Mechanism of Action

    Inhibits the production of certain prostaglandins, whichaccounts for its antiplatelet, anti-inflammatory, antipyretic,and analgesic actions. Aspirin inhibits plateletaggregation for the life of the platelet (7-10 days)
    Decreases impulse formation in the SA node, conductionthrough the AV node, and depresses left ventricularfunction. Thus, it depresses AV node and sinus nodeactivity and interferes with reentrant pathways, as well asaccessory bypass tracts, that cause SVT
  3. midaz, loraz, diaz
    Enhances action of GABA, an inhibitory neurotransmitter; Inhibits spread of electrical activity fromirritable focus during seizures, calms CNS. Also a musclerelaxant
    Diltiazem interferes with the entry influx of calcium intocardiac and vascular smooth muscle. In addition it slowsthe rate of the SA node and conduction velocity throughthe AV node. Diltiazem’s ability to relax coronaryarteries, as well as its negative inotropic and negativechronotropic qualities makes it a useful antianginal. It isalso used as an antihypertensive. However in theprehospital setting, we use it primarily as anantidysrhythmic so its ability to slow the conductionthrough the AV node is most pertinent.
    Dopamine stimulates alpha (α), beta-1 (β1), anddopaminergic receptors. It also acts indirectly bycausing release of norepinephrine from storage sites inthe sympathetic nerve endings. The effects ofdopamine are dose related. At low doses, β1 anddopaminergic receptors are stimulated. At high dosesalpha effects predominate
  6. EPINEPHRINE (1:1000, 1:10,000, RACEMIC)
    Epinephrine stimulates alpha (α) and beta (β)adrenergic receptors. Because of these effects the drugcauses: peripheral vasoconstriction (α); increasedinotropic, chronotropic, and dromotropic responses (β1);and bronchodilation (β2). Inhibits mast cell degranulation
  7. Insulin
    Promotes storage of glucose as glycogen, increasesprotein and fat synthesis, and inhibits the breakdown ofglycogen, protein, and fat. All types of insulin have thesame effect in the body. The differences lie in the onset,duration, concentration, source, and purity. Alsostimulates cellular uptake of potassium.
  8. LIDOCAINE (VISCOUS, 2%, 20%)
    As an antidysrhythmic, lidocaine suppresses automaticity, excitability, and spontaneous depolarization of the ventricles. As an anesthetic,lidocaine produces local anesthesia by inhibitingtransport of ions across neuronal membranes,preventing initiation and conduction of normal nerveimpulses
  9. Morphine
    Combines with opioid receptors in the brain. Peripheralvasodilation of veins and arteries resulting in enhancedcardiac function (not usually altering heart rate or bloodpressure at usual doses)
  10. Narcan
    Competitively displace opioid analgesics from theirreceptor sites, reversing their effects. Respiratorydepression, sedation, papillary miosis, and euphoriceffects will be reversed
  11. Nitro
    Causes vasodilation that reduces preload, reducingcardiac workload and myocardial oxygen demand.Dilates coronary arteries, resulting in improved perfusionto ischemic myocardium. Relief of ischemia alleviateschest pain.
  12. Sodium Bicarb
    When disassociated, bicarbonate binds with hydrogenion to decrease metabolic acidosis (mass action effect).When administered for TCA overdose, acts as adysrhythmic. Decreases the effects of hyperkalemia byshifting potassium into cells
  13. Succinylcholine
    Combines with cholinergic receptors in motor nerves tocause depolarization. Neuromuscular transmission isinhibited, causing temporary skeletal paralysis, untilsuccinylcholine is metabolized and cells becomerepolarized
  14. Vasopressin
    In high doses, vasopressin acts as a non-adrenergicperipheral vasoconstrictor. When given during CPR,vasopressin increases coronary perfusion pressure, vitalorgan blood flow, decreases defibrillation threshold
  15. Amiodarone
    Antidysrhythmic blocking sodium, potassium, andcalcium channels. It is also a weak, noncompetitive,alpha and beta blocking agent
  16. Atropine
    Atropine blocks the action of acetylcholine (ACh) at the post ganglionic receptor sites located in smooth muscle,secretory glands, the CNS, the SA and AV nodes, andcardiac muscle. Atropine’s effect is opposite that of theparasympathetic nervous system when stimulated.Actions of the drug can be dose dependant: low dosesdecrease sweating, salivation, respiratory secretions, andcause bronchodilation; intermediate doses cause pupildilation, loss of visual accommodation, an increase inheart rate, conduction velocity, and inotropy; and largedoses decrease GI secretions, and the motility of the GIand GU tracts
Card Set
Mechanism of Action
Mechanism of Action