Dyspnea

Victor J. Test

INTRODUCTION

Breathing is an involuntary action, controlled by the subconscious and normally does not prompt recognition by the conscious mind. Dyspnea is defined as an uncomfortable awareness or sensation associated with breathing. However, awareness of breathing is not synonymous with dyspnea, since the context of the awareness is crucial to determining if the sensation is uncomfortable or not. For example, a sprinter who completes a 400-m race may breathe quite hard; however, the work of breathing is expected in this setting and is not in itself an uncomfortable sensation.

Dyspnea is one of the more common complaints in pulmonary medicine and is more common in women and obese and older patients. The complaint of dyspnea is often difficult to elicit in clinical practice, since patients may provide disparate descriptions use such as “I can’t breathe,” “I am smothering,” “I get tired,” “I am puffed,” and “I am panting.” In addition, the evaluation of dyspnea may be delayed when patients and physicians attribute the symptom to aging, obesity, deconditioning, and/or smoking.

PRESENTATION

Dyspnea is an alarming symptom, even when compared to chest pain. Among patients who present with dyspnea and/or chest pain, all-cause mortality is much higher when dyspnea or dyspnea and chest pain are the presenting symptoms. In this group, mortality due to myocardial infarction and coronary revascularization is much higher when compared to patients who presented with chest pain alone.

Dyspnea is affected by numerous receptors and factors, as well as by one’s perceptions. The cerebral cortex interprets dyspnea-related data from chemoreceptors, muscles, skin, and the lung in order to place them in context. The medulla and subcortex receive input from the afferent receptors and central chemoreceptors as part of the control of breathing. The chest wall has mechanoreceptors in muscle spindles and tendon organs that are innervated by the anterior horn cells and project to the somatosensory cortex. The vagus nerve also has afferent nerves that relay information about lung inflation and volume changes. Chemorecepters in the carotid body and the medulla detect changes in pH, Pco₂, and Po₂. Myelinated nerves and unmyelinated C-fibers in the lung conduct information from the lungs, larynx, and trachea and send information via the vagus nerve regarding pulmonary stretch and air movement. Even the skin of the face and mucous membranes of the nasopharynx detect air flow and affect the sensation of dyspnea.

The differential diagnosis of acute onset of dyspnea is quite broad and includes asthma, anxiety-related hyperventilation, pneumothorax, pulmonary embolism, exacerbation of chronic lung disease, pulmonary edema, and myocardial ischemia. The evaluation of acute dyspnea should be guided by the history, physical examination, and judicious diagnostic testing. Basic diagnostic evaluation may include an electrocardiogram, chest radiography, complete blood count, and arterial blood gases. History and physical examination in conjunction with these diagnostic tests should establish the diagnosis of pulmonary edema, pneumothorax, and chest trauma. In a pure hyperventilation syndrome, arterial blood gases demonstrate respiratory alkalosis and normal alveolar–arterial gradient. The detection of myocardial ischemia and pulmonary embolism may be more difficult and generally mandates additional testing such as cardiac enzymes, D-dimer measurement, echocardiography, and thoracic imaging: either by contrast-enhanced computed tomography (CT) or ventilation–perfusion scanning. The Well’s Score or Geneva Score can help stratify the patient’s probability of having pulmonary embolism. Spirometry can identify airflow obstruction. The brain natriuretic peptide (BNP) and N-terminal pro-brain natriuretic peptide (NT-pro-BNP) are useful in identifying decompensated heart failure, although, it can increase in other conditions such as pulmonary embolism.

Chronic dyspnea is shortness of breath that has persisted for more than 3 weeks. As is the case in acute dyspnea, the diagnosis of chronic dyspnea can usually be identified with a careful history, physical examination, and a few basic tests such as chest radiography, electrocardiography, spirometry, and simple laboratory testing (complete blood count, chemistry, and thyroid testing). Elements of the history such as previous diagnoses may, however, be misleading in patients with chronic dyspnea. One study demonstrated that a historical diagnosis of reactive airway disease was associated with a positive predictive value (PPV) of only 0.55 for the final diagnosis of asthma. Similarly, a patient’s report of chronic obstructive pulmonary disease (COPD) was associated with a PPV of 0.45 for COPD. A history of smoking in patients with chronic dyspnea carried a PPV of 0.40 for COPD.

ETIOLOGY AND DIFFERENTIAL DIAGNOSES

Only gold members can continue reading. Log In or Register to continue