EMS Medications Flashcards
Epinephrine
Class: Adrenergic Agonist (Alpha-1,2;Beta-1,2); Inotropic Agent
MOA: Produces effects by activating adrenergic receptors with direct receptor binding
Effects: Pupil constriction, vasoconstriction, bronchodilation, urinary retention, and an increase in blood pressure
Purpose: Used during cardiac arrest, bradycardia, asthma/copd, anaphylaxis, croup, and epiglottis
Dopamine
Class: Adrenergic Agonist; Inotropic Agent
MOA: Produces effects by activating adrenergic receptors with direct receptor binding. Stimulates alpha-1, beta-1.
Purpose: Used for shock (except in cases of hypovolemia)
Phenylephrine
Class: Adrenergic Agonist
MOA: Produces effects by activating adrenergic receptors with direct receptor binding
Purpose: Used during nasal intubation to minimize bleeding from the nasal cavity.
*This drug only activates alpha-1
Albuterol
Class: Adrenergic Agonist
MOA: Produces its effect by activating adrenergic receptors with direct receptor binding
Purpose: Given for bronchoconstriction and hyperkalemia.
*Albuterol is a non-selective beta agonist (beta-1 and 2)
Terbutaline
Class: Adrenergic Agonist
MOA: Produces effects by activating adrenergic receptors with direct receptor binding. Beta-2 agonist.
Purpose: Given for bronchoconstriction
*This drug is a beta-2 agonist and NOT on the Denver Health Ambulance
Esmolol
Class: Adrenergic Antagonist; Beta Blocker
Vaughn William Class: 2
MOA: Produces a direct blockade of specific adrenergic receptor
(Beta Blockers). Also effects phase two and four (slow acting cells) of the cardiac potential sequence
Purpose: Helps to control heart rate and for arrhythmias
Atropine
Class: Muscarinic Antagonist (anti-cholinergic)
MOA: Produce a blockade at muscarinic receptor sites
Purpose: Given for bradycardia, dry secretions, and organophosphate poisoning
Atrovent
Class: Muscarinic Antagonist
MOA: Provides a blockade at muscarinic receptors
Purpose: Given for bronchoconstriction, and dry respiratory secretions
Pralidoxime (2PAM)
Class: Irreversible Cholinesterase Inhibitors
MOA: Causes a disassociation of organophosphates from the active center of acytelcholinesterase
Purpose: Given for organophosphate poisioning
Mivacurium; Pancuronium; Vecuronium; Rocuronium
Class: Neuromuscular Blocking Agents (Non-Depolarizing Agent)
MOA: Prevents acetylcholine from activating nicotinic (m) receptors on skeletal muscle thereby causing paralysis
Purpose: Causes paralysis
Succinylcholine
Class: Neuromuscular Blocking Agent (Polarizing Agent)
MOA: Produces a depolarizing neuromuscular state which holds the muscle in constant depolarization
Purpose: Causes paralysis in the muscle
Procainamide, Lidocaine, Dilantin
Class: Sodium Channel Blocker
Vaughn Williams Class: 1
MOA: Blocks some not all Na channels. Effects phase 0 of the cardiac potential sequence
Purpose: Used for arrhythmias
Amiodarone
Class: Potassium Channel Blockers
Vaughn Williams Class: 3
MOA: Blocks potassium channels, has effects on phase 1,2,3 when potassium is entering the cell. This will lengthen the overall time it takes to repolarize, which will lengthen the amount of time it takes for the heart to go below threshold.
Purpose: Given for V-fib and V-tach
Bonus points: It has a long half-life, about 45 days
Diltiazem, Verapamil
Class: Calcium Channel Blocker
Vaughn Williams Class: 4
MOA: Has effects on phase four (slow acting cells) and phase two of the cardiac action potential sequence
Purpose: Rate control, arrythmias
Nifedipine
Class: Calcium Channel Blocker
MOA: Blocks calcium channels, not allowing calcium to flow from the extracellular space into the intracellular space.
Use: Helps to maintain blood pressure
Vasopressin
Class: Vasopressor; Anti-diuretic
MOA: Causes potent vasoconstriction, but mostly promotes fluid retention. Synthetic version of ADH and much more potent. Holds onto Na which also holds H2O.
Note: This doesn’t directly effect the heart, but it indirectly effects it through pre-load and after-load.
Captopril (Capoten), Enalapril (Vasotec)
Class: Ace Inhibitors
MOA: Blocks ACE, inhibiting conversion of angiotensin-1 to angiotensin-2
Use: BP Control
Nitroglycerin
Trade name: NitroBid, Nitro-Quick, Nitrostat
Class: Vasodilator
MOA: Converts into Nitric oxide in the presence of sylphydryl group, which causes MOSTLY venus vasodilation through multiple biochemical reactions.
Use: Chest pain, CHF, and Hypertension
Epinephrine, Dopamine, and Norepinephrine
Class: Inotropic agents; Adrenergic Agonist
MOA: Improves contraction of heart cells by manipulating the cells to increase their intracellular Ca++
Uses: Shock, Cardiogenic shock
Digoxin
Trade name: Lanoxin
Class: Cardiac Glycside/Inotropic Agent
MOA: Slows down the Na/K pump, slows down its effectiveness. Increases the amount of Calcium in the cardiac cell.
Use: Slows heart rate and increases contraction
*Never give Calcium Gluconate to someone on Digoxin and this patient is at high risk of hyperkalemia
Adenosine
Trade name: Adenocard
Class: Cardiac Nucleotide/Anti-dysrhythmic
MOA: Binds to adenosine receptor on the membrane, inhibits beta-1 action through G-Protein. Opens potassium channels, blocks calcium channels. Slows AV conduction time.
Use: Used to prevent, treat, or suppress irregular heart rhythms
Use: The main target is the AV node, with slight effect on the SA node
Name the Vaughn Williams Class 1 drug group?
Sodium Channel Blockers
Name three Sodium channel blockers?
Procainamide
Lidocaine
Dilantin
Name the Vaughn Williams Class 2 drug group?
Beta Blocker
Name four Beta Blockers?
Esmolol
Labetalol
Propanaolol
Metoprolol (Not a Vaughn Williams Class)
Name the Vaughn Williams Class 3 drug group?
Potassium Channel Blocker
What is the main potassium channel blocker we use?
Amiodarone
Name the Vaughn Williams Class 4 drug group?
Calcium Channel Blocker
Name three Calcium channel blockers?
Diltiazem
Verapamil
Nifedipine (not a Vaughn William Class)
Labetalol
Trade name: Normodyne and Trandate
Class: Adrenergic Antagonist/Beta-blocker
Vaughn William Class: 2
MOA: Selectively antagonizes alpha-1, beta-1, and beta-2 receptors. Also effects phase two and four (slow acting cells) of the cardiac potential sequence
Purpose: Helps to control heart rate and for arrhythmias
Metoprolol
Trade name: Lopressor and Toprol XL
Class: Adrenergic Antagonist/Beta-blocker
MOA: Selectively blocks (antagonizes) beta-1. Also effects phase two and four (slow acting cells) of the cardiac potential sequence
Purpose: Helps to control heart rate and arrhythmias
Propranolol
Trade name: Inderal
Class: Adrenergic Antagonist/Beta-blocker
Vaughn William Class: 2
MOA: Non-selectively antagonizes (blocks) beta-1 and beta-2. Also effects phase two and four (slow acting cells) of the cardiac potential sequence
Purpose: Helps to control heart rate and for arrhythmias
Norepinephrine
Levophed
Class: Adrenergic Agonist/Vasopressor
MOA: Stimulates alpha- and beta-adrenergic receptors
Use: Hypotension, improve cardiac function during decompensation associated with CHF
Magnesium
Class: Mineral/Electrolyte; Anti-epileptic
Use: Blocks the NMDA receptor thus blocking the normal ion diffusion and blocking the propagation of the action potentials
Purpose: Given to pregnant women seizing before having the baby (pre-eclampsia)
Inapsine
Droperidol
Class: Anti-psychotic/Anti-emetic
MOA: Dopamine Antagonist (primary), also inhibits histamine (secondary), acetylcholine, adrenergic receptors. It blocks alpha-1, watch for hypotension
Use: Psychosis, or nausea
Haldol
Class: Anti-psychotic
MOA: Dopamine Antagonist
Use: Psychosis
Benadryl
Class: Acetylcholine and Histamine Antagonist; Muscarinic Antagonist
Use: Allergies, or sedation
Benadryl blocks acetylcholine but is not typically thought of as a muscarinic antagonist
Proper doses make you sleepy
High doses make you hyper, irritable, and agitated
Clonodine
MOA: Used to treat hypertension by blocking calcium influx on the presynaptic neuron this prevents some NE from being released from the vesicles
Use: Hypertension
Zofran
Class: Serotonin Antagonist/Anti-emetic
MOA: Used to treat vomiting by blocking the serotonin receptor in the VTZ (Vomiting trigger zone, Area postrimia)
Use: Decrease nausea and vomiting
Phenergan
Hydroxyzine
Class: Histamine Antagonist, Muscarinic Antagonist
Decrease nausea and vomiting associated with movement or balance and fix dystonic reactions through its antagonist actions of muscarinic sites. Can also have sedative effects.
Name three benzodiazapines
Versed (Midazalam)
Valium (Diazepam)
Ativan
Name three barbituates
Phenobarbital
Methoexital
Thiopental
Etomidate
Type: Anti-epileptic; Induction Agent; Sedative
MOA: Enhances GABA
Use: Reduce anxiety, promote sleep (hypnotic,sedative), RAS, muscle relaxation, amnesia, depresses vasomotor and respiratory centers in the medulla
How does versed,valium, ativan, phenbarbital, methoexital, and thiopental work? What do they do?
Type: Anti-epileptic
MOA: Enhances GABA, when Gaba is released it decreases activity in the brain
Use: Reduce anxiety, promote sleep (hypnotic,sedative), RAS, muscle relaxation, amnesia, depresses vasomotor and respiratory centers in the medulla
Lisinopril
Class: Ace Inhibitor
MOA: Blocks ACE which in turn allows the blood vessels to dilate. This med also decreases afterload on the heart.
Use: Treats high blood pressure, CHF
Fentanyl
Class: Narcotic Analgesic; Opioid Agonist
MOA: Strong agonist at both Mu and Kappa opioid receptors. 100 times for potent than morphine, blocks glutamate from being released.
Effects: Causes analgesia, respiratory depression, sedation, euphoria, and decreased GI motility
Use: Pain relief, sedation
Nubain; Stadol
Class: Opioid Agonist/Antagonist
MOA: Antagonist to Mu receptors and agonist to Kappa receptors. Blocks glutamate from being released.
Effects: Increases analgesia, sedation, and decreases GI motility.
Use: Moderate pain relief
Morphine Sulfate
Class: Narcotic Analgesic; Opioid Agonist
MOA: Strong agonist at both Mu and Kappa opioid receptors. Blocks glutamate from being released.
Effects: Causes analgesia, respiratory depression, sedation, euphoria, and decreased GI motility
Use: Pain relief, sedation
Demerol
Class: Narcotic Analgesic; Opioid Agonist
MOA: Strong agonist at both Mu and Kappa opioid receptors. Blocks glutamate from being released.
Effects: Causes analgesia, respiratory depression, sedation, euphoria, and decreased GI motility
Use: Pain relief, sedation
HcTZ (hydrochlorothiazide)
Class: Thiazide Diuretics
MOA: Blocks the Na+/Cl- transporter which holds these ions in lumen and are then excreted
Effects: Helps keep the body from absorbing to much salt, thereby preventing water retention
Use: Congestive heart failure, high blood pressure, kidney disorders, or edema
Compazine
Class: Dopamine Antagonist; Anti-psychotic; Anti-emetic
MOA: Blocks dopamine receptors
Effects/Use: reduces nausea/vomiting, also reduces psychosis
Mannitol
Class: Osmotic Diuretic
MOA: Prevents the reabsorption of water and sodium along the renal tubule. Circulating freely within the tubule, mannitol retains fluid, which is converted to urine and excreted from the body.
Effects: Causes potent diuresis
Use: Helps to reduce ICP, and edema
Calcium Gluconate
Class: Mineral/Electrolyte
MOA: Can be used to restore the balance of the cell
Effects: It increases the excitability/contractility the heart
Use: Helps to restore normal heart rhythm as a result of hyperkalemia.
Sodium Bicarbonate
Class: Mineral/Electrolyte; Antacid (buffering compound)
MOA: Changes the acid/buffer system, decreasing the acidity in the body (raising Ph). Can lower the respiratory rate in a patient hyperventilating.
Use: Used in cases of respiratory acidosis, treats aspirin overdoses, tricyclic anti-depressant overdoses, as well as cases of hyperkalemia
Oxygen
Class: Gas
MOA: Increased O2 concentration in the lungs helps to displace carbon monoxide from the heme group of hemoglobin. Increases aerobic production in the cell, increase ATP synthesis
Use: Many
Glucose
Dextrose 50%
Class: Carbohydrate
MOA: Absorbed by the cell and plays a large role in ATP production. This is a simple sugar so it acts extremely fast.
Use: Used to restore blood glucose levels.
Glucagon
Class: Hormone
MOA: Attaches to the G-protein in hepatocytes (liver cells) which ultimately causes a breakdown of glycogen into glucose. Don’t forget water follows glucose.
Use: Hypoglycemia, beta and calcium channel overdoses
What does the Muscarinic receptor do?
Increases glandular secretion
Slows the heart
Contraction of the sphincter of the iris (miosis, pupil constriction)
Contraction of the ciliary muscle (near vision)
What are the four Adrenergic receptors?
Alpha-1;Alpha-2;Beta-1;Beta-2
Where is alpha-1 located and what does it do?
Location: Eye, blood vessels, male sex organs, neck of bladder
Purpose: Dilates pupils (mydryasis), Vasoconstriction, Ejaculation, Bladder neck constriction
Where is alpha-2 located and what does it do?
Location: Pre-synaptic terminals on the nerves in the CNS
Purpose: Assists in activation of the sympathetic nervous system, primarily effects breathing and vasomotor responses
Where is beta-1 located and what does it do?
Location: Heart and Kidneys
Purpose: Heart: Increases HR, force of contraction and velocity of impulse through the AV node
Kidney: Causes a release of renin
Where is beta-2 located and what does it do?
Location: Lungs, uterus, muscles, and liver
Purpose: Lungs: Bronchial dilation
Uterus: Relaxation of the uterus
Muscles: Vasodilation
Liver: Glycogenelysis (Breakdown of glycogen into glucose)
What does the Mu receptor do?
When activated causes analgesia, respiratory depression, sedation, euphoria, and decreased GI motility
What does the Kappa receptor do?
Activates analgesia, sedation, and decreased GI motility
What are the effects of the Dopamine receptor?
Cognition Vomiting Voluntary movement Punishment Reward Sleep Mood Attention Working memory Learning
What does the histamine neurotransmitter effect?
Balance, vomiting, and the RAS
Narcan
Opioid Antagonist against Mu and Kappa receptors
Blocks Mu and Kappa receptors
Dobutamine
Class: Adrenergic Agonist/Inotropic Agent
MOA: Stimulates beta-1, allowing Ca to come into the cell.
Effects: Increased HR and force of contraction through the AV node. Also increases the release of renin in the kidneys.
