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INTRODUCTION

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Asthma is a heterogeneous disease of bronchial inflammation and bronchospasm. Status asthmaticus is a state of respiratory compromise characterized by bronchial inflammation and bronchospasm secondary to asthma with resultant prolonged expiratory phase, tachypnea, dyspnea, and work of breathing; it does not respond to conventional therapy and may lead to respiratory failure.1,2

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EPIDEMIOLOGY

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Asthma affects 8.7 million children in the United States with the highest prevalence in children 5 to 17 years of age.3

  • Blacks are disproportionately affected, and there is no gender predilection.

  • Seventy to eighty percent of children have allergic symptoms.

  • There are familial links, but asthma is more likely to develop if the mother has allergies or asthma rather than the father.3

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PATHOPHYSIOLOGY

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Asthma and status asthmaticus are due to increased inflammation of the lower airway leading to:

  • Airway irritability and bronchospasm

  • Overproduction of mucus

  • Mucosal edema

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Combined, these lead to airway obstruction via bronchoconstriction and mechanical obstruction.1

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RESPIRATORY MECHANICS IN ASTHMA

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PULMONARY CHARACTERISTICS OF ASTHMA

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  • Hyperinflation and increased functional residual capacity

  • Heterogeneous lung parenchyma

  • Airways can be affected in multiple ways2:

    • Complete obstruction of the airway (i.e., mucus plugging)

    • Partial obstruction present throughout the respiratory cycle

    • Partial obstruction present throughout expiration → prone to air trapping

    • No bronchial obstruction → prone to overdistention during an asthma exacerbation

    • V/Q mismatch occurs due to shunt physiology and increased dead space ventilation1

    • Areas of atelectasis secondary to mucus plugging lead to intrapulmonary shunt physiology

    • Areas of hyperinflation can lead to pulmonary blood flow obstruction and increased dead space ventilation

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CARDIOPULMONARY INTERACTIONS

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  • Extreme fluctuations in intrathoracic pressures during an acute asthma exacerbation can affect both the preload and the afterload on the heart.

  • High lung volumes and intrathoracic pressures increase the pulmonary vascular resistance.

  • High intrathoracic pressures decrease blood return to the right atrium (i.e., preload).

  • Negative inspiratory pressures increase afterload on the left ventricle.

  • These changes lead to pulsus paradoxus.

  • Changes in systolic blood pressure of more than 10 to 15 mmHg between inhalation and exhalation may be an indicator of impending respiratory failure.1

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DIAGNOSTIC CONSIDERATIONS

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DIFFERENTIAL DIAGNOSIS1,3

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Pneumonia – viral or bacterial, allergic bronchopulmonary aspergillosis, foreign body aspiration, cardiogenic pulmonary edema, anatomic lesions that may be fixed (e.g., airway web or hemangioma) or dynamic (tracheomalacia), immunodeficiency, bronchopulmonary dysplasia, vocal cord paralysis

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HISTORY AND PHYSICAL

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  • History

    • Acuity of symptoms, presence of fever, upper respiratory symptoms, exposures to allergens, personal or family history of asthma, allergies, eczema

    • Red flags: intensive care unit (ICU) admissions for asthma, history of mechanical ventilation, frequent emergency room visits1

  • Physical exam

    • Respiratory effort (i.e., accessory muscle use), dyspnea, breath sounds

    • Mental ...

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