Prehospital assessment and diagnosis

The approach to the dyspneic patient must always begin with a focus on immediate threats to survival, such as airway obstruction. Once this has been dealt with, provisional causes can be considered so as to guide specific therapy. Accurate diagnosis of the cause of dyspnea in prehospital settings remains difficult. Studies have shown that paramedics are able to determine the etiology of dyspnea with only moderate accuracy. In one of the more positive retrospective studies, a prehospital diagnosis of cardiac, pulmonary, or other as the cause of “difficulty breathing” agreed with that of the emergency department (ED) diagnosis 81% of the time [3]. However, Jaronik et al. studied 144 patients given furosemide in the field and noted that it was given appropriately only 58% of the time to patients with a subsequent diagnosis of congestive heart failure or an elevated B-type natriuretic peptide (BNP) level. It was given inappropriately 42% of the time, and for diagnoses in which it was potentially harmful 17% of the time [4]. Almost one-quarter of patients who received furosemide from EMS in this study subsequently required IV fluid therapy in the hospital [4]. Therefore, prehospital treatment must carefully find a balance between disease severity, diagnostic certainty, and the likelihood of harm.

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 end-tidal carbon dioxide (EtCO₂) levels. Some of the useful questions that can be asked by a medical oversight physician over the radio or phone include how many words the patient can speak at a time, whether there is associated diaphoresis, and if the patient appears to be fatiguing. If the initial assessment reveals the possibility of impending respiratory failure, appropriate supplemental ventilation should be considered, including the use of non-invasive positive pressure ventilation (NIPPV) or bag-valve-mask (BVM) ventilation in conjunction with oral/nasopharyngeal airways, supraglottic devices, or endotracheal intubation (ETI). An important early task is to question the family/caregivers and gather available paperwork regarding the patient’s wishes for life-sustaining treatment or end-of-life care.

Acute coronary syndrome is an important consideration among these disparate causes of shortness of breath. It can present as cardiogenic shock with ACPE but can also cause subjective dyspnea without severe impairment of cardiac function. Dyspnea associated with acute coronary syndrome may not be accompanied by chest discomfort and is more common in women, older individuals, and those with diabetes [5,6]. Dysrhythmias can also cause dyspnea and are readily diagnosed by cardiac monitoring. If time and the patient’s condition allow, a 12-lead electrocardiogram (ECG) may be useful in guiding treatment and destination decisions for the dyspneic patient. Severe sepsis can also present with respiratory distress due to increased oxygen consumption. Toxic exposures can cause respiratory distress either through direct irritation of the respiratory tract or secondarily by central 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 ETI and mechanical ventilation, it is important to continue to hyperventilate them to maintain their preexisting respiratory compensation for the underlying metabolic acidosis. This can be facilitated through the use of continuous EtCO₂ monitoring. Neuromuscular diseases such as myasthenia gravis and Guillain–Barré syndrome are rare causes of inadequate ventilation and respiratory failure. Although a diagnosis of exclusion, shortness of breath is also a common manifestation of anxiety disorders, panic attacks, and psychogenic hyperventilation. Having a patient breathe into and out of a paper bag, which is sometimes done by the uninformed for hyperventilation, actually decreases inspired oxygen and has no place in EMS.

The physical exam may be enhanced through the use of ultrasound of the chest in the patient with acute respiratory distress. Ultrasound is now commonly used in the ED for evaluation of pneumothorax, pleural effusion, pericardial effusion, large pulmonary embolism, cardiac function and volume status.

General treatment

As with most potential threats to life, initial therapy should begin with supplemental oxygen, application of monitoring devices, and often IV access. With standard use of SpO₂ monitoring, growing information suggests that oxygen therapy should be carefully titrated to a goal between 93% and 96% in patients with general respiratory distress, and to a goal of 88–92% in patients with known COPD [7,8]. A recent randomized controlled prehospital trial by Austin et al. showed decreased mortality among patients who were treated with a titrated oxygen regimen versus those treated with uncontrolled high flow oxygen. Mortality was reduced 58% in patients with any respiratory distress and 78% in patients with known COPD with the titration strategy [7].

Inhaled bronchodilators, including short-acting inhaled beta₂-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 ACPE, acute coronary syndrome, and cardiac arrhythmias 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 by Singer et al. revealed that 21% of patients ultimately diagnosed with acute decompensated heart failure (ADHF) exacerbation received SABA treatments by EMS or in the ED [9]. The authors also reported an association between bronchodilator use and a subsequent need for IV vasodilators and ETI. It is important to note, however, that no mortality difference was found between patients who did or did not receive SABAs. In addition, patients with combined ADHF and COPD were not studied separately. Fisher et al. reported six cases of acute myocardial infarction precipitated by bronchodilators [10].

Unfortunately, the relationship between cardiac manifestations and bronchodilator use is poorly understood and these cases likely reflect publication bias. SABAs are known to decrease serum potassium concentration by approximately 0.5 meq/L, which could precipitate 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. But in the final analysis and in the absence of well-designed trials to better guide the empirical use of bronchodilators in undifferentiated respiratory distress, it seems to make physiological sense to continue to include them in EMS protocols or at the discretion of a medical oversight physician.

Two forms of NIPPV have become standard for treatment of several forms of respiratory distress [11]. A mask is used to deliver ventilation support either at a constant pressure (CPAP) or with a higher pressure during inspiration (BiPAP). The use of NIPPV in the prehospital setting has become accepted as an early intervention, and studies of its use in this setting have demonstrated decreased mortality, reduced intubation rates, shorter intensive care unit (ICU) lengths of stay, and improved vital signs [11,12]. Although NIPPV has been most studied in COPD and ACPE, a recent systematic review and metaanalysis supports its use in all forms of undifferentiated acute respiratory failure [11]. NIPPV may also permit administration of a lower concentration of inspired oxygen, thereby decreasing the potential deleterious effects of hyperoxia [13]. It is important that prehospital providers understand the limitations of this intervention, including patient factors that are specific contraindications to its use. NIPPV is inappropriate for patients who require immediate ETI such as those who are unable to protect their airways, have altered mentation, or cannot tolerate the pressure mask. The patient must have an acceptable respiratory drive prior to application of NIPPV.