Respiratory Flashcards

1
Q

What is Pneumonia?

A

Acute inflammation of lungs which some or all alveoli are filled with fluid or cells

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2
Q

What are the SS of pneumonia?

A

Cough up green sputum, dyspnea, tachypnea, pleuritic pain, fever
Percussion: Dull sound
Presentation:
(1) Typical= sudden onset of symptoms, bacterial infection most common, fever, sputum, physical sign of consolidation
(2) Atypical (aka ‘walking pneumonia’) = few Sx, little sputum, minimal chest signs

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3
Q

What are the types of Pneumonia?

A
1. Inhalation
▪ Bacterial
▪ Viral
▪ Fungal
▪ Toxic chemicals: smoke, dust, gas
2. Hematogenous
▪ Occurs more often in immunosuppressed people
3. Aspiration
▪ Common in patients with swallowing disorders
➢ Supine body position increases risk
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4
Q

What are risk factors for developing pneumonia?

A

exposure to infectious agent, aspiration, impaired consciousness, alcohol abuse, post surgery, very
old/young and/or immunosuppressed, most are preceded by an upper respiratory infection followed by sudden and sharp chest pain

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5
Q

What is the treatment plan for Pneumonia?

A

(1) Poor gas exchange: Deep breathing, positioning
(2) Pain in cough or pleuritis (support cough, relaxation)
(3) retained secretion (mobilize ASAP, coughing, huffing, active cycle of breathing, improve chest expansion)
(4) Decreased mobility (Bed exercises, mobilize to tolerance level, upright position as much as possible)
(5) Active infection (Antibacterials/antibiotics, antifungal (if fungal infection))

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6
Q

What are preventions for pneumonia?

A
  • Vaccine.
  • Treatment of influenza.
  • Mobility (keep lungs clear of sputum).
  • Prevent aspiration (HOB at 30).
  • Universal precautions and overall health.
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7
Q

What is atelectasis?

A

Collapse of normally expanded and aerated lung tissue at any structural level involving all or part of the lung. Can be patchy, segmental or lobar distribution

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8
Q

Causes of Atelectasis

A
  1. Blockage of bronchus/bronchiole: Lung is prevented from expanding due to mucous or airway obstruction
  2. Compression which prevents alveoli from expanding due to pneumothorax, pleural effusion, space-occupying lesion (tumor)
  3. Post-anesthetic effects: Anaesthesia and prolonged recumbency, breathing at low lung
    volumes
  4. Poor ventilation: Due to paralysis, diaphragmatic disorders, hypoventilation
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9
Q

Signs of Atelectasis

A
  • Possible dyspnea, tachypnea, cyanosis
  • Chest X-Ray: shifting of lung structures toward collapse
  • Percussion: Dull
  • On Auscultation: Decreased breath sounds, fine crackles
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10
Q

Treatment for Atelectasis

A

Identify underlying cause:
o Suctioning/secretion removal techniques if due to secretions
o Chest tube if due to pneumo/hemo-thorax or extensive pleural effusion
• Positioning, mobility as tolerated and breathing exercises.

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11
Q

What is Acute Respiratory Distress syndrome (ARDS)

A

ARDS is not a single disease. It is a term given to the clinical manifestation of the common pathway of several indirect lung injuries. Other names may include adult respiratory disease syndrome, shock lung, wet lung or hyaline membrane disease.
• Acute respiratory failure with severe hypoxemia as a result of pulmonary or systemic problem.
• Lung injury characterized by increased permeability of alveolar capillary membrane.
• Leakage of fluid and blood into lung interstitium and alveoli - inflammatory reaction; alveolar edema and collapse.
• Can occur in adults and infants.

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12
Q

Risk factors for ARDS

A
  • Severe trauma.
  • Aspiration.
  • Embolism.
  • Indirect: happens after viral infection or pneumonia.
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13
Q

Treatment for ARDS

A

• Intubation and ventilator assistance.
Positive-end expiratory pressure (PEEP) to keep airways open
• Tackle underlying cause.
• Prone position.
• Secretion clearance if needed (manual or mechanical vibration).

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14
Q

Signs and Symptoms of ARDS

A

Key feature on X-ray = white out.

• Increased respiratory rate, shallow breathing, severe dyspnea, cyanosis, accessory

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15
Q

Why do you put someone with ARDS into prone?

A

The lung expands from the apex at the shoulder and goes down the rib 6 anteriorly, 8 medially and 10 posteriorly. There is more surface area available for gas exchange posteriorly. There are copious amounts of secretions in ARDS hence the white out. In supine, the posterior lung parenchyma (alveoli) are compressed by the abdominal content. When a patient with ARDS is placed prone, the posterior aspect of the lung is no longer subject to high pressure and posterior lung atelectasis decreases which increases V/Q marching and subsequent oxygenation

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16
Q

Why does Infant Respiratory Distress Syndrome happen?

A

Children have a lack of surfactant (helps lungs inflate with air and keeps the sacs from collapsing)

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17
Q

Risk for Infant respiratory distress syndrome? (IRDS)

A

prematurity, c-section, multiple babies, blue baby, stop breathing, grunts

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18
Q

What is the treatment for infant respiratory syndrome? (IRDS)

A

Deliver artificial surfactant

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19
Q

What is Lung Abscess?

A

Infection leading to necrosis of lung tissue and cavity formation

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20
Q

Signs of Symptoms for lung abcess

A

Purulent and foul smelling sputum
Cough
Fever
Chest pain

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21
Q

Treatment for lung abscess

A
Prolonged antibiotic use 
Drainage of abscess 
Deep breathing exercises
Supplemental O2 if needed
Mobility as tolerated 
Secretion removal if abscess if draining into airway
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22
Q

What is Tuberculosis?

A

Infection- mycobacterium tuberculosis
Inflammatory, systemic disease that affects lungs and may disseminate to involve kidneys, growth plates, meninges, avascular necrosis of hip joint, lymph nodes and other organs

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23
Q

How does Tuberculosis spread?

A

airborn droplets: when infected people sneeze, laugh, sing and cough

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24
Q

Signs and symptoms of TB

A
cough 3+ weeks 
weight loss 
fever
night sweats
fatigue 
bronchial breath sounds
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25
Q

How is TB detected?

A

Injected TB derivative into forearm: to determine of body’s immune response has been activated by TB before
+ve test: red/swollen site

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26
Q

Medical management of TB

A

There are 10 different drugs that have been approved to treat TB
Medication for 6-9 months

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27
Q

What are the Precautions for TB?

A

patient should have a PRIVATE, -ve pressure room

Patient should wear a surgical face mask when leaving the room

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28
Q

What is the PT treatment for TB?

A

Thorough Hx to be identify TB
Typically not treated in PT because medications are vital to curing TB
PT can provide percussions and postural drainage to clear secretions out of lung if needed
Self protection (N95, glove and gown)

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29
Q

What is Pneumothorax

A

Collapse of lung due to lung gathering in pleural space

Can be spontaneous due to lung disease or due to trauma

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30
Q

Signs and Symptoms of pneumothorax

A

Sudden chest pain and SOB

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31
Q

What is the percussion sound of a pneumothorax

A

hyper-resonance

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32
Q

What does the chest x-ray look like for a pneumothorax

A

hyperlucent lung, medialstinal shift away from the side of the pneumothorax

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33
Q

What does a pneumothorax sound like?

A

Decreased breath sounds

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34
Q

What is a tension pneumothorax

A

Can be quickly fatal
Increased pressure on heart can cause it to stop breathing
Need to remove seal of quickly insert a catheter needle

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35
Q

What is a hemothorax?

A

Collapse of lung due to blood gathering in the pleural space, usually due to trauma

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36
Q

What does a hemothorax sounds like?

A

Decreased breath sounds

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37
Q

What is flail chest?

A

Multiple rib fractures with free floating rib section

Results in inefficient ventilation and poor oxygenation

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38
Q

What happens during flail chest upon inhalation and exhalation?

A

On inspiration:
o Flail segment sucks in: lung, heart, mediastinum shift away, reducing air entry into the unaffected lung
• On expiration:
o Flail segment pushes outward: lung, heart, mediastinum pushed toward flail segment

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39
Q

What is the treatment for flail chest?

A

Pain control, airway clearance, O2, intubation, ventilation if needed

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40
Q

Is asthma is restrictive or obstructive lung disease?

A

Obstructive

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41
Q

What is Asthma?

A

Chronic inflammation of airways characterized by VARIABLE airflow limitation and airway hyper-responsiveness
Often reversible with bronchodilator (unlike COPD)

42
Q

What is the triad of asthma

A

eczema, allergies and asthma

43
Q

What are the 3 types of asthma

A

(1)Extrinsic: allergic or atopic
• Allergy to specific trigger.
• Mast cells release mediators which cause bronchospasm and hypersecretion.
• Usually childhood onset.
(2) Intrinsic: non-allergic
• No known allergic cause/trigger.
• Hypersensitivity to bacteria, virus, drugs, cold air, exercise, stress.
• Usually adult onset.
(3) Occupational:
• Related to exposure of workplace irritants.

44
Q

What are the SS of asthma

A
Wheezing
Breathlessness
Chest tightness
Coughing 
Coarse breath sounds 
Accessory respiratory muscle use
45
Q

What is treatment for Asthma?

A

Prevent triggers

Control symptoms pharmacologically- inhaled corticosteroids and bronchidilators

46
Q

What is Exercise induced asthma?

A

Acute, reversible, airflow obstruction that occurs 5-15 min after onset of exercise
S/S: During Xs: Coughing, wheezing, prolonged expiration, accessory muscle use
After Xs: cough, tightness or pain, SOB, nausea, stomachache

47
Q

What is the treatment of exercise induced asthma?

A

Keep patient upright and use inhaler prescribed

Lean forward and teach pursed lip breathing (SOS for SOB)

48
Q

What is COPD?

A

Destruction of the pulmonary vascular bed and hypoxic vasoconstriction results in increased pulmonary vascular resistance, leading to pulmonary hypertension and cor pulmonale (R sided head failure)

49
Q

What are the 2 types of COPD?

A
  1. Emphysema

2. Chronic Bronchitis

50
Q

What is Emphysema?

A

Destruction of air spaces distal to the terminal bronchioles with destruction of alveolar septa which causes MERGIN OF ALVEOLI INTO LARGER AIR SPACES. Results in reduced surface area needed for gas exchange.
There is also a loss of airways and capillaries
The elasticity of the alveolar septa are compromised, the airways collapse early and inspired air becomes trapped
= Decreased perfusion
= hyperventilation (patient breaths at high lung volumes)- uts the diaphragm at mechanical disadvantage (it’s flattened)

51
Q

How is Emphysema diagnosed?

A

Via diffusing capacity lung function test (measures exchange of gas across the alveoli using CO)

52
Q

What is Chronic Bronchitis?

A

= small airway remodeling

Productive cough, lasting for 3 months/yr for 2 consecutive yrs

53
Q

What are the S/S of chronic bronchitis?

A

long term irritation of the trochea/ bronchi, increased mucus production, decreased vital capacity

54
Q

What at the impacts on lung function of chronic bronchitis?

A

Impact on lung function:
▪ Airway wall increases due to inflammation and scarring resulting in smaller airway
▪ Increase in mucous also reduces size of lumen
▪ Damage to cilia increases infection susceptibility
▪ Increase in airway smooth muscle contraction can cause increase in bronchoconstriction

55
Q

What are the secondary effects of hyperinflation?

A

Increase in airway resistance and premature collapse of the airways upon exhalation leads to deceased expiratory flow and air trapping
More air enters on inspiration than exits on expiration
Alveolar destruction results in poor gas exchange

56
Q

What are the risk factors for COPD?

A
  • Age of onset: middle aged to older adults.
  • Smoking.
  • Occupational exposures.
  • Biomass smoke.
  • Genetic susceptibility.
57
Q

What are the S/S of COPD?

A
  • Airflow obstruction.
  • Dyspnea.
  • Chronic productive cough.
  • Wheeze.
  • Frequent exacerbations.
  • Fatigue.
  • Muscle weakness.
  • Deconditioned.
58
Q

How do you diagnose COPD?

A
  • Spirometry is most important test.

* Can also do chest x-ray, CT Scan, diffusing capacity (measures transfer gas from air in lungs into the blood).

59
Q

How is CO2 increased in COPD clients?

A

(1) Poor ventilation/perfusion matching:
➢ Poorly ventilated lung tissue (seen in clients with COPD) has low oxygen content which causes local vasoconstriction and diminished blood flow to that lung tissue
➢ Adding supplemental oxygen decreases this vasoconstriction
➢ Blood is then redistributed to areas of the lung with poor ventilation which reduces the amount of carbon dioxide that can effectively be eliminated from the system
(2) The haldane effect:
➢ Hemoglobin (Hb) carries more CO2 in deoxygenated blood (because there are fewer O2 molecules attached to the Hb)
➢ When supplemental oxygen is administered, CO2 molecules are forced off the hemoglobin and oxygen takes its place
➢ This causes an increase in PaCO2 levels within the blood
(3) Reduction of hypoxic drive:
➢ In healthy individuals, a rise in carbon dioxide causes an increase in the drive to breathe
➢ In some patients with COPD, this response has been blunted, leaving low oxygen levels as the stimulus of respiration (hypoxic drive)
➢ Giving supplemental oxygen can reduce their stimulus to breathe, causing respiration to slow (hypoventilation)
➢ Hypoventilation allows carbon dioxide to accumulate in the body
➢ Note: This mechanism alone does not cause respiratory failure in the COPD population when a high level of oxygen is administered

60
Q

What happens in Emphysema and Chronic Bronchitis?

A

Parenchymal inflammation, decreased elastic recoil, airway inflammation and remodeling
Hyperinflation and gas exchange

61
Q

What is Cystic Fibrosis?

A

Autosomal, recessively inherited genetic disorder
Abnormals Chloride and Sodium ions transport across epithelium of the respiratory, digestive and genital tracts (all exocrine glands)
Results in THICK mucus and scarring formation of cysts in the affected organs

62
Q

How can you test for Cystic Fibrosis?

A

Family Hx, 2 copies of abnormal gene
Sweat Test: Chloride content for sweat
Obstruction on lung function test
Chest X-ray: Linear opacities, thickened bronchial walls, consolidation due to atelectasis

63
Q

What is the clinical presentation of Cystic Fibrosis?

A

Respiratory symptoms are most common
-Reccurent chest infections, consolidation, atelectasis, thickened bronchial walls
-Breathlessness in later stages
finger clubbing
Delayed puberty and skeletal maturity
Infertility in males and reduced fertility in females
Symptomatic steatorrhea (thickened stools) due to pancreas dysfunction
Diabetes mellitus
liver disease
Osteoperosis
Chronic bacterial infection and progessive lung function leads to resp failure and early death

64
Q

What is the medical treatment for cystic fibrosis?

A
  • Bronchodilators.
  • Aggressive antibiotics to treat infections.
  • Oxygen supplementation.
65
Q

What is the treatment for cystic fibrosis?

A

1) Airway clearance techniques (selection depends on patient preference and their age):
o Birth - 5 years old:
▪ Aggressive bronchial drainage
▪ Chest vibration and percussion
o 6 years and older:
▪ Use of acapella device, flutter device, PEP mask
▪ Active cycle of breathing, autogenic drainage
2) Exercise:
o Posture
o Strength and endurance- Ensure you monitor SpO2 and avoid overexertion
3) Most critical part of treatment is secretion removal:
o Needed 2-3x/day
o Can time secretion removal after bronchodilator use

66
Q

What is Bronchiectasis?

A

Irreversible destruction (necrosis) and DILATION of the airways associated with chronic bacterial infection
Excess mucus production results in narrowed airways
History of repeated respiratory infections
Caused by CF, TB, endobronchial tumors
Eventually alveoli are replaced with scar tissue due to chronic inflammation

67
Q

Upon ausculation, what would you hear in bronchiectasis?

A

coarse crackle over affected lung

68
Q

What are treatments for bronchiectasis?

A

bronchidilator
antibiotics
regular secretion techniques

69
Q

What is a restrictive lung disease?

A

Loss of lung compliance (stiff, less compliant lung, NOT airway obstruction)
Can be due to intrinsic or extrinsic factors
Disorders that are intrinsic typically increase scarring

70
Q

What are the S/S of restrictive lung disease?

A
Dyspnea
Severe O2 desaturation 
Finger clubbing 
Dry/painful cough 
Rapid/shallow breathing
71
Q

What are the causes of intrinsic restrictive lung disease?

A

Pulmonary fibrosis: 2/3 no known cause, 1/3 TB.
Inhaling harmful particles, radiation therapy, meds. Scarring shown on CT scan
Idiopathic pulmonary fibrosis: scaring and fibrotic tissue.
Asbestosis: caused by inhaling harmful particle
Sarcoidosis: Granulomateous (accumulation of macrophages that form nodules)
Pneumoconiosis (coal workers lung)

72
Q

What are the causes of extrinsic restrictive lung disease?

A

(1) Neuromuscular: muscle weakness results in decreased respiratory muscle strength and a reduced vital capacity. Chest wall becomes stiff due to shallow breathing (ex. spinal cord lesion, polio, guillain-barre, ALS)
(2) Connective tissue disorders: Results in immobility of joints (ankylosing spondylitis, Rhumatoid arthritis)
(3) kyphosis: Increased curve in thoracic spine causing rigidity through chest wall
(4) obesity: chest wall restriction

73
Q

What is a pleural effusion?

A

Accumulation of fluid in pleural space due to disease which can impair breathing by limiting expansion of the lungs

74
Q

What are the 2 types of pleural effuction?

A

(1) Transudate: High fluidity and low protein (thin and clear). Commonly due to heart failure
(2) Exudate: low fluidity and high protein/ cells (mucus and opaque). Formation of fluid due to inflammation of pleura. Caused by infection, disease (ex. cancer) of the pleura

75
Q

S/S of pleural effusion

A

SOB

Chest P

76
Q

What is the percussion sound on pleura effusion

A

dull

77
Q

Upon auscultation of pleural effusion

A

Decreased or ABSENT breath sounds, may hear pleural rub

78
Q

How do we treat pleural effusion?

A

Chest tube drainage,
Deep breathing
Breath stacking
We DO NOT perform secretion clearance techniques as we cannot remove secretions that are NOT in the airways

79
Q

What is pulmonary Edema?

A

Increased fluid in extravascular spaces of the lung
Can initially occur only in the insterstitium and then progress into alveolar space
May be due to
(1) increased hydrostatic pressure due to heart failure or kidney failure (pushes fluid out of vessels)
(2) Increased alveolar permeability due to damage to alveoli epithelium (drug induced, ARDS, Inhalation or noxious gas)q

80
Q

What are the S/S of pulmonary edema?

A

Stiffer lung
Increased work to breath and dyspnea
Cough that produces a frothy pink tinged sputum

81
Q

Percussion sound of Pulmonary edema?

A

dull

82
Q

Auscultation of pulmonary edema?

A

fine crackles, wheezing

83
Q

What does a chest X-ray look like for pulmonary edema?

A

Fluffy looking white areas

84
Q

What are the medical treatments of pulmonary edema?

A

Oxygen, mechanical ventilation (if severe), vasodilators to decrease venous load, diuretics to decrease fluid overload

85
Q

What are the PT treatments for pulmonary edema?

A

Deep breathing, breath holds/stacking to allow for more O2 diffusion. Pt will be on diuretics and BP lowering medications to decrease pulmonary HTN which is the route cause of the problem. DO NOT perform secretion clearance techniques as this is NOT the cause of the problem

86
Q

What is a dull sound?

A

Normal if over the liver, heart of viscera

Cause- consolidation (eg pneumonia, atelectasis), pleural fluids (eg pleural effusion), pulmonary edema

87
Q

What is a hyper-resonant sound?

A

normal over the stomach
Indicates air in chest wall
Cause= hyperinflation (COPD, asthma attack, pneumothorax)

88
Q

What conditions produce fine crackle sounds?

A

Atelectasis, interstitial pulmonary fibrosis

89
Q

What conditions produce coarse crackle sounds?

A

Retained secretions (e.g. pneumonia, pulmonary edema)

90
Q

What conditions produce high or medium wheezing sounds?

A

Bronchospasm (e.g. asthma, COPD)

91
Q

What conditions produce low wheezing sounds?

A

Retained secretions in larger airways (e.g. bronchitis)

92
Q

Name 3 ways to evaluate vocal resonance

A

(1) Whispered Pectoriloquy- patient whispers a word and examiner hears the whisper lour and clear. An indication of lung consolidation
(2) Bronchophany - ‘99’ or ‘toy boat’. You can hear the words with greater intensity and clarity. An indication of lung consolidation
(3) Egophany - ‘e’ in a normal voice or ‘a’ in a high pitched . Indication of lung consolidation

93
Q

What conditions produce coarse crackle sounds?

A

Retained secretions (e.g. pneumonia, pulmonary edema)

94
Q

What conditions produce high or medium wheezing sounds?

A

Bronchospasm (e.g. asthma, COPD)

95
Q

What conditions produce low wheezing sounds?

A

Retained secretions in larger airways (e.g. bronchitis)

96
Q

Name 3 ways to evaluate vocal resonance

A

(1) Whispered Pectoriloquy
(2) Bronchophany - ‘99’ or ‘toy boat’
(3) Egophany

97
Q

What conditions produce fine crackle sounds?

A

Atelectasis, interstitial pulmonary fibrosis

98
Q

What conditions produce coarse crackle sounds?

A

Retained secretions (e.g. pneumonia, pulmonary edema)

99
Q

What conditions produce high or medium wheezing sounds?

A

Bronchospasm (e.g. asthma, COPD)

100
Q

What conditions produce low wheezing sounds?

A

Retained secretions in larger airways (e.g. bronchitis)

101
Q

Name 3 ways to evaluate vocal resonance

A

(1) Whispered Pectoriloquy
(2) Bronchophany - ‘99’ or ‘toy boat’
(3) Egophany