in prehospital settings remains difficult. Studies have shown that EMS professionals often struggle with determining the etiology of dyspnea [4, 5]. Prehospital treatment must find a balance between disease severity, diagnostic certainty, and the likelihood of benefit versus harm. Among 144 patients given furosemide in the field, it had been given appropriately only 58% of the time to patients with a subsequent diagnosis of congestive heart failure [6]. Inappropriate administration occurred 42% of the time and was potentially harmful 17% of the time [6].
Much of the assessment of disease severity comes from general observation of the patient, supplemented by physical examination and close monitoring of vital signs, cardiac rhythm, pulse oximetry (SpO2), and waveform capnography. Talking to a patient to assess how many words the patient can speak at a time, whether there is associated diaphoresis, and if the patient appears to be fatiguing can be helpful clues for potential deterioration. If the initial assessment reveals the possibility of impending respiratory failure, appropriate supplemental ventilation should be considered, including the use of noninvasive positive‐pressure ventilation (NIPPV) or bag‐valve‐mask ventilation in conjunction with oral/nasopharyngeal airways, supraglottic devices, or endotracheal intubation.
Once disease severity and the immediate needs have been addressed, the next step is to categorize the underlying cause. The four most common categories for respiratory distress are upper airway obstruction, small airway obstruction (e.g., chronic obstructive pulmonary disease [COPD] and asthma), cardiovascular etiologies (e.g., acute decompensated heart failure [ADHF], sympathetic crashing acute pulmonary edema [SCAPE], acute coronary syndrome, pulmonary embolism), and pneumonia. Additional medical conditions that can lead to acute respiratory distress are listed in Box 5.1.
Acute coronary syndrome is an important consideration among these disparate causes of shortness of breath. It can present as cardiogenic shock with acute pulmonary edema and cause subjective dyspnea without severe cardiac function impairment. Dyspnea associated with acute coronary syndrome may not be accompanied by chest discomfort and is more common in women, older individuals, and diabetics [7, 8]. Dysrhythmias can also cause dyspnea. They are readily diagnosed by cardiac monitoring. If time and the patient's condition allow, a 12‐lead ECG may guide treatment and destination decisions for the dyspneic patient. Sepsis can also present with respiratory distress due to fever, increased oxygen consumption, and compensation of underlying lactic acidosis. Toxic exposures can cause respiratory distress, either through direct irritation of the respiratory tract or secondarily by central or autonomic nervous system impairment of respiratory function. Tachypnea and subjective dyspnea may also be compensatory for an underlying metabolic acidosis, as with diabetic ketoacidosis or salicylate toxicity. If these acidotic patients require intubation and mechanical ventilation, it is important to continue to hyperventilate them after securing the airway to maintain their preexisting respiratory compensation. This can be facilitated through the early and continued use of continuous waveform capnography monitoring. Neuromuscular diseases such as myasthenia gravis and Guillain Barré syndrome are rare causes of inadequate ventilation and respiratory failure. Although diagnoses of exclusion, shortness of breath is also a common manifestation of anxiety disorders, panic attacks, and psychogenic hyperventilation.
Box 5.1 Common causes of respiratory distress in the EMS setting
Pulmonary
Asthma
COPD
Pneumothorax
Pleural effusion
Interstitial pulmonary fibrosis
Respiratory tract infections (e.g., pneumonia)
Cardiovascular
ADHF
Sympathetic crashing acute pulmonary edema
Acute coronary syndrome (STEMI, NSTEMI, unstable angina)
Pulmonary embolus
Pulmonary hypertension
Arrhythmias (e.g., atrial fibrillation)
Upper Airway
Foreign body obstruction
Infectious/inflammatory (e.g., epiglottitis, bacterial tracheitis, diphtheria, retropharyngeal abscess, peritonsillar abscess)
Allergic (e.g., angioedema)
Metabolic
Sepsis
Diabetic ketoacidosis
Toxic Ingestions
Salicylates
Ethylene glycol/methanol
Other
Anemia
Fever
Physiologic dyspnea of pregnancy
Psychiatric, hyperventilation, panic attack
Abdominal distension, obesity
Although auscultation of breath sounds is an integral part of the physical examination for respiratory distress, there can be much overlap in the cause of any one particular exam finding. Breath sounds must be interpreted in the context of the rest of the focused exam. For example, a common mistake is to equate “crackles” with an ADHF exacerbation and “wheezing” with asthma/COPD, although both findings can be found in either disease process. The examination should also include careful auscultation of heart sounds as well as palpation and inspection of the neck for jugular venous distension, chest for retractions and external injury, lower back for sacral edema, and extremities for edema or evidence of deep vein thrombosis (DVT) (Box 5.2).
Box 5.2 History and exam findings by disease state.
Asthma
Dyspnea with prolonged expiratory phase, tripoding position when severe, decreased breath sounds when very severe to diffuse wheezing, chest tightness.
Chronic Obstructive Pulmonary Disease
Cough increased or change in sputum production, dyspnea with prolonged expiratory phase, tripoding position when severe, decreased breath sounds when very severe to diffuse wheezing, barrel chest appearance.
ADHF with Volume Overload
Jugular venous distention, S3 or S4 heart sounds, pulmonary wheezing, pulmonary crackles (rales), lower extremity edema, sacral edema, weight gain.
ADHF with Low Cardiac Output State
Cool skin from peripheral vasoconstriction and low blood pressure.
Sympathetic Crashing Acute Pulmonary Edema
Severe respiratory distress developing rapidly over minutes to hours, pulmonary wheezing, pulmonary crackles (rales), significantly elevated blood pressure, may not present with volume overload.
Pneumonia
Unilateral decreased breath sounds, focal wheezing, unilateral or bilateral crackles (rales), fever, normotensive to hypotensive.
Pneumothorax
Pleuritic chest pain, unilateral decreased breath sounds, jugular venous distention, hypotension