Week 4: Respiratory Flashcards
Pulmonary acinus
The portion of lung distal to a terminal bronchiole and supplied by a first-order respiratory bronchiole or bronchioles
Top is the bronchi with a segmental bronchus and cartilage which goes down into the large subsegmental bronchi (~5 generations) which goes into the small bronchi (~15 generations) then the acinus begins with the bronchioles
Terminal bronchioles➡️ respiratory bronchioles (consists of 1st, 2nd, and 3rd orders) ➡️ alveolar ducts and sacs
Dead space
Gas exchange only happens in the alveoli
The area of lungs ventilated but where no gas exchange occurs is dead space
Anatomical dead space: internal volume of the upper airways including the nose, pharynx, trachea, and bronchi
Restrictive lung disorders
Limited full expansion= ⬇️residual volume & ⬇️ lung compliance
Inflammation/infection: acute bronchitis, pneumonia, TB, Adult Respiratory Distress Syndrome (ARDS)
Neuro: CNS depression-narcotics, neuromuscular disorders- Guillain-Barré syndrome, polio
Diffuse pulmonary disease: silicosis, fibrosis
Space-occupying lesions: tumors
Lung collapse: pneumothorax
Pleural disease: pleural effusion
Minute volume
Normal adult: 20 breaths/min
Consider various pathological situations
Vt = 300 mL or respiratory rate⬇️ or both
VT volume= 500 mL
Minute volume= VT* Respiratory rate
10,000 mL/min
The thorax
Parietal Pleura is attached to the wall and is always pulled outward
The visceral pleura is attached to the lungs and is always pulled inward due to the elastic recoil of the lungs
The sub-atmospheric pressure within the pleural space and the greater-than-atmospheric intrapulmonary pressure within the lungs allows the lungs to remain inflated
Intrapleural pressure is always:
Less than intrapulmonary pressure
Less than atmospheric pressure
Considered negative because of the pull of the two pleural membranes in opposite
Parietal pleura attached to the chest wall & visceral pleura attached to the lungs
Results in negative intrathoracic pressure
Holds lungs/alveoli open
Facilitates venous return
Restrictive signs and symptoms
Dyspnea: usually on exertion (DOE)
Dry hacking cough
Respiratory alkalosis initially (>7.45 pH, <35 CO2):
Caused by a compensatory ⬆️ in respiratory rate trying to offset ⬇️ lung volumes
Eventually lead to hypoxemia & if not corrected may lead to respiratory acidosis
Interstitial lung disease (ILD)
General term that includes a variety of chronic lung disorders including pulmonary fibrosis affecting the lung in 3 ways:
- The lung tissue is damaged in some known or unknown way
- The walls of the air sacs in the lung become inflamed
- Scarring (fibrosis) begins in the interstitium (tissue between the air sacs)➡️the lung becomes stiff
Symptoms (common and often ignored initially): breathlessness during exercise; a dry cough
Further testing is recommended to identify the specific type of ILD- unknown and known causes
ILD Etiology
Connective tissue diseases
Primary diseases
Occupational and environmental
Idiopathic pulmonary fibrosis (IPF)
Treatment or drug- ground glass appearance on CXR
Amiodarone induced interstitial lung disease
Occurs in 6-15% of patients
ILD Diagnosis
Bronchoalveolar lavage (BAL)
Lung biopsy
Blood tests
Pulmonary function tests (PFTs)
Chest X-ray
CT scan
ILD Treatment
Corticosteroids
Oxygen
Prevent complications
Pulmonary rehabilitation
Occupational lung diseases
Caused by microscopic substance inhaled in the workplace= lung damage (esp. with prolonged inhalation) (old hay- “farmers lung”)
More common among smokers who often have a more severe form
Categories: pneumoconioses- silicosis, black lung (coal miners)
Asbestos-related lung disease
Hypersensitivity diseases (occupational asthma, allergic alveolitis)
Occupational lung disease prevention
Education
Awareness of exposure
Dust control, eliminating cause
Protective equipment (think of farmers..)
Sarcoidosis
Restrictive lung disease
Systemic granulomatous disease, impact on several systems/organs; ~10% develop chronic form
Antigen-antibody reaction
Environmental etiology: African-American women in the US
Patho: growth of noncaseating granulomas & proliferation of lymph tissue
Initial symptoms vague, flu-like
Dx: CXR, biopsy, PFTs (I.D.?)
Tx: steroids, cytotoxic drugs, immune modifiers, cytokine inhibitors
Chronic form: cor pulmonale (pulmonary HTN➡️RV failure)
NRSG interventions: meds, NICs r/t manifestations, lung and heart involvement
What sarcoidosis affects in the body
CNS
Eyes
Lungs
Skin
Heart
Liver
Kidneys
Lymph glands
Joints
Chronic obstructive lung disease (COPD)
Airflow obstruction, ⬆️ residual volume (air trapping), ⬆️ airway resistance & compliance
- Bronchitis
- Emphysema
Common cause of death & increasing; now more women than men for chronic bronchitis & equalizing for emphysema
Pathogenesis for chronic bronchitis and emphysema
Tobacco smoke/ air pollution:=
Continual bronchial irritation and inflammation or breakdown of elastin in connective tissue of lungs (from alpha-antitrypsin deficiency)
Chronic bronchitis: bronchial edema, hypersecretion of mucus, chronic productive cough, bronchospasm
Emphysema: destruction of alveolar septa, airway instability
Leads to airway obstruction, air trapping, dyspnea, frequent infections
This leads to abnormal ventilation-perfusion ratio, hypoxemia, hypoventilation, right-sided heart failure
COPD Assessment
Subjective: dyspnea, cough, sputum, smoking
Objective:
- ⬆️RR, ⬆️HR
- Accessory muscle use (neck muscles & intercostals), nasal flaring, pursed lip breathing, prolonged expiration
- Barrel chest: 1:1 AP- Lateral diameter r/t ⬇️ lung compliance & air trapping
- ⬇️ fremitus, hyperresonnance with percussion
- diminished breath sounds, rales & heart sounds
- GI problems r/t ⬆️ lung capacity ➡️ epigastric fullness
- ruddy complexion: r/t normal CO2 from ⬆️RR (compensatory) or cyanosis from chronic hypoxemia
Chronic bronchitis pathophysiology
Significant airway obstruction d/t secretions, airway collapse, etc.
Limited capacity for airflow increase 2o air trapping & airway collapse
Minimal diffusion defect, but very significant ventilation-perfusion mismatch
Mismatch: hypoxia & hypercapnia; hypoxia triggers polycythemia = easily visible cyanosis
Chronic bronchitis
Chronic productive cough for >3 months/yr with no identifiable cause other than smoking
Mucous gland hypertrophy & hyperplasia= chronic irritation and mucous production and risk for infection
Hypoxemia & hypercapnia
Sputum: most frequent pathogens: S. Pneumoniae & H. Influenzae
CBC: erythrocytosis (polycythemia)
Emphysema pathophysiology
Minute volume to provide adequate alveolar ventilation despite dead space 2o reduction in alveolar surface area (compensation)
Diminished diffusion but minimal ventilation- perfusion (V/Q) mismatch
Hypoxia and hypercapnia are not significant as long as adequate minute volume is maintained
Emphysema
Destruction of alveolar walls, chronic over inflation
Lung compliance- loss of elastic recoil, larger lungs, larger volume relative to pressure changes with inhalation
Diffusing capacity- alveolocapillary membrane surface area for O2 and CO2 exchange
Airway resistance- air trapping occurs and diaphragm is distended & see use of accessory muscles to compensate
Dx: bronchitis & emphysema
PFTs: Forced expiratory volume (FEV) with bronchodilator has no improvement with emphysema
ABGs:
Chronic bronchitis- hypoxemia & hypercapnia
Emphysema- little hypoxemia & hypercapnia (hyperventilate to compensate)
CBC: compensate for hypoxemia (HGB & HCT)
Cor pulmonale
Right sided ❤️ failure as a result of pulmonary disease
⬆️pulmonary vascular resistance
Chronic bronchitis (irritation in the bronchial tubes) Tx
Antibiotics to treat acute infections
Bronchoactive drugs to help relax and open up air passages in the lungs
Anticholinergics for mucous gland secretions
Beta-agonists for bronchodilation
Methlxanthines (like theophylline) to increase muscle strength
Corticosteroids
Mucolytics
Eliminate sources of irritation and infection in the nose, throat, mouth, sinuses, and bronchial tubes
Avoid polluted air & dusty working conditions
Give up smoking
Emphysema medications
Bronchodilators: Beta-2 agonists- short acting with effects lasting from 3-6 hours including:
Albuterol (Proventil, Ventolin) Metaproterenol (Alupent, Metaprel) Pirbuterol (Maxair) Terbutaline (Brethine, Brethaire, Bricanyl) Bitolterol (Tomalate) Salmeterol (Serevent)
Theophylline (Theodur, Slo-bid, Uniphyl, Theo-24)
Ipratropium (Atrovent) [anticholinergic drug] acts to relax the bronchial muscles. It is a slow-acting drug with virtually no side effects
Corticosteroids (inhaled or oral)
Oxygen
Emphysema Tx
●Quitting smoking
●Bronchodilator drugs
●Antibiotics
●Exercise: including breathing exercises to strengthen the muscles used in breathing as part of a pulmonary rehabilitation program
●Treatment: with Alpha 1-Proteinase Inhibitor
●Only if a person has AAT deficiency-related emphysema
A1PI not recommended for those who develop emphysema as a result of smoking or other environmental factors
●Lung transplantation
●Lung volume reduction surgery
●A surgical procedure – resection of most severely diseased portions of the lung - to allow the remaining lung & breathing muscles to work better
NRSG Mx: COPD
Impaired gas exchange: low flow O2
Ineffective airway clearance: bronchodilators, use of MDI, coughing
Ineffective breathing pattern: positions to improve breathing, exhale with exertion
Activity intolerance: exercise training, pulmonary rehab, muscle reconditioning, sleep history
Imbalanced nutrition (less than body requirements): frequent small meals, low CHO
Risk for infection: respiratory infection=most common cause for admission; PT-family teaching (avoid crowds, get vaccinated, look for changes in sputum, etc.)
Ineffective coping: individual & family
COPD Preventing Complications
Low flow O2
Positioning: forward leaning, abdominal breathing with legs raising exercises to strengthen abdominal muscles
Muscle reconditioning exercises: start with 10 minutes BID & work up to 20 minutes
Postural drainage, percussion & vibration (CPT)
Improve nutrition, prevent infection
Environmental control: cool temp, low humidity
Assist with sleep, relaxation, and fear reduction
Pulmonary rehabilitation
A multidisciplinary continuum of services directed to those with pulmonary diseases & their families, usually by an interdisciplinary team of specialists, with the goal of achieving & maintaining the individual’s maximum level of independence & functioning in the community
Pulmonary rehab goals
Reduce work of breathing
Improve pulmonary function
Normalize ABGs
Alleviate dyspnea
⬆️efficiency of energy use
Correct poor nutrition
Improve exercise performance & ADLs
Restore a positive outlook
Improve emotional status
Lengthen survival
Asthma
Chronic inflammatory airway disorder; reversible reduction in airway diameter & airway resistance r/t:
Acute bronchoconstriction
Airway edema
Chronic mucus plug formation
Airway remodeling
Asthma costs
~1 in 12 people have asthma (25 million) & numbers are increasing every year
Asthma costs the US ~$56 billion in medical cost, lost school, and work days, and early deaths in 2007
Adults-4th leading cause of lost work
Asthma accounts for ~1.8 million ER visits, 10 million doctor visits, &~1/2 million hospitalizations per year
Asthma medications
Quick relief (rescue); maintenance
Bronchodilators: theophylline, Beta-2 agonists
Antiinflammatories: nonsteroids like Cromolyn (nasalcrom), corticosteroids
Leukotriene inhibitors/ receptor antagonists (block the stimulation of inflammation): accolate, singulair, zyflo
Stepwise approach (NAEPP)
Step 1: mild intermittent (Sx<2x/week)
Rescue: prn short acting inhaled B2 agonist (bronchodilator)
Step 2: mild persistent (Sx>2x/week, <1x/day)
Daily & rescue: step 1 & long-term inhaled steroid low dose daily or cromolyn (trade name nasalcrom)
Step 3: moderate persistent (daily Sx)
Daily & rescue: step 1 & long-term inhaled medium dose steroid daily plus bronchodilator
Step 4: severe persistent (continual)
Daily & rescue: step 3 long acting bronchodilator
Mild intermittent classification
Daytime symptoms less than or equal to 2 weeks
Nighttime symptoms less than or equal to 1 month
PEF (prediction) greater than or equal to 80%
Mild persistent
Daytime symptoms 2-4 weeks
Nighttime symptoms 2-4 months
PEF (predicted) greater than or equal to 80%
Moderate persistent
Daytime symptoms Greater than 4 weeks
Nighttime symptoms Greater than 4 months
PEF (predicted) 60-80%
Severe persistent
Daytime symptoms continuous
Nighttime symptoms frequent
PEF (predicted): less than 60%
Inhalation devices: nebulizer
Sometimes called a “compressor””
Changes liquid medication into fine droplets you inhale through a mask
Can be useful if you find it hard to use an inhaler
Useful for high doses of medications
Used in the hospital, especially the ED
Often used at home now
Asthma interventions
Identify triggers and avoid irritants
Use of peak flow meter
Use of inhalers- spacers, rinsing, timing, order
Pursed lip breathing
Cool air may help, avoid warm moist air
Environmental control: carpets, blinds, pillows, mattresses, pets, smoke, foods: nuts, milk, seafood, kiwi, avocados, air filters, shelf’s
Peak flow meter
Measures maximum speed of exhalation
Peak flow meter use
“Fast blast”
Teaching
Zones (green, yellow, and red)
Peak flow meter green zone
80-100% of your usual or “normal” peak flow- signals all clear
Peak flow meter yellow zone
50-80% of your usual or “normal” peak flow
Caution- your airways are narrowing and may require extra treatment
Your symptoms can get better or worse depending on what you do, or how & when you use your prescribed med
To be safe, call your doctor
Peak flow meter red zone
<50% of your usual or “normal” peak flow
Signals a medical alert
Immediate decisions and actions need to be taken
Severe airway narrowing may be occurring, contact your doctor now. The doctor can tell you what treatment to start
Asthma complications
Status asthmaticus
Respiratory failure
Status asthmaticus
An asthma attack that cannot be controlled with the usual meds
Ongoing attack➡️exhaustion of respiratory muscles & severe V/Q mismatch ➡️ respiratory failure & hypoxia
Unable to talk, moving very little air➡️barely/no audible wheezing or adventitious breath sounds; cyanotic; sensorium changes and pulses paradoxus
Treatment: medical emergency
Asthma presentations
It’s primarily an inflammatory disease that includes smooth muscle spasm, airway edema, and mucous plug
Cough Wheezing Anxiety Restlessness Oxygen desaturation Increased work of breathing
Asthma assessment
Findings consistent with impending respiratory failure:
Altered level of consciousness Absent breath sounds Central cyanosis Diaphoresis Inability to lie down Inability to speak
Beta agonists
Beta receptor agonists stimulate beta-2 receptors on bronchial smooth muscle and mediate muscle relaxation
Epinephrine/Isoproterenol➡️significant beta1 cardiovascular effects
Terbutaline/Albuterol➡️relatively selective beta2
Steroids
Methylprednisolone 2mg/kg x1, then 0.5-1mg/kg every 4-6
ABGs for status asthmaticus
Early status asthmaticus: hypoxemia, hypocarbia
Late: hypercapnia
Decision to intimate should not depend on ABG, but on clinical assessment
Risk factors for fatal asthma
Medical: previous attack with rapid/severe deterioration or respiratory failure or seizures/loss of consciousness
Psychosocial: denial/non-compliance, depression or other psychiatric disorder, dysfunctional family, inner city resident
Ethnic: non-white child
Up to 1/3 of children who die from asthma have only had mild asthma before and had not been classified as “high risk” until then
Status asthmaticus treatment
Humidified oxygen-to max saturation
Inhaled short-acting beta-2 agonists: large and frequent doses
Subcutaneous epinephrine-rescue if unresponsive to beta-2 agonist
Continuous bronchodilators (via MDI & nebulizers) until effective or reaching toxicity
Delay intubation for as long as possible
Corticosteroids: methylprednisolone 40 mg Q6h
Theophylline as it is an anti inflammatory med and has diaphragmatic effects
