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Antimucokinetic agents

-drugs that drecrease movement/production of mucus/fluid w/in tract
-infrequent clinical use

Parasympatholytic drugs

-atropine (belladonna alkaloids, scopolamine)
MOA: block muscarinic receptors
-decrease secretions or excess expectoration
-problems: impair mucociliary clearance, dry mouth, nasal stuffiness, causes lack of secretions everywhere not just respiratory

Mucokinetic agents

-agents that increase production of secretions
-prevent drying of secretions airway plugging
-increased effectiveness of cough
-prevent microbial colonizationof mucus plugging airways

Mucokinetic agents: Diluents

-saline solution (isotonic, hypotonic, hypertonic)
-aerosol delivery: suspension of particulate in gas (smaller size: deeper penetration)
-problems: risk of contamination, protective reflexes: cough, bronchospasm

Problems w/ diluents

-need effective cough
-caution if fluid restricted
-swelling or retained secretions
-cross contamination

Ethyl alcohol

-mucokinetic dilueting agent
-defoaming agent

What is the SAFEST and best way to maintain hydration of the resp tract?

-oral hydration! drink water, avoid caffeine, dairy

Mucotropic drugs

-act directly on broncial glands to increase volume and decrease viscosity of secretions
-used to increase ease of expulsion, enhance broncial drainage, enhance cough effectiveness
-not so effective in kids

Mucotropic drugs: Guaifenesin MOA

-works via gastropulmonary reflex: cause stomach irritation which activates the medullary center and increases broncial secretion
-side effects: vomiting

Mucotropic drugs: Iodinated glycerol

-works via gastropulmonary reflex + direct broncial stimulation
-SE: rashes, thyroid problems (to to the iodine)

Mucolytic agents

-agents that decrease tickness and stickiness of secretions (liquify mucus)

What makes resp. tract secretions thick?

-nuclear material

Consequenses of failure to remove secretions

-obstruction: retained secretions become almost inert masses: cough and ciliary clearance can't remove
-colonization by microbes


-mucolytic agent
-MOA: cleave disulfide bonds
-administered by aerosol
-use: removal of excessivly thick secretions: COPD, CF
-SE: n/v, rhinorhea, broncorhea, stomatitis
-caution: pt must be able to clear once liquified

Deoxyribonuclease (Dornavac)

-mucolytic agent
-use: secretions w/ significant nuclear material
-it is an enzye: so stability problems, expensive, and since from other species: hypersensitivity


-drugs affecting the cough reflex

Nonproductive cough

-not moving mucus
-exhaustive, disturbs sleep, break down of elastic fibers (long term), damage to epithelia (long term)

Common causes of non-productive cough

-dry air in heated rooms
-irritants (asthma, pulmonary edema)
-congestion of nasal mucosa
-treat the UNDERLYING problem causing cugh

Therapy goal w/ non-productive cough

-decrease frequency and intesity of the cough but NOT clearance

Narcotic antitussives

-codeine: most effect w/ fewest problems
-impair ciliary function, depresses respiration, broncial constriction, drug dependence, dry secretions


-non narcotic antitussive, number one used
-lacks resp/analgesic effects
-acts on medulary cough center


-ingredient in OTC sleep, cough, cold, decongestant and allergy medications
-anticholinergic: dries up secretions


MOA: peripheral local anesthetic effect, depression of medullary transmission
-problems: "pearls" containing liquid local anesthetic, caution pt about "chewing"


-sympathomimetic amines that vasoconstrict via alpha adrenergic stimulation
-improves ventilation, promotes drainage, reduces stuffy feeling
-topical: more effective, less systemic absorption
-oral: longer duration, less effective, less local irritation, no rebound effect

Decongestant SE

-systemic absorption of topicals: hypertension, tachycardia, hyperglycemia, mydriasis, CNS stim
-vasoconstriction may be followed by vasodilation: rebound effect (makes congestion worse)

Rationale for oxygen therapy

-insure tissue oxygenation
-reduce compensatory responses (hypoxia increases sympathetic tone
-need to eliminate hypoxia

Effects of hypoxia: cardiovascular funtion

-increase sypathetic activity: increase CO, tachycardia (chronic hypoxia decreases HR), increase in BP
-at 5% O2: circulatory failure
-pulomonary hypertension

Effects of 100% O2 on normal pt

-initial mild resp depression
-CNS long term: concurrent stim or depression
-decreased sympatetic tone: decrease CO, BP, HR
-vasoconstriction of coronaries and cerebral blood vessels
-no change in metabolism

Consequences of administering O2

-pulmonary atelectasis (absorption atelectasis)
-ear drum retration, vacuum type headache
-O2 apnea: chronic CO2 retention (COPD), loss of CO2 sensitivity following barbs, narcotics, brain injury

Oxygen poisoning

-cough, nasal stuffiness, sore throat, carinal irritation, burning on inspiration, frequent cough, severe pain on inspiration, dyspnea
-worse with more time
-after 24 hrs: ARDS

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