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
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
Smooth muscle constriction of bronchial
airways (bronchospasm)
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Excessive production of thick, whitish,
tenacious bronchial secretions
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Hyperinflation of alveoli (air-trapping)
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Mucus plugging and, in severe cases,
atelectasis
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Etiology

Extrinsic asthma
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
Intrinsic asthma

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Allergic or atopic asthma
Nonallergic or nonatopic asthma
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Figure 13-2. The immunologic mechanisms in asthma.
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Intrinsic Asthma
(Nonallergic or Nonatopic Asthma)
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Infections
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Exercise and cold air
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Industrial pollutants or occupational exposure
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Drugs, food additives, and food preservatives
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Gastroesophageal reflux
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Sleep (nocturnal asthma)
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Emotional stress
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Premenstrual asthma
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Figure 13-3. Factors triggering intrinsic asthma.
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Additional Risk Factors
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Residence in a large urban area, especially
the inner city
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Exposure to secondhand smoke
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A parent who has asthma
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Respiratory infections in childhood
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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
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Increased respiratory rate
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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
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Use of accessory muscles of expiration
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Pursed-lip breathing
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Substernal intercostal retractions
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Increased anteroposterior chest diameter
(barrel chest)
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Cyanosis
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Cough and sputum production
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Clinical Data Obtained at the
Patient’s Bedside
Pulsus paradoxus
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Decreased blood pressure during inspiration
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Increased blood pressure during expiration
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Clinical Data Obtained at the
Patient’s Bedside
Chest assessment findings
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Expiratory prolongation
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Decreased tactile and vocal fremitus
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Hyperresonant percussion
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Diminished breath sounds
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Diminished heart sounds
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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
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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

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TLC
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Arterial Blood Gases
Mild to Moderate Asthma Episode
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pH

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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

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C(a-v)O2
Normal
SvO2

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Abnormal Laboratory Tests and
Procedures
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Abnormal laboratory tests and procedures
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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
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Translucent (dark) lung fields
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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
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Green zone
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Yellow zone
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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
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Environmental control
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Respiratory care treatment protocols
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Oxygen therapy protocol
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Bronchial hygiene therapy protocol
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Aerosolized medication protocol
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Mechanical ventilation protocol
Medications commonly prescribed
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Xanthines
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Corticosteroids
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Anti-inflammatory agents
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Leukotriene inhibitors
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General Management of Asthma
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Slide 32
Monitoring
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Arterial blood gas measurements
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Pulse oximetry
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Serial PFTs
• PEFR
• FEV1
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Vital signs

Chest radiographs
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General Management of Asthma
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Slide 33
Patient compliance
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Asthma-symptom/medication-use diaries
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Serum theophylline levels
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Carboxyhemoglobin determinations
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Total (circulating) eosinophil counts
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No-show rates at physician offices
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Rate of medication use
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Frequency of emergency department visits and
hospitalizations
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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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