Prehospital Pharmacology
Advanced Care Paramedicine
Module: 6
Session: 5
Prehospital medicating
 Prescribed by GP
 Standing Orders
 Protocols
 Transfer orders (should be written)
 EMS administered
Ace Inhibitors
 Inhibits the effect of the Angiotensin
Converting Enzyme (ACE) in the lungs,
blocking the conversion of Angiotension I to
Angiotension II thus inhibits the release of
ADH and helps decrease blood pressure.
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Captopril
Enalapril
Quinipril
Benazepril
Lisinopril
Antibiotics
 Kills or disrupts/stops the growth and
development of bacteria
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Amoxicillin
Azithromycin
Bactrim
Ceclor
Ceftin
Ciprofloxacin
Clarithromycin
Cloxicillin
Dicloxicillin
Erythromycin
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Keflex
Metrodiazanole
Nitrofurantoin
Penicillin
PenVee
Rifampin
Suprax
Tetracycline
Vancomycin
Vantin
Antidysrhythmics
 Vaughn-Williams Classifications
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Class I
Class II
Class III
Class IV
Antidysrhythmics
 Class I
 Na Channel Blockers
 Slow the maximum rate of Phase 0 depolarization
 Slow conduction velocity
 Slow rate and force of contraction refractory period effects
 Mechanisms of Action
 Blocks Na influx through fast Na channels
Antidysrhythmics
 Differential effects:
Ia
 Increase duration of AP, prolonged repolarization, prolonged refractory
period, decreased membrane responsiveness
 Decreased depolarization of SA node thus decreased pacemaker
activity
 Also blocks K+ channels
Ib
 Decreased duration of AP, decreased membrane responsiveness in
ventricles
 Blocks activated and inactivated Na+ channels, depresses damaged
or depolarized cells (eg. post MI)
 Does not block K+ channels
Ic
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No effect or minimal increase in duration of AP & repolarization
Decreased membrane responsiveness
Decreased conduction velocity in atrial & ventricular cells
Also blocks K+ channels
Antidysrhythmics
 Class Ia
 Quinidine
 Procainamide
 Disopyramide
 Class Ib
 Lidocaine
 Tocainide (Mexilitine)
 Phenytoin
 Class Ic
 Flecainide
 Propanfenone
 Moricizine
Antidysrhythmics
 Class II
 Beta Blockers
 Mechanisms of Action
 Blockade of ß-receptors
 Inhibition of norepinephrine release (bretylium)
 Propranolol
 Metoprolol
 Atenolol
Antidysrhythmics
 Class III
 K Channel blockers
 Prolong action potential and affiliated refractory period
 Mechanisms of Action
 Do not alter normal fast Na conductance
 Do not compete for ß-receptors
 Bretylium
 Amiodarone (Has effects of all classes)
 Sotalol (no longer used – causes Torsades)
Antidysrhythmics
 Class IV
 Ca Channel Blockers
 Mechanisms of Action
 Selectively block slow Ca channels
 Inhibit slow inward Ca current during phase 2
 Decrease rate of phase 4 depolarization
 Effect on the “pacemaker in charge”
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 Depress conduction velocity in purkinji system and AV node
 Decrease contractility in myocardium
 Vasodilatation (lower intracellular Ca in arterial muscle)
Verapamil (Isoptin)
Diltiazem
Cardizem
Nifedepine
Plendil
Antihistamines
 Compete with histamine for H1 and H2
receptors thus decreasing the
histamines affect
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Chlorpheniramine
Cyproheptidine
Diphenhydramine
Hydroxizine
Promethazine
Antihypoglycemics
 Treat diabetes by increasing the amount of
sugar in the blood, and decreasing the
amount transported into the tissues
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Diabeta
Diabinese
Glypizide
Glyburide
Metformin
Tolinase
Antifungals
 Acts primarily by damaging the permeability barrier
in the membrane of the fungi. This leads to the
inability for the cell to construct an intact membrane
and leads to the death of the fungus
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Diflucan (Fluconazole)
Canesten (Clotrimazol)
Griseofluvin
Ketoconazole
Lamisil
Nizoral
Monostat
Sopranox
Tinactin
Antituberculosis
 Inhibits RNA synthesis in bacteria
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Ethambutol
Rifampin
Isoniazid
Pyrazinamide
Streptomycin
Antivirals
 Affects the reproduction of the virus.
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Acyclovir
Amatadine
Rimantadine
3TC
Acyclovir
Amatadine
AZT
DDI
Quinivere
Rimatadine
Zovirax
Anxiolytics
 Combat anxiety by binding with
receptors (GABA) in the cerebral
cortex and limbic regions.
 Valium
 Wellbutrin
 Xanax
Benzodiazepines
 Bind with receptors (GABA) to
decrease anxiety and prevent seizures
 Valium
 Versed
 Halcyon
Beta 1 Specific Blockers
 Compete for the ß-1 receptor sites
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Blocadren
Corgard
Lopressor
Tenormin
Bronchodilators
 ß-2 agonists
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Albuterol
Aminophylline
Atrovent (anti-cholinergic)
Metaproterenol
Ventolin
Cardiac glycosides
 Block ionic pumps in heart increasing
Ca concentrations and contraction,
decreasing rate and speed of
conduction
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Digitalis
Digitoxin
Digoxin
Lanoxin
Cholesterol lowering
 Prohibits the synthesis of cholesterol
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Lopid
Lozol
Mevacor
Zocor
Diuretics
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Causes body’s water balance to shift, excreting water and
some electrolytes
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Loop Diuretics
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inhibit reabsorption of sodium and chloride in the ascending Loop of
Henle, thus excreting water and potassium. Most potent of the
diuretics
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Thiazide Diuretics
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Affect the distal tubule blocking cotransport of Na-CL
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HCTZ
Potassium-sparing Diuretics
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Furosemide (Lasix)
Amiloride
Aldactone
Osmotic Diuretics
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pharmacologically inert nonelectrolyte which is freely filtered by the
renal glomerulus and not reabsorbed from the nephron. Osmotically
pulls large amounts of water from the cells which it carries with it
when it is excreted
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Mannitol
D50
Gastrointestinal
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Chlopromazine
Dimenhydrinate
Famotidine
Loperamide
Magnesium hydroxide
Omeprazole
Prochloperazine
Scopolamine
H2 blockers
 Blocks H2 receptors in the stomach
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Axid
Pepcid
Ranitidine
Tagamet
Cimetidine
Migraine therapy
 Typically decrease the vasodilatation
in the cranial vascualture relieving the
headache
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Inderal
Ergotamine
Fiorinol
Sumatripan
Narcotics
 Act on the CNS to slow down all body systems and
are used medically as cough suppressants or pain
relievers
 High potential for abuse and for dependency
 Narcotics can be classified into three groups:
 Natural origin
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Codeine, Morphine, Fentanyl
 Semi-synthetic
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Heroin
 Synthetic
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Merperidine (Demerol), Methadone, Hydromorphone
(Dilaudid)
Non-Narcotic analgesics
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Relieve pain without producing unconsciousness or impairing
mental capacities.
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Many of these drugs also have an antipyretic and/or an antiinflammatory effect
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Aspirin (ASA)
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Acetaminophen (Tylenol)
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Analgesic, antipyretic, and anti-inflammatory agent used for mild to
moderate pain. It is contraindicated in peptic ulcer disease. It acts as
a gastric mucosal irritant and has an anticoagulant effect.
Similar to aspirin, but has no anti-inflammatory action.
Ibuprofen
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Ibuprofen is indicated for the relief of mild to moderate pain. Has an
anti-inflammatory agent. It is not to be given to patients in the third
trimester of pregnancy or anyone with a history of gastrointestinal
bleeding
NSAIDS
 Non-Steroidal Anti-inflammatory Drug
 Inhibits the cyclooxygenase enzyme from
synthesizing prostaglandins
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Alleve
ASA
Ibuprofen
Indomethacin
Relafen
Toradol
Voltaren
Steroids
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Synthetic hormones
Possess anti-inflammatory (glucocorticoid) and/or salt-retaining
(mineralocorticoid) properties to varying degrees.
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Glucocorticoids
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Affect almost all body systems and cause varied metabolic effects
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Decrease inflammation
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Stabilization of leukocyte lysosomal membranes
Inhibition of macrophage accumulation in inflamed areas
Reduction of capillary permeability.
Suppress immune responses
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Promote gluconeogenesis
Redistribution of fat from peripheral to central areas of the body
Reduce intestinal absorption and increase renal excretion of Ca
Reduction of activity and volume of the lymphatic system
Decreased immunoglobulin and complement concentrations
Decreased passage of immune complexes through basement membranes
Mineralocorticoids
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Affect electrolyte and fluid balance by acting on the distal renal tubule to
promote Na reabsorption and K and H excretion.
Steroids
 Glucocorticoids
 Mineralocorticoids
 Short Acting
 Fludrocortisone
 Cortisone
 Hydrocortisone
 Intermediate Acting
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Methylprednisolone
Prednisolone
Prednisone
Triamcinolone
 Long Acting
 Betamethasone
 Dexamethasone
Education
 Previous Training was “ see this... give
this ”
 Education
A&P
Pathophysiology
Drug specifics
Drug specifics
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Class
Mechanism of action
Indications
Contraindications
Precautions
Side effects
Interactions
Dosage
Administration