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49 Cards in this Set
- Front
- Back
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Bumex |
Pharmacological properties/ action(s): Sulfonamide derivative structurally related to Furosemide with similar effects. Has faster rate of onset than Furosemide 40 times greater potency but shorter duration Produces only mild hypotension IV onset is rapid; peak effect in 15-30 minutes; duration is 3.5-4.0 hours Half Life is 60-90 minutes
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Tagament
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Pharmacologic properties/ action(s): Histamine H2 -receptor antagonist Cimetidine (Tagamet) competitively inhibits the action of histamine at the histamine H2-receptors.This antihistamine property functions to inhibit gastric acid secretion, and to inhibit the action of histamine from contributing to anaphylactoid reactions and/or anaphylaxis.
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Valium
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Pharmacologic action(s): Sedative-hypnotic; Anti-convulsant; anti-anxiety; Benzodiazepine Unknown exact mechanism
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Romazicon
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Pharmacologic properties/ action(s): Flumazenil, an imidazobenzodiazepine derivative, antagonizes the actions of benzodiazepines on the central nervous system. Flumazenil competitively inhibits the activity at the benzodiazepine recognition site on the GABA / benzodiazepine receptor complex. Flumazenil is a weak partial agonist in some animal models of activity, but has little or no agonist activity in humans. Flumazenil does not antagonize all of the central nervous system effects of drugs affecting GABA-ergic neurons by means other than the benzodiazepine receptor (including ethanol, barbiturates, or general anesthetics) and does not reverse the effects of opioids.
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Ativan
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Pharmacologic properties/ action(s): Lorazepam is a benzodiazepine family, and as such is a sedative, hypnotic. Lorazepam depresses the limbic system, thalamus, and hypothalamus resulting in calming effects. Lorazepam produces an amnesic effect and is also a muscle relaxant.
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Solumedrol
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Pharmacologic properties/ action(s): Methylprednisolone is a steroid. It has potent anti-inflammatory properties. The onset of action is several hours
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Phenergan
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Pharmacologic action: Blocks cholinergic receptors in the vomiting center, which may mediate nausea and vomiting; competes with histamine for the H1 receptor site. Blocks the effects of the hormone serotonin at the 5-HT3 -receptor sites (located in the vagal nerve terminals) that cause vomiting.
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Haldol
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Pharmacologic properties/ action(s): Antipsychotic agent or major tranquilizer (of the butyrophenone class). May block dopamine receptors in CNS, but exact mechanism has not been clearly established. It acts to have a profound calming effect on patients.
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Zofran
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Pharmacologic action: Ondansetron hydrochloride (HCl) is a selective blocking agent of the serotonin 5-HT 3 receptor type.
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Lasix
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Pharmacologic properties/ action(s): Furosemide is a potent loop diuretic. Lasix is sulfonamide derivative which inhibits the reabsorption of sodium and chloride in the proximal and distal renal tubules, as well as in the ascending loop of Henle. With IV administration, onset of diuresis is within 5 minutes; peaks in 30 minutes; and has a duration of 2 hours. |
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Vasopressin
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The naturally occurring antidiuretic hormone. Acts as a non-adrenergic peripheral vasoconstrictor. Acts by direct stimulation of smooth muscle V1 receptors (causes pallor of the skin, nausea, intestinal cramps, bronchial constriction, uterine contractions, and vasoconstriction). Half life is 10 – 20 minutes Increases coronary perfusion pressure, vital organ blood flow, and cerebral oxygen delivery V1 receptor interaction during CPR causes intense peripheral vasoconstriction, with less coronary and renal vasoconstriction, and cerebral vasodilatation
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Atropine
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Atropine is a potent antimuscinaric parasympatholytic It reduces vagal tone, increases automaticity of the SA node and increases AV conductions, thus increasing heart rate.
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Cardizem
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Calcium channel blocking agent Slows AV nodal conduction Increases AV nodal refractoriness Diltiazem inhibits the influx of calcium ions during membrane depolarization of cardiac and vascular smooth muscle, i.e. it slows AV nodal conduction time and prolongs AV nodal refractoriness. Diltiazem slows the ventricular rate in patients with a rapid ventricular response during atrial fibrillation or atrial flutter, converts PSVT to NSR and decreases total peripheral resistance in both SBP and DBP. Diltiazem is a negative inotropic agent (less potent than verapamil) and causes a reduction in myocardial oxygen consumption.
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Lidocaine
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Lidocaine is a class Ib antiarrhythmic agent. It blocks fast Na+ channels within the myocardium decreasing the slope of phase 0 of cardiac depolarization. Decreases ventricular automaticity and raises the ventricular fibrillation threshold. Lidocaine also blunts the rise in intracranial pressure resulting from laryngoscopy.
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Nitroglycerin
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Nitroglycerin causes relaxation of vascular smooth muscle. Nitroglycerin is a direct vasodilator which acts primarily on the venous system, although it also produces direct coronary artery vasodilatation as a result. There is a decrease in venous return which decreases the workload on the heart and thus, decreases myocardial oxygen demand. Sublingual Nitroglycerin spray is preferred as it is more reliably absorbed and bio-available.
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Sodium Bicarb
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Sodium bicarbonate is an endogenous anion that reacts with hydrogen ions to form water and carbon dioxide to buffer metabolic acidosis. An alkalizing agent used to buffer acids present in the body during and after severe hypoxia. Its effect is to raise the serum pH. This effect is favorable in the treatment of pre-existing metabolic acidosis, hyperkalemia, tricyclic anti-depressant/salicylate (aspirin)/or phenobarbital overdose. Sodium bicarbonate is effective only when administered with adequate ventilation and oxygenation.
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Epinephrine
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Epinephrine hydrochloride stimulates Alpha and Beta receptors. Effects include bronchodilation, increase in heart rate, increase in contractility, and increase in systemic vascular resistance.
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Dopamine
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Dopamine is a catecholamine. Dopamine stimulates dopaminergic, beta-adrenergic and alpha-adrenergic receptors of the nervous system. It exerts an inotropic effect on the myocardium resulting in an increased cardiac output. Dopamine produces less increase in myocardial oxygen consumption than does isoproterenol and its use is usually not associated with a tachyarrhythmia. Dopamine dilates renal and mesenteric blood vessels at low doses, renal dose, (1-2 mcg/kg/min) that may not increase heart rate or blood pressure.
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CaCl
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Calcium is a cation. Calcium ions increase the force of myocardial contraction and thus act to increase cardiac output. Calcium has a stabilizing effect on cardiac cell membranes when dangerously high potassium levels make the heart at risk for fibrillation.
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Magnesium
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Magnesium is a cation that is more than 98% contained within the intracellular compartment. Magnesium is a cofactor of membrane Na-K-ATP-ase (Na out, K in), and as such plays an integral role in maintaining intracellular potassium levels. Magnesium is essential for energy transfer and electrical stability. Magnesium also appears to be an outstanding antiarrhythmic, and it has been demonstrated that prophylactic administration of Magnesium Sulfate significantly reduces the incidence of potentially lethal ventricular arrhythmias in patients with AMI. It is also a CNS depressant effective in the management of seizures associated with toxemia of pregnancy (eclampsia).
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Glucagon
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Glucagon is a hormone. Glucagon, produced in the pancreas by the Alpha cells of the Islets of Langerhans, causes an increase in blood glucose concentrations. It is effective in small doses and no evidence of toxicity has been reported with its use. Glucagon acts only on liver glycogen, converting it to glucose. Glucagon effectively restores inotropy and chronotropy, via a cyclic-AMP mechanism, in patients with cardio-vascular toxicity secondary to beta-blockers, and to a more variable degree, to calcium channel blockers. |
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Adenosine (Adenocard)
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Antiarrhythmic—Slows impulse formation in the (SA) node, slows conduction time through the atrioventricular (AV) node, and can interrupt reentry pathways through the AV node. Adenosine depresses left ventricular function, but because of its short half-life, the effect is transient, allowing use in patients with existing poor left ventricular function |
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Albuterol sulfate solution, 0.083% (Proventil)
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Amiodarone (Cordarone)
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Antibiotic ointment (non-sulfa)
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Aspirin (chewable)
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Atropine sulfate
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Calcium chloride
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Diltiazem hydrochloride (Cardizem)
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Diphenhydramine hydrochloride (Benadryl)
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Dopamine hydrochloride (Intropin)
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Epinephrine, 1:1,000
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Epinephrine, 1:10,000
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Etomidate (Amidate)
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Furosemide (Lasix)
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Hydroxocobalamin (Cyanokit)
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Lidocaine hydrochloride, 2%
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Lidocaine hydrochloride, 20%
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Lorazepam (Ativan)
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Magnesium sulfate, 50%
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Methylprednisone sodium succinate (Solu-Medrol) |
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Morphine sulfate
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Naloxone (Narcan)
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Nitroglycerin
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Ondansetron (Zofran)
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Sodium bicarbonate, 8.4%
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Succinylcholine (Anectine)
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Tetracaine (Pontocaine)
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