• The onset of an asthma attack may be progressive over days or very sudden and unexpected, leading to respiratory arrest within minutes or a few hours (sudden asphyxic asthma). Bronchial obstruction results from mucosal inflammation, muscle spasm, and lumen occlusion by thick mucus.
• Sudden asphyxic asthma may have a distinct pathogenic mechanism and be attributable essentially to a bronchospasm.
• Expiratory air flow rate is reduced due to a decreased lung elastic recoil force, persistent contraction of inspiratory muscles, airways obstruction, and possible glottic aperture.
• Expiration time is so prolonged that inspiration begins before complete air exhalation, leading to progressive hyperinflation and positive end-expiratory pressure (auto-PEEP).
• Bronchial obstruction is associated with increased total lung capacity, functional residual capacity, and residual volume, and with decreased tidal volume and vital capacity.
• Deep negative intrapleural pressures developed during inspiration interfere with cardiovascular function; right ventricle preload and afterload are increased, left ventricle preload is depressed, and afterload is augmented. These alterations account for the development of pulsus paradoxus.
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