Let’s Talk About Code Drugs.

So you’re huffing and puffing as you finally reach the room at the very end of the hall in the remote regions of the orthopedic wing, situated just beyond the next zip code (or so it seems).  Someone yells out to you to hand them “the drugs”.  Now that all the blood flow has been redistributed to your muscles, you are tasked with composing yourself and thinking through your ACLS protocols.  This is at a time when you’re probably wishing you hadn’t just eaten that hamburger from the cafeteria while you attempt to collect your feeble and endorphin-clouded thoughts.  “Um”… you think to yourself.  Actually, you said that out loud and as everyone rushes around in fevered circles you take a deep breath and remember that awesome blog you read not too long ago.  So here you go… the skinny 411, quick and dirty run-through of the super-common meds you’ll be dolling out when the time comes!

These most common medications are arranged into class, indication, mechanism of action, dose, and adverse effect. (or you can just watch the video up top!)

ADENOSINE

  • Anti-arrhythmic
  • Used for Narrow complex Supraventricular tachycardia > 150 bpm
  • Used when Vagal maneuvers have failed (bear down, cough, carotid massage).
  • Slows conduction through the AV node.
  • 6 mg follow by 12 mg & 12 mg if unresponsive, rapid push with flush.
  • May cause flushing, chest pain, or bronchoconstriction.

Amiodarone

  • Anti-arrhythmic used to treats V-tach or V-fib that’s unresponsive to shock.
  • Used after defibrillation or cardioverson and when first line drugs like epinephrine and vasopressin have failed.
  • 300 mg IVP followed by 150 mg IVP if no conversion to Sinus Rhythm.
  • Then: 1 mg/min over 6 hours, then: 0.5 mg/min over 18 hours.
  • Should only be diluted with D5W and given with inline filter.

Atropine

  • Anticholinergic, speeds up heart.
  • Used for symptomatic bradycardia < 60 BPM with low BP, low LOC, chest pain, etc.
  • 0.5 – 1 mg every 3 – 5 minutes to total of 3 mg.
  • Transcutaneous pacing is the next intervention.

 Calcium Chloride

  • Extracellular ion
  • Used to prevent fatal arrhythmias associated with hyperkalemia and hypocalcemia. Signs include peaked T waves and widened QRS.
  • Returns resting membrane potential of myocardium closer to 0 mV which increases myocyte excitability and helps heart beat efficiently.
  • Give 1 mg slowly over 10 minutes.,
  • May cause hypotension or bradycardia.

Dobutamine

  • Inotropic agent
  • Used as a drip after filling pressure is optimized & w/ post resuscitation shock
  • Acts on Beta 1 (heart rate/contractility) & weak Beta 2 (lungs) & Alpha (vasoconstrict).
  • Increases cardiac output, BP, and heart rate while decreasing PVR.
  • 2-20 mcg/kg/min, titrate to response.
  • May cause tachycardia & increased myocardial oxygen consumption.

Dopamine

  • Inotropic agent
  • Used as drip for symptomatic bradycardia when atropine fails or post resuscitation.
  • Renal vasodilation, beta 1 adrenergic, and alpha adrenergic stimulation.
  • 10-20 mcg/kg/min, titrate to response.
  • May cause tachycardia & increases myocardial demand.

Epinephrine

  • Alpha & Beta adrenergic agonist
  • Used in pulseless arrest, bradycardia, and V-Tach/V-Fib.
  • Vasoconstricts & increases CO through increase HR, contractility, & conductivity through the AV node.
  • Given IV 1 mg every 3-5 min during arrest and V-tach & V-fib (no dose limit).
  • Given 2-10 mcg/min for bradycardia.
  • May cause increased myocardial demand.

 Magnesium Sulfate

  • Anti-arrhythmic
  • Used in Polymorphic VT or Torsade s de Pointes (lack of Mg from chronic ETOH).
  • Used to slow rate of SA node impulse.
  • 1 – 2 mg IV push
  • May cause decreased BP or build up in renal failure.

Vasopressin

  • Vasocontrictor & anti-diuretic hormone found naturally in body.
  • Used to increased blood pressure during vasodilatory shock.
  • 40 units IV push given to replace first or second dose of epinephrine.
  • May cause angina or allergic reaction.

 

A note on Vasopressin: Vasopressin has become a primary drug used during pulseless arrest. It increases blood pressure by creating moderate vasoconstriction and has been shown to be more effective than epinephrine in cardiac arrest. A major reason for vasopressin in place of epinephrine is its decreased risk for myocardial oxygen consumption and post arrest arrhythmias related to increased in heart rate and contractility (beta-1 effects). Vasopressin may also create cerebral vessel dilation thereby increasing cerebral perfusion.

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