The Advanced Practice Nurse's Role in Palliative Care and the Management of Dyspnea

Rose Anne Indelicato, MSN, APRN-BC, PCM-BC, OCN

Disclosures

Topics in Advanced Practice Nursing eJournal. 2006;6(4) 

In This Article

Breathing and Dyspnea

The etiology of dyspnea is multifactorial; the condition can result from impairment of 1 or more body systems.[1,15,16] Dyspnea is primarily related to disorders involving the pulmonary, cardiovascular, neurologic, and hematologic systems, as well as to psychological and spiritual issues (see Table 1 ).

Breathing is normally quite complex, involving the interaction of somatic and autonomic nerves. The respiratory center, located in the medulla and the pons, integrates peripheral and central afferent input, coordinating the diaphragm with intercostal and accessory muscles to generate the respiratory rhythm.[1,5,17]

Chemoreceptors and mechanoreceptors are found within the brain and in the periphery. These receptors respond to humoral and/or mechanical stimuli and vascular pressure. The central chemoreceptors, found within the medulla, are sensitive to small changes in pH and PCO2 levels within the blood. The peripheral receptors are located on the carotid and aortic bodies and are moderately sensitive to changes in PO2.[5,17]

Mechanoreceptors are found within the lungs, intercostal muscles, diaphragm, pulmonary artery, and the atria and right ventricle of the heart. They respond to a variety of stimuli including irritation, stretching, congestion, and vascular changes. The respiratory muscles include the diaphragm, intercostal muscles, and the sternomastoid muscle. Changes in muscle tension, chest wall tension, and the lungs, which occur during respiration, stimulate these mechanoreceptors. This information is then transmitted to the respiratory center.[5,17]

The pathophysiology of dyspnea is poorly understood. Dyspnea may result from 3 abnormalities that can occur within the processes of respiration: (1) an increase in the respiratory effort required to overcome a certain load (often seen in obstructive or restrictive lung disease, or pleural effusion); (2) an increase in the proportion of respiratory muscle needed to maintain a normal workload (as demonstrated with neuromuscular weakness or cachexia); or (3) an increase in ventilatory requirements (as seen in hyperemia, hypercapnia, metabolic acidosis, or anemia).[18] Patients may experience all 3 abnormalities simultaneously to differing degrees.[5]

Chemoreceptors play an important role in the transmission of information related to chemical changes (hypercapnia or hypoxemia). These receptors are highly sensitive to changes in carbon dioxide and oxygen. Once these changes have been detected, the patient reacts by breathing more forcefully and frequently. Signals from these receptors can initiate dyspnea independent of any increase in respiratory effort.[19,20,21]

Patients may also experience a magnification of the intensity of dyspnea due to cultural background, surrounding environment, previous life experiences, and psychological or spiritual distress.[5]

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