CONTROL OF BREATHING IN DISEASE STATES



Disordered respiratory control usually accom­panies other states and rarely in itself constitutes an independent clinical disorder.
Chronic Obstructive Pulmonary Disease (COPD). Patients with physiologically significant COPD have a reduced ventilatory response to hy­poxia and hypercapnia. While this was formerly thought to be entirely due to decreased chemo­sensitivity of the respiratory centers, most of these patients display an increased resting respiratory center drive. In hypercapnic patients this height­ened respiratory drive fails to translate into a suf­ficiently increased minute ventilation to maintain a normal Pco2 owing to the increased work of breathing and marked ventilation-perfusion mis­match. The level of hypercapnia is related in gen­eral to the degree of obstruction, although lung mechanics, resting respiratory drive, and the pat­tern of breathing are often similar in patients with and without C02 retention . Develop­ment of hypercapnia depends on poorly under­stood interactions of inherited respiratory drive, peripheral sensory receptor stimulation, associ­ated hypoxemia, degree of ventilation-perfusion mismatching, and the metabolic milieu.

Asthma. Patients with acute asthma display hy­perventilation and hypocapnia, presumably due to stimulation of lung sensory receptors. C02 re­tention is a late finding in the progression of a severe asthmatic attack. Indeed, eucapnia, rather than the expected hypocapnia, is a warning sign of impending deterioration.

Other disorders in which abnormal peripheral sensory receptor stimulation is thought to result in an increased respiratory drive with resultant dyspnea, tachypnea, and hypocapnia include re­strictive lung disease, pulmonary vascular dis­ease, and abnormalities of the chest wall.

Central Hypoventilation. This may occur sec­ondary to brain stem involvement by tumor, is­chemia, or inflammatory disease; a primary, idi­opathic form has also been described. Patients display decreased chemosensitivity, often with resting hypercapnia and cor pulmonale. Rarely the impairment of chemosensitivity may be so se­vere that the patient breathes adequately only when stimulated by wakefulness but hypoventi-lates and becomes apneic during sleep, when ros­tral neural influences are removed.
Obesity-Hypoventilation Syndrome. Some patients with obesity display chronic hypoven­tilation with hypoxia, hypercapnia, reduced chemosensitivity, and cor pulmonale. The hypo­ventilation may partly reflect the response to the increased load of fatty tissue on the chest wall, al­though hypoventilation is not directly related to the degree of obesity. Independent neural factors, yet undefined, are probably important. A sub­group called pickwickian have obesity, daytime hypoventilation, hypersomnolence, polycythe­mia, and cor pulmonale. All patients with the pickwickian syndrome probably have sleep apnea.

Breathing Pattern Abnormalities Associated with neurological Disease. Central neurogenic hyperventilation has been considered a charac­teristic feature of lower brain stem and upper pon­tine disease. Rarely is it an isolated finding, as most patients display associated pulmonary com­plications that could reflexly stimulate the res­piratory center through hypoxia or activation of intrapulmonary sensory receptors. Apneustic breathing consists of sustained inspiratory pauses, localizing damage to the mid pons, most commonly due to a basilar artery infarct. Biot’s or ataxic breathing, a haphazard random distribution of deep and shallow breaths, is caused by disrup­tion of the respiratory rhythm generator in the medulla.

Cheyne-Stokes respiration is characterized by regular cycles of crescendo-decrescendo changes in tidal volume separated by apneic or hypopneic pauses. Many affected patients have evidence of cardiac or neurological disease. In patients with cardiac disease the disturbance arises because of prolongation of the circulation time, which delays transmission of information concerning arterial Po2 and Pco2 to the respiratory centers, thus lead­ing to system instability with resulting oscilla­tions in tidal volume. It has no localizing value in patients with neurological disease but has gen­erally been considered to be an ominous sign. While this is sometimes the case, many patients display subtle evidence of Cheyne-Stokes respi­ration, especially during sleep, without serious consequences, and it is not an uncommon finding in otherwise normal elderly subjects.

Neuromuscular Disease. Respiratory center function is poorly defined in neuromuscular dis­ease. Decreased ventilatory capacity may result from impaired neural output or poor translation of this neural output into respiratory muscle con­traction. Typically, the patients display an in­creased respiratory rate and inability to take deep breaths, with consequent susceptibility to atelec­tasis. Paradoxical motion of the rib cage and ab­domen is commonly observed. Typical causes include inflammatory polyneuropathy, amyo­trophic lateral sclerosis, myasthenia gravis, and poliomyelitis. The features of diaphragmatic para­lysis are discussed in Chapter 26.