Palliative Care and the Management of Dyspnea

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]

Cite this: The Advanced Practice Nurse's Role in Palliative Care and the Management of Dyspnea - Medscape - Dec 31, 2006.

Etiology of Dyspnea ^[1,15,16]
Physiologic System	Disorder
Pulmonary	Asthma
	Adult respiratory syndrome
	Bronchial obstruction
	COPD (bronchitis, emphysema)
	Cystic fibrosis
	Interstitial lung disease
	Lung cancer
	Patient/ventilatory asynchrony
	Pleural effusion
	Pneumonia
	Pneumothorax
	Pulmonary embolism
	Chemotherapy toxicity
	Chest wall fractures related to metastatic disease
Cardiovascular	Congestive heart failure
	Fluid overload
	Superior vena cava syndrome
	Arrhythmias
	Cardiomyopathies
	Valvular or pericardial disease
	Congenital abnormalities
	Chemotherapy toxicity
Hematologic/Metabolic	Anemia
Hematologic/Metabolic	Electrolyte abnormalities
Neuromuscular	ALS
	Muscular dystrophy
	Multiple sclerosis
	Myasthenia gravis
	Reduced respiratory muscle force (deconditioning)
Psychological/Spiritual	Anxiety
	Depression
	Spiritual distress

ALS = amyotrophic lateral sclerosis; COPD = chronic obstructive pulmonary disease.

Scheduling of Opioids for the Management of Dyspnea ^{[1,41,60,80,81]}
	Opioid Naive*	Opioid Tolerant*
Mild dyspnea	Hydrocodone (5 to 10 mg) or codeine (30 mg) orally every 4 hours	Increase dose by 25% to 50%
Severe dyspnea	Morphine sulfate 5 mg orally every 4 hours, or oxycodone 5 mg orally every 4 hours, or hydromorphone 1 mg orally every 4 hours	Increase dose by 25% to 50%
Severe dyspnea	Parenteral morphine 2.5-5.0 mg subcutaneously or intravenously every 3-4 hours	Increase dose by 25% to 50%
Titration	Increase orally by increments of 50% to 100% every 24 hours as needed; titrate parenterally to effect	Increase by increments of 50% to 100% every 24 hours as needed

*If a patient is elderly or has severe pulmonary disease, such as COPD, start at 50% of the above doses and titrate more conservatively with increments of 25%. If the patient requires frequent dosing, the 24-hour total can be calculated and then converted into a sustained-release preparation, with the availability of a short-acting breakthrough dose every 2 hours as needed.

Benzodiazepine Therapy for the Management of Dyspnea ^[1,24]
Benzodiazepine	Dosage and Titration
Short-acting Formulations
Lorazepam	Starting dose: 0.5 to 1.0 mg orally every hour until the symptom is controlled, with routine dosing every 4-6 hours thereafter
Midazolam	Starting dose: 0.5mg IV every 15 minutes until dyspnea is controlled, then maintenance of a continuous subcutaneous or intravenous infusion
Long-acting Formulations
Diazepam	Starting dose: 2-10 mg orally every hour, then routinely every 6-8 hours
Clonazepam	Starting dose: 0.25-2.0 mg orally every 12 hours

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