would still cause an increase in blood pressure because its access to end organ receptors would be unaltered.

A nonselective alpha agonist (choice C) might not affect a second administration of epinephrine fifteen minutes later because the agonist effect would probably be gone. But, if there was still some agonist on board at the time of the second administration, it would only serve to enhance epinephrine's increase in blood pressure.

A nonselective beta receptor antagonist (choice E) would enhance epinephrine's increase in blood pressure. After administration of a beta antagonist such as propranolol, epinephrine would only produce alpha receptor stimulation. This would increase blood pressure to a greater extent than epinephrine alone.

 
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* Re:myocardial infarction
#530865
  vl2ss - 10/27/06 11:12
 
  hey got the wrong explanation dude!!  
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* Re:myocardial infarction
#530869
  saonew - 10/27/06 11:13
 
  hhhahaaa u right i am sleepy  
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* Re:myocardial infarction
#530871
  saonew - 10/27/06 11:13
 
  The correct answer is D. Lidocaine is a class IB antiarrhythmic indicated for the treatment of ventricular tachycardia. This agent blocks sodium channels and shortens the action potential duration. Both mexiletine and tocainide are classified as class IB antiarrhythmic agents that shorten the action potential duration and refractory period and improve the resting potential duration. These agents produce a modest suppression of sinus node automaticity, as well as AV node conduction.
Esmolol (choice A) is a class II antiarrhythmic agent that exerts its action as an ultrashort-acting beta-1 adrenergic blocking agent with cardioselective properties.

Diltiazem (choice B) and verapamil are calcium channel blocking agents and class IV antiarrhythmic agents. As antiarrhythmics, these agents decrease and slow SA and AV node conduction.

Both disopyramide (choice C) and procainamide (choice E) are class IA antiarrhythmics. They decrease myocardial excitability, conduction velocity, contractility, and automaticity. They also prolong the effective refractory period and block vagal stimulation of the AV node.

 
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