ALS Paramedic Pharmo

Platelet Aggregator Inhibitor

Suspected Acute Coronary Syndrome (ACS)

• -Hypersensitivity 
• -Active GI bleeds
• -Asthmatic with Pm Hx of sensitivity to ASA / NSAIDS

• 160mg chewed PO
• Repeat: NO Repeat

Inhibit the formation of Thromboxane A₂, which ihibits platelet aggregation.  ASA affects platelet function by inhibiting the enzyme prostaglandin cyclooxygenase in platelets, thereby preventing the formation of the aggregating agent thromboxane A2. 

Antianginal Vasodilator

Suspected ACS

• - Hypesensitivity
• - Systolic BP less than 100mmHg
• - Taken any Erectile Disfunction (ED) drugs withing 24 hrs
• - PT taking phosphodiesterase inhibitors
• - Right Ventricular Infarct 

0.4mg = 1 spray q 5 mins prn or until BP drops below 100 or more than 30mmgh in one dose.

• Reduction in left ventricular preload and afterload because of venous (predominantly) and arterial dilation with a more efficient redistribution of blood flow within the myocardium.
• Vasodilation (relaxes vascular smooth muscle) decreasing preload and afterload which results in decreased myocardial workload
• Increases use of coronary collaterals to enhance myocardial perfusion
• Relieves coronary vasospasm
• Dilates coronary arteries

Hyperglycemic   

Comfirmed Hypo - Glycemia

Decreased LOC (potential for aspiration)    

• 25 g PO, prn 
• Repeat: q 5 mins to a max to 50mg

Provides a quickly absorbed form of glucose to increase blood glucose levels

Protein Pancreatic Hormone / Insulin Antagonist (Antihypoglycemic)

Confirmed hypoglycemia in which an IV cannot be established

Hypersensitivity to glucagon, beef or pork proteins.

• 1 mg IM (1 unit)
• Repeat: q 15 minutes prn to max 2mg (2 units)

• Promotes hepatic glycogenolysis and gluconeogenesis.
• Stimulates adenylate cyclase to produce increased cyclic adenosine monophosphate (cAMP), which is involved in a series of enzymatic activities. The resultant effects are increased concentrations of plasma glucose, a relaxant effect on smooth musculature, and a positive chronotropic and inotropic myocardial effect via non-alpha and non-beta receptor
• Stimulates glycogen breakdown in the liver, converting glycogen to glucose which raises blood glucose levels.
• Onset of action is 5-20 minutes
• Hepatic stores of glycogen are necessary for glucagon to elicit an antihypoglycemic effect

Carbohydrate, Hyperglycemic, Hypertonic solution of 50% dextrose in H2O

Comfirmed Systomatic Hypoglycemia

Hypersesitivity

• 25g SIVP/IO in 50ml
• Repeat: q 5 minutes to a max of 50 g

• Increases blood glucose levels
• Hypertonic solution producing a transient movement of water from interstitial spaces into the venous system (osmotic diuretic)

Adrenergic Sympathomimetic

Anaphalaxis

No contraindications when used in emergency situations

• 0.3 mg IM 
• Repeat: q 5 mins to a max of 0.9 mg

Alpha 1 Effects

Peripheral vasoconstriction (increases perfusion pressure during CPR which improves coronary and cerebral perfusion)

Beta 1 Effects

• Positive chronotropic
• Positive inotropic
• Positive dromotropic
• Increases automaticity

Beta 2 Effects

• 1. Bronchodilation
• 2. Peripheral vasodilation (minimal)

Bronchodilator Effect

• Acts by stimulating beta2 – adrenergic receptors in the lungs to relax bronchial smooth muscle, thereby relieving bronchospasm. This action is believed to result from increased production of cyclic adenosine3,5-monophosphate and ensuing reduction in intracellular calcium concentration caused by activation of the enzyme adenylate cyclase that catalyzes the conversion of adenosine triphosphate (ATP) to cAMP. Increased cAMP concentrations, in addition to relaxing bronchial smooth muscle, inhibit release of
• mediators of immediate hypersensitivity from cells, especially from mast cells.

Allergy/Anaphylaxis Effects

Stimulates the release of cyclic adenosine monophosphate (cAMP). CAMP inhibits the release of mediators associated with allergic and anaphylactic reactions. These mediators are stored in granules within the cytoplasm of basophiles and mast cells. One of the involved mediators is histamine which is responsible for vasodilation and increased permeability of blood vessels.

Bronchodilator (sympathomimetic)    

Treatment of bronchospasm from (asthma, chronic bronchitis, COPD, anaphylaxis or emphysema)    

• Uncotrolled tachyarrythmias
• Hypersensitivity

• -Adult Dosage: 5mg mixed with ipratropium bromide via nebulized
• -Repeat: PRN

• -Pediatric: < 20kg, 2.5mg mixed with ipratropium bromide via nebulized. > 20kg, 5mg (same as adult dosage)
• -Repeat: PRN

• Salbutamol acts by stimulating beta2 receptors in the lungs to relax bronchial smooth muscle, thereby relieving bronchospasm. This action is believed to result from increased production of cyclic adenosine 3,5-monophosphate (cyclic 3,5-AMP; cAMP) and ensuing reduction in intracellular calcium concentration caused by activation of the enzyme adenylate cyclase that catalyzes the conversion of adenosine triphosphate (A TP) to cAMP. Increased cAMP concentrations, in addition to relaxing bronchial smooth muscle, inhibit release of mediators of immediate hypersensitivity from cells, especially from mast cells. Onset of action is 5-15 minutes.
• Mild Beta1 effects
• Mild peripheral vasodilation
• Beta2 selectively lost with high doses (Beta1 and Beta2 effects seen)

Anticholinergic Bronchodilator, Parasympatholytic

• Bronchospasm induce by anaphalaxys.
• Bronchospasm in general.

Use with caution in patients with know sensativity, but there are no containdications.

• Adult: 500mcg nebulized
• Repeat: PRN

• Pediatric: < 20kg = 250mcg nebulized
•                 > 20kg = 500mcg nebulized 
• Repeat PRN

• - Can also be administered via MDI with spacer, dose = 10 puff. 
• - Repeat: q 20 mins prn to total max of 30 puffs.

• Produces bronchodilation by competitive inhibition of cholinergic receptors on bronchial smooth muscle. This effect antagonizes the action of acetylcholine at its membrane-bound receptor site and thereby blocks the brochoconstrictor action of vagal efferent impulses
• Through blockade of acetylcholine, which inhibits parasympathetic stimulation, bronchial secretions are also decreased 
• Onset of action is 5-15 minutes, with a peak at 1-2 hours

Gaseous Analgesic

Pain management

• Inability to follow instructions.
• Intoxication.
• Head injury with altered LOC.
• Thoracic injury.
• ABD pain/distension.

Self administration via Demand Valve Mask

• Rapid reversible CNS depression and analgesia
• Inhaled anesthetics act on the lipid matrix of neuronal membranes or other lipophilic sites. This changes the membrane thickness, which in turn affect the gating properties of ion channels in neurons

Narcotic (opiate) Analgesic    

Pain management

• Systolic BP 90mmhg or less.
• Hypersensitivity.

0.1mg/kg IV/IM/IO to a max single dose of 5mg.

Repeat: PRN q 5 mins to a max total of 20mg.

• Opioid analgesics bind with stereospecific receptors at many sites within the CNS to alter processes affecting both the perception of pain and the emotional response to pain
• Analgesia (exerts its main effect by acting as an opioid agonist at specific opioid receptor sites in the CNS and other tissues).
• Maximum analgesia occurs 20 minutes after IV administration and 30-60 minutes after IM injection.
• Analgesia persists for 2.5-7 hours

Narcotic (opiate) Analgesic    

Pain management

• Hypersensitivity.
• MOAI (MonoAmine Oxidase Inhibitor) therapy within last 14 days.
• Systolic BP < 80mmHg.

• BP greater than 90mmHg.
• -1mcg/kg IV/IM/IO to a single max dose of 100mcg
• -Repeat: PRN q 3 mins to a total max of 250mcg

• BP between 80 and 90mmHg.
• -0.5mcg/kg IV/IM/IO to a single max dose of 25mcg
• -Repeat: PRN 5 mins to a total max of 250mcg

• Opioid analgesics bind with stereospecific receptors at many sites within the CNS to alter processes affecting both the perception of pain and the emotional response to pain
• Analgesic (immediate onset, 30-60 minute duration)
• CNS depressant – more potent, faster onset & shorter duration than morphine 

Nonsteroidal Anti-inflammatory Analgesic    

Pain Management, refractory to Fentanyl and Morphine

• Hypersensitivity to it or other NSAID's.
• Asthma.
• Renal failure.
• Suspected intracranial bleed.
• History of GI bleeding.

• With OLMC 30mg IV/IM
• Repeat: With OLMC

• Inhibits the activity of the enzyme cyclo-oxygenase, resulting in decreased formation of precursors of prostaglandin’s and thromboxanes from arachidaonic acid
• At analgesic doses little anti-inflammatory or antipyretic activity is seen.
• Ketorolac acts peripherally versus narcotics, which act upon the CNS, therefore, no CNS depression