This document provides an overview of the respiratory system including anatomy, physiology, clinical syndromes, examination techniques, and common respiratory complaints. Key points include: - The respiratory system includes the upper and lower respiratory tract, primary and accessory muscles of respiration, and lungs. - Respiratory physiology involves ventilation, oxygenation, and control centers in the brainstem and chemoreceptors. - The pulmonary exam follows inspection, palpation, percussion, and auscultation and evaluates the chest shape/movement, fremitus, expansion, and percussion notes to identify abnormalities. - Common respiratory complaints are cough, sputum production, shortness of breath, chest pain, and wheezing which

1. THE RESPIRATORY SYSTEM
1

2. THE LECTURE №1
Examination and investigation of patients with respiratory diseases.
Main Clinical Syndromes.
2

3. The anatomic respiratory
mechanism Upper respiratory tract:
-Nasal passages
-Oropharynx
-Retropharynx
-Epiglottis
-Trachea
*Supportive structures:
-Sternum and manibrium
-Clavicles
-Xiphoid process
-Costal cartilages
-Twelve pairs of ribs
-Twelve thoracic vertebrae
 Primary muscles of respiration:
-Diaphragm
-Intercostal muscles
*Accessory muscles of respiration:
-Sternocleidomastoid
-Trapezius muscle
-Abdominal muscles
*Lung parenchyma:
-Right lung with three lobes and two
fissures
-Left lung with two lobes, one fissure,
and the lingula
*Mediastinum and great vessels
3

4. The chest anatomy

ANTERIOR VIEW POSTERIOR VIEW
TracheaTrachea
4

5.  Vertebral fM line
l
f
M
l
i
n
e
5

6. The body lines
6

7. 7

8. Vertebral fM lineVertebral fM lineVertebral fM line
8

9. Respiratory physiology
 Ventilation=involves the movement of air back and forth from
the deepest reaches of the alveoli to the outside. Requires
anintact respiratory drive and mechanism (CNS, respiratory
muscles, supporting structures).
 Oxygenation=involves gas exchange across the alveolar-
pulmonary capillary membranes ( diffusion and perfusion,
exchange of oxygen and carbon dioxide).
 Respiratory control centers are located in the brainstem
specifically the pons.
 Chemoreceptors are located in the medulla oblongata and in
the carotid bodies.The chemoreceptos in the medulla
oblangata are very sensitive to hydrogen on concentration
while the chemoreceptors in the carotid body are sensitive to
arterial oxygen and carbon dioxide levels.
9

10. The Pulmonary History
 Again history will give you the most return as far as diagnosis.
 Key components specifically for the respiratory system:
 Cough
 Sputum production and characteristics
 Shortness of breath
 Chest pain
 Wheezing
 Fever
 Upper respiratory tract symptoms (sore throat, sinus congestion, etc.)
 Orthopnea
 Limitation of activity
 Diaphoresis
Risk factors
 Smoking
 Pets
 Sick contacts
10

11. Common Pulmonary Complaints
11

12. Cough
 Described in HPI with duration, productivity,
frequency, regularity
 Describe associated symptoms in HPI such
as fever, sick contacts, URI symptoms, GI
complaints
 Describe environmental factors that
exacerbate it
 Describe relieving factors
 Can be described in your physical (eg.
barking, rattling, etc.)
 All that coughs is not infection
12

13. Sputum Production
 Try to quantitate
 Note color
 Hemoptysis
13

14. Shortness of Breath
 What causes or worsens the shortness of
breath?
 What relieves the shortness of breath?
 Describe progression of shortness of
breath
 Relation to position
 Limitation of activity
 Associated pain or discomfort
 Associated cough, diaphoresis, ankle
edema, calf tenderness or cyanosis
14

15. Dispnea
Problem Chronic bronchitis Chronic
obstructive
Pulmonary disea
se(COPD)
Asthma
Process Exessive mucus
production in
brochi, followed by
chronic obstruction
of airways
Overdistention of
air spaces distal to
terminal
bronchiles, with
destruction of
alveolar septa and
chronic obstruction
of the airways
Bronchial
hyperresponsivene
ss involving release
of inflammatory
mediators,
increased airway
secretions, and
bronchoconstict-
ion
Timing Chronic productive
cough followed by
slowly progressive
dispnea
Slowly progressive
dyspnea; relatively
mild cough later
Acute episodes,
separated by
symptom-free
periods. Nocturnal
episodes common
15

16. Factors that
aggravate
Exertion, inhaled
irritants,
respiratory
infections
Exertion Variable, inclu-ding
allergens,Irritants,
respiratory
infections, exercise,
and emotion
Factor that Relieve Expectoration, rest,
through dyspnea
may become
persistent
Rest, through
dyspnea may
become persistent
Separation from
aggravating factors
Associated
symptoms
Chronic productive
cough, recurrent
respiratory
infections,wheezin
g may develop
Cough, with scant
mucoid sputum
Wheezing, cough,
tightness in chest
Setting History of smking,
air pollutants,
recurent
respiratory
infections
Hist. of smoking,
air pollutants,
deficiency in alpha
antitrypsin
Environmental and
emotional
conditions
16

17. Chest Pain
 PQRST
 Associated symptoms
 Patient's perception of the problem
 Many other diseases mimic angina
17

18. Pulmonary chest pain
Problem Tracheobronchitis Pleuritic pain
Process Inflammation of trachea
and large bronchi
Inflammation of the
parietal pleura, as in
pleurisy, pneumonia,
pulmonary infarction, or
neoplasm
Location Upper sternal or on aither
side of the sternum
Chest wall owerlying the
process
Quality Burning Sharp, knifelike
Severity Mild to moderate Often severe
18

19. Timing Variable Persistent
Factors that Aggravate Coughing Inspiration, coughing,
movements of the trunk
Factors that Relieve Lying on the involved
side may relieve it
-
Associated symptoms Cough Of the underlying illness
19

20. Past Medical History
 Thoracic trauma or surgery
 Previous pulmonary disorders and
hospitalizations
 Chronic pulmonary diseases (eg.
tuberculosis, bronchitis, emphysema,
asthma, cystic fibrosis)
20

21. Family History
 Cystic fibrosis
 Asthma
 Allergies
 Malignancy
 Genetic problems
 Deficiency of alpha-1 antitrypsin
21

22. Examination
 Patient should be shirtless. Women
should be draped (note: When patients
come in for nonrespiratory complaints is
recommended you do not listen through
the shirt, but for the sake of time you
can).
 Follow the traditional sequence:
 Inspection
 Palpation
 Percussion
 Auscultation
22

23. Inspection
 Under HEENT, examine the sinuses,
dentition, retropharynx, nares (flaring)
 Inspect the neck for tracheal deviation,
JVD and use of accessory muscles
 Examine in a side to side fashion
comparing one side to the other
 Shape and symmetry
 Anteroposterior diameter (eg. Barrel
chest)
 Pectus carinatum and pectus excavatum
23

24. Inspection (Continued)
 Cyanosis or pallor
 Clubbing
 Observe respiratory rate
 Note the breathing pattern
 Observe any retractions or use of
abdominal muscles for respiration
 Listen for audible wheezes or stridor
 Assess for prolonged expiratory phase
24

25. Descriptors of Respiration
 Dyspnea = difficult breathing with shortness of
breath
 Orthopnea = increasing shortness of breath when the
patient lies down
 Paroxysmal nocturnal dyspnea = sudden onset of
shortness of breath relieved by sitting or standing
 Platypnea = dyspnea increasing in the upright
posture (rarely seen)
 Tachypnea = persistent respiratory rate above 25 per
minute
 Hyperpnea = rapid and deep ventilation
 Bradypnea = respiratory rate < twelve respirations
per minute
25

26. Patterns of Respiration
Normal Respiration
Tachypnea
Bradypnea
Hyperpnea or Hyperventilation
Kussmaul Respirations
Cheyne-Stokes Respirations
Biot’s or Cluster Respirations
Ataxic Respirations
26

27. Inspection of the anterior
chest
Observe the shape of the patient's chest and the
movement of the chest wall. Note:
 Deformities or asymmetry
 Abnormal retraction of the lower interspaces
during inspiration. Supraclavicular retraction is
often present. (Severe asthma, COPD, or upper
airway obstruction)
 Local lag or impairment in respiratory
movement (underlying disease of lung or pleura)
27

28. Inspection of the posterior
chest
From a midline position behind the patient, note the shape of
the chest and how the chest moves, including:

Deformities or asymmetry
 Abnormal retraction of the interspaces during inspiration.
Retraction is most apparent in the lower interspaces.
 Inpaired respiratory movement on one or both sides or a
unilateral lag (or delay) in movement.
28

29. Path. chest
Barrel chest.
There is an increased
anterioposterior
diemeter.This shape is
normal during infancy,
and often accompanies
aging and chronic
obstructive pulmonary
diseases (emphysema
of lungs, bronchial
asthma).
29

30. Path. Chest.
Pigeon chest.
The sternum is
displaced anteriorly,
increasing the
anterioposterior
diameter.The costal
cartilages adjacent to
the protruding sternum
are depressed. Pectus
carinatum develops in
rickets and in chronic
childhood respiratory
illness in which it result
from repeated strong
contractions of
diaphragm while the
thorax is still pliable.

Depressed costal cartilages
30

31. Thoracic Kyphoscoliosis
Abnormal spinal
curvatures and vertebral
rotation deform the
chest. Distortion of the
underlying lungs may
make interpretation of
lung findings very
difficult. Kyphoscoliosis a
combination of both
shapes may be
idiopathic or secondary
to poliomyelitis or
Marfan syndrome.
Severe kyphoscoliosis
may reduce the lung
capacity and increase the
work of breathing
 Spinal convexity to the right
(patient bending forward)

Spinal convexity to the right (patient bending forward)
31

32. Traumatic Flail Chest
Multiple rib fractures
may result in
paradoxical
movements of the
thorax. As descent of
the diaphragm
decreases
intrathoracic
pressure, on
inspiration the
injured area caves
inward; it moves
autward.
32

33. Palpation
 Carefully palpate any area were pain
has been reported
 Masses or sinus tracts
 Respiratory expansion
 Assess forced expiratory time
 Crepitus
 Tactile fremitus
33

34. Palpation
 As you palpate the chest, focus on areas of tenderness and
abnormalities in the overlying skin, respiratory expansion,
and fremitus.
 Identify tender areas. Carefully palpate any area where
pain has been reported or where lesions or bruises are
evident.
 Assess any observed abnormalities such as masses or sinus
tracts (blind, infhmmatory, tubelike structures opening
onto the skin).

34

35. 
• Palpate and compare symmetric areas of the
lungs in the pattern shown in the photograph.
Identify and locate any areas of increased,
decreased, or absent fremitus. Fremitus is
typically more prominent in the interscapular
area than in the lower lung fields and is often
more prominent on the right side than on the
left. It disappears below the diaphragm.
 Tactile fremitus is a somewhat imprecise
assessment tool, but as
35

36. Palpation

Test chest expansion. Place your thumbs at about the level
of the 10th ribs, with your fingers loosely, grasping and
parallel to the lateral rib cage. As you position your hands,
slide them medially just enough to raise a loose fold of skin
on each side between your thumb and the spine.
 Ask the patient to inhale deeply.Watch the distance
between your thumbs as they move apart during
inspiration, and feel for the range and symmetry of the rib
cage as it expands and contracts.
 Causes of unilateral decrease or delay in chest expansion
include chronic fibrosis of the underlying lung or pleura,
pleural effusion, lobar pneumonia, pleural pain wit
associated splinting, and unilaten bronchial obstruction
36

37. 37

38. Feel for tactile fremitus. Fremitus refers to the palpable vibrations
transmitted through the bronchopulmonary tree to the chest wall as the
patient is speaking.To detect fremitus, use either the ball (the bony part of
the palm at the base of the fingers) or the ulnar surface of your hand to
optimize the vibratory sensitivity of the bones in your hand.Ask the patient
to repeat the words "ninety-nine" or "one-one-one." If fremitus is faint, ask
the patient to speak more loudly or in a deeper voice.
Use one hand until you have learned the feel of fremitus. Some clinicians
find using one hand more accurate.The simultaneous use of both hands to
compare sides, however, increases your speed and may facilitate detection
of differences.
38

39.  Fremitus is decreased or absent when the
voice is soft or when the transmission of
vibrations from the larynx to the surface c; the
chest is impeded. Causes include a very thick
chest wall; an obstructed bronchus; COPD;
separation of the pleural surface by fluid
{pleural effusion), fibrosis {pleural thickening),
air {pneumothorax), or an infiltrating tumor.
39

40. a scouring technique, it directs your attention
to possible abnormalities. Later in the
examination you will check any suggested
findings by listening for breath sounds, voice
sounds, and whispered voice sounds. All :
attributes tend to increase or decrease
together.
40

41.  Look for asymmetric fremitus: asymmetric
decreased fremitus in unilateral pleural
effusion, pneumothorax, neoplasm from
decreased transmission of low frequency
sounds; asymmetric increased fremitus in
unilateral pneumonia from increased
transmission.15
41

42. Percussion
42

43. Percussion
43

44. 44

45.  Percussion Notes. With your plexor or tapping
finger, use the lightest percussion that produces
a clear note. A thick chest wall requires stronger
percussion than a thin one. However, if a louder
note is needed, apply more pressure with the
pleximeter finger (this is more effective for
increasing percussion note volume than tapping
harder with the plexor finger).
45

46.  When percussing the lower posterior chest, stand
somewhat to the side rather than directly behind the
patient.This allows you to place your pleximeter finger
more firmly on the chest and your plexor is more
effective, making a better percussion note.
 When comparing two areas, use the same percussion
technique in both areas. Percuss or strike twice in each
location. It is easier to detect differences in percussion
notes by comparing one area with another than by
striking repetitively in one place.
 Learn to identify five percussion notes. You can
practice four of them on yourself.These notes differ in
their basic qualities of sound: intensity, pitch, and
duration.Train your ear to distinguish these differences
by concentrating on one quality at a time as you percuss
first in one location, then in another. Review the table
below. Healthy lungs are resonant.
46

47. Percussion Notes and their
characteristic
Relative
Intensity
Relative
Pitch
Relative
Duration
Example of
Location
Pathologic
Examples
Flatness Soft High Short Thigh Large
pleural
effusion
Dullness Medium Medium Medium Liver Lobar
pneumonia
Resonance Loud Low Long Healthy
lung
Simple
chronic
bronchitis
Hyperreso-
nance
Very load Lover Longer Usually
none
COPD,
pneumotho
rax
Tympany Loud High Gastric air
bubble or
puffed-out
Large
pneumotho
rax 47

48. Percussion
 Be sure to percuss between ribs not
over the bones
 Assess diaphragmatic excursion
48

49. While the patient keeps both arms
crossed in front of the chest, percuss the
thorax in symmetric locations on each
side from the apex to the base.
Percuss one side of the chest and then
the other at each level in a ladder-like
pat-tern, as shown by the numbers
below. Omit the areas over the
scapulae— the tickness of muscle and
bone alters the percussion notes over
the lungs. Identify and locate the area
and quality of any abnormal percussion
note.
 “
"LADDER" PATTERN FOR PERCUSSION AND AUSCULTATION
49

50.  Identify the descent of the diaphragm, or
diaphragmatic excursion. First, determine the
level of diaphragmatic dullness during quiet
respiration. Holding the pleximeter finger above
and parallel to the expected level of dullness,
percuss downward in progressive steps until
dullness clearly replaces resonance. Confirm this
level of change by percussion near the middle of
the hemothorax and also more laterally.
50

51.  Note that with this technique, you are identifying
the boundary between the resonant lung tissue and
the duller structures below the diaphragm.You are
not percussing the diaphragm itself.You can infer
the probable location of the diaphragm from the
level of dullness.
 Now, estimate the extent of diaphragmatic
excursion by determining the distance between the
level of dullness on full expiration and the level of
dullness on full inspiration, normally about 5 or 6
cm.
51

52. 52

53.  Dullness replaces resonance when fluid or solid tissue
replaces air-containing lung or occupies the pleural
space beneath your percussing fingers. Examples
include: lobar pneumonia, in which the alveoli are filled
with fluid and blood cells; and pleural accumulations of
serous fluid {pleural effusion), blood {hemothorax), pus
{empyema), fibrous tissue, or tumor.

 Generalized hyperresonance may be heard over the
hyperinflated lungs of COPD or asthma, but is not a
reliable sign. Unilateral hyperresonance suggests a large
pneumothorax or possibly a large air-filled bulla in the
lung.

53

54.  An abnormally high
level suggests pleural
effusion, or a high
diaphragm as in
atelectasis or
diaphragmatic
paralysis.
Location and sequence of
percussion
Resonant
Level of diaphragm
Dull
54

55. Auscultation
 Use the diaphragm, not the bell
 Involves:
n Listening to sounds generated by
breathing
n Listening for adventitious sounds
n If abnormalities are suspected listen to
transmitted sounds (Vocal Resonance)
55

56. Auscultation
56

57.  Auscultation
Auscultation is the most important examination
technique for assessing air flow through the
tracheobronchial tree.Together with percussion, it
also helps the clinician assess the condition of the
surrounding lungs and pleural space. Auscultation
involves (1) listening to the sounds generated by
breathing, (2) listening for any adventitious (added)
sounds, and (3) if abnormalities are suspected,
listening to the sounds of the patient's spoken or
whispered voice as they are transmitted through
the chest wall.
57

58.  Sounds from bedclothes, paper gowns, and the
chest itself can generate confusion in
auscultation Hair on the chest may cause crack-
ling sounds. Either press harder or wet the hair.
If the patient is cold or tense, you may hear
muscle contraction sounds—muffled, low
pitched rumbling or roaring noises. A change in
the patient's position may eliminate this noise.
You can reproduce this sound on yourself by
doing aValsalva maneuver (straining down) as
you listen to your own chest.
58

59. Vocal Resonance
 Bronchophony = greater clarity
increased on this spoken words while
auscultating
 Whispered pectoriloquy = hearing a
whispered while auscultating
 Egophony = “e to a” changes
59

60. Breath Sounds (Lung Sounds), You will learn to identify patterns of breath
sounds by their intensity, their pitch, and the relative duration of their
inspiratory and expiratory phases. Normal breath sounds are:
 Vesicular, or soft and low pitched.They are heard through inspiration,
continue without pause through expiration, and then fade away about
one third of the way through expiration.
 Bronchovesicular, with inspiratory and expiratory sounds about equal in
length, at times separated by a silent interval. Detecting differences in
pitch and intensity is often easier during expiration.
 Bronchial, or louder and higher in pitch, with a short silence between
inspiratory and expiratory sounds. Expiratory sounds last longer than
inspiratory sounds.
The characteristics of these three kinds of breath sounds are summarized in
the next table.Also shown are the tracheal breath sounds—very loud,
harsh sounds that are heard by listening over the trachea in the neck.
60

61.  Listen to the breath sounds with, the
diaphragm of a stethoscope after instructing the
patient to breathe deeply through an open
mouth. Use the pattern suggested for
percussion, moving from one side to the other
and comparing symmetric areas of the lungs. If
you hear or suspect abnormal sounds, auscultate
adjacent areas so that you can fully describe the
extent of any abnormality. Listen to at least one
full breath in each location. Be alert for patient
discomfort resulting from hyperventilation (e.g.,
lightheadedness, faintness), and allow the
patient to rest as needed.
61

62.  Note the intensity of the breath sounds.
Breath sounds are usually louder in the lower
posterior lung fields and may also vary from
area to area. If the breath sounds seem faint,
ask the patient to breathe more deeply.You
may then hear them easily.When patients do
not breathe deeply enough or have a thick
chest wall, as in obesity, breath sounds may
remain diminished.
62

63. Characteristics of Breath
SoundsDuration of
Sounds
Intensity of
Expiratory
Sound
Pich of
expiratory
Sound
Locations
where
heard
normality
Examples
of
abnorma-
lity
Vesicular Inspiratory
sounds last
longer than
expiratory
ones
Soft Relatively
low
Over most
of both
lungs
Bronchovesi
cular
Inspiratory
and
expiratory
sounds are
about equal
Intermedia-
te
Intermedia-
te
Often in the
1st and 2 nd
interspaces
anteriorly
and
between
the scapulae
It
bronchoves
or bronchial
breath
sounds are
heard in
locations
distant
63

64. Bronchial Expiratory
sounds last
longer
then
inspiratory
ones
Loud Relatively
high
Over the
manubriu
m, if heard
at all
From
those
listed,
suspect
that air-
filled lung
has been
replaced
be fluid-
filled or
solid lung
tissue.
Tracheal Inspiratory
and
expiratory
sounds are
about equal
Very loud Relatively
high
Over the
trachea in
the neck
64

65.  Breath sounds may be decreased when
airflow is decreased (as in obstructive lung
disease or muscular weakness) or when the
transmision of sound is poor (as in pleura,
effusion, pneumothorax, or COPD).
65

66. Adventitious or Added Breath
Sounds
Crackles (or Rales) Wheezes and Rhonchi Examples of abnormalites
DISCONTINUOUS CONTINUOUS Crackles may be from
abnormalites of the lungs
(pneumonia, fibrosis, early
congestive heart failure) or
of the airways (brochitis,
bronchiectasis).
Intermittent, nonmusical,
and brief
>or =250 msec, musical,
prolonged(but not
necessarily persisting
throughout the respiratory
cycle)
Like dots in time Like dashes in time
Fine crackles: soft, high-
pitched, very brief (5-10
msec)
Wheezes: relatively high
pitched (>=400Hz) with
hissing or shrill quality
Wheezes suggest narrowed
airways, as in asthma, COPD
or bronchitis.
Coarse crackles: somewhat
louder, lower in pitch,
brief(20-30 msec)
Rhonchi: relatively low-
pitched(>=200Hz) with
snoring quality
Rhonchi suggest secretions
in large airways
66

67.  Timing in the respiratory cycle
 Location on the chest wall
 Persistence of their pattern from breath to
breath
 Any change after a cough or a change in the
patient's position
67

68.  Clearing of crackles, wheezes, or rhonchi
after coughing or postion change suggests
inspissated secretions, as in bronchitis or
atelectasis.
68

69.  When lung tissue loses its air, it transmits high-
pitched sounds much better. If the
tracheobronchial tree is open, bronchial breath
sounds may replace the normal vesicular sounds
over airless areas of the lung.This change is seen
in lobar pneumonia when the alveoli fill with
fluid, red cells, and white cells— a process called
consolidation. Other causes include pulmonary
edema or hemorrhage. Bronchial breath sounds
usually correlate with an increase in tactile
fremitus and transmitted voice sounds.These
findings are summarized below.
69

70. Normal Air-Filled Lung
Breath Sounds:
Predominantly vesicular
TransmittedVoice
Sounds:
Spoken words muffled
and indistinct
Spoken "ее" heard as
"ее"Whispered words
faint and indistinct, if
heard at all
Tactile Fremitus:
Normal
70

71. Airless Lung, as in Lobar
Pneumonia
Breath Sounds:
Bronchial or bronchovesicular
over the involved area
TransmittedVoice Sounds:
Spoken words louder, clearer
(bronchophony)
Spoken "ее" heard as "ay"
(egophony Whispered words
louder, clearer (whispered
pectoriloquy)
Tactile Fremitus:
Increased
71

72. Adventitious (added) Sounds
 Crackles (rales)
 Wheezes
 Rhonchi
 Rubs
 Stridor
 Grunting
72

73. Crackles (rales)
 Described as fine, medium or coarse
 Other terms used are sibilant (high-
pitched) and sonorous (low-pitched)
 If heard, determine if it clears with
coughing
73

74. Rhonchi
 Sometimes described as a sonorous
or low pitched wheeze
 Deeper, rumbling, more pronounced
during expiration
 If heard, determine if they clear with
coughing
74

75. Wheezes
 High-pitched, musical sound, almost
whistle like
 Heard most of the time on expiration
 All that wheezes is not asthma
75

76. Friction Rub
 It has a dry, crackly, grating, low
pitched sound
 heard both on expiration inspiration
76

77. Stridor
 Usually upper respiratory foreign
body or mass
 Can be both inspiratory and
expiratory
77

78. Grunting
 Usually seen in infants
 Sign of respiratory distress
 Usually seen with accessory muscle
usage.
78

79. Theme: Laboratory and
instrumental inspection of
patients with diseases of
respiratory organs
79

80. The information block
 Concept about the basic methods of research
of organs of breath. At diseases of organs of
breath necessary, and informative are: the
general analysis of the sputum, research of a
pleural liquid, function of external breath,
(pulmonary function test), chest Xray
changes, bronchoscopy, spirometry and on
occasion - biopsy, oximetry.
80

81.  Sputum - pathological separated the breath
organs, thrown out at cough and expectorate. At
the HEALTHY PERSON (which not smoke!) no
sputum. Structure of the sputum: mucus, a
serous liquid, blood cells, cells of respiratory
ways, elements of destruction of tissues,
crystals, microorganisms, the helminths.The
daily quantity can fluctuate in limits from 1 ml to
1000 ml and more. Excretion of large quantity of
the sputum at change of position of the patient
is characteristic for bronchiectesis.
81

82. The characteristic of sputum
Mucous sputum- colourless, slightly whitish, viscous - at an acute
bronchitis. Serous sputum- colourless, liquid, foamy - at a lung
hypostasis. Mucopurulent sputm- yellow or greenish colour,
viscous - at a chronic bronchitis, a tuberculosis and etc.
Purulent - homogeneous, semi-fluid, yellowish-green it is
characteristic for an lung abscess has ruptures into a bronchus.
Blood-stained sputum - purely blood - at pulmonary bleedings (a
tuberculosis and a lung cancer, at a syndrome bronchoectasis).
Mucous with blood foamy (heamoptysis) pink - at a syndrome
left ventricular failure warm insufficiency with the stagnation
phenomena in a small circle of blood circulation. Mucous –blood
stained - at a syndrome thromboemboly a pulmonary artery (a
lung infarction), "rusty" sputum - at a syndrome of consolidation
or inflammatory of the lung tissues (a primary or acute
pneumonia).
82

83.  The smell of the sputum - is absent is more
often. A fetid smell - a sign of a suppuration
and destruction of a pulmonary tissues - at a
syndrome of purulent disintegration (or
fusions) a pulmonary tissues (a lung
gangrene, a lung cancer, a lung abscess),
sputum with an unpleasant smell (foetuг ех
ores) - at an bronchiectasis.
83

84.  Microscopic research of the sputum spend at small,
then at the big increase: kurshman”s spirals , Sharco-
Layden”s crystals , eosinophyls - at a syndrome of
bronchial obstruction (a bronchial asthma). Elastic
fibres - at a syndrome destruction (fusion) of a
pulmonary tissues (a lung abscess), a tuberculosis, a
lung cancer. Atipical cells - at tumours of bronchial
tubes and lungs, fungate- at long treatment with
antibiotics. Erythrocytes - at destruction of a tissues of a
lung, a syndrome inflammatory a pulmonary tissues
(pneumonia), a syndrome thromboamboly a pulmonary
artery ( a pulmonary infarction) and at a syndrome left
ventricule failure in a small circle of blood circulation.
Leukocytes - at inflammatory and нdestruction
diseases of lungs.
 Showing of the sputum - are necessary for definition of
a kind and virulence activators, definition of sensitivity
(stability) of microbes to medical drugs ( antibiotics).
84

85. Color
 Yellowish green indicates inflammation
(infection or allergy).
 Presence of blood suggests acute infection,
tuberculosis, tumor pulmonary infarct.
Sputum Gram stain and culture are indicated in:
 Lower respiratory tract infection
(pneumonia).
 Aspergillus lung disease.
Sputum AFB (acid fast bacilli)
 For tuberculosis, samples of early morning are
 sent three consecutive days.
Sputum cytology
 Required for diagnosis of bronchogenic carcinoma. If patient is not
producing sputum, it can be induced by inhalation of nebulized
hypertonic saline. It can also be obtained during bronchoscopy in
bronchial washing.
85

86. SPUTUM
 White -Mucoid
 Grey -Mucoid (Just inhalation)
 Black -Mucoid +• coal dust (melanoptysis)
 Yellow or green -Purulent
 Rusly -Altered blood (pneumococcal
pneumonia)
 Pink frothy -Pulmonary edema
 Blood-stained -Hemoptysis
86

87. Examination of sputum
Quantity
 Scanty: Bronchitis, early stage of pneumonia,
asthma.
 Moderate amount: Chronic bronchitis,
tuberculosis.
 Large amount: Brpnchiectasis, chronic
bronchitis, and lung abscess.
Appearance
 Watery: Pulmonary congestion, pulmonary
edema
 Mucoid: Acute & chronic bronchitis, asthma
 Mucopurulent: All infections of lungs &
bronchi
 Purulent: Bronchiectasis, lung abscess,
pulmonary tuberculosis
Color
 Blackish: due to inhalation of carbon
 Rusty (khaki): due to altered blood mixed
 with sputum in lobar pneumonia
 Reddish:,indicates hemoptysis
 Frothy pink: in pulmonary edema
 Sticky brown to red: in Klebsiella infection
87

88. HEMOPTYSIS
 The expectoration of blood or blood stained
sputum is known. as hemoptysis.The source of
blood should be-below the vocal cords.The lungs
are supplied with dual circulation. Pulmonary
arteries arise from right ventricle and supply
pulmonary parenchyma .while the bronchial
arteries arise from aorta"or intercostals arteries
and supply airways, blood-vessels, hila and
visceral pleura.The bronchial circulation is only
1-2% of total pulmonary blood flow but is more
common source of bleeding. Bonchial blood flow
dramatically increases in inflammation.
88

89. Causes
From airways in
 Bronchitis
 Bronchiectasis
 Bronchial adenoma
 Bronchogenic carcinoma
From pulmonary vasculaturc
 Mitral stenosis
 Pulmonary infarction
 Left ventricular failure
 A-V malformation
From pulmonary parenchyma
 Pneumonia
 Bleeding disorders.
 Autoimmune diseases e.g. Goodpasture's
syndrome andWegncr's syndrome
Massive hemoptysis: more than 200-600 ml of blood in 24 hours. Occurs in
bronchicctasis. tuberculosis, pulmonary infarction.
89

90. ARTERIAL BLOOD-GAS ANALYSIS
(ABGs)
Measurement of P02 and PC02 and H+
concentration in arterial blood is valuable in
assessment of hypoxemia or acid-base balance
in respiratory failure, and asthma.
 Procedure
 Heparinize the syringe with 0.1 ml heparin to
prevent clot formation.
 Draw blood from radial or brachial or femoral
artery.
 The sample should be immersed in ice bag
immediately to prevent metabolism that can
reduce PO2 and increase PCO2.
90

91. Normal values
 PH: 7.35-7.45
 PO2: 80-105mmHg
 PCO2: 35-45 mmHg
 HCO3: 22-26 mmol/L
 O2 saturation: 95-100%
91

92. Primary respiratory acidosis
 High PC02 and low pH
 Causes are type II respiratory failure (due to
COPD and hypoventilation).
Compensated respiratory acidosis
 High PC02 but pH becomes normal as the kidney
starts to compensate with renal bicarbonate
retention.Therefore the patient presents with
primary respiratory acidosis (raised PC02),
normal pH, and compensatory metabolic
alkalosis (raised bicarbonate).
92

93. Primary respiratory alkalosis
 Low PCO2 and high pH.
 Causes are hyperventilation intentionally or
unintentionally.
Compensated respiratory alkalosis
 Low PC02, normal pH and low bicarbonate as
a compensatory response from the kidney.
93

94. Primary metabolic acidosis
 Low bicarbonate, low pH.
 Causes are chronic renal failure, diabetic
ketoacidosis and lactic acidosis.
Compensated metabolic acidosis
 Lungs try to maintain pH to normal by rapid
respiratory rate, blowing off CO2 and causing
respiratory alkalosis".Therefore the picture is
low bicarbonate, almost normal pH and low
C02.
94

95. Pleural fluid
 . Research of a pleural fluid - after reception
by its method of a pleural puncture or during
operation intervention on respiratory organs .
 A diagnostic pleural puncture spend in 7 - 9
intercostals, in a zone dullness of percussion
sound, more often - between scapular and
posterior axillary lines, a needle enter on an
upper edge of an underlaying edge of costal.
95

96.  The characteristic of a pleural fluid.
Organoleptics and microscopic investigation
of fluid.The received pleural fluid can be
inflammatory exudate and not inflammatory
(more often - stagnant) character
(transudate).
96

97.  Transudate - the accumulation of not
inflammatory fluid in a pleural cavity
(hydrothorax), light yellow colour,
transparent, without a smell, is not
coagulation at standing, alkaline reactions,
protein - no more ЗО g/l, relative density - not
above 1,015, Rivalt”s test is negative
97

98.  Exudate - an inflammatory liquid, sometimes
opalesce(a tuberculosis!), at standing forms a
clot, protein - more ЗО g/l, Rivalt”s test - it is
positive (at the expense of protein-
seromucyne), relative density above 1,015.
Variants of exudate: serous exudate (at an
serous pleurisy),serous - purulent (at a
pneumonia and a tuberculosis), purulent and or
putridity (at purulent process in a pleura cavity -
empyema), heamorragic ( hemothorax) - at the
malignant , the closed traumas of a thorax, the
wounding of a thorax, the hemorragic diathesis.
98

99. PROCEDURE OF THERAPEUTIC
PLEURAL ASPIRATION
 Carefully sterilize the skin over the aspiration site.
Sterile gloves, cap, gown and mask must be worn.
 Anaesthetize the skin, muscle and pleura with 2%
lignocaine,
 Make a small incision, then push a 28 French gaugeArgylc catheter into the pleural space.
 Attach to three-way tap and 50 ml syringe.
 Aspirate up to 1000 ml. Stop aspiration if patient
becomes uncomfortable - shock may ensure if too
much fluid is withdrawn too quickly.
Pleurodesis
Tetracyclinc 500 nig or bleomycin 15 units in 30-50 ml
sodium chloride 0.9% solution is instilled into the pleural
cavity to achieve pleurodesis in recurrent/malignant
effusion.
99

100. Complications of pleural
aspiration
 Pleural shock: due to vagal stimulation as a
complication of pain.
 Air embolism
 Pulmonary edema: if fluid is removed too
quickly.
 Pneumothorax: if lung is ruptured.
 Empyema: if introduction of infection into
pleural space.
 Rupture of intercostals vessels.
100

101. X-ray INVESTIGATION of syndromes
at diseases of respiratory system
 Postero-anterior (PA) view is the routine film.
 Antero-posterior (AP) is taken if the patient is
unable to stand. Cardiac shadow is larger in
AP view. .'•• -1
 Lateral view is required to localize the site of
abnormality visible on PA view.
 Lordotic view is required to look lung apices
as in pulmonary tuberculosis.
 Lateral decubitus view is taken to confirm
pleural effusion.
 Chest x-ray should be taken in full
inspiration, if taken in expiration lower parts
of lungs are not clear.
 X-ray reading should be in sequence (inside
to outside) starting from trachea to
mediastinum, heart, hila, diaphragm,
costophrenic angle, cardiophrenic. angle, lung
apices, lung parenchyma, pleural . Space,eleton and then soft tissues.
101

102. It is better to look the name, date, position of
patient and quality of x-ray but during exams
examiners usually do not like that students start
from these features due to lack of time;
therefore
start from saying " x-ray chest PA view
showing .
 Following points should be noted in chest X-ray:
Trachea
 Central or deviated
102

103. Mediastinum
 Look for the widening of mediastinum
 Shifting of mediastinum due to pull or push
phenomenon.
Heart
 Size, shape and position of heart, aortic knuckle.
Hilar shadow
 Size and shape of hilar shadow, prominent
hilar lymphadenopathy unilateral or bilateral.
 Pulmonary artery shadow
Diaphragm
 • Elevated or flat.
 • Gas under the right diaphragm indicates gut
• perforation.
 • Obliteration of costophrenic angle - in pleural
effusion.
103

104. Lung field
 Lung apices for haziness due to tuberculosis.
 Homogenous or patchy infiltrates.
 Reticulonodular pattern of tuberculosis
 Fibrosis
 Cavities, bullae
 Prominent vascular markings.
 Round opacities.
Pleural space
 • Wide pleural space, no lung marking in
pncumothorax.
 • Pleural thickening
Skeletal deformities
Bones deformities, fracture.
Soft tissue shadow
Look for subcutaneous emphysema
104

105. CT SCAN
 CT scan demonstrates size and position of a
pulmonary nodule or mass and whether
calcification or cavitation is present in it.
 CT scan is also valuable in bronchial
carcinoma staging to demonstrate
mediastinal, pleural or chest wall invasion.
 High - resolution CT • scanning involves
sampling the lung parenchyma with thin 1-2
mm thickness throughout the lung. It is
particularly effective in the diagnosis of
interstitial lung disease, bronchiectasis and
emphysema.
105

106. VENTILATION-PERFUSION SCAN
 Ventilation - perfusion (V/Q) scan is required
for the diagnosis of pulmonary embolism in
which there is diminished perfusion relative
to ventilation.
106

107. ULTRASOUND
 It is required for detection of pleural effusion
especially that is loculated
107

108. MEDIASTINOSCOPY
 The mediastinoscope is introduced through a
small incision at the suprastcrnal notch to
give a view of upper mediastinum. Biopsy of
some mediastinal nodes is possible and will
reveal the presence or absence of malignant
cells in the enlarged lymph nodes previously
detected by CT, allowing accurate staging of
the disease.
108

109. FIBREOPTiC BRONCHOSCOPY
There are two types of bronchoscdpes; flexible
fiberoptic and rigid type. Flexible bronchoscope is
commonly used and requires only local anesthetic
solution while rigid type requires general anesthesia.
 Trachea and large bronchi are inspected; distortion
or obstruction can be seen.
 Abnormal tissue in the bronchial lumen or wall can
be biopsied.
 Bronchial brushing, washings or aspirates can be
taken for cytological or bacteriological
examination.
109

110. Indications
 • Lesion requiring biopsy seen on x-ray chest
 • Hemoptysis
• Strider
 • Positive sputum cytology for malignant cells
with no chest X-ray abnormality
 Collection of bronchial secretions for bacteriology,
especially tuberculosis
 Recurrent laryngeal nerve palsy of unknown
etiology
 Infiltrative lung disease (to obtain a transbronchial
biopsy)
 Investigation of collapse lobes or segments
 Aspiration of mucus plug.
110

111. Procedure
 After overnight fasting atropine 0.6 mg IM given 30
min before procedure.Topical 2% lignocaine gel is
applied to nose, nasopharynx, and pharynx. IV
sedation with diazepam 10 mg. Bronchoscope is
passed through the nose, nasopharynx, and pharynx
under direct vision. Lignocaine 2 ml of 4% is
dropped through the instrument on to the vocal
cords. Bronchoscope is passed through the cords
into the trachea. All segments and subsegmental
orifices should be identified. Biopsies and brushing
should be taken.

111

112. Changes of pulmonary function tests (PFT) at
main syndromes of RESPIRATORY SYSTEM
diseases
112

113. 1. The SYNDROME of BRONCHIAL OBSTRUCTION is
characterised by change (decrease) in high-speed
indicators PFTs: decrease forced vital capacity (FVC)
and the maximum ventilation of lungs (TLC-total lung
capacity), the forced expiratory volume for the first
second (FEV1), instant maximum volume speeds at an
exhalation at level of 50-75 % of volume of forced vital
volume of the lungs, average volume speed in the
interval of an exhalation at level from 20-75 % of
volume of forced vital volume of the lungs, and also
FEV1/FVC (Tiffno-Votchal”s index); at
pneumotachometry (PTM) and peak-floumetry (PFM)
- decrease in the maximum speed of an exhalation.
 The increase in high-speed indicators PFTs (an Tiffno –
Votchal”s index and indicators PTM of an exhalation)
after inhalation broncholytics drugs more than 15 %
from initial testifies about bronchospastic genesis an
obstruction syndrome.
113

114. 2.The SYNDROME of CONSOLIDATION of the
PULMONARY tissues is characterised by change
of capacitor indicators: reduction of indicators of
respiratory volume (CV), inspiratory reserve
volume (IRV) an expiratory (ERV) and vital
capacity of lungs (VC), increase indicators
residual volume of lungs (RV) and increase in the
total volume capacity of lungs and functional
residual capacity of lungs (FRC). Important:
change sizes variable depending on volume of
the damage pulmonary tissues - from any (small
volume or the centre), to expressed - at lobar
pneumonia.
114

115. 3.The SYNDROME of HYPERINFlATION of LUNG
tissues is characterised by change of capacitor
indicators: decrease of indicators of respiratory
volume (RV), inspiratory reserve volumes of a
breath (IRV) and expiratory (ERV) and vital
capacity of lungs (VCL), increase in indicators of
residual volume of lungs (RVL) and increase in
the total lung capacity (TLC) and functional
residual capacities of lungs (FRC).
115

116. 4.The SYNDROME of ACUTE and CHRONIC
RESPIRATORY INSUFFICIENCY. Changes
pulmonary function tests - depend on the reason
which have caused pulmonary insufficiency (see
above).The syndrome of pulmonary (respiratory)
insufficiency is characterised by reduction of
saturation of oxygenation of blood in lungs.
Adequate indicators of this syndrome are: degree
of saturation of blood oxygen (a method
oxyhemometry), concentration of carbonic gas and
carbonic acid in blood, degrees of recycling of
oxygen tissues - oxygen operating ratio (OOR2),
relations of pulmonary ventilation and perfusion.
The Syndrome is caused or obstructon syndrome
(its any variant), or an obstruction syndrome (its any
variant), or a combination of these syndromes.
116

117. OXYHEMOMETRY
 Gives representation about degree of
saturation of blood oxygen on colour change
of blood (direct invasive methods), or a colour
transparency of a living tissue (for example,
an ear lobe, a finger, etc.), appeared through
by monochromatic light. Indicators
oxyhemometry can be less then 98 % there
are less also characterised oxygen
insufficiency (debts) of blood.
117

118. BRONCHOSCOPY
The most informative and solely method allowing in vital to examine an internal
surface of bronchial tubes to study a relief of a mucous membrane both its
folds configuration of orifices and some bronchial tubes and to take a byopsy
material for microscopic investigation. Bronchoscopy it is applied as:
 - Diagnostic bronchoscopy - for finding-out of the nature of pathological
changes in a mucous membrane of bronchial tubes (character of an
inflammation of a mucous membrane of bronchial tubes, erosion, ulcers of a
mucous membrane of bronchial tubes, and tissues , suspicious on a bronchial
tube tumour).
 - Medical byopsy ( for treatment)- for evacuation (aspiration) pathologically
their secrets and alien bodies from a gleam of a bronchial tube, introduction
in bronchial tubes of medicinal substances, removal of polyps of bronchial
tubes, treatment of bronchoectasys , also it is central the located abscesses
of a lung, performance of some kinds of operative interventions.
Bronchoscopy at a syndrome of bronchial obstruction - hyperaemia and
moderate puffiness of a mucous membrane, the insignificant deformation of
bronchial tubes moderately expressed bleeding of mucous membrane,
presence of a pathological secret
118

119. Bronchoscopy at a syndrome of consolidation of a lung tissues
characterises changes in the bronchial tubes corresponding to
a site of consolidation of a pulmonary tissues: are sharply
expressed hyperaemia, puffiness and bleeding a mucous
membrane, sputum in a bronchial tube gleam. Are possible
deformation of a corresponding bronchial tube and distal
departing bronchial orifices. Changes in other bronchial tubes
can and not to be (for example, at a primary pneumonia) or
pathological changes in other organs are expressed slightly
(for example, at a acute pneumonia and chronic bronchitis)
Bronchoscopy at a syndrome of presence of a cavity in a lung – its
local process , corresponds to bronchial tubes, by dran an
abscess: hyperaemia of the mucous membrane of bronchial
tubes , the expressed puffiness, sharp deformation draning
bronchial tubes and them orifices (edema), expressed bleeding
of walls draning bronchial tubes, plicatea if the mucous
membrane is absent, vascular drawing of a mucous membrane
is not visible.

119

120. BYOPSY
 - At varies as for finding-out of the nature of pathological
changes in a mucous membrane of bronchial tubes and a
pulmonary tissues - diagnostic bronchoscopy, and for
evacuation (aspiration)of pathological secrets and alien
bodies from a gleam of a bronchial tube, introduction in
bronchial tubes of medicinal substances, performance of
some kinds of operative interventions - medical
bronchoscopy.
 On a way of manufacture byopsy it is divided into 3 groups:
endobronchial (pick out, various types curetage a mucous
membrane of bronchial tubes), transbronchial -
transbronchial punctures, catheterisation bronchial tubes
and aspiration byopsy. The definitive diagnosis and
inspection terms quite often depends on a choice of a way
byopsy.
120