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N5 471 > Week 4: Respiratory > Flashcards

Week 4: Respiratory Flashcards

1
Q

Pulmonary acinus

A

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

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2
Q

Dead space

A

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

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3
Q

Restrictive lung disorders

Limited full expansion= ⬇️residual volume & ⬇️ lung compliance

A

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

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4
Q

Minute volume

A

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

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5
Q

The thorax

A

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

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6
Q

Intrapleural pressure is always:

A

Less than intrapulmonary pressure

Less than atmospheric pressure

Considered negative because of the pull of the two pleural membranes in opposite

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7
Q

Parietal pleura attached to the chest wall & visceral pleura attached to the lungs

A

Results in negative intrathoracic pressure

Holds lungs/alveoli open

Facilitates venous return

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8
Q

Restrictive signs and symptoms

A

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

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9
Q

Interstitial lung disease (ILD)

A

General term that includes a variety of chronic lung disorders including pulmonary fibrosis affecting the lung in 3 ways:

  1. The lung tissue is damaged in some known or unknown way
  2. The walls of the air sacs in the lung become inflamed
  3. 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

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10
Q

ILD Etiology

A

Connective tissue diseases

Primary diseases

Occupational and environmental

Idiopathic pulmonary fibrosis (IPF)

Treatment or drug- ground glass appearance on CXR

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11
Q

Amiodarone induced interstitial lung disease

A

Occurs in 6-15% of patients

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12
Q

ILD Diagnosis

A

Bronchoalveolar lavage (BAL)

Lung biopsy

Blood tests

Pulmonary function tests (PFTs)

Chest X-ray

CT scan

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13
Q

ILD Treatment

A

Corticosteroids

Oxygen

Prevent complications

Pulmonary rehabilitation

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14
Q

Occupational lung diseases

A

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)

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15
Q

Occupational lung disease prevention

A

Education

Awareness of exposure

Dust control, eliminating cause

Protective equipment (think of farmers..)

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16
Q

Sarcoidosis

A

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

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17
Q

What sarcoidosis affects in the body

A

CNS

Eyes

Lungs

Skin

Heart

Liver

Kidneys

Lymph glands

Joints

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18
Q

Chronic obstructive lung disease (COPD)

A

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

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19
Q

Pathogenesis for chronic bronchitis and emphysema

A

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

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20
Q

COPD Assessment

A

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
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21
Q

Chronic bronchitis pathophysiology

A

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

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22
Q

Chronic bronchitis

A

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)

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23
Q

Emphysema pathophysiology

A

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

24
Q

Emphysema

A

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

25
Q

Dx: bronchitis & emphysema

A

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)

26
Q

Cor pulmonale

A

Right sided ❤️ failure as a result of pulmonary disease

⬆️pulmonary vascular resistance

27
Q

Chronic bronchitis (irritation in the bronchial tubes) Tx

A

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

28
Q

Emphysema medications

A

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

29
Q

Emphysema Tx

A

●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

30
Q

NRSG Mx: COPD

A

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

31
Q

COPD Preventing Complications

A

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

32
Q

Pulmonary rehabilitation

A

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

33
Q

Pulmonary rehab goals

A

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

34
Q

Asthma

A

Chronic inflammatory airway disorder; reversible reduction in airway diameter & airway resistance r/t:

Acute bronchoconstriction
Airway edema
Chronic mucus plug formation
Airway remodeling

35
Q

Asthma costs

A

~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

36
Q

Asthma medications

A

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

37
Q

Stepwise approach (NAEPP)

A

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

38
Q

Mild intermittent classification

A

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%

39
Q

Mild persistent

A

Daytime symptoms 2-4 weeks

Nighttime symptoms 2-4 months

PEF (predicted) greater than or equal to 80%

40
Q

Moderate persistent

A

Daytime symptoms Greater than 4 weeks

Nighttime symptoms Greater than 4 months

PEF (predicted) 60-80%

41
Q

Severe persistent

A

Daytime symptoms continuous

Nighttime symptoms frequent

PEF (predicted): less than 60%

42
Q

Inhalation devices: nebulizer

A

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

43
Q

Asthma interventions

A

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

44
Q

Peak flow meter

A

Measures maximum speed of exhalation

45
Q

Peak flow meter use

A

“Fast blast”

Teaching

Zones (green, yellow, and red)

46
Q

Peak flow meter green zone

A

80-100% of your usual or “normal” peak flow- signals all clear

47
Q

Peak flow meter yellow zone

A

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

48
Q

Peak flow meter red zone

A

<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

49
Q

Asthma complications

A

Status asthmaticus

Respiratory failure

50
Q

Status asthmaticus

A

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

51
Q

Asthma presentations

A

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
52
Q

Asthma assessment

A

Findings consistent with impending respiratory failure:

Altered level of consciousness 
Absent breath sounds
Central cyanosis
Diaphoresis 
Inability to lie down 
Inability to speak
53
Q

Beta agonists

A

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

54
Q

Steroids

A

Methylprednisolone 2mg/kg x1, then 0.5-1mg/kg every 4-6

55
Q

ABGs for status asthmaticus

A

Early status asthmaticus: hypoxemia, hypocarbia

Late: hypercapnia

Decision to intimate should not depend on ABG, but on clinical assessment

56
Q

Risk factors for fatal asthma

A

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

57
Q

Status asthmaticus treatment

A

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

N5 471 (5 decks)

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