This clinical review feature article is presented in conjunction with the Department of Emergency Medicine Education at the University of Texas Southwestern Medical Center, Dallas.
>> Identify the most common causes of respiratory distress seen in the prehospital setting.
>> Identify the management options and the goals for prehospital treatment of shortness of breath.
>> Discuss the benefits of CPAP for respiratory distress.
Anticholinergic: Any drug that blocks the effects of the parasympathetic nervous system, causing the bronchioles to relax.
Coronary artery bypass graft: A surgical procedure in which a donor vessel (usually the saphenous vein from the leg) is grafted to a coronary artery before and after a blockage, thus restoring circulation.
Continuous positive airway pressure (CPAP): A method of noninvasive ventilation that provides a continuous level of pressurized air.
Diuretic: Any drug that increases the formation rate of urine.
Exacerbation: Worsening or increase in severity of a disease.
Florid respiratory failure: Fully developed or the complete clinical manifestation of respiratory failure.
Sympathetic response: A response of the sympathetic nervous system, or the “fight or flight” response, which causes increased heart rate, bronchodilitation and increased blood pressure.
A 9-1-1 call is received for a 68-year-old male with breathing problems. Upon arrival, the crew finds the patient confused but able to speak in short phrases. Initial vital signs are: BP 148/89, pulse 110 sinus rhythm, respiratory rate 28 and labored, O2 saturation 84% on room air and a fingerstick glucose of 145.
The patient’s oxygenation and work of breathing improve markedly with 100% O2 by non-rebreather face mask. Physical examination is remarkable for increased work of breathing with rhonchi found bilaterally at the lung bases (worse on the left). No wheezing is present.
The patient’s medical problems include coronary artery disease, coronary artery bypass graft, congestive heart failure (CHF), diabetes, chronic obstructive pulmonary disease (COPD) and obesity. His wife states that he’d been having increased difficulty breathing over the past 24 hours accompanied by a mild cough and confusion. He tells the crew he hasn’t had a fever or chest pain, and he’s unsure if he’s taken all of his medications over the past few days. A 12-lead ECG shows normal sinus rhythm with no ST-segment elevation or T-wave inversions. The patient is transported to the nearest hospital for further evaluation and treatment.
Complaints of respiratory distress, including shortness of breath, account for approximately 13% of all EMS calls.(1) Numerous diseases present with shortness of breath, including pneumonia, decompensated heart failure, COPD exacerbations, pneumothorax, pulmonary embolism, cardiac tamponade, anaphylaxis and asthma.
For optimal recall, it’s easiest to group the many causes of shortness of breath into five main categories: cardiac, pulmonary, central nervous system (CNS) abnormalities, neuromuscular disorders and those secondary to blood disorders.
Unfortunately, many patients have multiple, coexisting medical problems, which makes correctly diagnosing the cause of respiratory distress difficult, if not impossible, without X-rays and laboratory studies. As illustrated in this case, the exact cause of a patient’s respiratory distress may not be evident, even after a thorough history and physical exam. Often, more than one disease process contributes to a patient’s symptoms. For example, a COPD exacerbation may be due to pneumonia, causing hypoxia, which then reflexively increases heart rate, thus cardiac demand is increased, which can lead to decompensation of heart failure.
Even in the more controlled setting of the emergency department (ED), physicians with access to lab tests and diagnostic imaging may have difficulty determining the exact cause of a patient’s breathing problems. Therefore, EMS providers are faced with the challenging task of quickly determining the most likely cause of respiratory compromise and administering appropriate therapies while avoiding possibly harmful treatments—all without the benefit of the many diagnostic studies available in the ED.
Three very common causes of respiratory distress seen in the prehospital setting are COPD, pneumonia and heart failure. Diagnosis of these disorders by EMS relies primarily on the patient’s history and physical exam findings. Unfortunately, there’s significant overlap of signs and symptoms in these disease processes. All may present with dyspnea, cough, hypoxia and abnormal breath sounds, including wheezing, rhonchi and rales.
Pneumonia is a common respiratory disease often seen in elderly individuals and those with chronic medical problems causing immunosuppression (HIV, autoimmune disease, cancer and chemotherapy). But it’s also seen in children and young adults. There are 2–4 million cases of community-acquired pneumonia in the U.S. each year, and it’s this country’s seventh leading cause of death.(2)
Patients with pneumonia typically present with productive cough, fever and abnormal breath sounds in the affected lung area. More severe cases will also have hypoxia and tachypnea.
Confusion, decreased functional status, or abdominal or back pain may be the presenting symptoms in the elderly or immunocompromised patient. Unfortunately, there’s no one physical finding that’s reliable enough to accurately diagnose pneumonia, but it should be considered a likely diagnosis in a patient who complains of shortness of breath, fever, chills and a new productive cough with thick sputum production.
Heart failure is the inability of the heart to pump a sufficient amount of blood to adequately perfuse the body to meet its metabolic needs. Heart failure is increasingly common as people age, and is usually a result of years of hypertension, prior myocardial infarction (MI), valvular disease or longstanding obstructive lung disease. It’s often associated with atrial fibrillation.
Approximately five million people in the U.S. have a diagnosis of heart failure, with more than a half a million more diagnosed each year. The five-year mortality rate after the diagnosis of heart failure is nearly 50%.(3)
Common elements in the history of a patient with heart failure are prior episodes of heart failure, lower extremity edema, weight gain, increasing dyspnea with exertion, sleeping elevated by multiple pillows (orthopnea) and nighttime waking with shortness of breath (paroxysmal nocturnal dyspnea).
The patient’s medications often include furosemide (Lasix) or another diuretic and digoxin, and Coumadin if heart failure is associated with atrial fibrillation. Most patients with heart failure have symptoms that have worsened over days to weeks. However, acute heart failure with flash pulmonary edema and rapid progression to florid respiratory failure may occur with acute myocardial infarction (AMI), pulmonary embolus or such cardiac dysrhythmias as atrial fibrillation with rapid ventricular response.
COPD is a chronic disease of airway obstruction and inflammation usually caused by exposure of lung tissue to cigarette smoke or another inhaled toxin. COPD exacerbation contributes to 20% of hospitalizations in people older than 65. A patient with a COPD exacerbation will usually complain of worsening shortness of breath and increased cough and sputum production over the past few days.
Exacerbations are more common in the winter, and are often due to viral or bacterial lung infections. COPD exacerbations are almost never hyper-acute. Patients generally seek medical care after a period of worsening symptoms. A sudden onset of dyspnea in a patient with COPD should prompt an evaluation for a more acute illness, such as heart failure, pneumonia, AMI, pulmonary embolus or arrhythmia.(4)
Standard treatments for respiratory distress include oxygen, albuterol nebulization (with or without ipratropium), nitroglycerin, Lasix, morphine and continuous positive airway pressure (CPAP) or endotracheal (ET) intubation, depending on the presumed cause of distress. In all cases of respiratory compromise, oxygen by either face mask or nasal cannula should be administered, and its effect on oxygen saturation monitored. The use of capnography may aid in evaluating and monitoring the adequacy of the patient’s ventilatory status.
The goal for the patient’s oxygenation should be an O2 saturation of greater than 95% for all patients except for those with COPD, in which case a goal of 92% is appropriate. Aspirin should be administered to any patient in whom AMI is suspected if they have no reported aspirin allergy. Assisted ventilation is required in any patient with poor ventilatory effort or apnea. A capnography waveform above or below 40 should alert you to difficulty with the patient’s exchange of carbon dioxide and may be your earliest alert for the need to bag the patient. The role of morphine, nitroglycerin, Lasix, CPAP, ET intubation and albuterol/ipratropium nebulization in specific disease entities is discussed below. A 12-lead ECG should be performed if possible on all patients with shortness of breath over the age of 50–55, and in any adult patient suspected of having myocardial ischemia.
Nitroglycerin: This arterial and venous vasodilator decreases both preload and afterload, oxygen consumption and cardiac workload. It may also decrease blood pressure and coronary spasm. Nitroglycerin is highly effective in pulmonary edema and should be used aggressively in this setting as long as the patient’s blood pressure remains above approximately 110/70 mmHg.
Nitrates shouldn’t be used in patients with hypotension, recent use of phosphodiesterase inhibitor erectile dysfunction medications (Viagra, Cialis, Levitra) or history of severe aortic stenosis. Higher doses of nitroglycerin may cause headaches. Nitroglycerin can also cause profound hypotension in patients having an inferior MI with right ventricular involvement.
Albuterol/Ipratropium (Combivent): Albuterol, or albuterol combined with ipratropium, causes bronchodilation and decreases airway secretions. These two bronchodilators are useful in asthma, COPD and anaphylaxis to decrease wheezing and airway obstruction. Although the anticholinergic ipatropium is only somewhat beneficial in asthma, it should always be used if possible in COPD where its benefits are equal to or better than albuterol. Remember, beta agonist bronchodilators can be harmful to patients with dyspnea due to causes other than asthma or COPD.
Outcomes have been shown to be worse for patients who have dyspnea due to heart failure, but no history of COPD, and were given bronchodilator therapy than those who didn’t receive bronchodilator therapy.(5) Therefore, bronchodilator therapy should be reserved for patients who are wheezing or have a history of COPD or asthma.
Morphine: Patients with respiratory distress due to acute pulmonary edema in heart failure will have a significant sympathetic response, including increased blood pressure and heart rate, along with “air hunger.” Morphine was previously thought to help blunt this sympathetic response, thus decreasing discomfort and lessening pulmonary congestion by reducing preload and cardiac demand. However, no controlled study has shown that morphine has any beneficial effects in pulmonary edema, and evidence now suggests it may be harmful. In one study, patients with a heart failure exacerbation who received morphine were more likely to require mechanical ventilation and had a higher mortality rate when compared to those who did not receive morphine.(6) Therefore, morphine shouldn’t be used in cases of decompensated heart failure unless the patient also has severe ischemic chest pain that’s refractory to nitroglycerin.
Furosemide (Lasix): Furosemide is a common, effective treatment of pulmonary edema due to heart failure. It’s a diuretic that works by increasing excretion of sodium and water by the kidneys. Onset of action with normal kidney function and blood pressure is usually within 30 minutes and is marked by increased urine output.
Although furosemide is appropriate in heart failure due to volume overload and pulmonary edema, there are many cases in which the use of this drug is harmful to a patient in respiratory distress. A study in Michigan found that approximately 40% of the patients who received furosemide from EMS for presumed CHF did not ultimately have a hospital diagnosis of heart failure. Even more concerning is that 17% of the patients who received inappropriate furosemide administration had diseases, such as sepsis, pneumonia or dehydration, that were made worse by it.
Additionally, many patients given furosemide actually required IV fluids in the ED. Urban EMS providers should keep in mind that a short delay for furosemide administration until a more definitive diagnosis of heart failure can be made (with an ED chest X-ray and laboratory studies) will decrease the risks associated with inappropriate administration of furosemide without significantly delaying the potential benefits of the treatment. Lasix administration in the field should follow the maximal dosing of nitroglycerin and be subjected to careful consideration whether the patient has a high probability of heart failure.
CPAP: Mechanical ventilation and positive pressure ventilation by bag valve mask, ET intubation or CPAP decrease work of breathing, allow increased gas exchange and decrease cardiac afterload. ET intubation has been the standard treatment for patients needing immediate ventilatory support. Most patients with severe respiratory failure due to heart failure will be awake and will therefore require sedation and paralytics, such as rapid sequence intubation (RSI) prior to ET intubation. Many EMS systems don’t allow RSI, thus leaving awake nasotracheal intubation or bag-mask ventilation as the only options.
CPAP is a promising addition to airway management and has been shown to significantly reduce the need for ET intubation, thus decreasing the associated adverse outcomes and complications. CPAP provides continuous positive pressure to the airways and helps recruit alveoli, stenting them open to improve oxygenation and decrease ventilation/perfusion mismatch.
In one prehospital study, patients with severe respiratory distress attributed to pulmonary edema not responsive to standard treatment of O2, nitrates and furosemide were either intubated or underwent a trial with CPAP. ET intubation was required in 25% of patients in the control group compared to only 9% of patients who were put on CPAP first. The authors reasoned that CPAP use in six patients would prevent the need for intubation in one patient.(7)
Another prehospital study found a similar benefit of CPAP in decreasing need for ET intubation, with an absolute reduction of ET intubation of 30% and absolute reduction of mortality of 21% when patients with failing respiratory efforts received CPAP rather than intubation.(8)
Initiating CPAP in the field seems to have many benefits but is associated with some financial cost. When the cost of equipment, training and consumables (face masks and tubing) averaged over five years are taken into account, the cost per CPAP application in one typical urban EMS system was $89. Cost per life saved,with CPAP (assumed to save 0.75 lives per 1,000 people) is $490.9 Hospital costs were estimated to be reduced by $4,075 for each patient who was able to avoid ET intubation with CPAP use. Thus, the big cost savings to the hospital, and ultimately the patient, is the decreased length of hospital and intensive care unit stays when CPAP is used. Intubated patients in this study had an average hospital stay of 10.82 days compared to just 5.84 days for those for whom intubation was avoided.(9)
Heart failure: The standard treatment of heart failure in the prehospital setting is evolving, and the efficacy and role of many therapies that have been considered standard are now being questioned. Therapy should center on adequate oxygenation, close monitoring and the aggressive use of nitrates. Patients with severe distress will also benefit from CPAP application.
Pneumonia: The primary treatment of shortness of breath due to pneumonia in the prehospital setting is preventing hypoxia with the application of supplemental oxygen. These patients need early treatment with antibiotics for improvement of symptoms and disease resolution. Often, pneumonia can exacerbate COPD; thus, albuterol and Atrovent nebulization may be helpful in decreasing wheezing and dyspnea.
COPD: Infection and medication non-compliance are common causes of COPD exacerbations, so treatment is aimed at addressing the underlying infection with antibiotics and decreasing bronchospasm with albuterol and Atrovent. The goal of prehospital treatment of COPD is to decrease bronchospasm and hypoxia.
Bronchospasm is treated with albuterol and Atrovent, along with magnesium, which may also be very helpful as a bronchodilator in severe bronchospasm due to COPD. Hypoxia is treated with supplemental O2 to increase oxygen saturation to about 92%. Oxygen saturation greater than 92% in patients with severe, chronic COPD has been associated with decreased drive to breath and apnea. CPAP should be used for patients with severe exacerbations of COPD. If CPAP isn’t available and the patient continues to decline, assisted ventilation with bag-valve mask or ET intubation may be necessary. Although signs of respiratory failure must always be carefully monitored for, some feel capnography may provide the earliest signs.
Dyspnea is a very common symptom seen by EMS providers. Treatment of shortness of breath can often be challenging given the difficulty in determining the etiology of a patient’s symptoms. Providers must focus on those therapies proven to benefit the patient and avoid those that may cause harm.
For heart failure patients, we recommend avoiding morphine, Lasix and potentially bronchodilators while providing supplemental O2, nitrates and CPAP. We don’t support the routine use of Lasix in the prehospital setting, because of the potential for harm to the patient with dyspnea due to causes other than heart failure. Supplemental oxygen and bronchodilators remain the main treatments for COPD. Assisted ventilation with CPAP or ET intubation is indicated in any patient with respiratory failure. JEMS
1. Maio RF, Garrison HG, Spaite DW, et al. Emergency medical services outcomes project I (EMSOP I): Prioritizing conditions for outcomes research. Ann Emerg Med. 1999;33:423–432.
2. Moran GJ, Talan DA. Rosen’s emergency medicine: Concepts and clinical practice. In JA Marx (Ed.), Pneumonia. St. Louis: Mosby Elsevier, 2010.
3. O’Brien JF, Falk JL. Rosen’s emergency medicine: Concepts and clinical practice. In JA Marx (Ed.), Heart Failure. St. Louis: Mosby Elsevier, 2010.
4. Swadron SP, Mandavia DP. Rosen’s emergency medicine: concepts and clinical practice. In JA Marx (Ed.), Chronic Obstructive Pulmonary Disease. St. Louis: Mosby Elsevier, 2010.
5. Singer AJ, Emerman C, Char DM, et al. Bronchodilator therapy in acute decompensated heart failure patients without a history of chronic obstructive pulmonary disease. Ann Emerg Med. 2008;51:25–34.
6. Peacock WF, Hollander JE, Diercks DB, et al. Morphine and outcomes in acute decompensated heart failure: An ADHERE analysis. Emerg Med J. 2008;25:205–209.
7. Hubble MW, Richards ME, Jarvis R, et al. Effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema. Prehosp Emerg Care. 2006;10:430–439.
8. Thompson J, Petrie D, Ackroyd-Stolarz S, et al. Out-of-hospital continuous positive airway pressure ventilation versus usual care in acute respiratory failure: a randomized controlled trial. Ann Emerg Med. 2008;52:232–241.
9. Hubble MW, Richards ME, Wilfong DA. Estimates of cost-effectiveness of prehospital continuous positive airway pressure in the management of acute pulmonary edema. Prehosp Emerg Care. 2008;12:277–285.
This article originally appeared in May 2010 JEMS as “Shortness of Breath: Prehospital treatment of respiratory distress.”