Dyspnea is common in patients with COPD and other lung diseases, so common that it is addressed in the general questionnaires patients complete on every visit. Responses to those very general questionnaires can disguise the patient’s own experience with dyspnea.
“Dyspnea is a subjective experience that is different for every patient,” said Denis O’Donnell, MD, MBBCh, FCCP, professor of medicine at Kingston Health Services Centre and Queens University. “You can’t depend on general questionnaire responses; you have to address the patient’s own experiences, problems, and problem times. When you adjust treatment to the patient’s specific problems, you can have a very direct impact on their life.”
Dr. O’Donnell explored the physiology of dyspnea and how physiology can affect treatment choices during the Distinguished Scientist Honor Lecture in Cardiopulmonary Physiology “Helping the Dyspneic Patient: Clinical Physiology Matters” on Sunday, October 18. The session is available for viewing on the virtual CHEST 2020 meeting platform through January 18, 2021, for registered attendees.
Effective treatment depends on how the physiology of dyspnea can affect each patient individually.
Recent research has confirmed early suggestions that dyspnea is an imbalance between respiratory demand and respiratory capacity. The increasing urge to breathe outpaces inspiratory capacity, feeding a growing air hunger that leads to panic if not satisfied.
“The urge to breathe increases very quickly in dyspnea,” Dr. O’Donnell said. “If there is not an immediate expansion in tidal volume, the patient becomes very uncomfortable very quickly.”
Treating dyspnea effectively means safely decreasing the drive to breathe, increasing inhalation capacity, or both, he continued. Increasing inspiratory drive is largely driven by increasing CO2 levels.
The primary drivers of the growing need to breathe are hypoperfusion in the lungs and increasing CO2 production from early metabolic acidosis.
Hypoperfusion is the result of microvascular injury in COPD, interstitial lung disease, and other conditions. Microvascular injury reduces the alveolary-capillary surface area for gas exchange and reduces the volume of blood in the alveolar-capillary bed.
Most patients have a heterogenous distribution of reduced alveolar perfusion and gas exchange rather than reductions in distinct areas, Dr. O’Donnell noted. He called it “physiologic dead space.”
Deflating the lungs can improve inspiratory capacity, whether deflation is accomplished using bronchodilators, exercise training, oxygen therapy, lung volume reduction surgery, or some combination. Even a small reduction in capacity, 0.5 L, can have a major impact on dyspnea symptoms.
The most effective approach depends on the patients’ most troublesome symptoms and when those symptoms occur. Dr. O’Donnell suggested charting each patient’s dyspnea by cause and time of day to help identify appropriate interventions.
Some patients are particularly bothered with nighttime symptoms, waking multiple times to use a rescue inhaler. One solution could be a long-acting bronchodilator at night before sleeping. CPAP or BiPAP might also help the patient sleep through the night.
For patients whose dyspnea is worsened by exercise, exercise training can be particularly helpful. Exercise training reduces lactate acidosis to improve dyspnea and improves exercise capacity while it improves self-efficacy and reduces both anxiety and depression.
Inspiratory muscle training can also improve symptoms. So can oxygen, regardless of reimbursement status in a particular jurisdiction.
Oxygen can reduce chemoreceptor activity and reduce the urge to breath, improve breathing patterns, reduce dynamic lung hyperinflation, delay peripheral muscle fatigue, and improve cardio-circulatory function.
“The message is that we can’t tackle dyspnea with a single intervention,” Dr. O’Donnell said. “It is always multiple interventions.”