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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.
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Anatomic Alterations of the Lungs

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

Allergic or atopic asthma

Intrinsic 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 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.


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Additional Risk Factors

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).

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Figure 9-10. Bronchospasm clinical scenario (e.g., asthma).


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Figure 9-11. Excessive bronchial secretions clinical scenario.


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Clinical Data Obtained at the Patients Bedside


Vital signs

Increased respiratory rate Increased heart rate, cardiac output, blood pressure

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Clinical Data Obtained at the Patients Bedside


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 Patients Bedside


Pulsus paradoxus

Decreased blood pressure during inspiration Increased blood pressure during expiration

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Clinical Data Obtained at the Patients Bedside


Chest assessment findings

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.


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Figure 2-17. As air trapping and alveolar hyperinflation develop in obstructive lung diseases, breath sounds progressively diminish. Copyright 2006 by Mosby, Inc.

Clinical Data Obtained from Laboratory Tests and Special Procedures

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Pulmonary Function Study: Expiratory Maneuver Findings


FVC PEFR FEVT MVV FEF25%-75% FEF50% FEF200-1200 FEV1%

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Pulmonary Function Study: Lung Volume and Capacity Findings


VT N or RV FRC TLC N or

VC

IC

ERV

RV/TLC ratio

N or

N or

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Arterial Blood Gases


Mild to Moderate Asthma Episode

Acute alveolar hyperventilation with hypoxemia


PaCO2 HCO3 (Slightly) PaO2

pH

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Time and Progression of Disease Disease Onset


100 90 80 Point at which PaO2 declines enough to stimulate peripheral oxygen receptors

Alveolar Hyperventilation

PaO2 or PaCO2

70 60 50 40 30 20 10 0

PaO2

Figure 4-2. PaO2 and PaCO2 trends during acute alveolar hyperventilation.
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Arterial Blood Gases


Severe Asthmatic Episode (Status Asthmaticus)

Acute ventilatory failure with hypoxemia

pH

PaCO2

HCO3PaO2 (Significantly)

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Time and Progression of Disease


Disease Onset
100 90 80 Pa02 or PaC02 70 60 50 40 30 20 10 0 Figure 4-7. PaO2 and PaCO2 trends during acute ventilatory failure.
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Alveolar Hyperventilation

Acute Ventilatory Failure

Point at which PaO2 declines enough to stimulate peripheral oxygen receptors

Point at which disease becomes severe and patient begins to become fatigued

Oxygenation Indices
QS/QT DO2 VO2 Normal C(a-v)O2 Normal

O2ER

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)

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Charcot-Leyden Crystals

Needle shaped crystals Represents breakdown products of eosinophils

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Radiologic Findings
Chest radiograph

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.
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Table 13-1. Asthma Classification Based on SeverityExcerpts


Disease Symptoms

Step 4:
Step 3: Step 2:

Continual symptoms
Daily symptoms 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.
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Table 13-2. Asthma Zone Management SystemExcerpts

Green zone

80% to 100% of personal best PEFR

Yellow zone

50% to 80% of personal best PEFR

Red zone

<50% of personal best PEFR

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General Management of Asthma


Environmental control Respiratory care treatment protocols


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

Monitoring

Arterial blood gas measurements Pulse oximetry Serial PFTs PEFR FEV1 Vital signs Chest radiographs

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General Management of Asthma

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

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Number of red zone days per months (see Table 13-2)


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Classroom Discussion
Case Study: Asthma

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