Auscultation

Front 1

Breath sounds are produced by ..

Back 1

Breath sounds are produced by
1. Airflow patterns
2. Associated pressure changes within the airways
3. Solid tissue vibrations within the lungs

Front 2

Disease states alter auscultatory findings by

Back 2

Disease states alter auscultatory findings by
1. Altered vibration of solid structures
2. Airflow through narrowed airways
3. By abrupt changes in airway pressure

Front 3

Sound damping

Back 3

Sound damping.
Body structures or cavities that produce resonance selectively transmit or amplify breath sounds that are similar in frequency (impedance matching -> consolidated tissue and chest wall) and absorb, or damp, those with other frequencies (impedance mismatch -> high-pitched breath sounds are absorbed as they're transmitted through the lungs and thorax. Pleural effusion, empyema..)

Front 4

Classification of breath sounds

Back 4

Classification of breath sounds
1. Tracheal and bronchial
(<- Turbulent airflow, loud, through expiration and inspiration, over trachea and mainstem bronchi. Heard anteriorly from 2-4th intercostal space parasternally and 3-6th intercostal pace paravertebrally)

3. Vesicular
(Faint, best heard through inspiration and at the beginning of inspiration)

(4. Bronchovesicular - In between)

Front 5

Voice sounds
a. What
b. Bronchophony
c. Egophony
d. Whispered pectoriloquy

Back 5

Voice sounds
a. What
I. Vibrations produced by speech that are transmitted to the chest wall through the tracheobronchial tree

b. Bronchophony (Phone - voice)
I. Voice sounds auscultated over the chest wall
II. In a healthy individual it is similar to voice sounds heard through the neck

c. Egophony
I. Voice sounds transmitted through the chest wall that have selectively amplified higher-pitched frequencies

d. Whispered pectoriloquy
I. High-pitched whispered sounds transmitted through airless, consolidated lung tissue

Front 6

How to document auscultation findings

Back 6

How to document auscultation findings
1. Location - By anatomic thoracic landmarks and whether its bi or unilateral

2. Intensity - Loud, soft, absent, diminished, distant

3. Duration - Timing in the respiratory cycle
I. Inspiratory, expiratory or both
II. Early, late, prolonged

4. Pitch - High or low

Front 7

Adventitious sounds

Back 7

Adventitious sounds
I. Added sounds that are heard with normal and abnormal breath sounds
II. Classified as crackles or wheezes and subclassified byduration and pitch

Front 8

Briefly describe the differences between breath sounds heard over the trachea and mainstem bronchi and those heard over other chest wall areas

Back 8

Sounds heard over the trachea land large airways are characterized as high-pitched, harsh, loud, and tubular (hollow) with a long expiratory phase. These sounds are thought to reflect the turbulent airflow patterns in the first divisions of the large airways.

Sounds heard over other chest wall areas are softer and have a shorter expiratory phase.

Front 9

Tracheal and bronchial breath sounds
a. Characteristics
b. Where are they heard
c. Heard best using the diaphragm or the bell

Back 9

Tracheal and bronchial breath sounds
a. Characteristics
I. Inspiratory:expiratory ratio of 1:2-1:3
II. Loud, harsh, high-pitched, tubular
(200-2000Hz)

b. Where are they heard
I. Anteriorly parasternally from 2nd-4th intercostal space
II. Posteriorly in 3rd-6th intercostal space paravertebrally

c. Diaphragm

Front 10

Vesicular breath sounds
a. Characteristics
b. Where are they heard
c. Heard best using the diaphragm or the bell

Back 10

Vesicular breath sounds
a. Characteristics
I. Inspiration is heard clearly and expiration is heard but fades quick. The I:E ratio is 3:1 to 4:1
II. Softer, lower-pitched
(200-600 Hz)

b. Over the entire lung

c. Low-pitch --> Diaphragm or bell

Front 11

Bronchovesicular breath sounds
a. Characteristics
b. Where is it heard
c. Best heard with bell or diaphragm

Back 11

Bronchovesicular breath sounds
a. Characteristics
I. Pitch and duration are midway between those of vesicular and tracheobronchial - Low-pitch, softer and less harsh than bronchial breath sounds
II. I:E ratio of 1:1

b. Where is it heard
I. Anteriorly and posteriorly over the large central airways
II. Can be heard in the outer fields in children up to 6 years
(Due to their thin chest walls and muscles that don't diminish breath sounds to the same extent as the thicker chest walls of adults)

c. Diaphragm or bell

Front 12

What happens to normal breath sounds when lung density increases?

Back 12

Transmission of breath sounds from large airways is enhanced. ->
1. Breath sounds are louder and more tubular
2. Expiration is significantly louder and longer -> I:E can change to 1:1 to 1:2 (Bronchial breath sounds)

(Increased density from consolidation. This happens because little high-frequency sound is lost through attenuation or filtration. As lung tissue density increases the impedance between the fluid-filled lung tissue and the pleurae and chest wall, these three medial become well matched, which decreases the normal filtering of high-frequency sounds. Consequently, breath sounds are transmitted more readily to the chest wall surface and are louder and more tubular than normal breath sounds heard over the same area).

Front 13

Bronchial breath sounds - Associated conditions

Back 13

Bronchial breath sounds
a. Associated conditions - All that increase lung density
1. Consolidation
I. Pneumonia
(Increase by fluid accumulation)

2. Atelactasis
(Increase density by lung collapse)

3. Fibrosis
(Increase density by fibrotic scarring)

Front 14

Lung consolidation
a. Mechanism
b. Causes
c. Findings

Back 14

Lung consolidation
a. Mechanism - Exudation of alveoli

b. Cause - Most commonly pneumonia

c. Findings - Over area
I. Decreased chest wall movement
II. Dull percussion
III. Bronchial breath sounds (Loud, harsh, IE 1:1 to 1:2)

(Can be auscultated using either the bell or the diaphragm of the stethoscope)

(Can be heard over upper lobe even without a patent bronchus due to the proximity to the trachea)

Front 15

Atelactasis
a. Mechanism
b. Causes
c. Findings

Back 15

Atelactasis
a. Mechanism
I. Prolonged shallow breathing or uncleared secretions that occlude the airway -> Incomplete expansion of that lung area

b. Causes
1. Postoperative patients
2. Immobile patients
3. Bronchiectasis
4. Pneumonia

c. Findings
I. Decreased chest wall movement
II. Dull percussion
III. Bronchial breath sounds
(Loud, high-pitched, IE 1:1)

(They are not heard over an atelactatic lower lobe if the bronchus is obstructed)

(Can be heard equally well using either the diaphragm or the bell)

Front 16

Lung fibrosis
a. Mechanism
b. Causes
c. Findings

Back 16

Lung fibrosis
a. Mechanism - Abnormal formation of fibrous connective tissue

b. Causes
1. Smoke inhalation
2. Asbesosis
3. Idiopathic in most cases

c. Findings
I. Decreased chest wall movement
II. Dull percussion
III. Bronchial breath sounds

(Usually heard over the lower lung regions. The lung bases are auscultated over the 5th intercostal space anteriorly, 5-6th intercostal space in anterior axillary line, 7-9th intercostal space posteriorly)

(Heard equally well with either the diaphragm or bell)

Front 17

Abnormal voice sounds
a. Mechanism of sound
b. Conditions when they're heard more clearly, why
c. Types

Back 17

Abnormal voice sounds
a. Mechanism of sound
I. When voice sounds pass through normally inflated, air-filled lungs, vowel tones, which contain many high-frequency sounds, are diminished and filtered. Like other high-frequency sounds, voice sounds are also selectively reflected back toward the lung tissue at the pleurae
II. Consequently, transmitted voice sounds are normally heard as low-pitched, unintelligible mumble over healthy lung and pleural surfaces because most of the vowels are filtered out

b. Conditions when they're heard more clearly, why
I. Heard more clearly over consolidated or atelactatic lung tissue areas because less filtering takes place, thus enhancing transmission

c. Types
1. Bronchophony
2. Egophony
3. Whispered pectoriloquy

Front 18

Bronchophony
a. What
b. Procedure

Back 18

Bronchophony
a. What
I. The clear, distinct, intelligible voice sound heard over dense, airless lung tissue
(Mechanism: dense, airless lung tissue transmits high-frequency vowel sounds more easily because of impedance matching)

b. Procedure
I. The patient is asked to repeat the words "ninety-nine" several times
(Over healthy lung tissue, the words are unintelligible. Over a consolidated area, however, the high-frequency sounds are easily understood as words)

Front 19

Why are bronchophony heard over dense, airless upper lobes but not dense, airless lower lobes?

Back 19

Because the upper lobe surfaces are in direct contact with the trachea, leading to direct transmission of tracheal breath sounds.

Front 20

Whispered petoriloquy
a. What
b. Procedure

Back 20

Whispered petoriloquy
a. What
I. The clear, distinct, intelligible, whispered voice sound heard over airless, consolidated, or atelactatic lung tissue
(In a healthy person, normal lung tissue filters the high frequencies of whispered vowel sounds, making the unintelligible during auscultation.)

b. Procedure
I. The patient is asked to whisper words such as "one-two-three" several times
(Over healthy lung tissue, the words are unintelligible, over the atelactatic/consollidated are, the high-frequency vowel sounds are easily understood as words)

(Typically discernible over atelactatic lung segments or areas of patchy consolidation where bronchial sounds or bronchophony isn't completely audible)

Front 21

Egophony
a. What
b. Procedure

Back 21

Egophony
a. What
I. A voice sound that has a nasal or bleating quality when heard over the chest wall
II. Produced over consolidated or atelactatic areas becaue impedence matching enhances breath sound transmission in such areas
III. Also heard about the upper level of the fluid in cases of pleursiy with effusion
(Ego - goat. A peculiar broken quality of the voice sounds, like the bleating of a goat.

b. Procedure
I. The patient is asked to say the letter "E" several times
II. Over healthy lung tissue, the letter sounds as it normally does. Over the consolidated area, it sounds like "A-ay", and has a high-pitched, nasal quality

Front 22

What constellation of auscultatory findings is typical in patients with consolidation

Back 22

What constellation of auscultatory findings is typical in patients with consolidation
1. Bronchial breath sounds
2. Bronchophony
3. Whispered pectoriloquy
4. Egophony

Front 23

Absent and diminished breath sounds
a. Mechanism
b. Which conditions are associated with diminished or absent breath sounds

Back 23

Absent and diminished breath sounds
a. Mechanism
I. Limited airflow into lung segments
(Less air movement -> Less turbulent airflow)

II. When breath sounds are reflected at the visceral and parietal pleura because of an impedance mismatch
(A mismatch occurs when sounds are transmitted through two types of media with significantly different acoustic properties)

b. Which conditions are associated with diminished or absent breath sounds
1. Shallow breathing
I. Postoperative patients
II. Patients with rib fractures
II. Decreased LOC from CNS injuries or drug overdoses

2. Diaphragmatic paralysis
(Ventilation of the lung bases is limited -> Diminished breath sounds)

3. Airway obstruction

4. Pneumothorax
(Sharp, stabbing chest pain, dyspnea, absent breath sounds, inaudible egophony, bronchophony, and whispered pectoriloquy, and hyperresonance. If diminished breath sounds are heard, they have a low pitch)

5. Pleural effusion

6. Hyperinflated lungs
7. Obesity
8. PEEP during assisted ventilation

Front 24

Pleural effusion - Findings

Back 24

Pleural effusion - Findings
1. Diminished (low-pitched) breath sounds
2. --> Atelactasis -->
I. Dull percussion
II. Can be heard at the upper border of the effusion - Egophony, bronchophony, whispered pectoriloquy

(Occasionally, loud bronchial breath sounds may have sufficient intensity to be transmitted through a small pleural effusion)

(Mechanism: Acoustical mismatch)

Front 25

Egophony
a. What
b. Procedure

Back 25

Egophony
a. What
I. A voice sound that has a nasal or bleating quality when heard over the chest wall
II. Produced over consolidated or atelactatic areas becaue impedence matching enhances breath sound transmission in such areas
III. Also heard about the upper level of the fluid in cases of pleursiy with effusion
(Ego - goat. A peculiar broken quality of the voice sounds, like the bleating of a goat.

b. Procedure
I. The patient is asked to say the letter "E" several times
II. Over healthy lung tissue, the letter sounds as it normally does. Over the consolidated area, it sounds like "A-ay", and has a high-pitched, nasal quality

Front 26

What constellation of auscultatory findings is typical in patients with consolidation

Back 26

What constellation of auscultatory findings is typical in patients with consolidation
1. Bronchial breath sounds
2. Bronchophony
3. Whispered pectoriloquy
4. Egophony

Front 27

Absent and diminished breath sounds
a. Mechanism
b. Which conditions are associated with diminished or absent breath sounds

Back 27

Absent and diminished breath sounds
a. Mechanism
I. Limited airflow into lung segments
(Less air movement -> Less turbulent airflow)

II. When breath sounds are reflected at the visceral and parietal pleura because of an impedance mismatch
(A mismatch occurs when sounds are transmitted through two types of media with significantly different acoustic properties)

b. Which conditions are associated with diminished or absent breath sounds
1. Shallow breathing
I. Postoperative patients
II. Patients with rib fractures
II. Decreased LOC from CNS injuries or drug overdoses

2. Diaphragmatic paralysis
(Ventilation of the lung bases is limited -> Diminished breath sounds)

3. Airway obstruction

4. Pneumothorax
(Sharp, stabbing chest pain, dyspnea, absent breath sounds, inaudible egophony, bronchophony, and whispered pectoriloquy, and hyperresonance. If diminished breath sounds are heard, they have a low pitch)

5. Pleural effusion

6. Hyperinflated lungs
7. Obesity
8. PEEP during assisted ventilation

Front 28

Pleural effusion - Findings

Back 28

Pleural effusion - Findings
1. Diminished (low-pitched) breath sounds
2. --> Atelactasis -->
I. Dull percussion
II. Can be heard at the upper border of the effusion - Egophony, bronchophony, whispered pectoriloquy

(Occasionally, loud bronchial breath sounds may have sufficient intensity to be transmitted through a small pleural effusion)

(Mechanism: Acoustical mismatch)

Front 29

Hyperinflated lungs
a. Associated conditions
b. Mechanism of impeded breath sound transmission
c. Sound characteristics
d. Associated signs of COPD

Back 29

Hyperinflated lungs
a. Associated conditions
1. COPD
2. Severe asthma
3. Obesity
4. PEEP
(Increase FRC)

b. Mechanism of impeded breath sound transmission
I. Premature dynamic compression of the large central airways and loss of elastic tissue --> Limited airflow during expiration --> Hyperinflated state -->
II. The trapped air create a mismatch between the pleurae, chest wall, and the hyperinflated lung tissue

c. Sound characteristics
I. Soft and low-pitched (-> Diaphragm)
II. Throughout inspiration and expiration

d. Associated signs of COPD
1. Dyspnea
2. Hyperresonant percussion note
3. Prolonged expiratory phase
4. Inaudible voice sounds (egophony, bronchophony, whispered pectoriloquy)

Front 30

Classification of adventitious sounds according to the American Thoracic Society

Back 30

Classification of adventitious sounds according to the American Thoracic Society
1. Crackles
I. Discontinuous
a. Coarse crackles/Rales/Coarse rales
(Explosive, loud, low-pitched)
b. Fine crackles/Fine rales/Crepitations
(Explosive, shorter in duration, higher in pitch, less intense than coarse crackles)

II. Continuous

2. Wheezes
I. Discontinuous
II. Continuous
a. Wheezes/Sibilant rales or rhonchi
(High-pitched, hissing or coughing sound, musical quality)
b. Low-pitched wheezes/Sonorous rales or rhonchi
(Low-pitched, resemble snoring. Caused by fluid/secretions partially blocking the large airway)

Front 31

Crackles
a. What
b. Mechanism
c. Documentation

Back 31

Crackles
a. What
I. Short, explosive popping sounds that are described according to their pitch, timing, and location
II. These characteristics change according to the etiology

b. Mechanism - 2 Theories
1. Air bubbling through secretions
I. Like in severe pulmonary edema and chronic bronchitis
(Can't explain why its only heard in expiration and not enough pressure to occur in smaller airways due to viscosity of secretions and surface tension)

2. Sudden, explosive openings of airways
I. Atelactasis and interstitial lung disease, lung bases of elderly people (and sometimes in other healthy individuals)
(At the end of expiration, peripheral airways in the lung bases close. At the beginning of inspiration, these peripheral airways remain closed, and inspired air flows to each lung apex first)

c. Documentation
I. Early,mid or late inspiration or expiration
II. Pitch - high or low
III. Density - Profuse or scanty

Front 32

Dependent lung region

Back 32

Dependent lung region
I. The lowest part of the lungs according to gravity

(Gravity and lung’s weight act on ventilation by increasing pleural pressure at the base (making it less negative) and thus reducing the alveolar volume. The lowest part of the lung in relation to gravity is called the dependent region. At the dependent region smaller volumes mean the alveoli are more compliant (more distensible) and so capable of wider oxygen exchanges with the external environment. The apex, though showing a higher oxygen partial pressure, ventilates less efficiently since its compliance is lower and so smaller volumes are exchanged.)

Front 33

Late inspiratory crackles
a. Sound characteristics
b. Associated conditions

Back 33

Late inspiratory crackles
a. Sound characteristics
I. High-pitched, explosive
II. Variable intensity

b. Associated conditions
1. Atelactasis
2. Resolving lobar pneumonia
3. Interstitial fibrosis
4. Left-sided heart failure

Front 34

Atelactasis
a. Seen in which patients
b. Mechanism of causing adventitious sounds
c. Sound characteristics
d. Other findings

Back 34

Atelactasis
a. Seen in which patients
1. Postoperative patients
2. Immobile patients
3. Patients with impaired diaphragmatic function
4. Premature infants with surfactant deficiency
(Elderly are more prone due to regressive changes in the musculoskeletal system and decreased respiratory forces)

b. Mechanism of causing adventitious sounds
I. Shallow breathing -> Gravitational forces close airways and deflate lung bases
II. Mucus plugging
= Sudden opening of collapsed small airways and alveoli

c. Sound characteristics
I. High-pitched
II. Explosive
III. Heard late in inspiration
IV. Vary in intensity

d. Other findings
1. Decreased chest wall movement
2. Dull percussion note
3. Bronchial breath sounds
4. Voice sounds - Bronchophony, egophony, whispered pectoriloquy

(Heard over the posterior bases of both lungs (8-10th intercostal space. Not audible at mouth. May clear partially with coughing. Dependent on position (dependent lung regions.))

Front 35

(Resolving) Lobar pneumonia
a. Mechanism
b. Sound characteristics
c. How can they be differentiated from inspiratory crackles from atelactasis

Back 35

(Resolving) Lobar pneumonia
a. Mechanism
I. In resolving lobar pneumonia many alveoli are still filled with exudate, but the surrounding alveoli are areated
II. Opening of the alveoli (snapping sound) at increased pressure creates the crackles

b. Sound characteristics
I. High-pitched
II. Late inspiratory

c. How can they be differentiated from inspiratory crackles from atelactasis
I. Not affected by coughing or position changes

Front 36

Interstitial fibrosis
a. Associated conditions
b. Sound characteristics
c. First heard where

Back 36

Interstitial fibrosis
a. Associated conditions
1. Inhalation of heavy metals
2. Nitrofurantoin
3. Some chemotherapeutic agents
4. Prolonged inhalation of high concentrations of oxygen
5. Idiopathic (Most common)
6. Asbestosis
7. Pulmonary sarcoidosis
(Noncaeating granulomatous disease of unknown origin that occur in lungs and other organs)
8. Rheumatoid arthritis
9. Scleroderma/Systemic sclerosis

b. Sound characteristics
1. Late inspiratory
2. Short, discontinuous
3. High-pitched

c. First heard where
1st heard in the midaxillary area over the lateral lung bases (7-8th intercostal)
2nd heard over the posterior bases...

(Can be first be detected on dependent basilar regions because it is due to the natural dependent effect and fibrosis)

Front 37

Left-sided heart failure
a. Mechanism
b. Sound characteristics

Back 37

Left-sided heart failure
a. Mechanism
I. Left-sided heart failure -> Fluid accumulation in lung interstitium -> Pressure causing narrowing on smaller airways -> Delayed opening on inspiration
(More severe form cause pulmonary edema with alveolar flooding)

b. Sound characteristics
1. Late inspiration
2. Fine intensity
3. Low-pitched

(Change to a loud rattling over inspiration and expiration as the patient's condition worsens, can be heard throughout the chest)

(In the patient with heart failure, auscultate the lung bases first because crackles may not be audible after continued deep breaths)

Front 38

Coarse crackles
a. Mechanism
b. Sound characteristics
c. Associated conditions

Back 38

Coarse crackles
a. Mechanism
I. Common in diffuse airway obstruction
II. Thought to be produced by the intermittent closure of large bronchi and the corresponding flow of a bolus of air through the obstructed area

b. Sound characteristics
1. During early inspiration and during expiration
2. Can be heard over any chest wall area
3. Lower pitch than fine crackles
4. Loud
5. Unaffected by position, but can disappear after a cough

c. Associated conditions
1. Chronic bronchitis
(Excessive mucus production, over all chest surface and at mouth)
2. Bronchiectasis

Front 39

Expiratory polyphonic wheezes
a. Mechanism
b. Associated conditions
c. Sound characteristics

Back 39

Expiratory polyphonic wheezes
a. Mechanism
I. Believed to be caused by the dynamic compression of large airways during expiration.
(Can sometimes be auscultated in healthy individuals during a maximal forceful expiration)

b. Associated conditions - Conditions with widespread airflow obstruction
1. Asthma
2. Chronic bronchitis

c. Sound characteristics
1. Expiratory
2. Widespread - Throughout the lung
3. Loud musical
4. High pitch (-> Diaphragm)

Front 40

Fixed monophonic wheezes
a. Mechanism
b. Associated conditions
c. Sound characteristics

Back 40

Fixed monophonic wheezes
a. Mechanism
I. Generated by the oscillation of a large, partially obstructed bronchus

b. Associated conditions - Conditions that partially obstruct a bronchus
1. Tumor
2. Foreign body
3. Bronchial stenosis
4. Intrabronchial granuloma

c. Sound characteristics
1. Low-pitched, constant pitch
2. Single musical tone

(Can be reduced by change in position or coughing)

Front 41

Sequential inspiratory wheezes
a. Mechanism
b. Associated conditions
c. Sound characteristics

Back 41

Sequential inspiratory wheezes
a. Mechanism
I. Generated by airways that open late in inspiration in unaeraeted lung regions --> The rapid inflow of air precipitates airway wall vibrations --> Sequential inspiratory wheezes
(Along with crackles from sudden opening of alveoli)

b. Associated conditions - Bases (Unaerated) of
1. Interstitial fibrosis
2. Abestosis
3. Fibrosing alveolitis

c. Sound characteristics
1. Inspiratory - More predominant in late
2. Monophonic
3. Loud intensity
4. High pitch

(Usually heard over lateral (7-8th intercostal) and posterior (8-10th intercostal) lung bases)

Front 42

Random monophonic wheezes
a. Mechanism
b. Associated conditions
c. Sound characteristics

Back 42

Random monophonic wheezes
a. Mechanism
I. From airways narrowed by bronchospasm or mucosal swelling
II. Louder are more widely transmitted the more centrally/in larger airways they are produced

b. Associated conditions - Status asthmaticus

c. Sound characteristics
1. Loud
2. Continuous
3. Prolonged expiration
4. High-pitch

(Random monophonic wheezes produced in the large central airways are loud and widely transmitted through the lung. They can be heard at a distance from the mouth. Random monophonic wheezes produced in the peripheral airways are weaker and are filtered as they're transmitted to the chest wall; these sounds are audible only over the chest wall)

(As status asthmatics becomes more severe, all wheezes heard over the chest wall surfaces disappear because of a combination of air trapping and severe airway narrowing causes the site of dynamic airway compression to move toward the lung periphery - this phenomenon is called a silent chest. Silent chest is associated with hypercapnia and acidosis)

(Status asthmatics can first present with expiratory monophonic wheezes that can be heard at the mouth -> continuous wheeze -> Gradually more silent)

Front 43

Stridor
a. Mechanism
b. Associated conditions
c. Sound characteristics

Back 43

Stridor
a. Mechanism
I. Laryngeal spasm and mucosal swelling -> Contract the vocal cords and narrow the airway

b. Associated conditions
1. Whooping cough
2. Laryngeal tumors
3. Tracheal stenosis
4. Aspiration of foreign object
5. Severe URTIs
6. Acute epiglottitis
(Worsens in supine)

c. Sound characteristics
1. Loud, monophonic, musical - 'Crowing sound'
2. Inspiratory, can progress to continuous
3. Can be heard without stethoscope
4. High-pitch
(Can easier be heard by auscultating the larynx)

Front 44

Asbestosis
a. Abnormal breath sounds
b. Abnormal heart sounds

Back 44

Asbestosis
a. Abnormal breath sounds
1. End-inspiratory high-pitched crackles
2. Advanced: Continuous inspiratory crackles
3. Pleural friction rub

b. Abnormal heart sounds
1. Severe -> Paradoxical S2 split, Right ventricular heave

Front 45

Asthma
a. Abnormal breath sounds
c. Abnormal heart sounds
c. Additional findings in status asthmaticus

Back 45

Asthma
a. Abnormal breath sounds
1. Diminished breath sounds
2. Expiratory wheezes
I. Musical
II. High-pitched
III. Polyphonic

c. Abnormal heart sounds - None

c. Additional findings in status asthmaticus
1. Continuous wheezes
I. Loud
II. Random monophonic
2. Prolonged expiration
3. Severe -> Silent chest

Front 46

Atelectasis
a. Abnormal breath sounds
c. Abnormal heart sounds

Back 46

Atelectasis
a. Abnormal breath sounds
1. Bronchial breath sounds
I. High-pitched
II. Hollow/tubular
2. Late inspiratory crackles
I. Fine
II. High-pitched
3. Wheezes
4. Diminished breath sounds
5. Voice sounds: Bronchophony, ego phony, whispered pectoriloquy
6. I:E ratio: I > E

(All findings are focal to the atelectasis)

c. Abnormal heart sounds - None

Front 47

Bronchial stenosis - Abnormal breath sounds

Back 47

Bronchial stenosis - Abnormal breath sounds
1. Continuous wheezes
I. Loud
II. Low-pitched
III. Monophonic
IV. Can disappear when in supine or when turning from side to side

Front 48

Bronchiectasis - Abnormal breath sounds

Back 48

Bronchiectasis - Abnormal breath sounds
1. Midinspiratory crackles
I. Low-pitched
II. Profuse
2. Scattered wheezing

Front 49

Chronic bronchitis - Abnormal breath sounds

Back 49

Chronic bronchitis - Abnormal breath sounds
1. Early inspiratory crackles
I. Scanty
II. Low-pitched
III. Not affected by the patient's position

2. Expiratory wheezes
I. Loud
II. Musical
III. High-pitched
IV. Polyphonic

Front 50

COPD
a. Abnormal breath sounds
b. Abnormal heart sounds

Back 50

COPD
a. Abnormal breath sounds
1. Diminished, low-pitched, breath sounds
2. Wheezes
I. Sonorous (Low-pitched, 'snoring')
II. Sibilant (High-pitched, 'musical')
3. Inaudible voice sounds (bronchophony, egophony, whispered pectoriloquy)
4. Prolonged expiration
5. Fine inspiratory crackles

b. Abnormal heart sounds
1. Paradoxical S2 split
2. Right ventricular heave

Front 51

Fibrosing alveolitis - Abnormal breath sounds

Back 51

Fibrosing alveolitis - Abnormal breath sounds
1. Continuous sequential wheezes
I. Loud
II. High-pitched

Front 52

Interstitial pulmonary fibrosis - Abnormal breath sounds

Back 52

Interstitial pulmonary fibrosis - Abnormal breath sounds
1. Late inspiratory fine crackles
I. Not affected by coughing, but may appear with position change, deep inhalation, or holding breath

2. Bronchial or broncho-vesicular breath sounds
I. High-pitced
II. Lower lung-regions
III. Continuous

3. Continuous sequential wheezes
I. Loud
II. High-pitched

Front 53

Laryngeal spasm - Abnormal breath sounds

Back 53

Laryngeal spasm - Abnormal breath sounds - Inspiratory stridor

Front 54

Pleural effusion - Abnormal breath sounds

Back 54

Pleural effusion - Abnormal breath sounds
1. Absent or diminished breath sounds
I. Low-pitched

2. Occasionally bronchial breath sounds

3. Contralateral normal breath sounds

4. Voice sounds at upper border of the pleural effusion
I. Bronchophony
II. Egophony
III. Whispered pectoriloquy

Front 55

Pneumonia - Abnormal breath sounds

Back 55

Pneumonia - Abnormal breath sounds
1. Bronchial breath sounds
I. High-pitched
II. Tubular

2. Voice sounds - Bronchophony, egophony, whispered pectoriloquy

3. Late inspiratory crackles
I. Not affected by coughing or positional changes

4. I:E ratio 1:1

(All findings are focal)

Front 56

Pneumothorax - Abnormal breath sounds

Back 56

Pneumothorax - Abnormal breath sounds
1. Absent or diminished breath sounds
I. Low-pitch

2. Inaudible voice sounds

3. Normal breath sounds heard on contralateral side

Front 57

Pulmonary edema
a. Abnormal breath sounds
b. Abnormal heart sounds

Back 57

Pulmonary edema
a. Abnormal breath sounds
1. Continuous crackles
2. Wheezes

b. Abnormal heart sounds
1. S3
2. S4

Front 58

Whooping cough - Abnormal breath sounds

Back 58

Whooping cough - Abnormal breath sounds - Stridor

Front 59

Crackles
A common finding in certain cardiovascular and pulmonary diseases, crackles are characterized by short, explosive, or popping sounds usually heard during inspiration. They may be described as coarse (loud, low-pitch) or fine (less intense, high-pitch). Crackles are believed to result either when air bubbles through secretions in the airway or when the airways open suddenly and explosively
a. Common signs and symptoms
b. Differential diagnosis

Back 59

Crackles
a. Common signs and symptoms
1. Tachycardia
2. Tachypnea
3. S3
4. Cough
5. Circulatory collapse
6. Hypoxia

b. DDx
1. Pneumonia, bacterial
I. Additional S&S: Diffuse fine to coarse moist crackles, productive cough, dyspnea, decreased breath sounds, chills, fever and malaise
II. DX: PE, labs (sputum, Gram stain, CBC, ABG), CXR
III. TX: Antibiotics, hydration, O2, suctioning
IV. F/U: Daily assessment if treated as outpatient, return visit 1 week after hospitalization and CXR 6 weeks after recovery

2. Pulmonary embolism
I. Additional S&S: Blood-tinged sputum, acute dyspnea, Anginal or pleuritic chest pain, low-grade fever, diaphoresis
II. DX: ABG, VQ scan, spiral chest CT, pulmonary angiogram, pulmonary function tests
III. TX: O2, Thrombolytics, Anticoagulants, vena cava filter, embelectomy
IV. F/U: Pulmonologist

3. Left-sided heart failure
I. Additional S&S: Dyspnea, orthopnea, cyanosis or pallor, arrhythmias, pulsus alternans
II. DX: Labs (ABG, electrolytes), CXR, echo, ECG, pulmonary artery catheterization
III. TX: Airway management, ventilation, O2, medications (Diuretics, digoxin, morphine, vasodilators, ACEi)
IV. F/U: Cardiologist

4. Pulmonary edema
I. Additional S&S: Pink and frothy sputum, exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea
II. DX: Labs (ABG, electrolytes), CXR, echo, ECG, pulmonary artery catheterization
III. TX: Airway management, medication (diuretics, digoxin, morphine, vasodilator, ACEi), low sodium diet
IV. F/U: Cardiologist

5. ARDS

6. Acute asthma

7. Bronchiectasis

8. Chronic bronchitis

9. Interstitial lung fibrosis

10. Legionnaire's disease

11. Lung abscess

12. Pneumonia

13. Psittacocis

14. Pulmonary tuberculosis

15. Sarcoidosis

16. Silicosis

17. Tracheobronchitis

Front 60

Pleural friction rub/crackles
Coarse, grating sound that may be auscultated over one or both lungs during inspiration or expiration. Indicates inflammation of the visceral and parietal pleural lining. The resultant fibrinous exudate cases the pleural surfaces to lose their ability to glide silently over each other during breathing. Patients with pleural friction rub typically have sharp inspiratory pain, causing them to splint the affected side in an attempt o reduce muscle and chest wall movement
a. Common signs and symptoms
b. DDx

Back 60

Pleural friction rub/crackles
a. Common signs and symptoms
1. Decreased breath sounds
2. Inspiratory crackles
3. Dyspnea
4. Tachypnea

b. DDx
1. Asbestosis
I. Additional S&S: Pleuritic chest pain, exertional dyspnea, dry cough, history of recurrent RTI
II. DX: P&H, ABG, CXR, PFT
III. TX: Chest physiotherapy, O2, medication (ATB, digoxin, diuretics, mucolytic inhalation agents)
IV: F/U: Pulmonologist

2. Pulmonary emboli
I. Additional S&S: Anxiety, chest pain, fever, productive cough, hypoxia
II. DX: P&H, ABG, Imaging (Spiral chest CT, VQ scan, angiography), ECG
III. TX: O2, medication (analgesics, anticoagulants, fibrinolytics), vena cava filter, embolectomy)
IV. F/U: Pulmonologist

3. Pneumonia
I. Additional S&S: Pleuritic pain, fever and chills, productive cough
II. DX: P&H, Labs (CBC, Sputum culture and sensitivity, ABG), CXR
III. TX: Chest physiotherapy, O2, medication (ATB, antipyretics, bronchodilators)
IV. F/U: Reevaluate in 48h, 2-3w, repeat CXR in 4w

4. Pleurisy/Pleuritis
I. Additional S&S: Sudden intense and unilateral chest pain, pain on lower lateral chest, pain aggravated by movement
II. DX: P&H, CXR, ECG
III. TX: Bed rest, medication (Analgesic, anti-inflammatories), thoracentesis
IV. F/U: Pulmonologist if treatment is ineffective

5. Lung cancer

6. Rheumatoid arthritis

7. SLE

8. Pulmonary tuberculosis

9. Radiation therapy

10. Thoracic surgery

Front 61

Low-pitched wheezes
Continuous and low-pitched, producing a snoring sound. Typically produced when fluid or secretions narrow the large airways, and often change in sound or disappear with coughing. Rough and rumbling. Mainly expiratory.
a. Synonyms
b. Common S&S
c. DDx

Back 61

Low-pitched wheezes
a. Synonyms
1. Rhonchi
2. Sonorous rales
3. Sonorous rhonchi

b. Common S&S
1. Tachycardia
2. Tachypnea
3. Dyspnea

c. DDX
1. Pulmonary edema
I. Additional S&S: Dyspnea, paroxysmal nocturnal dyspnea, non-productive cough, crackles, S3, cyanosis
II. DX: P&H, ABG, Imaging studies (CXR, CT, MRI)
III. TX: O2, Medication (Diuretics, morphine)
IV: F/U: Cardiologist

2. Pneumonia
I. Additional S&S: Dyspnea, cyanosis, productive cough, fever and chills, myalgia, headache, pleuritic chest pain, decreased breath sounds, fine crackles
II. DX: P&H, Labs (CBC, ABG, sputum gram stain), CXR
III. TX: ATB, O2
IV. F/U: Reevaluate in 1w

3. Emphysema
I. Additional S&S: Exertional dyspnea, barrel chest, clubbing, decreased breath sounds, weight loss, mild and chronic productive cough, accessory muscle use, grunting expiration
II. DX: P&H, labs (ABG, serum alpha-1 antitrypsin deficiency), CXR, PFT
III. TX: Smoking-cessation, medication (diuretics, bronchodilators, corticosteroids)
IV. Pulmonologist

4. Bronchitis
I. Additional S&S: Exertional dyspnea, barrel chest. Acute: chills, sore throat, low-grade fever, myalgia. Chronic: Coarse crackles, prolonged expiration, chronic productive cough, increased accessory muscle use, fluid retention
II. DX: P&H, ABG,CXR, PFT
III. TX: Smoking cessation, ATB, nebulizer treatment, O2, chest physiotherapy
IV. F/U: Pulmonologist

5. ARDS
I. Additional S&S: Crackles, retractions, fluid accumulations, dyspnea
II. DX: P&H, ABG, CXR
III. TX:O2, treat underlying cause
IV. F/U: Pulmonologist

6. Asthma

7. Bronciectasis

8. Pulmonary coccidioidomycosis

9. Bronchoscopy

10. Foreign body aspiration

11. Iatrogenic

Front 62

Stridor
A loud, musical respiratory sound. Results from an obstruction in the trachea or larynx, and may be heard without a stethoscope. Usually heard during inspiration, this sign may also occur during expiration in severe upper-airway obstruction. Stridor may signal a life-threatening condition requiring prompt emergency interventions.
a. Common S&S
b. DDX

Back 62

Stridor
a. Common S&S
1. Dyspnea
2. Tachypnea
3. Tachycardia
4. Diaphoresis
5. Retractions
6. Decreased breath sounds
7. Prolonged inspiration and expiration
b. DDX
1. Spasmodic croup
I. Additional S&S: Hoarseness, wheezing, barking cough that occurs while sleeping, nasal flaring, cyanosis, anxious and frantic appearance, non-febrile
II. DX: History of repeated episodes, P&H, Absence of signs of infection
III. TX: O2
IV. F/U: Allergist

2. Acute laryngotracheobronchitis
I. Additional S&S: Wheezing, infrequent barking, low/moderate -grade fever, runny nose, red epiglottitis
II. DX: P&H
III. TX: O2, ATB
IV. F/U: Return after one week after treatment or hospitalization

3. Epiglottitis
I. Additional S&S: Barking cough, high-grade fever, dysphagia, severe respiratory distress, nasal flaring, cyanosis
II. DX:Labs (throat culture, blood culture, CBC), lateral neck X-ray
III. Airway protection, medication (corticosteroids, ATB), IV fluids
IV. F/U: Return one week after hospitalization

4. Anaphylaxis
I. Additional S&S: Wheezing, angioedema, nasal edema and congestion, circulatory collapse
II. DX: P&H - History of allergen exposure
III. Airway and O2 maintenance, mediation (epinephrine, antihistamine, nebulized albuterol, corticosteroids), allergy testing
IV. F/U: Reevaluate in 24h

5. Airway trauma

6. Hypocalcemia

7. Inhalation injury

8. Laryngeal tumor

9. Mediastinal tumor

10. Retrosternal thyroid gland

11. Thoracic aortic aneurysm

12. Foreign body aspiration

13. Prolonged intubation

Front 63

Wheezing
Wheezes are high-pitched, continuous musical sounds that result when air passes rapidly through a narrowed bronchus that oscillates between being barely open to being completely closed. May signal a medical emergency requiring immediate medical intervention.
a. Common S&S
b. DDX

Back 63

Wheezing
a. Common S&S
1. Audible or auscultated wheezing
2. Dyspnea
3. Chest tightness
4. Apprehension
5. Tachypnea
6. Tachycardia
7. Diaphoresis
8. Nasal flaring
9. Accessory muscle use

b. DDX
1. GERD
I: Additional S&S: Hematemesis, Abdominal pain, pyrosis/heartburn, flatulence, dyspepsia, postural regurgitation
II. DX: Labs (Electrolytes, CBC, stool guaiac), Imaging (Barium swallow, upper GI series, endoscopy), biopsy
III. TX: Diet and lifestyle modification, medication (H2-blockers, antacids, PPIs), blood transfusion

2. Chronic bronchitis
I. Additional S&S: Wheezing that varies with severity location and intensity, prolonged expiration, coarse crackles, scattered rhonchi, hacking/productive cough, clubbing, cyanosis, edema
II. DX: PFT, Labs (CBC, ABG), CXR
III. TX: Smoking cessation, medication (pneumococcal vaccination, influenza vaccination, beta-2 agonist therapy, bronchodilator, corticosteroids), avoidance of environmental irritants, avoidance of beta-adrenergic blockers and antihistamines, early treatment of infections, O2

3. Anaphylaxis
I. Additional S&S: Stridor, angioedema, retractions
II. DX: PE, History of allergen exposure
III. TX: Symptomatic of ABC, medication (Epinephrine, antihistamines, inhaled albuterol, corticosteroids)

4. Asthma
I. Additional S&S: Cough (dry or productive), prolonged expiration, retractions, rhonchi
II. DX: Allergy skin testing, PFT, Labs (CBC, ABG), CXR
III. TX: Avoidance of allergens, tobacco, and beta-adrenergic blockers, medication (Inhaled beta-2 agonists, inhaled corticosteroids, leukotriene receptor antagonists, systemic steroids)

5. Obstructive lung disease

6. Partial obstruction from a
I. Tumor
II. Foreign body
III. Secretions

7. Use of a beta-adrenergic blocker

8. Extrinsic pressure
I. Goiter
II. Tension pneumothorax

9. Bronchial adenoma

10. Bronchiectasis

11. Bronchogenic carcinoma

12. Inhalation injury

13. Wegener's granulomatosis

Front 64

What two pulmonary diseases are commonly associated with massive hemoptysis?

Back 64

What two pulmonary diseases are commonly associated with massive hemoptysis?
1. Active pulmonary TB
2. Bronchiectasis

Front 65

Examination of the chest - Orientation lines

Back 65

Examination of the chest - Orientation lines
Anterior surface
1. Midsternal line - Connects the suprasternal notch/jugular fossa with the pubic symphysis
2. Parasternal lines
3. Midclavicualr lines
5. Axillary lines - Anterior, Middle, Posterior

Posterior surface
6. Scapular line - Over the lower angle of the scapula
7. Paravertebral line
8. Midspinal line

Front 66

Inspection of the chest - Overview

Back 66

Inspection of the chest - Overview
1. Shape of the chest
2. Respiratory movements
3. Soft parts - Signs of neoplastic process, Breasts

Front 67

Abnormal chest shapes
a. Barrel chest
b. Pigeon breast/Pectus carinatum
c. Funnel breast/Pectus excavatum
d. Kyphoscoliosis

Back 67

Abnormal chest shapes
a. Barrel chest
I. Consequence of prolonged obstructive lung disease
II. The chest is permanently in an 'inspired position'
III. The sternum is arched out, the spine can be kyphotic
IV. Ribs: More horizontally, widened intercostal spaces, blunted epigastric angle
V. Shallow respiratory movements

b. Pigeon breast/Pectus carinatum
I. Protruding sternum
II. Characteristic for rickets
(With rachitic rosary bilateral knobs at the costochondral junctions)

c. Funnel breast/Pectus excavatum
I. Usually without clinical significance

d. Kyphoscoliosis
I. Common in childhood rickets
II. Can compromise ventilation --> Hypoxic vasoconstriction --> Cor pulmonale kyphoscolioticum

(Chest deformities: congenital heart disease/early valvular disease --> bulge/vossure on chest, TB --> retractio hemithoracis (from fibrotic and adhesive changes)

Front 68

Respiratory movements
a. How can one see evidence of diseases of the pleura, such as pleuropneumonic adhesions, pleural effusions or pneumothorax
b. Respiratory rate in adult
c. Tachypnea - Causes

Back 68

Respiratory movements
a. How can one see evidence of diseases of the pleura, such as pleuropneumonic adhesions, pleural effusions or pneumothorax --> The movements of the chest on the affected side may be diminished or absent

b. Respiratory rate in adult - 16-20

c. Tachypnea - Causes
1. Pulmonary disease
2. Cardiac disease
3. Neurological disease
4. Anemia
5. Toxic and metabolic processes
6. Excitement and nervousness
7. Fever
8. Exercise
9. Hypoxia from circulatory insufficiency

Front 69

Respiratory movements
a. Cheyne-Stokes periodic respiration - Causes
b. Biot's breathing
c. Sighing respiration

Back 69

Respiratory movements
a. Cheyne-Stokes periodic respiration - Causes
1. Heart failure
2. Uremia
3. Severe pneumonia
4. Increased ICP - Cerebral hemorrhage

b. Biot's breathing
I. Irregular irregular breathing with apneic periods
II. Seen in meningitis, encephalitis
III. Caused by decreased sensitivity of the respiratory center

c. Sighing respiration
I. The normal respiratory rhythm is interrupted by a long deep inspiration, usually followed by a sigh and a prolonged expiration
II. Seen in neurasthenic/neurotic individuals

Front 70

Examination of the breasts
a. Inspection - Overview
b. Palpation - Overview

Back 70

Examination of the breasts
a. Inspection - Overview
1. Overall size
2. Shape
3. Bilateral symmetry
(Asymmetry due to cystic enlargement, mastitis, or neoplasm)
4. Skin appearance
5. Condition of the nipple
6. Skin retraction

b. Palpation - Overview
1. Structure
2. Density/Consisteny --> Masess/lumps?
a. Size
b. Shape
c. Regularity
d. Blunt or sharp surface
e. Mobility

Front 71

Examination of the breasts
a. Gynecomastia - Causes
b. Skin - Evaluate
c. Nipples - Evaluate
d. Secretion - Evaluate

Back 71

Examination of the breasts
a. Gynecomastia - Causes
1. Endocrine disturbances
2. Obesity
3. Hormonal treatment with female steroids
4. Liver cirrhosis

b. Skin - Evaluate
1. Color
(Redness --> Swollen breast)
2. Swelling
3. Bulges - Lumps
4. Dimples ('smilehull')
5. P'eau d orange/Skin of orange
(Adenocarcinoma, mastitis --> Lymphatic blockage --> Edema --> retractions)

c. Nipples - Evaluate
1. Changes - Size, position, redness, fissures
2. Recent (Weeks, months) changes are important
3. All unilateral changes are suspicious for malignancies

d. Secretion - Evaluate
1. Purulent (yellow, green, gray) --> Mastitis
2. Small amount of clear or cloudy secretion --> Usually harmless
3. Blood secretions from the same nipple --> Cancer
4. Abnormal lactation --> Endocrine (pituitary, thyroid)

Front 72

Palpation of the breast
a. Method
b. What is evaluated in a lump
c. Benign cyst or fibroadenoma - Characteristics
d. Adenomatosis, Cancer - Characteristics

Back 72

Palpation of the breast
a. Method
I. Supine and standing
II. Examine bimanually to compare
III. Circular movements and gentle pressure against the chest wall, stepwise in small areas
IV. Evaluate structure and density/consistency
V. Ask for tenderness
VI. Complete by examining axillary lymph nodes

b. What is evaluated in a lump/mass
1. Size
2. Shape
3. Regularity
4. Surface/Margins - Blunt or sharp
5. Mobility - Against the rest of the gland, the chest wall, and the covering skin

c. Benign cyst or fibroadenoma - Characteristics
I. Distinctly circumscribed
II. Smooth
III. Rounded, oval, or polycystic node/lump

d. Adenomatosis, Cancer - Characteristics
I. Irregular and ragged surface
II. Indistinct margins

Front 73

Vocal/Tactile/Pectoral fremitus
a. Fremitus
b. Vocal/tactile/Pectoral fremitus - What, method

Back 73

Vocal/Tactile/Pectoral fremitus
a. Fremitus (Fremo - To roar, resound)
I. A vibration imparted to the hand resting on the chest or any other part of the body

b. Vocal/tactile/Pectoral
fremitus - What, method
I. The perception of vibration of the chest wall caused by phonation of the patient
II. The patient loudly pronounces certain words (one-two-three) to cause resonance, the examiner places the palms bilaterally over corresponding areas on the hemithoraces and compares vibrations
(Dependent on proper functioning of the vocal cords, unobstructed trachea and bronchi, elastic chest wall. Best felt over the right upper lobe, as this point is closest to the trachea)

Front 74

Vibratory/Vocal/Tactile/Pectoral fremitus
a. Causes of increased fremitus
b. Causes of decreased or absent fremitus

Back 74

Vibratory/Vocal/Tactile/Pectoral fremitus
a. Causes of increased fremitus
1. Larger infiltrative processes of the lungs as found in pneumonia

b. Causes of decreased or absent fremitus
1. Pleural
a. Pleural exudates/effusions
b. Pneumothorax
c. Massive adhesions
(Asses borders by palpating with the ulnar surface of the hand during phonation)

2. Bronchial obstruction causing local atelactasis
a. FAO
b. Tumor

3. Lung emphysema
(Not enough normal lung tissue to transmit the sound)

Front 75

Pleural friction rub
a. What
b. Where is it best palpated
c. Differential diagnosis

Back 75

Pleural friction rub
a. What
I. Tactile perception of the rub between the pleural layers in pleuritis

b. Where is it best palpated
I. At the lower edges of the lung in the midaxillary line
(Where the movements between the pleural layers are largest. Both during expiration or inspiration)

c. Differential diagnosis
I. Broken rib

Front 76

Percussion
a. Pattern of percussion on the back
b. Characteristics of the percussion sound over normal lungs

Back 76

Percussion
a. Pattern of percussion on the
back
1. Start up in the neck (backside of supraclavicular notch)
2. Percuss along the scapular and paravertebral lines in a comparative fashion toward the bottom of the lungs

b. Characteristics of the percussion sound over normal lungs
1. Sonorous, resonant, clear
2. Slightly hyperresonant toward the lung bases

(In the front one used to start in the supraclavicular notch and proceed in the midclavicular lines)

Front 77

Topographic percussion
a. Delineation of the inferior percussion borders
b. Where is the largest displacement during respiration

Back 77

Topographic percussion
a. Delineation of the inferior percussion borders
1. In the front and sides - In relation to the ribs and intercostal spaces
(Parasternal line -> 6th rib
Medioclavicular line -> 6th intercostal space (not on left due to heart)
Midaxillary line -> 8th rib)

2. In the back - In relation to the vertebral spinous processes
(Scapular line -> 10th rib, Paravertebral line - Left -> T11, Right -> T10)
(One prominent vertebra on the back -> C7, 2 -> Lower is C7, 3 -> Middle is C7)

b. Where is the largest displacement during respiration - In the midaxillary lines (Up to 8 cm)
(2nd scapular lines (4cm), 3rd - front)

Front 78

Topographic percussion
a. Bilateral diminished respiratory movements and percussory displacement - Causes
b. Unilaterally diminished percussion displacement - Causes

Back 78

Topographic percussion
a. Bilateral diminished respiratory movements and percussory displacement - Causes
1. Pulmonary emphysema
2. Ascites
3. Elevated diaphragm in pregnancy
4. Massive bilateral pleuropulmonary adhesions

b. Unilaterally diminished percussion displacement - Causes
1. Pleural effusion
2. Pneumothorax
3. Pleuropulmonary adhesions
4. Atelactasis of the lower lobe
5. Phrenic nerve paresis
6. Elevated diaphragm, ie due to a suphrenic abscess

Front 79

Bronchial/Tubular breathing
a. Description of sound
b. Mechanism of sound
c. Physiologically heard at

Back 79

Bronchial/Tubular breathing
a. Description of sound
I. Sounds like a throaty ''kh''
II. Short inspiratory phase and long expiratory phase

b. Mechanism of sound
I. Originates from air rushing through the larynx and vibrating the air column in the larynx and trachea

b. Physiologically heard at
1. Over the larynx and trachea in the supraclavicular fossa and over the upper part of the sternal manubrium

2. In the vicinity of C7

3. To the right of Th4

4. In the axilla
(Particularly in children)

Front 80

Pathologic vesicular breathing

Back 80

Pathologic vesicular breathing
1. Increased/Intensified vesicular breathing
I. Hyperventilation - Kussmauls..
II. Unilateral compensation for pathologic process on the other side
a. Massive lobar pneumonia
b. Pneumothorax
c. Massive pleural effusion

2. Weakened/Decreased vesicular breathing
I. Quiet breathing in obese patient
II. Hypoventilation secondary to pain from trauma or pleuritis
III. Large pleuropulmonary adhesions
IV. Pleural effusion
V. Pneumothorax
VI. Emphysema
(Due to numerical reduction of pulmonary alveoli and loss of elasticity, the lungs are in a hyperinflated position with reduced ventilation)
VII. Obstructive atelactasis

3. Inaudible breathing
I. Extremely weakened ventilation
II. Large pneumothoraces
III. Massive pleural effusions
IV. Massive atelactases

4. Vesicular breathing with prolonged expiration
I. Bronchial asthma
II. Bronchiolitis
III. Emphysema
(When the prolonged expiration is a consequence of bronchiolar resistance due to spasm, swelling, and/or the presence of secretion)

Front 81

Pathologic bronchial/tubular breathing
a. Mechanism
b. Causes
c. Amphoric breathing
d. Compressive breathing

Back 81

Pathologic bronchial/tubular breathing
a. Mechanism
I. Occurs if the vesicular/alveolar areas are compromised, but the bronchial tree is unobstructed

b. Causes - Mostly pathologic with airless alveoli
1. Alveoli filled with
I. Blood in pulmonary infarction
II. Inflammatory exudate in pneumonia
III. Tumorous tissue
2. If the alveoli are compressed from the outside
I. Fluid in the pleural cavity

c. Amphoric breathing
I. Tubular breathing heard over a large pulmonary cavity that communicates with a bronchus

d. Compressive breathing
I. Observed at/above the border of a large pleural effusion
II. Caused by pressure of the pleural fluid upon the adjacent lung tissue
III. Can be considered an intermediate between bronchial and vesicular breathing
IV. Best audible during expiration

Front 82

Adventitious breath sounds/Rales
a. What
b. Types

Back 82

Adventitious breath sounds /Rales
a. What
I. Sounds heard on auscultation of abnormal lungs
II. Rales are not modifications of normal breath sounds, but arise from the flow of air and the presence of
1. Liquid or semiliquid material in the alveoli, bronchioli and bronchi
2. Bronchospasm

b.Types
1. Dry rales
I. Sibilant rales (High pitched: whistles)
II. Sonorous rales (Low pitched: rhonchi)

2. Moist rales/Crackles
I. Crackling - Fine bubbles
II. Crepitant - Medium bubbles
III. Coarse/Gurgling rales - Large bubbles
(Also sometimes called rhonchi)

Front 83

Dry rales
a. Mechanism
b. Types
c. Heard in which diseases

Back 83

Dry rales
a. Mechanism
I. They arise in medium or larger bronchi if they are filled with thick or viscous exudate adhering to the bronchial wall
II. The exudates vibrates like a string or a pseudomembrane during respiration
II. Spasms of bronchi may contribute to their development

b. Types
1. Sibilant/Whistling/Wheezing - High-pitched
2. Sonorous/Musical - Low-pitched

c. Heard in which diseases
1. Acute and chronic bronchitis
2. Bronchial asthma - Then called wheezes

(Present on inhalation and exhalation)

Front 84

Moist rales/Crackles
a. Description of the sound
b. Moist crackles/rales are heard in
c. A flood of crackling (and crepitant) rales are heard in

Back 84

Moist rales/Crackles
a. Description of the sound
I. Compared to the sound of bursting bubbles on top of a liquid

b. Moist crackles/rales are heard in
1. Pneumonia
2. Bronchopneumonia
3. Bronchiectasis

c. A flood of crackling (and crepitant) rales are heard in
1. Pulmonary edema

(Some distinguish between accentuated and unaccentuated according to their intensity. Accentuated rales are "clear" and appear to be closer. Unaccentuated rales seem to be "flat" and coming from a distance. The difference is due to the presence or absence of an infiltrative process at the origin of the rales: infiltration of the tissue transmits the crackling sound better than tissue filled with air. The rales are accentuated in pneumonia. Continuous accentuated rales over one or both lower lobes may be indicative of bronchiectasis)

Front 85

Inspiratory crepitations
a. Description of the sound
b. Causes

Back 85

Inspiratory crepitations
a. Description of the sound
I. Similar to the sound of hair rubbed between the thumb and the index finger
II. Resemble fine, clear, sharp crackling rales which create a continuous hum toward the end
III. Only inspiratory

b. Cause
1. Physiologic in shallow breathing
(In shallow breathing some of the alveolar sacs in the lung bases collapses, but during the first deep breaths their walls expand by the rushing air that causes the crackling sounds. After a few deep breaths this phenomenon disappears)

2. Pathologically
I. Pneumonia
(A small amount of exudate causes the walls of the alveoli to stick together. With the flow of inspired air the alveolar walls are forcefully separated, causing the crackling sound)
(Lobar pneumonia: Early -> Crepitus indux, Late -> Crepitus redux)
II. Pulmonary infarction
(III. Tuberculous infiltrate in the subclavicular area after coughing if the lung apices are involved)

Front 86

Syndrome of bronchial obstruction - Chronic and acute bronchitis
a. Mechanism
b. Findings

Back 86

Bronchitis - Chronic and acute
a. Mechanism
I. Swelling
II. Increased mucus production
III. Bronchospasm

b. Findings
1. Percussion - Resonant
2. Auscultation
I. Vesicular breathing
II. Prolonged exhalation
III. Sibilant dry rales/Wheezes (High-pitced)
IV. Copious sputum --> Moist rales/Crackles

Front 87

Syndrome of bronchial obstruction - COPD - Findings

Back 87

Syndrome of bronchial obstruction - COPD - Findings
1. Percussion is hyperresonant
2. Auscultation
I. Vesicular, but weakened
II. Prolonged expiration
III. Wheezes and whistles are audible
IV. Moist rales/crackles can be heard if copious mucus production

(The prolonged expiration is caused by bronchial obstruction and decreased elasticity of the lung in emphysema)

Front 88

Syndrome of bronchiectasis
a. What
b. Mechanism
c. Findings

Back 88

Syndrome of bronchiectasis
a. What
I. A disease characterized by dilatation of the lumina of the small bronchi
II. Localized and diffuse bronchiectasis

b. Mechanism
I. Secretions, usually purulent, accumulate in the dilated bronchi
II. Mostly acquired not congenital

c. Findings
1. Percussion - Resonant
2. Auscultation
I. Vesicular breathing
II. Moist accentuated crepitant or coarse crackles/rales

(Confirmed by bronchography, recurrent pneumonia is a common complication. Composite symptomatology when combined with COPD)

Front 89

Syndrome of lung consolidation
a. Causes
b. Findings in the presence of a patent bronchus

Back 89

Syndrome of lung consolidation
a. Causes
1. Lobar pneumonias
2. Pulmonary infarctions
3. Neoplasms
4. Atelactasis

b. Findings
1. Percussion dullness or flatness
2. Increased fremitus pectoralis
3. Bronchial breathing
4. Accentuated moist crackling or crepitant rales
5. Increased bronchophony

(In atelactasis where the supplying bronchus is obstructed, vesicular breathing is reduced/absent, fremitus and bronchophony are weakened)

Front 90

Bronchophony
a. What
b. Where is decreased bronchophony found
c. Pectoriloquy - What
d. Pectoriloquy - Causes

Back 90

Bronchophony
a. What
I. Auscultation of voice sounds - Voice is transmitted through the airways to the chest wall
II. Ask the patient to repeat certain words (''coockoo'') and compare both sides of the chest
III. Over normal healthy lung tissue the spoken words are very indistinct and unclear. Heard somewhat better in the areas of physiologic bronchial breathing

b. Where is decreased bronchophony found
I. Over a pleural exudate
II. Over a pneumothorax
III. In obstructive atelactasis
IV. Over massive pleural thickenings

c. Pectoriloquy (Loquor - To speak)
I. Exaggerated bronchophony
II. Syllables can be heard and distinguished clearly
III. Use whispered voice

d. Pectoriloquy - Causes: Consolidation
1. Pneumonia
2. Pulmonary infarction

Front 91

Pneumonia
a. Anatomical types
b. Acute pneumonia: Inflammation, scant serous exudation of the alveoli. Physical findings
c. Next phase - Exudation entirely fills the alveoli. Physical findings
d. Next phase: Leukocytic enzymes dissolves the alveolar exudate which then gets absorbed -> Aeration resumes. Physical findings

Back 91

Pneumonia
a. Anatomical types
1. Alar - Affect entire right or left wing of the lung
2. Lobar

b. Acute pneumonia: Inflammation, scant serous exudation of the alveoli. Physical findings
1. Percussion - Resonant, mildly dulled over consolidation
2. Vesicular breathing, sometimes weakened
3. Crepitus indux - Initial crepitations

c. Next phase - Exudation entirely fills the alveoli. Physical findings
1. Flat percussion sounds
2. Bronchial breathing
3. Accentuated rales
4. Fremitus, increased bronchophony (can be pectoriloquy)

d. Next phase: Leukocytic enzymes dissolves the alveolar exudate which then gets absorbed -> Aeration resumes. Physical findings
1. Percussion - Dullness, resonant
2. Vesicular breathing
3. Crepitus redux - Final crepitations
(4. Pleural rub - If the pleura is involved in the inflammation)

Front 92

Atelactasis
a. What
b. Types
c. Physical findings in extensive atelactasis due to obstruction of a main bronchus

Back 92

Atelactasis (Ateles - Incomplete, Ektasis - Extension)
a. What
I. Non-distension/expansion of the lung tissue
(In a stricter sense it means non-aeration of lung tissue that has not yet breathed - neonate atelactasis)

b. Types
1. Neonate atelactasis
2. Acquired obstructional atelactasis
I. Foreign object
II. Blood clot
III. Mucus clot
IV. Neoplasm compressing externally

c. Physical findings in extensive atelactasis due to obstruction of a main bronchus
1. Flat percussion sound
2. Absent vocal fremitus
3. Inaudible respiration
4. Absent pectoriloquy

(If it only affects a small portion of the lung (ie a lung segment), other lung areas expand and compensate, which then cannot be identified by the physical diagnosis)

Front 93

Cavitary (Cavity) syndrome
a. What
b. Detectable by physical findings only if the cavity is larger than ... and ...
c. Method of diagnosis

Back 93

Cavitary (Cavity) syndrome
a. What
I. Cavity in the lung
II. Mostly caused by tuberculosis or a lung abscess

b. Detectable by physical findings only if the cavity is larger than 6 cm and near the lung surface and surrounded by infiltrated/condensed tissue

c. Method of diagnosis - Radiology

Front 94

Syndrome of diminished lung volume
a. Acute volume diminution
b. Chronic volume diminution

Back 94

Syndrome of diminished lung volume
a. Acute volume diminution
I. When an entire lung collapses

b. Chronic volume diminution
I. Develops if the aerated lung is replaced by fibrous tissue - Seen in
1. Fibrous tuberculosis
2. Extensive pleuropulmonary adhesions
3. Other fibrotic processes of the lung

(Can affect single lobe (-> intercostal retractions, internal structures pulled toward it (ie esophagus, trachea)) or a whole lung (hemithorax reduced in size, retracted, ribs are closer, the spinal column is curved toward the affected side, the heart, trachea, and esophagus are pulled toward the diseased side)

Front 95

Syndrome of enlarged lung volume - Acute
a. Cause
b. Physical findings

Back 95

Syndrome of enlarged lung volume - Acute
a. Cause - Acute asthmatic attack

b. Physical findings
I. Inspection
1. Prolonged expiration
2. Orthopneic position (erect or sitting)
3. Respiration is labored
4. The chest is in inspiratory position
5. Respiratory excursions are diminished

II. Percussion
1. Hyperresonance
2. Inferior borders are percussed lower caudally

III. Auscultation
1. Vesicular with prolonged expiration
2. Musical rales - Wheezes/whistles (high-pitched), rhonchi (low-pitched)
(The basic breathing then become inaudible)

Front 96

Syndrome of enlarged lung volume - Chronic lung volume enlargement
a. Cause
b. Physical findings

Back 96

Syndrome of enlarged lung volume - Chronic lung volume enlargement
a. Cause - Pulmonary emphysema (En- in, Physa - Bellows)

b. Physical findings
I. Inspection
1. Barrel chest in inspiratory position
2. Filled out supraclavicular fossae

II. Percussion
1. Hyperresonant
2. Lower lung borders extended caudally (Sometimes to L1)
3. Respiratory excursions are diminished

III. Auscultation
1. Weakened, reduced breath sounds
2. Prolonged expiration
(Decreased elasticity)
3. Soft to inaudible heart sounds

Front 97

Syndrome of effusion in the pleural cavity (Fluidothorax)
a. Types
b. Distribution of pleural effusion
c. Only effusions over ... can be detected by physical examination

Back 97

Syndrome of effusion in the pleural cavity (Fluidothorax)
a. Types
1. Exudate - Inflammatory effusion
2. Transudate - Non-inflammatory fluid in cardiac failure
3. Hemorrhagic fluid - Hemothorax
4. Purulent fluid - Empyema/Pyothorax

b. Distribution of pleural effusion
1. Gravity -> Costophrenic angles
(Lowest point)
2. Areas with highest lung elasticity -> Areas farthest from the hilum -> Space between the scapular and anterior axillary lines - Contains most of the fluid

(Curve of Damoiseau - Tip of curve lies in axilla - descends anteriorly to the sternum and posteriorly to the spine. Seen in inflammatory effusions)

c. Only effusions over 200-400 mL can be detected by physical examination

Front 98

Syndrome of effusion in the pleural cavity (Fluidothorax) - Physical findings on affected side

Back 98

Syndrome of effusion in the pleural cavity (Fluidothorax) - Physical findings on affected side
I. Inspection
1. Hemithoracic expansion
(In large effusions in thin patients)
2. Fuller intercostal spaces
3. Shallower respiratory excursions

II. Percussion
1. Dull, flat
2. Skodaic resonance/Skoda's sound - Strip with tympanitic resonance above the upper border of the dullness
(Corresponds to the area with distended alveoli above the compressed lung)

III. Auscultation
1. Respiration above the fluid is faint, over the lung bases inaudible
2. Vocal fremitus and bronchophony are caudally diminished or absent

Front 99

Pneumothorax
a. Complete and partial pneumothoraces
b. External and internal pneumothoraces
c. Open, closed, tension pneumothoraces

Back 99

Pneumothorax
a. Complete and partial pneumothoraces
I. Complete - the entire lung retracts to its hilus
II. Partial - Collapses only partially due to adhesions between the pleurae

b. External and internal pneumothoraces
I. External - If the pleural space is connected with the ambient atmosphere from chest injuries
II. Internal pneumothorax - Due to disruption of visceral pleura from perforation of
1. Tuberculous focus
2. Lung abscess
3. Emphysematous bleb
4. Lung cyst

c. Open, closed, tension pneumothoraces
I. Open - The communicating hole remains open during inhalation and exhalation
II. Closed - The communicating hole closes due to the lung collapsing
III. tension - The communicating hole remains open during inhalation only
(Right-sided tension pneumothorax is particularly dangerous, because pressure is exerted upon the SVC, the right atrium and ventricle, which all have thin walls)

Front 100

Pnemuothorax - physical findings

Back 100

Pneumothorax - Physical findings
I. Inspection
1. Expansion of the hemithorax
2. Distended intercostal spcaces and bulging supra- and infraclavicular fossae
3. The affected hemithorax don't participate in respiratory excursions

II. Palpation
1. Reduced or absent fremitus

III. Percussion
1. Hyperresonant to tympanitic
2. Metallic character in higher intrathoracic pressure

IV. Auscultation
1. Inaudible or very faint breathing
2. Vocal fremitus and bronchophony are absent in a complete pneumothorax and reduced in a partial pneumothorax

(In a left-sided pneumothorax cardiac dullness is absent and heart sounds are faint or absent)

Front 101

Mediastinal syndrome
a. What
b. Causes
c. Symptoms

Back 101

Mediastinal syndrome
a. What
I. Combination of symptoms and signs due to increased pressure in the mediastinum from enlarged organs or other structures

b. Causes
1. Enlarged lymph nodes - Malignant lymphoas, lymphogranuloma, paramalignant lymphomas
2. Thyroid gland - Hyperplasia, tumor
3. Parathyroid gland - Hyperplasia, tumor
4. Thymus - Hyperplasia, tumor
5. Various cysts
6. Aneurysms of the aorta
7. Connective tissue tumors
8. Neurogenic neoplasms

c. Symptoms
I. Respiratory
1. Cough
(If the pressure-causing structure lies in the vicinity of tussigenic zones (trachea, large bronchi. Dry, irritative and paroxysmal cough)
2. Stridor
3. Inspiratory dyspnea
(Next to trachea or main bronchus)

II. Neurologic
1. Hoarseness due to compression of the recurrent laryngeal nerve
2. Compression of the phrenic nerve -> Paresis/Palsy of the diaphragm
3. Horner's syndrome from pressure on the superior cervical sympathetic ganglion

III. Symptoms from vascular impingement
1. SVC syndrome
(Engorgement in the face, neck and arms, cyanosis and edema of the neck and face (Collar of stokes), conjunctival congestion)

IV: Symptoms from pressure on the esophagus -> Dysphagia

Front 102

Lung condensation
a. Respiratory movements of the thorax
b. Mediastinal displacement
c. Percussion
d. Auscultation/Breath sounds
e. Adventitious breath sounds
f. Bronchophony and pectoral fremitus

Back 102

Lung condensation
a. Respiratory movements of the thorax
I. Reduced on affected side
b. Mediastinal displacement
I. No

c. Percussion
I. Dullness

d. Auscultation/Breath sounds
I. Bronchial

e. Adventitious breath sounds
I. Crackles (Accentuated rales)

f. Bronchophony and pectoral fremitus
I. Increased

Front 103

Pleural effusion
a. Respiratory movements of the thorax
b. Mediastinal displacement
c. Percussion
d. Auscultation/Breath sounds
e. Adventitious breath sounds
f. Bronchophony and pectoral fremitus

Back 103

Pleural effusion
a. Respiratory movements of the thorax
I. Reduced to absent on affected side

b. Mediastinal displacement
I. To healthy side

c. Percussion
I. Dull to flat

d. Auscultation/Breath sounds
I. Vesicular
II. Weak to absent

e. Adventitious breath sounds
I. Occassionally friction rub

f. Bronchophony and pectoral fremitus
I. Decreased

Front 104

Pneumothorax
a. Respiratory movements of the thorax
b. Mediastinal displacement
c. Percussion
d. Auscultation/Breath sounds
e. Adventitious breath sounds
f. Bronchophony and pectoral fremitus

Back 104

Pneumothorax
a. Respiratory movements of the thorax
I. Reduced to absent on the affected side

b. Mediastinal displacement
I. To healthy side

c. Percussion
I. Hyperresonant

d. Auscultation/Breath sounds
I. Vesicular
II. Weak to absent

e. Adventitious breath sounds
I. None

f. Bronchophony and pectoral fremitus
I. Weak to absent

Front 105

Emphysema
a. Respiratory movements of the thorax
b. Mediastinal displacement
c. Percussion
d. Auscultation/Breath sounds
e. Adventitious breath sounds
f. Bronchophony and pectoral fremitus

Back 105

Emphysema
a. Respiratory movements of the thorax
I. Symmetrically reduced

b. Mediastinal displacement
I. No

c. Percussion
I. Hyperresonant

d. Auscultation/Breath sounds
I. Vesicular
II. Weak
III. Prolonged expiration

e. Adventitious breath sounds
I. No

f. Bronchophony and pectoral fremitus
I. Reduced

Front 106

Acute asthma
a. Respiratory movements of the thorax
b. Mediastinal displacement
c. Percussion
d. Auscultation/Breath sounds
e. Adventitious breath sounds
f. Bronchophony and pectoral fremitus

Back 106

Acute asthma
a. Respiratory movements of the thorax
I. Symmetrically reduced

b. Mediastinal displacement
I. No

c. Percussion
I. Resonant to hyperresonant

d. Auscultation/Breath sounds
I. Vesicular
II. Prolonged expiration

e. Adventitious breath sounds
I. Whistles

f. Bronchophony and pectoral fremitus
I. Normal

Front 107

Bronchitis
a. Respiratory movements of the thorax
b. Mediastinal displacement
c. Percussion
d. Auscultation/Breath sounds
e. Adventitious breath sounds
f. Bronchophony and pectoral fremitus

Back 107

Bronchitis
a. Respiratory movements of the thorax
I. Normal

b. Mediastinal displacement
I. No

c. Percussion
I. Resonant

d. Auscultation/Breath sounds
I. Vesicular
II. Prolonged expiration

e. Adventitious breath sounds
I. Whistles and wheezes

f. Bronchophony and pectoral fremitus
I. Normal

Front 108

Bronchiectasis
a. Respiratory movements of the thorax
b. Mediastinal displacement
c. Percussion
d. Auscultation/Breath sounds
e. Adventitious breath sounds
f. Bronchophony and pectoral fremitus

Back 108

Bronchiectasis
a. Respiratory movements of the thorax
I. Normal

b. Mediastinal displacement
I. No

c. Percussion
I. Resonant

d. Auscultation/Breath sounds
I. Vesicular

e. Adventitious breath sounds
I. Accentuated wet rales

f. Bronchophony and pectoral fremitus
I. Normal

Front 109

Atelactasis
a. Respiratory movements of the thorax
b. Mediastinal displacement
c. Percussion
d. Auscultation/Breath sounds
e. Adventitious breath sounds
f. Bronchophony and pectoral fremitus

Back 109

Atelactasis
a. Respiratory movements of the thorax
I. Reduced on affected side

b. Mediastinal displacement
I. To affected side

c. Percussion
I. Flat

d. Auscultation/Breath sounds
I. Vesicular
II. Reduced to absent

e. Adventitious breath sounds
I. No

f. Bronchophony and pectoral fremitus
I. Reduced to absent

Front 110

The principal symptoms of pulmonary diseases

Back 110

The principal symptoms of pulmonary diseases
1. Dyspnea
2. Cough
(Most frequent symptom in diseases of the respiratory system)
3. Hemoptysis
4. Chest pain
5. Cyanosis

Front 111

Dyspnea
a. Causes
b. Classification
c. Orthopnea

Back 111

Dyspnea
a. Causes
1. Pulmonary
2. Cardiovascular
3. Anemias
4. Neuro-psychiatric

b. Classification
1. Expiratory
2. Inspiratory
3. Mixed

c. Orthopnea
I. The patient assumes a half-sitting or sitting position to better utilize the auxiliary respiratory muscles
II. Typical for dyspnea in cardiovascular disease. Can also be seen in attacks of bronchial asthma, large pleural effusions, and pneumothoraces

Front 112

Dyspnea
a. Expiratory dyspnea - Causes and findings
b. inspiratory dsypnea - Causes and findings

Back 112

Dyspnea
a. Expiratory dyspnea - Causes and findings
I. Causes
1. Bronchial asthma
2. Pulmonary emphysema

II. Findings
1. Prolonged expiration
2. Wheezes, whistles, musical rhonchi

b. inspiratory dsypnea - Causes and findings
I. Causes - Obstruction of the upper respiratory airways
1. Laryngeal tumor
2. Tumor growing in the trachea or the main bronchus
3. Goiter
4. Edema
5. Hematoma of the glottis
6. Epiglottitis
7. Croup
8. Foreign body aspiration

II. Findings
1. Inspiratory retractions - Jugular fossa, supraclavicular fossa, intercostal spaces, epigastrium

Front 113

Cough
a. Tussigenic zones
b. Function
c. Paroxysmal cough

Back 113

Cough
a. Tussigenic zones
1. Larynx
2. Carina trachea
3. Bronchi - 1st and 2nd order
4. Parietal pleura

b. Function
1. Maintains the patency of the airways
2. Removes pathologic products and foreign objects from them

c. Paroxysmal (Paryoxysmos - Irritation) cough
I. A severe attack of coughing, as may accompany whooping cough, bronchiectasis, or a lung injury

Front 114

Cough
a. Dry, unproductive cough
b. Wet, productive cough - Evaluate
c. Wet, productive cough - Distinction according to macroscopic appearance

Back 114

Cough
a. Dry, unproductive cough
I. If there is no material to be removed from the airways
II. Causes
1. At the onset of acute inflammation
2. Pneumothorax
3. In pressure upon tussigenic structures from enlarged structures
4. In incipient heart failure
(Old, heavy smoker, dry cough, hemoptysis -> Bronchogenic cancer)

b. Wet, productive cough - Evaluate
1. When is it most abundant during the day
(Early morning -> bronchiectasis)
2. Macroscopic appearance
3. Presence of blood
4. Volume/24h
5. Lab tests - Cytology, microscopic, bacteriologic

c. Wet, productive cough - Distinction according to macroscopic appearance
1. Serous
(Watery, thin, frothy, copious, can be blood-tinged (pink). <- Pulmonary edema)

2. Mucous
(Glassy, tenacious (seig). <- Acute bronchitis, end of asthmatic attack (scant, mucoid))

3. Mucopurulent
(Yellowish or greenish. <- Chronic bronchitis, bronchiectasis, TB..)

4. Purulent
(--!!--. <- Bronchiectases, lung abscesses, pulmonary TB..)

5. Putrid
(Typical for anerobic infections - pulmonary gangrene)

(In croupus (lobar) pneumonia a rusty sputum is produced (sputum croceum))

Front 115

Hemoptysis
a. Hemoptysis
b. Massive hemoptysis/Hemoptoe
c. Classification

Back 115

Hemoptysis
a. Hemoptysis
I. Coughing out of blood alone or mixed with sputum
II. Usually develops from damage to a smaller blood vessel

b. Massive hemoptysis/Hemoptoe
I. Spitting or coughing up pure blood from the respiratory tract
II. From damage to a larger blood vessel
III. It can be life-threatening by causing either exasnguination or suffocation

c. Classification
1. Bleeding from pulmonary tuberculosis
(Early infiltrative stage - bleeding from necrosis of a small pulmonary branch. Necrotic lymph node ruptures into a bronchus, and the node communicates with a blood vessel)

2. Bleeding from non-tuberculous causes
(Bronchogenic cancer (necrosis of tumorous tissue or erosion of vessel), bronchiectasis (the damaged bronchial wall is replaced by granulation tissue which is prone to bleeding), coagulation disorders (congenital or drug-induced), early pneumonia (later a rusty/prune-juice sputum develops)

3. Bleeding from circulatory disturbances
(Pulmonary infarction (dark brownish red blood), pulmonary hypertension disorders (mitral stenosis))

Front 116

Cyanosis
a. The amount of reduced hemoglobin in the blood must increase above
b. Contributing cause to cyanosis in chronic lung diseases

Back 116

Cyanosis
a. The amount of reduced hemoglobin in the blood must increase above 50 g/L
b. Contributing cause to cyanosis in chronic lung diseases - secondary polycythemia (polygobulia)

Front 117

Auskulteringspunkt

Back 117