physiology.
Pulmonary Embolism with Infarction
Dyspnea, pleuritic chest pain, hemoptysis, possibly decreased oxygen saturations.
Pulmonary Embolism with Saddle Embolism
Syncope, hypoxemia, jugular venous distention, acute right heart strain on ECG, dilated right ventricle on portable echocardiogram.
The physical exam may be enhanced by point‐of‐care ultrasound of the chest in the patient with acute respiratory distress. Ultrasound can help differentiate many conditions, including acute pulmonary edema, pneumothorax, pleural effusion, pericardial effusion, and pneumonia. (See Chapter 69.) B‐lines, which are vertical lines extending from the pleural line to the bottom of the ultrasound image, are indicative of the interstitial lung fluid that is present in ADHF and SCAPE [9]. An absence of lung sliding on the affected side is highly sensitive and specific for the detection of pneumothorax [10, 11].
Figure 5.1 Normal capnographic waveform
Capnography plots the concentration of exhaled CO2 throughout the respiratory cycle and provides a continuous assessment of metabolism, circulation, and ventilation. A normal capnogram is shown in Figure 5.1. End‐tidal CO2 (EtCO2) refers to the concentration of CO2 at the end of exhalation. The displayed EtCO2 value represents the highest measurement in a ventilation cycle, which, under a normal physiological state, is between 35 and 45 mmHg. Waveform capnography has become the criterion standard for confirming correct endotracheal tube placement and assessing for effective ventilation with advanced airways. It also a valuable noninvasive method for continuously monitoring a spontaneously breathing patient’s ventilatory and circulatory status.
Capnography can be used to monitor the response to treatment in some patients. With asthma and COPD, small airway obstruction leads to prolonged expiration and a “shark fin” appearance of the capnogram [12, 13]. Normalization of the capnograph waveform indicates favorable response to treatment. Alternatively, increasing EtCO2 levels may be indicative of worsening respiratory failure in these patients.
EtCO 2 may help differentiate the causes of respiratory distress. Lower EtCO2 levels may be more likely to be associated with a diagnosis of ADHF rather than COPD [14]. In patients with hyperglycemia, prehospital EtCO2 levels were significantly lower in patients eventually diagnosed with diabetic ketoacidosis [15].
General treatment
Initial therapy should begin with supplemental oxygen, application of monitoring devices, and vascular access. Evidence suggests that oxygen therapy should be carefully titrated to a SpO2 goal of 94%‐98% in patients with general respiratory distress and to a goal of 88%‐92% in patients with known COPD [16].
Inhaled bronchodilators, including short‐acting inhaled β2‐agonists (SABAs) and anticholinergics, are commonly included in protocols for respiratory distress of unclear etiology. Although there is usually little downside to their use, especially if a component of bronchospasm is suspected, SABAs can be potentially harmful in those with ADHF, acute coronary syndrome, and cardiac dysrhythmias, due to their chronotropic, inotropic, and vasoactive effects on the cardiovascular system. A review of the Acute Decompensated Heart Failure National Registry Emergency Module (ADHERE) database revealed that 21% of patients ultimately diagnosed with ADHF exacerbations received SABA treatments by EMS or in the emergency department [17]. There was an association between bronchodilator administration and a subsequent need for IV vasodilators and intubation [17]. Additionally, cases of acute MI precipitated by bronchodilator use have been reported [18]. SABAs are known to decrease serum potassium concentration by approximately 0.5 meq/L, which could precipitate or worsen hypokalemia‐associated dysrhythmias. In addition, SABAs may temporarily worsen hypoxemia by increasing the ventilation/perfusion mismatch. Inhaled anticholinergics, such as ipratropium, are not absorbed systemically and have no cardiovascular toxicity. Prehospital studies supporting their use as bronchodilators are limited [19].
Two forms of NIPPV have become common for treating several respiratory distress etiologies [20]. (See Chapter 6.) A mask is used to deliver ventilation support either at a constant pressure (continuous positive airway pressure) or with a higher pressure during inspiration (bilevel positive airway pressure). Prehospital NIPPV has resulted in decreased mortality, reduced intubation rates, shorter ICU lengths of stay, and improved vital signs [20, 21]. Although NIPPV has been most studied in COPD and ADHF, a systematic review and meta‐analysis supports its use in all forms of undifferentiated acute respiratory failure [22]. NIPPV may also permit administration of a lower concentration of inspired oxygen, thereby decreasing the potentially deleterious effects of hyperoxia [23]. It is essential that EMS clinicians understand the limitations of this intervention, including patient factors that are specific contraindications to its use. NIPPV is inappropriate for patients who require immediate intubation, such as those who cannot protect their airways, are vomiting, have altered mentation, or cannot tolerate the pressure mask. The patient must also have an acceptable respiratory drive prior to the application of NIPPV.
Advanced airway management with supraglottic airways or endotracheal intubation is the final common pathway for most individuals with severe respiratory distress who have failed to respond to the strategies discussed above.
Asthma
Asthma is a chronic inflammatory lung disorder characterized by acute attacks of airway hyper‐responsiveness with reversible obstruction. Precipitating factors include upper respiratory tract infections, exposure to allergens, high pollution indices, and failure to use preventive and maintenance therapies. The disease affects nearly 25 million individuals (and minority communities disproportionally) in the United States [24]. Although there are hallmark features of an acute exacerbation, assessment of asthma exacerbations can be challenging and potentially misleading (Box 5.2). For example, the absence of wheezing may indicate either severely restricted airflow or clinical improvement following appropriate treatment. A multicomponent guide can help assess the severity and monitor the effectiveness of the treatment of asthma (Table 5.1) [25]. Extreme (both low and high) values of initial prehospital EtCO2 were associated with poor outcomes among adult asthma patients in one study [26].
Oxygen should be provided to relieve hypoxemia and titrated to a SpO2 of 94%‐98%. The initial drug of choice for treatment is a SABA, which acts by relaxing bronchial smooth muscle and increasing mucociliary clearance. Nebulization is the preferred route of administration in the acute setting with either intermittent or continuous delivery. SABAs can also be administered through metered dose inhalers and spacer devices. The use of subcutaneous or intramuscular epinephrine (a nonselective beta‐agonist) has declined with the availability of SABAs, but epinephrine remains useful when the patient is critically ill or when the inhaled SABA cannot be delivered effectively. An anticholinergic bronchodilator agent, such as ipratropium, can be added to the SABA for more severe exacerbations. Patients who fail to respond promptly and completely to inhaled bronchodilators benefit from the administration of systemic corticosteroids. The benefits of prehospital corticosteroid administration have not been proven through randomized controlled clinical trials. Nonrandomized observational studies, however, have shown that EMS delivery of corticosteroids is associated with faster resolution