Drugs to Treat Respiratory Conditions

NSG 220

Structures of the Respiratory System

The upper respiratory tract consists of:


Paranasal sinus


Larynx trachea

The lower respiratory tract consists of:





This week we will review drugs that effect the respiratory system. We will discuss drugs that are used to treat upper respiratory tract illnesses and lower respiratory tract illnesses.

The upper respiratory tract consists of:


Paranasal sinus


Larynx trachea

The lower respiratory tract consists of:





Covering of the lungs-visceral (lining covering the organ/lung) and parietal (lining of the body cavity) layer, pleural space between the visceral and parietal layer which contains fluid eliminating friction.

We have diseases that affect the airway and as well illnesses that affect the airway such as the common cold, allergic rhinitis, sinus infections.

We know that when a person takes a breath, the thorax increases in size, pressure inside intrapleural and intrapulmonic layers(always negative) decrease, air rushes from the atmosphere all the way to the alveoli.


Acute & Chronic Respiratory Diseases and Illnesses

Acute Respiratory Illnesses

Allergic Rhinitis

Common cold

Obstructive Airway Diseases


Chronic Bronchitis


Class of Meds to discuss

Bronchodilators (inhaled)

corticosteroids (intranasal),

antihistamines (oral and intranasal), and

sympathomimetics (oral and intranasal)

*mast cell stabilizers

*Not discussed but treat asthma

Obstructive Airway- difficulty exhaling air- limitation of airflow due to partial or complete obstruction (once air is in difficult to exhale)

Restrictive- difficulty inhaling air (reduced expansion of the lung)


Obstructive Airway Diseases


Chronic inflammation of the airways

Caused by environmental triggers (medications, air pollution, allergens)

Smooth muscles around bronchioles spasm causing narrowing of airways

Increased mucous production

Initially reversible - long term is irreversible due to edema, fibrosis & scarring causing thickening of the “basement membrane”

COPD (group of diseases)


Structural changes- destruction of alveolar septa and elasticity of bronchial walls

Enlarged, weakened air spaces

Chronic Bronchitis “Inflammation of bronchial tubes”

Productive cough

3 months each year for 2 or more years

Called obstructive disease because you can get air out compared to restrictive diseases where you can’t get air in (osis- sarcoidosis)



Albuterol- beta 2 agonist

1st given for severe attacks “only rescue inhaler”

Acts quickly, but doesn’t last long (short acting)

Give before steroid inhaler

Ipratropium- “anticholinergic effect”

Given 2nd during severe/acute attacks

Reduces mucous secretions

Methylxanthines (Theophylline)

Can be toxic due to narrow therapeutic range. Over 20 mcg/ml considered toxic


Beta 2 agonist dilates the bronchi opening up airways/ relax smooth muscles

Also works on beta- 1 which causes the heart to beat fast – will also feel jittery, anxious

Nursing Implications:

Avoid giving patient NSAIDs (worsens asthma)

Avoid Betablockers (can cause bronchospasms)- decreased response to beta-agonist

During severe respiratory attacks “A-I-M”

Use in sequence




Beta 2 agonist- short acting (SABAs) to provide quick relief, given orally or by inhaler

Asthma can be treated with bronchodilators, which are beta-2 receptors agonists (stimulators) which causes the lungs to expand. People with heart conditions, however, are given the opposite: beta-receptor antagonists. Beta blockers block the effects of the hormone epinephrine.

**Remember the lungs are constricted during an asthma attack. Epinephrine is floating around to expand the lungs. But when a non-specific beta blocker is given, it blocks the bronchodilators which stimulates the lungs to open action. *** So avoid all beta blockers

Some betablockers are cardioselective and others are non-cardioselective meaning that they can block beta-1 (heart) or beta-2 (lung) receptors. If given to a person with asthma, it would block effects of bronchodilator (beta-2) resulting in narrowing of the airways.

AIM – Albuterol (1st fastest), Ipratropium (, Methyl-prednisone (Solumedrol)- slow steroid reduces inflammation

Anticholinergics becareful when giving to patients who are already dry, “fluid volume deficit”

Methylxanthines- can be toxic 10-20 mcg/ml therapeutic range. Over 20 mcg/ml is considered toxic so frequent blood draws must be obtained. Avoid given with beta-blockers

**Do not take with Ciprofloxacin or Cimetidine- can increase toxicity risk.

Avoid caffeine.


Steroids & Anti-inflammatory Drugs (Beclomethasone, Fluticasone)

Methylprednisolone & Beclomethasone

Corticoid inhaler works directly on respiratory system reducing inflammation

Usually always given in the event of an asthma attack despite improvement

Mechanism of Action (MOA)

Reduce Swelling & Inflammation

Nursing implications

Onset of medication is slow –not a rescue medication

Increases blood glucose “sones”

Suppress the immune systems, slow wound healing

**Remember glucocorticosteroids (prednisone, dexamethasone, hydrocortisone) are for total body swelling, corticosteroids are respiratory specific

Leukotriene Inhibitors (Montelukast)**


Suppresses the effects of leukotrienes (ultimately reducing inflammation)

Nursing Implications

Given in combination with steroids & albuterol

Long term management of chronic resp conditions

Takes 1-2 weeks for drug to reach therapeutic effect

** most commonly used


Things to teach patient:


The only rescue inhaler to be used during an acute episode (neb or INH)

Can make the pt. feel “jittery/shaky” and heart rate usually increases during/after treatment


Increase fluid intake

If pill form, make sure the patient does not swallow pills


Caffeine increases stimulation-increase chances of arrythmias

Always take in the morning due to restlessness

Antibiotics- Ciprofloxacin and Levofloxacin increase risk of toxicity “seizures”

Allergic Rhinitis

Most common allergic disorder

Inflammatory disorder of the upper airway

Symptoms: sneezing, rhinorrhea (runny nose), pruritis (itching), conjunctivitis, sinusitis, and nasal congestion (dilation and increased permeability of nasal blood vessels.

Triggers: airborne allergens

Two types:

Seasonal “hay fever” occurs during spring and fall due to outdoor allergens (fungi, pollen, grasses, trees)

Perennial (nonseasonal) triggered by indoor allergens usually in the home (dust mite and pet dander).

Drugs to Treat Upper Respiratory Symptoms

Decongestant (Sympathomimetics)

 Oral: Pseudoephedrine** (Sudafed),

Nasal Sprays & drops: Phenylephrine (Neo-Synephrine), Oxymetazoline (Afrin)

Mechanism of Action: Stimulates alpha-adrenergic receptors causing vasoconstriction of the capillaries in the nasal mucosa

Adverse reactions: Palpitations, tachycardia, hypertension

Side effects: Drowsiness, GI irritation, Dry mouth**

Nursing Implications

Rebound congestion can occur with intranasal administration.

Avoid taking with other medications that act as sympathomimetics.

** Pseudoephedrine has the potential to be abused. Patients must purchase with a photo ID and maybe subjected to limited amounts to be purchased. (also counted at medical facilities)

Expectorants: Dextromethorphan, Guaifenesin

Mechanism of Action: Liquefy mucus by increasing respiratory tract secretions via oral absorption; available in oral preparations

Adverse reactions: GI irritation, Skin Rash, dizziness, irregular heart rate

Side Effects: Fatigue, constipation

Nursing Implications:

Promote increasing po fluids

Encourage coughing and deep breathing

Assess Respiratory Status

Have suction available


Caused by

Mycobacterium tuberculosis, Mycobacterium leprae, Mycobacterium avium

Slow growing requiring prolonged treatment

Spread through droplets propelled in the air




Caused by- because of these drug toxicities can occur and non-compliance makes it difficult to treat.

People don’t have any symptoms and don’t know they have it (90% of people) . Referred to as latent





Foreign born


Immunity to M. Tuberculosis develops within weeks

Reactivation can occur in 5-10%


Disease requires prolong therapy usually 3-9 months depending on treatment regimen

Protection against TB can be confirmed by inoculation with bacillus Calmette-Guérin (BCG) vaccine

Caused by- because of these drug toxicities can occur and non-compliance makes it difficult to treat.

People don’t have any symptoms and don’t know they have it (90% of people) . Referred to as latent


Tuberculosis can be…

Latent (Inactive)

Not contagious, patient doesn’t have symptoms

Bacteria is inactive causing no symptoms

Can develop into active TB (5-10% of population with inactive TB) w/o treatment

Must be treated


Contagious until the TB medications have been taken for two weeks

**Yes, you can catch TB more than once!

Person with latent TB may have a negative CXR, but a positive TB test

Reinfection is common


Treating TB- Latent vs. Active

Active TB

Goal: Treat and prevent reactivation

Drug Treatment

Isoniazid (see Latent TB info)


(elevates LFTs

Urine, tears & sweat may turn orange)

Pyrazinamide (elevates LFTs)


optic neuritis – inflammation causing vision impairment

Active TB always treated with 2 or more drugs

Mutation causing resistance.

Resistance to one drug only. So should treat with 2 different drugs to prevent reactivation

Latent TB

Drug Treatment

Isoniazid (INH) (active & latent)*

metabolized in the liver/excreted by the kidneys

teach patients to reduce or eliminate consumption of alcohol to reduce risk of hepatotoxicity.

Can cause liver damage- monitor liver function panel

isoniazid alone taken daily for 6 or 9 months

taken weekly for 3 months when combined with rifapentine

administered IM and PO

Rifampin (RIF) daily

for those who have isoniazid-resistant TB or cannot take isoniazid for other reasons

take for 4 months

Isoniazid plus rifapentine (3 months)

Once weekly

*primary prescribed agent

Don’t forget education….

Isoniazid can cause damage to the liver cells and cause hepatic necrosis.

Teach patients to identify

signs of hepatitis (jaundice, anorexia, malaise, fatigue, nausea) and notify provider immediately.

peripheral neuropathy (tingling, numbness, burning, or pain in the hands or feet), and instruct them to notify the prescriber if these occur. “

Can suppress the metabolism of certain drugs such as phenytoin causing toxic levels. Dosage may need to be adjusted.

Monitor labs

Monitor phenytoin levels

Monitor liver function test (i.e. AST)

Nursing Implications

Monitor Liver function test & Kidney function test

INH is metabolized in the liver and excreted by the kidneys


Cautioned in patients with renal impairment

Can reduce the effects of other drugs (increase metabolism- breaking down fast and not working).

Women taking birth control should use another form of oral contraceptive.

Phenytoin (Dilantin)- suppresses metabolism and can cause elevated levels

Adverse reactions:


Dose-related peripheral neuropathy

Rifampin – red-orange tinged body fluids “harmless”



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