Transcript Document
Chapter 13
Asthma
Figure 13-1. Asthma. DMC, Degranulation of mast cell; SMC, smooth muscle constriction;
MA, mucus accumulation; MP, mucus plug; HALV, hyperinflation of alveoli.
Slide 1
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Anatomic Alterations of the Lungs
Slide 2
Smooth muscle constriction of bronchial
airways (bronchospasm)
Excessive production of thick, whitish,
tenacious bronchial secretions
Hyperinflation of alveoli (air-trapping)
Mucus plugging and, in severe cases,
atelectasis
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Etiology
Extrinsic asthma
Intrinsic asthma
Slide 3
Allergic or atopic asthma
Nonallergic or nonatopic asthma
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Figure 13-2. The immunologic mechanisms in asthma.
Slide 4
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Intrinsic Asthma
(Nonallergic or Nonatopic Asthma)
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Infections
Exercise and cold air
Industrial pollutants or occupational exposure
Drugs, food additives, and food preservatives
Gastroesophageal reflux
Sleep (nocturnal asthma)
Emotional stress
Premenstrual asthma
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Figure 13-3. Factors triggering intrinsic asthma.
Slide 6
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Additional Risk Factors
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Residence in a large urban area, especially
the inner city
Exposure to secondhand smoke
A parent who has asthma
Respiratory infections in childhood
Low birth weight
Obesity
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Overview of the Cardiopulmonary
Clinical Manifestations Associated
with ASTHMA
The following clinical manifestations result from
the pathophysiologic mechanisms caused (or
activated) by Bronchospasm (see Figure 9-10)
and Excessive Bronchial Secretions (see Figure
9-11)—the major anatomic alterations of the lungs
associated with asthma (see Figure 13-1).
Slide 8
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Figure 9-10. Bronchospasm clinical scenario (e.g., asthma).
Slide 9
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Figure 9-11. Excessive bronchial secretions clinical scenario.
Slide 10
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Clinical Data Obtained at the
Patient’s Bedside
Vital signs
Slide 11
Increased respiratory rate
Increased heart rate, cardiac output,
blood pressure
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Clinical Data Obtained at the
Patient’s Bedside
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Use of accessory muscles of inspiration
Use of accessory muscles of expiration
Pursed-lip breathing
Substernal intercostal retractions
Increased anteroposterior chest diameter
(barrel chest)
Cyanosis
Cough and sputum production
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Clinical Data Obtained at the
Patient’s Bedside
Pulsus paradoxus
Slide 13
Decreased blood pressure during inspiration
Increased blood pressure during expiration
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Clinical Data Obtained at the
Patient’s Bedside
Chest assessment findings
Slide 14
Expiratory prolongation
Decreased tactile and vocal fremitus
Hyperresonant percussion
Diminished breath sounds
Diminished heart sounds
Wheezing and rhonchi
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Figure 2-12. Percussion becomes more hyperresonant with alveolar hyperinflation.
Slide 15
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Slide 16
Figure 2-17. As air trapping and alveolar hyperinflation develop in obstructive
lung diseases, breath sounds progressively diminish.
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Clinical Data
Obtained from Laboratory Tests
and Special Procedures
Slide 17
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Pulmonary Function Study:
Expiratory Maneuver Findings
Slide 18
FVC
FEVT
FEF25%-75%
FEF200-1200
PEFR
MVV
FEF50%
FEV1%
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Pulmonary Function Study:
Lung Volume and Capacity Findings
VT
RV
FRC
N or
N or
IC
N or
ERV
N or
RV/TLC ratio
VC
Slide 19
TLC
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Arterial Blood Gases
Mild to Moderate Asthma Episode
pH
Slide 20
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 PaCO2 trends during acute alveolar hyperventilation.
Slide 21
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Arterial Blood Gases
Severe Asthmatic Episode (Status Asthmaticus)
Acute ventilatory failure with hypoxemia
pH
Slide 22
PaCO2
HCO3PaO2
(Significantly)
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Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
Acute 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 ventilatory failure.
Slide 23
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Oxygenation Indices
QS/QT
DO2
VO2
Normal
O2ER
Slide 24
C(a-v)O2
Normal
SvO2
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Abnormal Laboratory Tests and
Procedures
Abnormal laboratory tests and procedures
Sputum examination
• Eosinophils
• Charcot-Leyden crystals (see next slide)
• Casts of mucus from small airways
called Kirschman spirals
• IgE level (elevated in extrinsic asthma)
Slide 25
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Charcot-Leyden Crystals
Needle shaped crystals -
Represents breakdown products of eosinophils
Slide 26
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Radiologic Findings
Chest radiograph
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Increased anteroposterior diameter
Translucent (dark) lung fields
Depressed or flattened diaphragm
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Figure 13-4. Chest X-ray of a 2-year-old patient during an acute asthma attack.
Slide 28
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Table 13-1. Asthma Classification
Based on Severity—Excerpts
Disease
Symptoms
Step 4:
Continual symptoms
Step 3:
Daily symptoms
Step 2:
Symptoms > than twice weekly
Step 1:
Symptoms < than twice weekly
From McCance KL, Huether SE: Pathophysiology: The biologic basis for disease in adults and
children, ed 4, St. Louis, 2002, Mosby.
Slide 29
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Table 13-2. Asthma Zone Management
System—Excerpts
Green zone
Yellow zone
50% to 80% of personal best PEFR
Red zone
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80% to 100% of personal best PEFR
<50% of personal best PEFR
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General Management of Asthma
Environmental control
Respiratory care treatment protocols
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Oxygen therapy protocol
Bronchial hygiene therapy protocol
Aerosolized medication protocol
Mechanical ventilation protocol
Medications commonly prescribed
Xanthines
Corticosteroids
Anti-inflammatory agents
Leukotriene inhibitors
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General Management of Asthma
Slide 32
Monitoring
Arterial blood gas measurements
Pulse oximetry
Serial PFTs
• PEFR
• FEV1
Vital signs
Chest radiographs
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General Management of Asthma
Slide 33
Patient compliance
Asthma-symptom/medication-use diaries
Serum theophylline levels
Carboxyhemoglobin determinations
Total (circulating) eosinophil counts
No-show rates at physician offices
Rate of medication use
Frequency of emergency department visits and
hospitalizations
Number of red zone days per months (see Table 13-2)
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Classroom Discussion
Case Study: Asthma
Slide 34
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