COCAINE

 

  1. Initially cocaine is reported to cause vagotonic effect followed by  hyperadrenergic state that manifests with sympatomimetic  S &S: tachycardia, BP, diaphoresis, mydriasis, agitation, presence of bowel sounds that distinguishes  it from anticholinergic toxidrom.
     
  2. Cocaine both  inhibits the reuptake of norepinephrine and epinephrine as well as stimulates presynaptic release of norepinephrine.

S & S:

  1. CNS : delirium, CVA, SZ
     
  2. Pulm: Bronchospasm, Alveolar hemorrhage, Hypoxia, Pneumotorax
     
  3. CV: MI, Arrhythmia, Dissection. These occur 2ry to coronary vasoconstriction, accelerated atherosclerosis, platelet aggregation, thrombi formation,O2 demand. Neither signs & symptoms, nor EKG, nor labs are 100% reliable in assessment. Duration, location, and quality of chest pain are not predictable of MI. Although most of the symptoms occur within 24 hrs, cocaine withdrawal can also be the cause of  myocardial ischemia. Other causes of  cocaine induced chest pain  must be ruled out: pntx, pneumomediastinum, PE, pericarditis, aortic dissection.
     
  4. GI : PUD, Mesenteric ischemia
     
  5. Renal: failure 2ry to rhabdomyalisis                  

DX:

  1. EKG  interpretation
    1. Cocaine induces QRS prolongation.
       
    2. 50-80%  of EKGs are abnormal and about 50% of EKGs meet thromolitic criteria despite the fact that pts do not  rule-in for MI. Abnormalities are 2ry to the fact that most of the pts are young and have frequently J point and ST elevation  caused by early repolarization. MI can be found in normal and abnormal EKG, making sensitivity of EKG < 50%.
       
  2. Cardiac  markers i.e. CPK, are frequently  ­2ry to motor activity.
     
  3. Rhabdomyalisis – increase CPK in thousands. Follow creatinine closely.

Treatment:

  1. CP/Angina/MI
    1. Benzo - this helps to  control high  BP and HR
    2. O2
       
    3. Nitro - antagonizes vasoconstriction
       
    4. Mg ++ recommended by ACLS
       
    5. ASA (with or without Heparin) - administered  to prevent further thrombosis. Yet as compared  to traditional MI, pts with cocaine abuse are prone to intracranial bleeds such as SAH.
       
    6. If pain persists after the above attempts,  blocker - phentolamine 1mg  IV is given to reverse vasoconstriction
       
    7. If tachycardia persists after above measures Ca Channel Blockers are given. Do not administer  b -blockers.
       
    8. MSO4 is also used to control pain
       
    9. Drugs to avoid: beta-blockers - these medications will  potentiate  the alfa-effect. Even Labetolol that has both anti-a and  anti-b effect, the  b- blocking effect predominatesleaving unopposed a effect.
       
  2. Arrhythmias - Most common is tachyarrhythmia  followed by VT.
      
    1. Atrial  tachycardias are treated with O2, Benzoes and CCB.
       
    2. Ventricular Tachycardia is generally   treated with Lidocaine. In case of cocaine use, both cocaine and Lidocaine share the same pharmacological  properties and can, in theory, aggravate arrhythmias. The studies so far didn't confirm and validate this theory and Lidocaine continues to be used as per standard ACLS protocol. Another medication used for VT is NaHCO3  that antagonizes  prolonged QRS/QT caused by cocaine.
                                                                                                                                                                                                                                                     
  3. Cocaine induced agitation - Commonly, agitated pts in ER are treated with Haloperidol. This, as a  Dopamine -2  receptor  blocker  will exaggerate catecolamine release, has anti-cholinergic effect and could exacerbate  arrhythmias and lower sz threshold. Thus, the treatment of choice for agitated pt on cocaine is not Haloperidol  but Benzo.
     
  4. Cocaine induced HTN - treated with Benzo, Nitroglycerin or Nitroprusside drip and Phentolamine 1 mg IV
     
  5. Other Complications -listed in  the beginning and are treated in the usual fashion.

 

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