Haley Respiratory

Reversible airflow limitation

Asthma

Irreversible airflow limitation

COPD

For COPD and asthma management, why do we teach about risk factors and triggers?

So patients can avoid them which will prevent worsening symptoms or exacerbations → improve quality of life

Chronic inflammatory airway disorder causing bronchial spasms; airways are overly sensitive and narrow easily. Is reversible

Inflammation → airway narrrowing → difficulty breathing

Asthma

Asthma risk factors

• Genetics

• Nose/sinus problems

• Allergens

• Cigarrete smoke/air pollution (pollen, dust, mold, furry pets)

• GERD → triggers bronchoconstriction

• Psychological factors (anxiety/panic

• Drugs & food aditives (e.g. NSAIDs, tartar, yellow dye, sulfiting agents)

• Exercise (cold environment or dry air → wear mask)

• Respiratory tract infections/immune response

Theory that suggests children/infants who grow up in very clean environments have less developed immune systems, making them more prone to allergies/asthma later in life

Hygeine hypothesis

Pathophysiology of asthma

• Inflammatory cells release mediators; allergens cross-link IgE antibodies on mast cells/eosinophils, triggering the release of leukotrienes, histamine, cytokines, prostaglandins, and nitric oxide

• Vasodilation → runny nose

• Nerve cells → itching

• Smooth muscle cells → bronchospasms

• Goblet cells → inflammation causes mucus production

• All lead to muscle spasms and secretions that obstruct airflow, esp during exhalation

Early phase response (asthma)

Asthma response that triggers within minutes after exposure to irritant or allergen; resolves in 1-2 hrs, but symptoms can recurr 4-6 hrs after initial trigger due to influx of inflammatory mediators

Late phase response (asthma)

Body activates more inflammatory cells which continues airway inflammation and symptoms. Can last for 24 hrs+

• Treat w/ corticosteroids

Clinical manifestations of asthma

• Wheezing (not a reliable indication of severity)

• Cough

• Dyspnea

• Chest tightness

Very little/no wheezing or decreased breath sounds →

Silent chest; red flag for impending respiratory failure

• Most extreme form of an acute asthma attack.

• Is characterized by hypoxia, hypercapnia, and ARF.

• Unresponsive to treatment with bronchodilators and corticosteroids.

• They may have chest tightness, a severely marked increase in SOB or sudden inability to speak.

• Hypotension, bradycardia, and respiratory and/or cardiac arrest may occur if we do not recognize that the patient is getting worse.

Status Asthmaticus

Diagnostic study of asthma

• Physical exam

  • Lung sounds

  • Respiratory effor

  • Color

• Diagnostic tests

  • ABGs

  • Pulmonary function tests

  • Allergy testing

Taking a hx for diagnosing asthma

• Ask patient if they’ve had similar attacks

• Whether or not the attacks are linked to a trigger

Diagnostic Assessment of asthma

• History and physical assessment

• Spirometry, including response to bronchodilator therapy

• Peak expiratory flow rate (PEFR)

• Chest x-ray

• Pulse oximetry

• Allergy skin testing (if indicated)

• Blood level of eosinophils and IgE (if indicated)

Simple way to measure how fast a person can exhale; often used to confirm asthma and monitor control of asthma over time

PEFR

PFT for diagnosing asthma; patients must avoid tkaing bronchodilators upt 6-12 hours before this test

Spirometry test

Asthma meds

• Corticosteroids

• Bronchodilators

• Leukotriene modifiers

• Inhalers

• Anticholinergics (acute)

• 1st line controller drugs

• Reduce airway inflammation and prevent bronchospasms

• Can block late phase inflammatory response

• Must be taken consistently for long-term control

ICS

ICS SE

• Hoarseness

• Oral thrush

• Dry cough

• Risks lower if patient uses a spacer and rinse mouth after each use

Albuterol =

SABA

SABA (albuterol) indication

• Works within minutes to relieve acute symptoms

• Do not treat inflammation → consistent use of SABAs = read flag that astham is not well-controlled

LABAs (salmeterol) nursing considerations

• ALWAYS pair with ICS (take ICS first)

Leukotriene modifiers

• Provide additional anti-inflammatory effects

• Not as strong as ICS

• Do not work for acute attacks; take every day for long-term control

MDIs VS DPI

• Metered dose inhalers → tell patient to press and breathe slowly (can use spacers)

• Dry powdered inahlers → inhale quickly and deeply (do not need spacers)

• TEACH BACK METHOD

Nursing care of the asthma patient

• Goal of care is to achieve and maintain control of asthma symptoms

• Nurse’s role is to prevent or reducing asthma attacks is educating the patient and their caregivers (identify and avoid triggers)

• Trigger & irritant management

• Therapy & medication education

Chronic, slowly progressive respiratory disorder that is not fully reversible (is irreversible) and causes airflow limitation

COPD

Risk factors for COPD

• Smoking (#1 cause)

• Pollution/occupational hazards

• Male

• Aging adult (50-60’s after decades of exposure)

Pathophysiology of COPD

• Chronic inflammation of the airways; leads to lung remodeling and destruction of lung tissue

• Involves airflow limitation that cannot be completed reversed with forced inhalation. Main cause is loss of elastic recoil and airflow obstruction

• Progession leads to worsening airflow limitation, air trapping, and impaired gas excahnge

• Main inflammatory cells are neutrophils, macrophages, and lymphocytes

How does “barrel shape” chest develop in COPD patients?

As COPD worsens, residual air in the lungs increases, leading to air trapping. This causes the chest to hyper inflate and take on the “barrel shape”. This also reduces the effectiveness of the respiratory muscles

COPD is chronic inflammation of the airways. True or false?

True

COPD clinical manifestations

• Dyspnea on exertion or at rest

• Clubbing, cyanosis

• Barrel chest & accessory muscle use

• Impaired exercise toleranc & fatigue

• Chronic cough

• Chronic sputum production

• Dyspnea (heaviness in chest, difficulty taking deep breath, gasping/labored breaths)

• Hx of exposure to risk factors

• Patient shifts to chest breathing

• Advanced COPD → weight loss, anorexia, fatigue

RSHF caused by pulmonary HTN → emergency

Cor pulmonale

S&S of ccute exacerbation of COPD

• Sudden worsening of baseline symptoms

  • Cough

  • Sputum changes

  • Increased dyspne

  • ARF (caused by acute exacerbation or if meds are abruptly stopped)

Body produced excess RBCs due to chronic hypoxia

Polycthemia vera

COPD Assessment

• Physical exams

  • Respiratory status (rate, effort, O2 sat, use of accessory muscles)

  • History (do they have chronic cough, sputum production, dyspnea, smoking hx, any exposure to irritants)

  • Impact on daily life (fatigue, weight loss, inability to do ADLs, nutrition)

• Diagnostic tests

  • Spirometry (reduced FEV1 and reduced FEV1/FVC ratio)

  • Chest X-ray (flattened diaphragm due to hyperinflated lungs)

  • ABG’s (help understand severity)

  • 6 min walk test → assess exercise tolerance (if drop below 88% → red flag for COPD)

Purse-lipped breathing

• Natural response from COPD patients when SOB, where patients inhale through nose and exhale slowly through pursed lips (like blowing out a straw) → keeps airways open longer which improves exhalation and reduces work of breathing; improves O2 exchange

• Teach patients this breathing technique for symptom relief

Pulmonary fibrosis effect on FEV1/FVC ratio

Restrictive disease reduces both numbers, but ratio remains normal

COPD meds

• O2 therapy (keep O2 sat above 90%; keep it between 88% and 92%)

• Bronchodilaotrs (1st line meds for most COPD patients)

  • Beta agonists and anticholinergics

• Rofumilast (Daliresp)

• Mucolytics

Why is giving too much O2 bad for COPD?

Some patients retain CO2, and giving them too much O2 can reduce their drive to breath which can worsen CO2 retention and lead to respiratory acidosis

Oral anti-inflammatory drug that helps reduce exacerbations in people with COPD and chronic bronchitis

• Long-term daily; not for acute symptoms

Rofumilast (Daliresp)

Breathing techniques

• Pursed-lip breathing → improves O2 exchange

• Diaphragm/belly breathing → strengthens diaphragm and makes breathing more efficient

• High-fowlers

• Tripod breathing

Nursing care for COPD

• Overall goal is symptom releif, ability to perform ADLs, improved exercise tolernace, prevent complications, and slow diseae progression

• Nurse must support patient’s self-management of COPD through education, monitoring, and promoting lifestyle changes

• Meds and how to use inhalers/meds correctly

• Follow O2 therapy guidelines

Energy conservation for COPD patients

• Plan rest periods

• Spread out activites to help reduce fatigue and dyspnea

Single most important lifestyle change for COPD

Smoking

Inflammation of the bronchi; hallmark feature is chronic, productive cough that lasts longer than 3 months in 2 consecutive years.

• “Blue bloaters”

  • Cyanotic, overweight, may have peripheral edema

  • Mucus + infllamation

Chronic bronchitis

Destruction of the alveolar walls which leads to loss of elastic recoil and air trapping.

• “Pink puffers”

  • Thin/weight loss, purse-lipped breathing, severe dyspnea with minimal cyanosis until late in disease, barrel chest

Emphysema

Treatment approach to COPD

• Start with bronchodilators (1st line)

• Use ICS or combination inhalers if symptoms persist or exacerbations occur

Chronic productive cough & airway obstruction due to production of excess mucus (airway problem) →

Chronic bronchitis

Normal FEV1/FVC ratio

70-85% (0.70-0.85)

COPD FEV1/FVC ratio is classified as

< 0.70 (70%)

FEV1/FVC ratio is preserved, but TLC is decreased

Restrictive disorders (e.g. fibrosis)