I.

Respiratory Drugs: Include Bronchodilators (Beta) Anticholinergics, Xanthines, Corticosteroids, Antihistamines, Mucolytics, and Cough Suppressants: Three concerns are bronchoconstriction, mucus production, inflammation, and histamine response,
A. Bronchodilators: Beta Agonists, Non Selective,
1. Beta Agonist: Albuterol, levalbuterol, metaporterenol, isoetharine, terbutaline, recemic epi, epi, isoproterenol

B. Anticholinergics: Also called parasympatholytics, decrease secretions andexpectorate, temporary bronchodilation

1. Atropine sulfate, ipratropium

C. Xanthine Derivitives: Metabolites of caffeine, theophylline, and theobromide. Phosphodiesterase inhibitors which relax bronchial smooth muscle, stimulate cardiac and CNS, mild diuretic. Used in ER settings
1. Theophylline

D. Corticosteroids: Imrove responsiveness of airway muscles to beta agonists, stabalize membranes to reduce histamine effects, anti inflammatory (not bronchodilator), longer onset of action, aerosolized can worsen acute symptoms.
1. Methylprednisolone, hydrocortisone, dexamethasone

E. Antihistamines: Mast cells cause histamine production and storage and are abundant in small blood vessels and bronchial smooth muscle, H1 and H2 receptors cause increased blood flow, increased capillary permeability, edema, vasodilation, bronchoconstriction.
1. Diphenhydramine,

F. Mucolytics: Promote coughing and removal of airway exudate, used for bronchopulmonary disease (cystic fibrosis, atelactasis)
1. Acetylcysteine

G. Cough Suppressants: Antiussives decrease cough reflex, opiods and non opiods, and expectorants

II. Electrolytes and Vitamins: Chemical substances that dissolve in water into charged particles. Also used as antidotes
1. Calcium Chloride/ Gluconate, Mag Sulfate, potassium chloride, Sodium Bicarb,

III. CNS Depressants: Include Narcotic Analgesics, Anesthetics, Sedatives/ Hypnotics which include Barbituates, Benzodiazepines, and Phenothiazines that together make up the anticonvulsants.
A. Analgesics in general mean decrease perception of pain not decreased sensation. They are divided into opiod/ narcotic (agonist, antagonist, agonist-antagonist) and Non Opiods (Salicylates, NSAIDS, Adjunts) B. Agonists Bind to receptor Site and cause the expected response, Antagonists bind to site but do not initiate the response, and Agonist-Antagonist bind to the site and cause some of the expected response but block parts of it (partial agonist or competitive agonism. C. Narcotic Analgesics: Opiods aka Narcotics are morphine like drugs. They act on endorphine receptors to decrease ability to propagate pain impulses. General actions include Analgesia, Resp Depression, Constipation, Urinary retention, Cough Suppresion, Euphoria, Sedation, Miosis, Decrease Preload and afterload, Increase ICP. Morphine is the prototype and Naloxone is the Opiod Antagonist Prototype which compete for and block the opiod receptor site but has a shorter half life than most opiods. Adjunct medications are not actually analgesics but potentiate them, they are Benzos, Antihistamines, and Caffeine.
1. 2. Morphine Sulfate, fentanyl, meperidine hydrachloride, hydromorphone, Naloxone (Antagonist)

D. Non Opiod Analgesics: Salicylates, NSAIDS (inhibit COX responsible for synthesis of protaglandins which increase pain)
1. Aspirin (Salicylate) acetameniphen, ketorolac.

E. Anesthetics: Loss of sensation, usually with loss of consciousness due to decreased propagation of neural impulses. They can be local or general and usually used for when they need the patient awake.
1. Nitrous oxide

F. Sedative Hypnotics cause sedation and decrease anxiety and inhibitions. Classed as Barbiturates and Benzos and Alcohol. They promote the effectiveness of GABA receptors in the CNS. Benzos only promote GABA but Barbiturates promote and stimulate GABA which is the chief inhibitory neurotransmitter. Anti Seizure Meds decrease propagation of action potentials and stabilize cell membranes.
1. Barbiturates produce anesthesia and hypnosis without analgesia. Their MOA is unknown but believed to act of RAS. They are very short action and are used as premeds for RSI. They are far more addicting then benzodiazepines and GABA (opposite of EPi and nor epi) are turned on by barbiturates which depress nerves. a) Phenobarbital, amobarbital, pentobarbital, secobarbital

2. Benzodiazepines: Receptors found in the cerebellum mediate anxiety and sedation, receptors in the hippocampus cause muscle relaxation and decreased memory and sensation.

a)

Diazepam, lorazepam, midazolam

b) Other anticonvulsants: phenytoin(decreases voltage frequency) and Mag Sulfate which produces neuromuscular blockade in the CNS

G. Antipsychotics are aimed at regulating neurotransmitters: Act on dopamine, seratonin, and nor epi by balancing the excitatory and inhibitory effects of these. Dopamine receptors are for movement emotion and cognition. Dopamine disorders include schizo, ADD, Terets. Two drugs used as antipsychotics are phenothiazines (low potency) and butyrophenones (high potency) They block dopamine, block chemo receptor trigger zones, block vagus nerve, alpha blockers. Cause dystonia
1. 2. Phenothiazines: chlorpromazine, prochlorperazine Butyrophenones: droperidol, haloperidol

IV.

ANS Control Drugs: Sympathetic and Parasympathetic

A. ANS Control: Cholinergic (Parasympathomimetic or Anticholinergic) Adrenergic = Sympathomimetic or Catecholamines. Adrenergic blockers are called Sympatholytics. B. Cholinergic Fibers: Nicotinic effects= inc HR BP via PVR and Skeletal Muscle Contraction= Twitching C. Muscarinic effects of ACH: Vasodilation, Bradycardia, SLUDGE M which can be blocked by
1. Atropine Sulfate.

D. ANS Sympathetic: Adrenirgic fibers increase CO, BP, Regulate Body Heat, Bronchodilation. Act on Alpha and Beta, Three natural,
1. epi, nor epi, dopamine.

E.

Vasopressors are sympathomimetics done and winning

1. Epi, vasopressin, dopamine, doputamine, norepi, isoprterenol, amrinone, milrinone

V.

Antihypertensives:
A. Diuretics affect volume, loop diuretics, thiazides, potassium-sparing diuretics, osmotic diuretics
1. Furosemide, hydrochlorothiazide, mannitol

B. ACE Inhibitors prevent vasoconstriction from preventing the development of Angiotensin 2 (benazapril, captopril, enalapril, lisinopril) C. Vasodilator (nitrates)
1. NTG, amyl nitrate, nitroprusside, hydralazine

VI.

Paralytics (Neuromuscualr Blockers)

A. Depolarizing mimic effects of ACH causing depolarization then paralysis (fassiculations)
1. Succinylcholine

B.

Nondepolarizing block the uptake of ACH preventing depolarization

1. Vecuronium, pancuronium, rocuronium

VII. Cardiac Drugs!

A. Cardiac function depends on the amount of adequate ATP and Calcium along with coordinated electrical stimulus. Calcium links the electrical and mechanical events, increases inotropy, automaticity, and vasoconstricts. B. C. D. Two types of action potentials: Fast= Na and K Slow= CA in SA, AV nodes ALL antidysrhythmics can CAUSE dysrhythmias Vaughn- Williams Classification: Class I (a b and c), II, III, IV

E. Class I: Sodium Channel Blockers decrease Na + movement, decrease conduction and repolarization rate, decrease excitability, for ventricular dysrhythmias. They Relax the Heart
1. 1a agents slow conduction through ventricles, decrease repolarization rate, widening the QRS and QT interval. May promote torsades des pointes. a) procainamide

2. 1b Agents also slow through ventricles, increase the v-fib threshold, reduce automaticity a) lidocain, phenytoin

3. 1c Agents Slow conduction through the ventricles, atria, and conduction system. They decrease repolarization rate and decrease contractility, Rare last chance drug a) flecanide, propafenone

F. Class II Beta Blockers: Beta 1 receptors in the heart attach to Ca channels. Gradual Ca influx is responsible for automaticity. Beta Blockers decrease the Ca influx and are similar to Class IV. Used to treat tachydysrhythmias caused by sympathetic stimulation and HTN, SVT, and Angina
1. Propanolol, metoprolol, atenolol, labetalol, carvedilol.

G. Class III Potassium Channel Blockers: Decrease K+ efflux during repolarization, prolongs repolorization which extends refractory period. Prototype is Amiodorone.
1. Amiodorone, bretylium,

H. Class IV Calcium Channel Blockers: Similar to Beta Blockers, decrease SA/AV automaticity, useful in breaking re-entry circuit (slowing SVT, a-fib and a-flutter) Prime Side Effect, Hypotension and bradycardia.
1. Verapamil, diltiazem hydrochloride, nifedipine.

I.

Misc. Agents
1. Adenosine prolongs the P-R interval, decreases Ca+ influx and increases K+ efflux thereby hyperpolarizing the membrane and decreasing conduction velocity Chemical Cardioverter 2. Digoxin Cardiac Glycosides = Positive Inotrope, negative chronotrope for CHF A- Fib and A- Flutter. Narrow Therapuetic range!