Recently I had another episode of food allergy with shortness of breath as a symptom. Also some time ago, I experienced dyspnea a couple of times because of obstructive sleep apnea. Needless to say, such disruption of a vital function is a disturbing experience. I was reminded of an old, asthmatic friend who suffered recurrent respiratory emergencies and died of COPD. I ran into him after many years, and, holding up two fingers together, he said, “Me and the Reaper are like that.”

Although “shortness of breath” defines dyspnea, a more comprehensive definition would be “a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity, deriving from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses.” (American Thoracic Society)

While the pathogenesis of dyspnea is not completely clear, it is thought to be based on the concept of a regulatory circuit that consists of afferent information relayed centrally (from chemoreceptors for pH, CO2, and O2 as well as from mechanoreceptors in the musculature and the lungs, and a corresponding ventilatory response).

The ventilation/perfusion ratio (V/Q) refers to the relation of oxygen movement to degree of blood saturation in the lung capillaries. Most conditions associated with respiratory discomfort are characterized by increases in ventilation in response to derangements in ventilation-perfusion matching as well as increases in dead space, the presence of metabolic acidosis, or stimulation of pulmonary or chest wall receptors.

The peripheral chemoreceptors, located in the carotid bodies and aortic arch, sense changes in the partial pressure of oxygen in arterial blood and are also stimulated by acidosis and hypercapnia. The central chemoreceptors, located in the medulla, respond to changes in pH and arterial tension of carbon dioxide (PaCO2).

Throughout the airways, lungs, and chest wall are a variety of mechanoreceptors that assist the body in monitoring changes in pressure, flow, and volume in the respiratory system. Stimulation of such receptors in the face and upper airway, which are largely innervated by the trigeminal nerve, can reduce the intensity of dyspnea.

Most of the causes are pulmonary, cardiac, hematological, and psychogenic. (However, Diagnosis Pro, an online expert system, listed 497 distinct causes in October 2010!) I’ll just focus on the first two here; specifically, congestive heart failure and chronic obstructive pulmonary disorder.

Heart failure is a complex clinical syndrome in which the heart cannot pump enough blood to meet the body’s requirements. It results from any disorder that impairs ventricular filling or ejection of blood to the systemic circulation. Patients usually present with fatigue and dyspnea, reduced exercise tolerance, and flued retention (pulmonary and peripheral edema). Heart failure remains a highly prevalent disorder worldwide with a high morbidity and mortality rate. It has an estimated prevalence of 26 million people worldwide and contributes to increased global healthcare costs.

Coronary artery disease and diabetes mellitus have become the predominant predisposing factors for heart failure. Other structural causes include hypertension, valvular heart disease, uncontrolled arrhythmia, myocarditis, and congenital heart disease. The most common causes of decompensated CHF are inappropriate drug treatment, dietary sodium restriction, and decreased physical activity.

The main pulmonary causes of dyspnea, as noted, are COPD and asthma. The former is comprised of emphysema and chronic bronchitis, and is now the third leading cause of death in the U.S. Characterized by inflammation and persistent obstruction to airflow through the lungs, usually caused by harmful inhaled particles (e.g., those of tobacco smoke), the disease manifests itself by dyspnea, a productive cough, frequent chest infections, and persistent wheezing. It can sometimes be asymptomatic. Treatment includes smoking cessation, of course, inhalers, pulmonary rehabilitation, and, in rare cases, surgery. COPD cannot be cured or reversed but for some people, treatment can keep it under control. For others, it may worsen despite treatment.

According to the National Institutes of Health, 1 in 6 people with COPD have never smoked. The common factors that participants who didn’t smoke but had COPD shared were: being 40+, having asthma, and having had a severe respiratory disease as a child. Also, indoor and outdoor pollutants can cause COPD in people who don’t smoke. Symptoms tend to be similar for smokers and non-smokers. Some research has found that the severity of COPD is lower in people who don’t smoke than in those who do.

One more thing about my late friend with the asthma. Before he entered hospice, he suffered his worst crisis, which led to his being put on a ventilator for over a month. He struggled mightily to attain some semblance of recovery. Once he was free, we met at a coffee shop. “I’m not what I was,” he said, “but I’m still here.”

. – Rylan Dray, Ph.D. – March 2023

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