Surges of muscle sympathetic nerve activity during obstructive apnea are linked to hypoxemia.

Obstructive sleep apnea (OSA) is associated with oscillations of arterial blood pressure (BP) that occur in phase with irregularities of respiration. To explore the role of the sympathetic nervous system in these responses, we studied muscle sympathetic nerve activity (MSNA; peroneal microneurography), an index of vasoconstrictor nerve traffic, and BP during awake regular breathing and during spontaneous apneas in patients with OSA. To determine the role of the arterial chemoreflex, we also examined the effects of 100% O2 (hyperoxia) on MSNA and BP. In awake regularly breathing patients with OSA (n = 12), resting MSNA was markedly higher than in an age-matched control population (n = 15) [41 +/- 23 (SD) vs. 24 +/- 17 bursts/min; P < 0.05] and was unchanged during hyperoxia (n = 9). Apneas during sleep (n = 8) were associated with surges in MSNA followed by transient rises in BP when breathing resumed. In contrast to room air apneas, hyperoxic apneas of similar duration were associated with attenuated MSNA responses (+82 +/- 84% vs. +5 +/- 25% compared with awake baseline; P < 0.05; n = 6), even though O2 did not affect sleep stage and the occurrence of arousal. Thus the BP oscillations that occur with apnea during sleep may in part be mediated by intermittent surges of sympathetic activity resulting in vasoconstriction. Because the MSNA responses to obstructive apnea are blunted during O2 administration, they appear to be linked to intermittent arterial hypoxemia and stimulation of arterial chemoreceptors.

Ventilatory pattern after hypoxic stimulation during wakefulness and NREM sleep.

The ventilatory after-discharge mechanism (VAD) may stabilize ventilation (VE) after hyperventilation but has not been studied in detail in humans. Several studies conducted during wakefulness suggest that VAD is present, although none has been conducted during sleep, when disordered ventilation is most common. We conducted two experiments during wakefulness and non-rapid-eye-movement (NREM) sleep in 14 healthy young men to characterize the ventilatory response after termination of a 45- to 60-s 10-12% O2 hypoxic stimulus. Eight subjects had triplicate hypoxic trials terminated by 100% O2 during wakefulness and NREM sleep. Hypoxia caused a drop in arterial O2 saturation to 78.5 +/- 0.5%, an increase in VE of 4.4 +/- 0.6 l/min, and a decrease in end-tidal PCO2 of 4.4 +/- 0.4 Torr during wakefulness, with no significant differences during sleep. When the hypoxia was terminated with 100% O2, VE was variable within and between subjects during wakefulness. During sleep, all subjects developed hypopnea (VE < 67% baseline) with a mean decrease of 65.5 +/- 7.8% at the onset of hyperoxia (P < 0.05 compared with baseline VE). We hypothesized that this uniform decrease in VE might be due to the nonphysiological hyperoxia employed. We therefore studied six additional subjects, all during NREM sleep, with identical hypoxic stimulation of breathing terminated by 100% O2 or room air. We again found that termination of hypoxia with 100% O2 produced uniform hypoventilation. However, when the identical stimulus was terminated with room air, no hypoventilation occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Dyspnea in the patient with chronic obstructive pulmonary disease. Etiology and management.

We have summarized much of the known information regarding the pathogenesis of dyspnea in the COPD patient and have reviewed a great many of the therapeutic options that have been investigated. It should be obvious that we are really in the early stages of our understanding about this symptom, and that we know very little about how to decide which treatment options are likely to succeed in any individual. At this time, there is no substitute for a careful assessment of each treatment modality that is instituted using a measurement tool, and the value of a comprehensive assessment as outlined cannot be overemphasized.

The medical evaluation of elderly patients with major depression.

Elderly patients hospitalized for management of major depression frequently have an extensive medical evaluation to determine if physical illness is masquerading as, or serving as the precipitating event for, the depression. The purpose of this study was to determine the incidence of newly discovered medical problems and the yield of various diagnostic modalities in such elderly depressed patients. Of 100 depressed geropsychiatric inpatients, the most frequent new diagnoses included: electrolyte abnormalities (6 patients), bacteriuria (13), medication reactions (7), exacerbation of previous thyroid disease (6), new thyroid function abnormalities (3), and renal failure, Parkinson's Disease, and chronic obstructive lung disease (2 each). One patient had a cerebellar hemangioblastoma, and 4 had acute illnesses. A workup including CBC, blood chemistries, urinalysis, and thyroid function tests frequently yielded abnormal results. When used as screening tests, head CT scanning, electroencephalography, and chest radiography did not affect management. We conclude that elderly depressed patients have a high prevalence of undiscovered physical illnesses, but that history, physical examination, and simple laboratory evaluation may be sufficient to guide their workups.