The respiratory system consists of the lungs and chest wall and has two functions: ventilation and gas exchange. Ventilation refers to the movement of air into and out of the lungs and is required for effective gas exchange. Ventilation requires the synchronized activities of both nervous and muscle tissue. The muscles of respiration (and their innervation) are typically divided into the inspiratory group (diaphragm [C3-C5], external intercostals [T1-T12], and scalenes [C4-C8]) and the expiratory group (abdominals [T7-L1] and internal intercostals [T1-T12]). During quiet breathing, the inspiratory muscles are active, with the diaphragm generating most of the tidal volume, and expiration is predominantly passive. When quiet breathing is unable to keep pace with the metabolic demands of the body (e.g., during exercise or respiratory muscle failure), the accessory muscles of inspiration (trapezii, sternocleidomastoids, serrati, pectorals, levator scapulae, and the costal levators) are recruited and expiration becomes active; thus, ventilation increases.

All levels of the neuraxis are involved in respiration, and for the most part, it occurs without voluntary effort (i.e., it is automatic). Automatic respiration occurs via two neuronal groups located within the brain stem: one is situated near the floor of the fourth ventricle (the medullary center), and the other is located within the pons (the pontine pneumotaxic center). The medullary neurons have inherent automaticity, and the pontine neurons help coordinate the cyclical respirations. Through synapses with motor neurons innervating respiratory muscles, these neurons are responsible for spontaneous respiration. Voluntary respiration, which involves corticospinal tract innervation of the same respiratory motor neurons, can override automatic breathing. Under normal circumstances, respiratory regulation reflects the PaCO 2 and pH and, to a lesser extent, the PaO2 . Chemoreceptors within the carotid and aortic bodies transmit this information to the respiratory centers in the brain stem (via cranial nerves IX and X, respectively), and respiration is adjusted accordingly.

The term hypoxic encephalopathy refers to the neurological findings resulting from impaired gas exchange or ventilation (e.g., anoxic anoxia, anemic anoxia, and histotoxic anoxia) and differs from the term hypoxic-ischemic encephalopathy, which refers to neurological dysfunction related to cerebral hypoperfusion (i.e., ischemic anoxia). With hypoxic-ischemic encephalopathy, in addition to hypoxia, there is loss of substrate (e.g., glucose) and impaired waste removal. Anoxic anoxia refers to reduced arterial partial pressure of O 2 (e.g., at high altitudes), whereas anemic anoxia relates to reduced hemoglobin availability for O 2 transport (e.g., in anemia and carbon monoxide intoxication). Histotoxic anoxia occurs when, in the setting of adequate O 2 availability, the tissue's ability to use O 2 is impaired (e.g., cyanide toxicity).

Pathogenesis and Pathophysiology. Ventilatory failure results in hypercapnia as well as hypoxemia, a combination that causes cerebral vasodilation, increased cerebral blood flow (CBF), and occasionally, increased ICP. Although hypoxemia probably contributes to the observed neurological features, the degree of CO 2 retention is more closely correlated. y Acute, moderate hypercapnia (5 to 10 percent CO2 in the inspired air) increases arousal and excitability. At higher levels of CO 2 , an anesthetic effect occurs, followed by a convulsant effect at the highest levels. y , y Because CO2 freely crosses the blood-brain barrier (BBB), thereby producing a cerebrospinal fluid (CSF) acidosis, respiratory acidosis is more neurologically disabling than is metabolic acidosis. Fortunately, several compensatory mechanisms exist to enhance the nervous system's tolerability of respiratory insufficiency. The CNS compensates by increasing O 2 extraction, CO2 release, and CBF. These processes arise in conjunction with systemic alterations at the level of the kidney and with polycythemia. y Should compensatory mechanisms fail, hypoxia, hypercapnia, and acidosis develop and produce neurological sequelae. Sustained hypoxia produces brain edema and cell death, abnormalities that can precipitate cardiac arrhythmias and hypotension. Again, isolated hypoxic encephalopathy is seldom seen in humans. y

Clinical Features and Associated Disorders. Pulmonary disease causes both hypoxemia and hypercapnia, and distinguishing which neurological features are related to which state is difficult. The clinical features observed reflect the body's ability to compensate and the acuteness of the situation. The neurological manifestations are most closely related to the rapidity of onset and degree of hypercapnia, although hypoxia and cerebral edema may also contribute. y Compensatory mechanisms may render individuals asymptomatic, even in the setting of significant degrees of hypoxia and hypercapnia. When these mechanisms cannot keep pace, clinical features of respiratory insufficiency manifest. Initially, patients with respiratory insufficiency may complain of sleep disturbances, daytime somnolence, and early morning headache, a reflection of nocturnal hypoventilation with resultant CO 2 retention and vasodilation; however, these symptoms are nonspecific and can occur with CHF or respiratory muscle weakness. y Mental status changes are common early and include drowsiness, forgetfulness, and inattentiveness. Later, lethargy, obtundation, and coma may appear. y Tremor and asterixis are frequently seen, whereas myoclonus and seizures are uncommon and are observed only with severe and prolonged respiratory insufficiency. y Tendon reflexes may be brisk or depressed, upper motor neuron features may be present, and papilledema occurs in up to 10 percent of patients. y

Differential Diagnosis and Evaluation. Respiratory impairment may be caused by dysfunction of gas exchange or ventilation (...Xa„bie.. .3.8-6.). Differentiation between these


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