Chapter 17
Tuberculosis
A
B
C
D
Figure 17-1. Tuberculosis. A, Early primary infection. B, Cavitation of a caseous tubercle and new primary
lesions developing. C, Further progression and development of cavitations and new primary infections.
Note the subpleural location of some of these lesions. D, Severe lung destruction caused by tuberculosis.
Slide 1
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Anatomic Alterations of the Lungs
(Three categories)

Primary tuberculosis


Postprimary tuberculosis


Secondary or reinfection TB
Disseminated tuberculosis

Slide 2
Primary infection stage
Extrapulmonary TB
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Anatomic Alterations of the Lungs
(Mainly Postprimary TB)
Slide 3

Alveolar consolidation

Alveolar-capillary destruction

Caseous tubercles or granulomas

Fibrosis and secondary calcification of the
lung parenchyma

Distortion and dilation of the bronchi

Increased bronchial airway secretions
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Etiology

In human, TB primarily caused by
Mycobacterium tuberculosis

Others

Slide 4

Mycobacterium bovis

Mycobacterium ulcerans

Mycobacterium kansasii

Mycobacterium avium-intracellulare
Highly aerobic organisms
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Diagnosis

Slide 5
Intradermal tuberculin skin testing

Mantoux test

Injection of purified protein derivative (PPD)
• Wheal <5 mm: negative
• Wheal 5 mm to 9 mm: considered suspicious
• Wheal 10 mm or greater: positive
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Diagnosis

Acid-fast stain and sputum culture

Ziehl-Neelsen stain
• Reveals bright red acid-fast bacilli against a blue background

Fluorescent acid-fast stain
• Reveals luminescent yellow-green bacilli against a dark brown
background

Slide 6
A culture is necessary to differentiate M. tuberculosis
form other acid-fast organisms
• Results take as long as 6 to 8 weeks
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Diagnosis

Identification of Mycobacterium species

Polymerase chain reaction (PCR)
• Quick identification of organisms in expectorated or
bronchoscopically obtained sputum

Slide 7
Deoxyribonucleic acid (DNA) probe
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Nontuberculosis Mycobacteria


Slide 8
Mycobacterial infection caused by species
other than M. tuberculosis are called
nontuberculosis mycobacteria (NTM)—also
called:

Mycobacteria other than tuberculosis (MOTT)

Atypical mycobacterial infection
Found in soil and water
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Overview of the Cardiopulmonary
Clinical Manifestations Associated
with TUBERCULOSIS
The following clinical manifestations result from
the pathophysiologic mechanisms caused (or
activated) by Alveolar Consolidation (see
Figure 9-8), and Increased Alveolar-Capillary
Membrane Thickness (see Figure 9-9)—the
major anatomic alterations of the lungs
associated with tuberculosis (see Figure 17-1).
Slide 9
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Figure 9-8. Alveolar consolidation clinical scenario.
Slide 10
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Figure 9-9. Increased alveolar-capillary membrane thickness clinical scenario.
Slide 11
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Clinical Data Obtained at the
Patient’s Bedside
Vital signs
Slide 12

Increased respiratory rate

Increased heart rate, cardiac output,
blood pressure
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Clinical Data Obtained at the
Patient’s Bedside
Slide 13

Chest pain/decreased chest expansion
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Cyanosis
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Digital clubbing

Peripheral edema and distention

Distended neck veins

Pitting edema

Enlarged and tender liver
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Digital
Clubbing
Figure 2-46. Digital clubbing.
Slide 14
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Distended
Neck Veins
Figure 2-48. Distended neck veins (arrows).
Slide 15
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Figure 2-47. Pitting edema. From Bloom A, Ireland J: Color atlas of diabetes, ed 2,
London, 1992, Mosby-Wolfe.
Slide 16
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Clinical Data Obtained at the
Patient’s Bedside
Slide 17

Cough, sputum production, and hemoptysis
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Chest assessment findings
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Increased tactile and vocal fremitus
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Dull percussion note
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Bronchial breath sounds

Crackles, rhonchi, and wheezing

Pleural friction rub

Whispered pectoriloquy
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Figure 2-11. A short, dull, or flat percussion note is typically produced over areas of
alveolar consolidation.
Slide 18
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Figure 2-16. Auscultation of bronchial breath sounds over a consolidated lung unit.
Slide 19
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Figure 2-19. Whispered voice sounds auscultated over a normal lung
are usually faint and unintelligible.
Slide 20
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Clinical Data Obtained from
Laboratory Tests and Special
Procedures
Slide 21
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Pulmonary Function Study:
Expiratory Maneuver Findings
FVC

FEVT
N or 
FEF25%-75%
N or 
FEF200-1200
N
PEFR
MVV
FEF50%
FEV1%
N
Slide 22
N or 
N
N or 
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Pulmonary Function Study:
Lung Volume and Capacity Findings
VT
Slide 23
RV
FRC
TLC
N or 



VC

IC

ERV

RV/TLC%
N
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Arterial Blood Gases
Mild to Moderate Tuberculosis

pH

Slide 24
Acute alveolar hyperventilation with
hypoxemia
PaCO2

HCO3 (Slightly)
PaO2

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Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
100
90
PaO2 or PaCO2
80
Point at which PaO2
declines enough to
stimulate peripheral
oxygen receptors
70
60
PaO2
50
40
30
20
10
0
Figure 4-2. PaO2 and PaC02 trends during acute alveolar hyperventilation.
Slide 25
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Arterial Blood Gases
Extensive Tuberculosis with Pulmonary
Fibrosis

Chronic ventilatory failure with hypoxemia
pH
Normal
Slide 26
PaCO2

HCO3PaO2
 (Significantly) 
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Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
Chronic Ventilatory Failure
100
90
Pa02 or PaC02
80
70
Point at which PaO2
declines enough to
stimulate peripheral
oxygen receptors
Point at which disease
becomes severe and patient
begins to become fatigued
60
50
40
30
20
10
0
Figure 4-7. PaO2 and PaCO2 trends during acute or chronic ventilatory failure.
Slide 27
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Acute Ventilatory Changes on
Chronic Ventilatory Failure
Slide 28

Acute alveolar hyperventilation on chronic
ventilatory failure

Acute ventilatory failure on chronic ventilatory
failure
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Oxygenation Indices
QS/QT
DO2
VO2


Normal
O2ER

Slide 29
C(a-v)O2
Normal
SvO2

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Hemodynamic Indices
(Severe Tuberculosis)
Slide 30
CVP
RAP
PA
PCWP



Normal
CO
SV
SVI
CI
Normal
Normal
Normal
Normal
RVSWI
LVSWI
PVR
SVR

Normal

Normal
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Abnormal Laboratory Tests
and Procedures
Slide 31

Positive tuberculosis skin test (PPD)

Positive acid-fast bacillus stain of sputum
and sputum culture
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Radiologic Findings
Chest radiograph
Slide 32

Increased opacity

Ghon’s complex
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Cavity formation
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Pleural effusion

Calcification and fibrosis

Retraction of lung segments or lobe

Right ventricular enlargement
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Figure 17-2. Cavitary reactivation TB showing a left upper lobe cavity and localized pleural thickening
(arrows). (From Armstrong P et al: Imaging of diseases of the chest, ed 2, St. Louis, 1995, Mosby.)
Slide 33
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General Management of
Tuberculosis
Pharmacologic agents

Slide 34
Consists of 2 to 4 drugs for 6 to 12 months

First-line agents (first 9 months)
• Isoniazid (INH) and rifampin (Rifadin)
• INH most effective

Often supplemented with:
• Ethambutol
• Streptomycin
• Pyrazinamide
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General Management of
Tuberculosis

Slide 35
Respiratory care treatment protocols

Oxygen therapy protocol

Bronchopulmonary hygiene therapy protocol

Hyperinflation therapy protocol

Mechanical ventilation protocol
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Classroom Discussion
Case Study: Tuberculosis
Slide 36
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