© Springer International Publishing Switzerland 2016
Antonio M. Esquinas (ed.)Noninvasive Mechanical Ventilation10.1007/978-3-319-21653-9_3636. Noninvasive Mechanical Ventilation in Asthma Exacerbation: Key Practical Aspects and Clinical Evidence
(1)
Department of Anesthesiology and Reanimation, Cerrahpasa Medical School, Istanbul University, Istanbul, Turkey
Keywords
Noninvasive ventilationAcute asthma attackCOPDRespiratory failureAbbreviations
BiPAP
Bi-level positive airway pressure
COPD
Chronic obstructive pulmonary disease
CPAP
Continuous Positive Airway Pressure
FEV1
Forced expiratory volume in 1 s
GINA
Global initiative for asthma
NIV
Noninvasive mechanical ventilation
PEEP
Positive end-expiratory pressure
36.1 Introduction
Asthma is highly prevalent worldwide (estimated to account for 1 in every 250 deaths) and its exacerbations can lead to acute respiratory failure. A mortality rate of 27 % has been reported in invasively ventilated patients. Approximately 5–10 % of asthmatic patients experience at least one severe acute asthma episode in a given year, and there are approximately 2 million emergency department visits and 500,000 hospital admissions annually worldwide [1].
The major physiological changes in severe acute asthma are associated with the onset or worsening of limitation of the air flow as a result of bronchospasm, mucosal edema, and mucus hyperproduction, which are triggered by bronchial flogosis and hyperresponsiveness. Like in COPD exacerbations, the increase in airway resistance prolongs the exhalation time required to empty the lung, producing air trapping (dynamic hyperinflation with increased auto-positive end-expiratory pressure (PEEP)), reduced FEV1 (<60 %), and reduced lung elastic recoil [2].
The severity assessment of an asthma attack has been suggested by the Global Initiative for Asthma (GINA) [3]
36.2 Criteria for Defining Severe Acute Asthma
36.2.1 Clinical Signs
Clinical signs include the following: breathlessness at rest; wheezing (life-threatening respiratory arrest is imminent if the chest is silent); use of accessory respiratory muscles (life-threatening respiratory arrest is imminent if paradoxical thoracoabdominal movement is present); limited ability to talk; and agitation (life-threatening respiratory arrest is imminent if confusion or coma are present).
36.2.2 Physiologic Signs
Physiologic signs include the following: respiratory rate > 30 breaths/min; heart rate > 120 beats/min (life-threatening respiratory arrest is imminent if bradycardia is present); pulsus paradoxus >25 mmHg (life-threatening respiratory arrest is imminent if pulsus paradoxus is present); post-bronchodilator peak expiratory flow <60 % of patient’s best or predicted, or <100 l/m; FEV1 < 30 % of patient’s best or predicted Level; and SpO2 < 90 %, PaO2 < 60 mmHg, and PaCO2 > 45 mmHg on room air.
The NIV therapy is used routinely in the acute exacerbations of COPD, and its efficiency has been proved. It is known that the efficacy of bronchodilator therapy also increases as the airways and alveoli open during NIV application [4]. It is curious that even the physiopathologies of COPD and asthma exacerbations are so alike; NIV therapy is not used routinely during the asthma attacks. A reason for this is the lack of strong prospective, randomized clinical studies with large number of patients that suggest the use of NIV in asthma exacerbations. Although all clinical studies show that administration of NIV during asthma exacerbations increases FEV1, PaO2, and peripheral oxygen saturation values and decreases the work of breathing, none of those studies recommend use of NIV during exacerbations strictly [5–9].
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