admission rates [27]. It has also been suggested that early use of corticosteroids may enhance the effectiveness of SABAs [28]. Corticosteroid options include prednisone (oral), dexamethasone (oral, IM, IV), and methylprednisolone (IV). Oral steroids as part of an evidence‐based protocol for pediatric asthma were associated with shorter hospital care times, lower hospitalization rates, and less need for critical care in admitted patients [29]. For severe exacerbations that fail to respond to inhaled bronchodilators and systemic corticosteroids, adjunctive therapies, such as IV magnesium sulfate or heliox, if available, should be considered. The beneficial actions of magnesium include smooth muscle relaxation and an anti‐inflammatory effect [30]. A 2014 Cochrane review concluded that a single infusion of 1 or 2 g IV MgSO4 over 15 to 30 minutes reduced hospital admission and improved lung function in adults with acute asthma who had not responded sufficiently to oxygen, nebulized SABAs, and IV corticosteroids in the emergency department [31]. Capnography waveforms in asthma may have a shark fin (Figure 5.2), which can facilitate diagnosis and assessment of response to treatment.
Although NIPPV for acute exacerbations of asthma is traditionally viewed as a last resort due to the fear of worsening air trapping and secondary barotrauma, studies of its use in the emergency department and ICU settings in children and adults have shown benefit [32, 33]. A retrospective study of pediatric patients who were placed on bilevel PAP and given SABAs in the emergency department, with initial disposition plans for ICU admission, found that 22% of the patients tolerated bilevel PAP and were able to be downgraded to ward admission [34]. None required subsequent ICU admission. All of these patients had improved SpO2 levels as well as respiratory rates, and there were no bilevel PAP–related adverse events [33].
Table 5.1 Asthma severity guide
Source: Based on National Heart, Lung and Blood Institute, National Institutes of Health. Guidelines for the diagnosis and management of asthma (EPR‐3). 2007. National Heart, Lung, and Blood Institute; National Institutes of Health; US Department of Health and Human Services.
| Parameter | Mild | Moderate | Severe |
|---|---|---|---|
| Shortness of breath | Walking | Talking | At rest |
| Ability to speak | Full sentences | Phrases | Words |
| Accessory muscle use | Rare | Common | Always |
| Mental status | Agitation (variable) | Agitated (usually) | Agitated to somnolent |
| Heart rate (bpm) | 100 | 100‐120 | >120 |
| Respiratory rate | Increased | Increased | >30 |
| EtCO2 (mmHg) | 20‐30 | 30‐40 | >40 |
| Lung sounds | End expiratory wheezing | Full expiratory wheezing | Absent or biphasic wheezing |
bpm, beats per minute; EtCO2, end‐tidal CO2
Figure 5.2 A capnogram depicting bronchospasm with a characteristic “shark fin” appearance.
Source: Based on Egleston CV, Ben Aslam H, Lambert MA. Capnography for monitoring non‐intubated spontaneously breathing patients in an emergency room setting. J Accid Emerg Med. 1997; 14:222–4.
If rapid sequence intubation is necessary for an asthma patient, the preferred induction agent is ketamine due to its inherent bronchodilator properties. Once intubated, ventilation should be provided at reduced volumes and rates to prevent air trapping and secondary barotrauma. The inspiratory‐to‐expiratory ratios should be adjusted to provide a prolonged expiratory phase. Permissive hypercarbia is generally well‐tolerated in these individuals. All NIPPV and intubated asthma patients should be monitored closely for signs of secondary barotrauma, such as tension pneumothorax and pneumomediastinum.
Chronic obstructive pulmonary disease
COPD is characterized by persistent expiratory airflow limitation. The underlying pathophysiology involves a complex process of chronic inflammation, remodeling of the small airways with the destruction of alveoli, and an increase in extracellular matrix production. The disease is manifested through a response to noxious particles and gases, including cigarette smoke and environmental pollutants, though genetic factors may also play a role [20, 35, 36]. It has significant social and economic effects and is the fourth leading cause of death in the United States [37–39].
Acute exacerbations are often precipitated by bacterial or viral respiratory tract infections, exposure to pollutants or allergens, or medication noncompliance. The clinical presentation is similar to that of asthma (Box 5.2). Patients typically develop worsening shortness of breath, more frequent and severe cough, and possibly increased sputum production [40]. Clinical examination often reveals wheezing.
Patients with COPD should receive titrated oxygen with a goal to maintain SpO2 between 88% and 92%, which is associated with reduced mortality [16]. Continuous capnography can aid in the detection of impending respiratory failure. Increasing EtCO2 levels indicate a deteriorating condition. As with asthma, capnographic waveforms may take the form of a shark fin appearance (Figure 5.2) and can assist with the prehospital diagnosis and assessment of response to treatment [12].
As with asthma, the primary treatments during acute exacerbations are directed toward reversing airway obstruction with SABAs and anticholinergic agents [41]. Corticosteroids are associated with decreased rates of treatment failure and relapse [42]. Antibiotics are also important adjuvant therapy for COPD exacerbations and are associated with a reduction in treatment failure and mortality in selected patients [43]. NIPPV has become established as a lifesaving therapy in the treatment of COPD exacerbations [20, 21, 44]. If it is necessary to intubate a COPD patient, appropriate settings for mechanical ventilation include decreased respiratory rates, lower tidal volumes, and an increased expiratory phase. As with asthma, these patients must be monitored closely for evidence of secondary barotrauma [21, 45].
Acute decompensated heart failure and SCAPE
Heart failure results from a structural or functional cardiac abnormality that leads to impaired ventricular filling or cardiac output. Chronic heart failure is typically caused by myocardial ischemia, cardiomyopathy, longstanding uncontrolled hypertension, or underlying valvular heart disease. A common way to classify heart failure is based on systolic function. Patients with impaired cardiac filling are classified as having heart failure with preserved ejection fraction, whereas those