Prehospital Care for Dyspnea
Prehospital dyspnea has a large differential diagnosis, including many potential causes that overlap, and the wrong treatment may have unwanted consequences and complications. Narrowing the differential diagnosis in the prehospital setting is important.
Dyspnea, the sensation of breathlessness and the patient’s reaction to it, is often described by patients as difficulty breathing or chest tightness. It accounts for a large portion of chief complaints reported by patients who call 9-1-1 for ambulance services.1 In a University of Washington study of adults transported to any of 16 area hospitals from 2002–2006, the most common primary discharge diagnoses among respiratory distress patients were congestive heart failure (16%), pneumonia (15%), and COPD (13%).2
Dyspnea is a nonspecific symptom with many possible causes and degrees of severity, making the evaluation of these patients challenging. Accurate diagnosis differentiation and early appropriate treatment is needed for improved outcomes, as studies have shown early and late mortality with prehospital dyspnea patients that was possibly related to lack of intervention.3
Patients with shortness of breath are a complex and seriously ill group with a broad range of possible causes; most studies show the highest mortality associated with circulatory diseases, followed by respiratory diseases and then other factors.4
The differential diagnosis for causes of dyspnea can involve a variety of systems, including the respiratory, cardiovascular, and endocrine. Anything that can increase a derangement in oxygenation and/or ventilation can cause dyspnea. Origins can involve many body systems, such as pathology affecting the head and neck region; pulmonary/thoracic, cardiovascular/hematologic, and neuromuscular/CNS causes; and metabolic/toxic and infectious causes.
The four most common factors that contribute to increased work of breathing include a need for increased ventilation, increased airway resistance, decreased pulmonary compliance, and decreased elastic recoil of the lungs. Increased respiratory drive can occur during severe hypoxia and acidosis when the CNS is acted upon by centrally acting stimuli such as toxins or central CNS events. An increase in lung resistance or decreased compliance commonly occurs as the result of diseases such as asthma and/or COPD.1
Two of the most common causes of dyspnea are cardiac and respiratory. These can be difficult to distinguish and will be the focus of the remainder of this article.
Barring complete respiratory failure, misdiagnosis and treatment of cardiac causes of dyspnea have by far the higher mortality and morbidity risk to the patient. Such misdiagnoses may stem from the expectation that wheezing is always derived from a respiratory cause.
Cardiac asthma, a condition secondary to heart failure that is often misdiagnosed as bronchial asthma, is marked by dyspnea, wheezing, cough, frothy or bloody sputum, and rales. The term was coined in 1833 by physician James Hope to describe the lack of oxygenation that resulted in an increased desire to breath. It is now better described as breathlessness and wheezing, commonly during the night, that results in congestion of the lungs secondary to heart failure.
Although we have better defined the process, we have not improved our differentiation, especially in the prehospital setting. Focusing on the subtle differences in the symptoms can make differentiation of the problem easier.
Cardiac asthma is more common in the elderly. Due to progression of the disease, exacerbations usually occur at night and with abrupt onset. Patients commonly report a sudden onset of severe dyspnea that wakes them from their sleep. Bronchial asthma, on the other hand, is from a underlying inflammatory process and occurs in a younger population that reports a gradual progression and worsening of symptoms.5 Progressive worsening of symptoms over hours and days is more consistent with many chronic conditions, such as COPD and pneumonia1 Is it imperative to accurately distinguish the nuances because the treatments are different and incorrect treatment for the latter can exacerbate cardiac asthma.
COPD, chronic obstructive pulmonary disease, is the second-most-common cause (after cardiac) of dyspnea in the prehospital setting. COPD can be one of the hardest to differentiate, especially in patients with a dual diagnosis and the frail stability of its chronic end stages.
Patients with COPD typically have cough and sputum for at least three months in at least two consecutive years. There is a chronic inflammation that leads to the destruction of lung parenchyma and thereby to overinflation of the lungs and a decline in elastic restorative forces. This commonly affects patients over age 40 with a current or past history of smoking.6
Although it is ideal to develop a differential diagnosis for dyspnea in the prehospital patient before initiating treatment, acuity of a patient’s distress does not always allow time for narrowing. Decreased mental alertness, inability to speak one-syllable words, and certain types of body positioning signal significant distress and the need for rapid interventions. Once airway and breathing are stabilized, causes can be investigated.1
After initial stabilization it is important to obtain a focused HPI. Historical features of symptoms and clinical timeline can help identify the most likely cause of a patient’s dyspnea. For example, a sudden onset with correlated fevers, cough, and unilateral abnormal breath sounds is most indicative of pneumonia, whereas a sudden onset with decreased oxygen saturations plus/minus sharp chest pain may represent a pulmonary embolism.
Key features to consider include the progression of symptoms, past medical history, associated symptoms, and things that may improve or worsen the dyspnea. Chronic or progressive dyspnea is more likely to be pulmonary or cardiac in origin, whereas sudden-onset dyspnea is more concerning for a diagnosis of pulmonary embolism or pneumothorax. CHF tends to be worse lying flat and can be associated with an increase in blood pressure as well as lower-extremity edema and weight gain.
Has the patient been around anyone sick recently or missed any cardiac medications? A concise but thorough review of symptoms and provoking/alleviating factors can provide a wealth of information.
Early EtCO2 Monitoring
Although the HPI and physical exam findings will help narrow the diagnosis of most patients, there are a couple of tools, such as end-tidal CO2 (EtCO2) waveform capnography and ultrasound, that can provide a clearer picture of the etiology to the patient’s dyspnea.
End-tidal CO2 measures exhaled carbon dioxide. This can be affected by the patency of an airway, ventilation quality, and the ability of gases to exchange through the lungs and throughout the body. End-tidal CO2monitoring thus provides a breath-to-breath update of the patient’s ventilation/respiration status, whereas pulse oximetry only gives feedback on tissue oxygenation and can take minutes to reflect respiratory failure. Capnography is the measurement of the carbon dioxide concentration in the atmosphere and was first used for monitoring internal environments in World War II. Although developed for use in medicine in the 1950s, it was not actively used in practice until the 1980s, when smaller, more practical machines allowed its use in the anesthesia field.16
Normally the capnography waveform takes the shape of a rounded rectangle. That is created by exhalation (when the graph goes up) and inhalation (when the graph goes down) as a patient breathes. Although in its most simplistic form end-tidal capnography is a graphic representation of how much CO2 a person is exhaling, the CO2 measurement as well as the shape of the waveform can give us diagnostic clues to the underlying lung disease that may be present. Different disease processes of the heart and lungs can change different phases of waveform capnography and thus the overall appearance of the patient’s waveform.17
For example, the disease pathology of obstructive pulmonary disease (COPD/asthma) subsequently leads to hypoventilation, retention of carbon dioxide, and its waveforms have a sharper upslope in the initial expiratory phase due to air trapping, commonly referred to as a shark-fin appearance.7 Pulmonary edema caused by heart failure, conversely, is characterized by poor alveolar oxygen exchange and increased ventilation. Research has shown emergency department EtCO2 measurements were significantly lower in CHF patients compared to those with COPD, and many other studies have consistently shown lower levels were associated with and predicted CHF, especially under 40 mmHg.7
Capnography isn’t without its limitations. One is that EtCO2 levels do not always correspond to PaCO2 levels in an arterial blood gas. Patients with abnormal lung function due to severe lung disease commonly have a widened gradient or difference between the end-tidal CO2 and the arterial blood CO2. So in a patient with severe obstructive lung disease, EtCO2 is more useful to trend ventilatory status over time rather than a single number as a spot check.15
Additionally, although there are limited diagnostic resources available to prehospital providers, EMS use of ultrasound in the prehospital setting is rapidly expanding. Prehospital ultrasound has robust clinical applications that may reduce morbidity and mortality and improve outcomes. It isn’t without barriers, but it is a new tool that can help refine medical decision-making. It has an application in distinguishing cardiac vs respiratory causes of dyspnea.
In pulmonary edema, a commonly missed diagnosis, the accumulated interstitial pulmonary fluid can be identified on ultrasound. Interstitial pulmonary fluids are identified as vertical hyperechoic lines that arise from, and run perpendicular, to the pleura. These lines extend deep into the lung parenchyma and the presence of three or more B lines in at least two bilateral lung zones is indicative of pulmonary edema.9
The Pathophysiology of Heart Failure
Pulmonary edema is most commonly a result of heart failure. There are two types of heart failure, one with preserved ejection fraction and the other with reduced. Acute pulmonary edema, and thus heart failure, is underidentified by paramedics, and studies support that we have room to grow in differentiating our dyspneic patients and providing them aggressive treatment.10 This can be achieved by the growth of the prehospital provider from mere technicians to clinicians. The most common factors associated with missed acute decompensated heart failure were a reported previous history of COPD and no prior history of CHF.
This is important, as giving beta-agonists to patients with congestive heart failure has been shown to lead to adverse outcomes, including death.11 Difficulties in differentiating heart failure from other causes of acute respiratory distress—e.g., pneumonia, COPD, ACS—limits the utility of initiating focused therapies beyond just stabilization in the prehospital setting. When differentiation cannot be ascertained, prehospital management should focus primarily on stabilization of the patient’s respiratory status and avoid targeted medical therapy.9
In the prehospital setting, initial rapid assessment involves the measurement of oxygen saturation and application of supplemental oxygen if needed. The most appropriate initial management goals for all patients with prehospital dyspnea are adequate oxygenation and ventilation, supplemental oxygen, NIPPV (or, in severe cases, emergent endotracheal intubation), and mechanical ventilation, along with hemodynamic stabilization.
Patients with acute respiratory decompensation without contraindications often respond well to noninvasive positive pressure ventilation en route to the hospital. Early application of this therapy can prevent deterioration and help avoid the need for intubation. A meta-analysis of multiple studies found a reduction in both morbidity and mortality with the use of continuous positive airway pressure in prehospital patients with acute respiratory failure. Positive-pressure ventilation also plays a critical role in the stabilization and management of severe COPD exacerbations and thus can be a crucial step in resuscitation of the undifferentiated dyspnea patient.
Obtain a 12-lead EKG to assess for cardiac ischemia, since acute coronary syndrome can present with acute onset of heart failure. The presence of ST-segment elevation myocardial infarction would alter the immediate hospital management and may also change the destination hospital. Common treatments for congestive heart failure in the ED include diuretics, nitrates, morphine, and, in severe exacerbations, the use of BiPAP. Current prehospital treatments are similar but vary per state and local protocols.
Patients with elevated blood pressure and symptoms of heart failure can be started on sublingual nitroglycerin prior to arrival at the ED. Although limited, there have been studies showing the safety of high-dose prehospital sublingual nitroglycerin for systolic blood pressures greater than 180–200 mmHg, with rare incidences of hypotension.
The patient in acute heart failure can present with hypotension due to decreased cardiac contractility, along with intravascular volume depletion. Patients with systolic pressures greater than 80 mmHg will typically find no benefit from inotropes; more benefit may come from small fluid boluses to optimize intravascular volume. Monitor these patients closely for fluid responsiveness.9
In the hypertensive patient, consider nitroglycerin SL or IVP and IV loop diuretics. Nitroglycerin promotes systemic and cardiac venous vasodilation, which results in increased blood flow to the heart, reduces cardiac preload, and decreases myocardial wall stress. It is extremely effective at restoring the balance of oxygen and nutrients to the ischemic heart.
Nitroglycerin can be given in much higher doses to the hypertensive heart failure patient than those presenting with chest pain, as it rapidly counteracts the patient’s sympathetic overdrive and improves their respiratory function. Sublingual nitroglycerin, in combination with infusion and/or IVP, has allowed more rapid stabilization and reduction of blood pressure in the ED setting.9
Although starting and administering nitroglycerin drips in the prehospital setting is not logistically practical, some protocols utilize IV push-dose vasodilators at 100-mcg/ml increments with prehospital success or a rapid succession of SL spray/tablets that will deliver 400 mcg per tablet or spray dose.
Loop diuretics may still be beneficial to appropriate patient populations. One of the primary goals of heart failure treatment is to improve pulmonary vascular congestion. Patients with heart failure with demonstrated symptoms of fluid overload should be treated with IV diuretics early in their clinical course. These play an important role in the treatment of failure-induced fluid overload.9
Furosemide, one of the most commonly used IV diuretics in heart failure, inhibits the reabsorption of sodium and chloride and causes diuresis, which improves symptoms by reducing preload in the heart. Furosemide isn’t without potential adverse effects and can lead to hypotension, electrolyte disturbances, gout exacerbations, reversible hearing loss, and worsening renal function.5
Unfortunately, until there is improved ability to accurately diagnose acute heart failure with hypervolemic patients, the risk of harm outweighs the benefit prehospital diuretics may provide. With improved diagnostic tools, a role for prehospital furosemide may reemerge in the future.12,13
Recognition & Management
First impressions created by EMS play an important role in building rapport with hospital staff on clinical acumen and teamwork. A biased initial diagnosis and wrong course of care can contribute to initiation bias and bad momentum for the prehospital patient. This can result in prolonged treatment with wrong and potentially harmful therapy, delays, and inappropriate care.
Acute dyspnea of unknown origin has been found to be an independent predictor of mortality, with a 30-day mortality of 2.55.14 The entire healthcare team needs to improve our early diagnosis and treatment of these patients; start in the prehospital setting.
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