N203 RESPIRATORY AGENTS
Normal Pulmonary Function:
Co2 out, O2 in
Pressure changes, diffusion across membranes, pressure gradients. Compliance: alveoli and airways stretch. Naturally humidified to 100%. Surfactant; decreases surface tension between alveoli—who would rather collapse. Pons and respiratory centers [pons and medulla] in the brain, diaphragm innervated by the phrenic nerve, which respond to baro receptors and chemo receptors [that notice O2, CO2, H2 levels.] Peripheral chemoreceptors: carotid and aortic arch also check chemicals going by. These are responsive especially to O2. Volume: around 500mLs. People post op get atelectasis [collapsed alveoli], pneumonia, etc because it hurts to take a deep breath. Lungs love to get involved when pts come in for any pathology—being still in bed the lungs are likely to get pathological too. Pts lung sounds can change day to day. That’s the “outlier:” a pt who gets complications in the hospital and is there for 3 weeks instead of the 3 day stay for their surgery.
Concerns about using supplemental O2: low O2 is sensed by peripheral chemoreceptors [at aortic arch and carotids] and triggers increased ventilation. Putting a person on supplemental O2 can thereby have the opposite effect of depressing respiration.
Bronchial smooth muscles: are on bronchi and bronchioles, and respond to bronchoconstrictive PNS signals from the vagus nerve, and bronchodilate in response to SNS neurotransmitters [epinephrine.]
II. Drugs for Common Upper Respiratory Disorders
Runny nose: is rhinorrhea or rhinitis due to the common cold or to hayfever.
Pharm treatments for the common cold: antihistamine [H1] blockers, simpathomimetic decongestants, antitussives, and expectorants.
H1 versus H2: There’s H1 and H2—H2 are in the gastric, the H1 are in the upper respiratory. Histamine is an immune inflammatory agent released from the mast cells.
A. Antihistamines
2. Prototype: Diphenhydramine (Benadryl)
Action: compete with histamine for H1 receptor sites, prevent histamine (allergic) response.
Indication: allergic rhinitis, itching, sleep aid, antitussive
Contraindication: acute asthmatic attack, severe liver disease
Adverse effects: agranulocytosis, hemolytic anemia, thrombocytopenia [so please don’t take this long term]
side effects: drowsiness, N & V, urinary retention, blurred vision, hypotension
patient teaching; avoid other CNS depressants, driving. Don’t take this long term.
Prototype: Loratadine: Claritin: has fewer side effects, it’s a second generation drug.
Action: compete with histamine for H1 receptor sites, prevent histamine (allergic) response. Non-sedating b/c It has poor affinity to CNS H1 receptors.
Use: Relief of symptoms of seasonal allergic rhinitis; idiopathic chronic urticaria [hives].
Adverse: Hypotension, hypertension, palpitations, syncope, tachycardia
Education: Avoid CNS depressants.
B. Decongestants
1. action: produce vascular constriction of nasal mucosal capillaries
2. administration: nasal spray or drops
3. caution; frequent use can lead to rebound nasal congestion from irritation of mucosa; use less than 5 days
4. adverse effect: HTN, hyperglycemia
Prototype: Sinex
Action: alpha-adrenergic agonist; mydriatic; decongestant. Potent, synthetic, direct-acting sympathomimetic with strong alpha-adrenergic and weak beta-adrenergic cardiac stimulant actions. Produces little or no CNS stimulation.
Use: Used topically for rhinitis of common cold, allergic rhinitis, and sinusitis. Also : Parenterally to maintain BP during anesthesia, to treat vascular failure in shock, mydriatic for ophthalmoscopic examination or surgery.
Adverse effect: HTN, tremor, sneezing, severe visceral or peripheral vasoconstriction
C. Antitussives [anti-cough]
Prototype: Dextromethorphan Hydrobromide (Robitussin DM)
Action: suppress cough reflex by inhibiting cough control center in medulla; reduces viscosity of tenacious/stringy secretions.
Use: Temporary relief of cough spasms in nonproductive coughs due to colds, pertussis, and influenza.
Contraindications: COPD, chronic productive cough
Adverse effects: hallucinations, CNS depression with very large doses
D. Expectorants
Best expectorant: adequate hydration. Expectorants loosen bronchial secretions so they can be expectorated
Prototype: Guaifenesin (Robitussin, Mucinex)
Action: Enhances reflex outflow of respiratory tract fluids by irritation of gastric mucosa.
Use: loosen mucus: Aids in expectoration by reducing adhesiveness and surface tension of secretions.
Contraindications: Cough due to CHF, ACE inhibitor therapy, or tobacco smoking.
Adverse effects: none. Nausea and dizziness, the end.
III. Drugs for Acute and Chronic Lower Respiratory Disorders
A. COPD
1. “Bronchial asthma is a COPD” [not included in Lemone/Burk book]
Asthma is bronchoconstriction set off by some stimulant—bronchial asthma is a chronic histamine reaction. “Clinically asthma is diagnosed when a patient has reversible airway obstruction." This is manifested by:
- Bronchospasm - wheezing, dyspnea, cough
- Mucous hypersecretion - mucus plugs, V/Q mismatch
- Airway edema - decreases airway diameter
- Airway inflammation - makes airway stiff (decreased compliance)
- Hyperactive airway - irritants can precipitate acute bronchospasm
Mild asthma is generally a seasonal condition or occurs sporadically. Wheezing and breathlessness may be experienced when triggered by events such as exercise. The attacks are mild, with symptoms presenting themselves only during the attacks. Treatment: a bronchodilator and used only to alleviate symptoms when they occur.
Moderate asthma usually occurs a couple times per week. Symptoms may present at night, may be triggered by exercise. An asthma attack may require emergency care. Treatment: may include a beta-agonist to be used when symptoms occur. Preventative treatment, such as an inhaled steroid, may be prescribed for administration between asthma attacks.
Severe asthma: continuous symptoms and/or frequent asthma attacks. These asthmatics must change their lifestyle to accommodate the condition. Overall activity levels are affected, and hospitalization and emergency care may be frequently required. Severe asthma has many triggers. Treatment: preventative medications, as well as medications to treat attacks.
Brittle asthma: is rare, unpredictable; attacks are very severe and can be life threatening. Treatment: Preventative and episodic medication is prescribed--Nebulizers and bronchodilators, and steroid tablets are used for long-term asthma maintenance and control.
2. Emphysema: oft from smoking but also sometimes from bad working conditions, coal, asbestos, steel workers. Also some genetic component from mutation of the Alpha-1-antitrypsin protein that prevents alveoli breakdown.
3. Chronic bronchitis: usually from smoking—these guys cough and rattle every morning and hack up sputum.
4. Factors Leading To Bronchoconstriction
· environment: what are they? Pollen, air pollution, temp changes, humidity, work, stifling perfume, etc.
· pollutants: what are they?
· allergic substances: what are they? Dust, animals, etc.
· drugs: such as? Asprin and NSAIDS [why? I don’t get it…]
COPD’ers get pneumonia b/c they don’t move as much air, low gas exchange, stagnant fluid in the lungs, all COPD’ers are always immunosuppressed because of chronic pathology. ‘Exacerbation’ is a flare up of symptoms: like pneumonia
B. Sympathomimetics
Prototype: Metaproterenol (Alupent)
Action: Hit Beta 2 receptors: bronchodilation, relaxation of smooth muscles of bronchi. “Potent synthetic beta-adrenergic agonist that acts selectively on beta2-adrenergic receptors to relax smooth muscle of bronchi, etc.
Drug-drug interaction: increased with other sympathomimetics; Epinephrine, other sympathomimetic bronchodilators may compound effects of metaproterenol; MAO inhibitors, tricyclic antidepressants potentiate action of metaproterenol on vascular system; decreased effect of beta blockers
Given: PRN, Inhaler, PO, etc. Patient may use tablets and aerosol concomitantly.
Adverse effects: tremors, tachycardia, dysrhythmias, HTN, cardiac dysrhythmias, cardiac arrest, paradoxical bronchoconstriction.
RN Assessment: Listen to lungs before and after inhaler treatment.
Dyspnea: sense of breathlessness. DOE: dyspnea on exertion
PEOPLE ON ANTIINFLAMATORIES ARE ALWAYS AT RISK FOR INFECTION—BECAUSE WE ARE BLOCKING THEIR IMMUNE SYSTEM.
Inhaled drugs have local effects, therefore fewer systemic effects
C. Methylxanthine (Xanthine) Derivatives
Prototype: theophylline
Action: relaxes smooth muscle by direct action, particularly of bronchi and pulmonary vessels, but also GI.
Stimulates medullary respiratory center with resulting increase in vital capacity.
Stimulates myocardium, thereby increasing force of contractions and cardiac output,
Stimulates all levels of CNS, but to a lesser degree than caffeine.
Bad bad: narrow therapeutic range, not as effective as other inhalers— These are not inhaled, they are IV or
Adverse effects: tachycardia, convulsions/seizure, dysrhythmias, cardiac arrest, CNS reactions, resp arrest, circulatory failure
D. Leukotriene Receptor Antagonists
1. effects of leukotrienes: inflammation in lungs:
2. Not to be used with acute asthmatic attack; used for prophylaxis and maintenance
Prototype: Montelukast ( Singulair)
Not for: acute asthma attack; used for prophylaxis and maintenance
Action: Leukotriene Receptor Antagonist; interrupts smooth muscle contraction/bronchoconstriction
adverse effects: none known!
Bronchodilators and Steroids are for acute asthma attack
E. Glucocorticoids (Steroids) for acute attack:
1. MDI [inhaler]
2. IV
3.
Beclomethasone (Vanceril) inhaler
Type: glucocorticoid, long acting
Use: for Rx of asthma, COPD, allergies
2. Action: suppresses inflammation and adrenal function
Side effects: Candidal infection of oropharynx, Dry mouth, itchy nose, etc.
Adverse: with excessive doses: symptoms of hypercorticism.
If ‘steroid dependent COPD’er,’ that’s a serious disease. If we see that, we have to make sure a steroid is ordered for them in order to keep their airways open. Don’t let them be abruptly stopped.
Hyperglycemia and hypertension always go with gluco [sugar] corticoids]
Mast Cell Stabilizer
F. Nedocromil: inhaler
Action: antiinflammatory; mast cell stabilizer: Inhibits activation of and mediators released from inflammatory cells (e.g., neutrophils, mast cells, monocytes).
Use: Don’t use for acute asthma attack. prophylaxis of bronchial asthma; inhibits histamine release; maintenance.
Adverse: none
Mucolytics: These are basically expectorants: they thin the mucus by acting like detergents. You need to see what the thickness of mucus is. If someone’s got thick mucus, you need to get them hydrated. Tenacious mucus is stringy.
IV. Case Scenarios
A. Your roommate has a cold, coughing all night so you can’t sleep. What drug and nondrug interventions are indicated?
Anti tussives, have them sit up, get OOB, vapo-rub,
B. Your patient has COPD with pneumonia. What drug and nondrug interventions are indicated?
Oxygen first. Get their pulse ox, in case they are CO2 retainers. Be upright for max lung expansion, or be comfortable. Use an incentive spirometer for breathing exercise. There’s a good chance the patient is dehydrated. Sympathomimetics, antibiotics, need to know the hx, might need steroids, need RT involved, and humidification. Think worst case: pt deteriorates and ends up on a vent.
C. Your 8 yo son plays CYO basketball. Every game he gets an asthma attack. What interventions are indicated?
Inhaler.
Objectives: Upon completion of this class, the student will be able to:
1. Compare antihistamine [blocks inflammatory immune response], decongestant [like sympathomimetics—sinex], antitussive [robitussin that depresses CNS cough center], and expectorant drug groups [mucinex or robitussin that thin mucus and irritate bronchial walls to get lung butter out];
2. Describe the nursing process with these agents;
3. Differentiate the drug groups used to treat COPD and asthma and the desired effects of each; glucocorticoids, xanthine derivatives [these are bad], mucolytics, Leukotriene Receptor Antagonists, sympathomimetics, Mast Cell Stabilizer
4. Contrast the therapeutic effects of these meds for for COPD and asthma; Leukotriene antagonists [leukotriene causes bronchconstriction, so we block it], glucocorticoids [block inflammatory response], Nedocromil [chills out the Mast cells by blocking their activating chemicals], antihistamines [blocks H1 receptors to prevent allergic reaction/inflammation], and mucolytics [get the lung butter thinner and expectorated]
5. Describe the nursing process with safe use of these agents.
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