Perhaps no other sensation can evoke such fear as the inability to breathe. Dyspnea rivals sensations like hunger or thirst.1 There are numerous causes for dyspnea that range from the benign to life-threatening, and the emergency physician must quickly distinguish the innocuous from the grave. The question is, at what cost? Which patients need only reassurance, and which require an extensive (and expensive) diagnostic work-up?
Patient anxiety may be a major source of diagnostic confusion. A diagnosis of anxiety provides a simple explanation for many cases of dyspnea seen in the ED. But while anxiety can produce breathlessness, lifethreatening diseases also generate hyperventilation in patients and physicians alike. This issue of Emergency Medicine Practice will decrease your trepidation in dealing with this common complaint.
Dyspnea is the perception of the inability to breathe comfortably.2 Although dyspnea is subjective, it has a physiologic basis. Chemoreceptors and stretch receptors interact with the brain and lungs to modulate respirations. Of note, respirations are the only vital sign subject to voluntary control.
Chemoreceptors detect changes in blood oxygen and carbon dioxide and subsequently trigger the respiratory drive centers. Decreased ventilation and increased lung deadspace both elevate PCO2. Lung deadspace expands when lung units are ventilated but not perfused, such as in pulmonary embolism. While elevations in CO2 are a crucial stimulant of respiratory drive, this mechanism is often blunted in patients with chronic lung disease. Other chemoreceptors are responsible for detection of acidosis, which will also increase respiratory drive.
Hypoxemia also modulates respirations through chemoreceptors. When the carotid body senses a minute fall in oxygen tension, it stimulates the brainstem to increase ventilation. The most common cause of hypoxemia is pulmonary ventilation-perfusion mismatch. This imbalance between pulmonary blood flow and alveolar ventilation is usually due to diseases of the heart or lung. Shunt is an extreme form of ventilation-perfusion mismatch and occurs when ventilation to a lung unit is interrupted despite persistent blood flow.3,4 Thus, the blood shunts past this "dummy" area of lung without exchanging gases. During shunt, the body compensates with reflex pulmonary vasoconstriction, which attenuates blood flow to non-ventilated lung units. While b2-adrenergic agents can reverse this vascular response, supplemental oxygen cannot correct hypoxemia produced by shunt.
Heightened airway resistance, elevated lung deadspace, and abnormal lung stiffness all increase the work of breathing.3,5,6 Mechanoreceptors in the face, upper airway, chest wall, and lungs are responsible for a feedback loop that modulates this sensation; vagal J receptors in the lung are important mediators.5 Researchers believe that the mismatch between lung volume and tension in the muscles of respiration is another important factor in patients with increased work of breathing.1
Even "psychogenic" dyspnea has a physiologic basis. Changes in brain neurochemistry and unusual responsiveness to PCO2 may be responsible for the breathlessness of panic disorders.7
A wide range of conditions can produce "shortness of breath." Dyspnea is merely a symptom and does not connote a specific condition or diagnosis. Emergency physicians should consider dyspnea in terms of organ systems. These include the airway, the lungs, the heart, the blood (including metabolic causes), and neuromuscular causes. (See Table 1.) Muscular weakness can produce dyspnea, and causes include myasthenia gravis, Guillain- Barr® syndrome, and thyrotoxicosis.8,9 Gastroesophageal reflux is responsible for approximately 4% of chronic undifferentiated dyspnea.10,11
In three prospective studies, 207 patients underwent comprehensive laboratory and physiological testing for chronic dyspnea. A cardiac or pulmonary problem was the primary etiology in three-quarters of the cases.10-12 In these settings, most cases of dyspnea were due to one of the following processes: hyperactive airways or chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), acute pneumonia, or acute pulmonary embolism (PE).
Although it is difficult to track the prevalence of isolated dyspnea in adult ED, approximately 2-3% of all ED patients complain of respiratory distress.13,14
Many patients have dyspnea in conjunction with another symptom, such as diaphoresis, chest pain, palpitations, cough, or fever. These associated symptoms may provide important clues to the etiology.
An important goal in emergency medicine is detection of serious or life-threatening causes of dyspnea. For this reason, psychogenic dyspnea should be diagnosed after exclusion of organic causes. This does not require extensive diagnostic testing in all cases. History, physical, and simple ED tests may obviate the need for further studies. Patients previously in good health with dyspnea who are younger than 40 are diagnosed with psychogenic dyspnea in one-third of ED visits.10
Another important goal is detection of PE. Pulmonary embolism is of special import, not just because of potential lethality, but because patients may not appear critically ill. While there are other serious causes of dyspnea, such as pulmonary edema, profound acidosis, and pericardial tamponade, these patients appear supremely distressed. They present with dramatic findings on examination and are unlikely to be discharged by even the unwary clinician. On the other hand, the patient with pulmonary embolism may exhibit only modest findings, inviting a superficial evaluation.
The history, physical examination, and chest film will accurately predict the cause of dyspnea in about twothirds of patients.11These three basic investigations will frequently determine the need for other studies. The Clinical Pathway "Management Of Unexplained Dyspnea" summarizes the approach to patients with dyspnea.
History will provide important clues to the diagnosis and the need for further investigation. Determine the patient's risk for serious disease. Of particular importance is the patient's age, past medical conditions, and associated symptoms.
2. "But the pulse ox was normal!"
3. "But he had CHF the last time he came to the ED."
4. "Here it is right in the chart……No chest pain'!"
5. "I knew he was pulled out of a burning building…that's why I got the pulse ox."
6. "Even the radiologist said the chest film showed pneumonia."
7. "The radiologist said the chest x-ray was normal."
8. "After I gave him the high-flow oxygen, he calmed down a lot…he even went to sleep. So I turned out the lights and let him rest."
9. "I didn't get the V/Q scan because her obstetrician said she didn't need it."
10. "I should have ordered the chest x-ray and a pulse ox."
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, each reference will note (in bold type following the reference) pertinent information about the study, such as the type of study and the number of patients in the study. In addition, the most informative references cited in the paper, as determined by the author, will be noted by an asterisk (*) next to the number of the reference.