O bstructive sleep apnea (OSA) is a common disorder that affects sleep and quality of life. Because many people with OSA cannot or will not comply with the standard treatment with a continuous positive airway pressure (CPAP) mask, alternative treatments have been sought. Upper-airway stimulation using unilateral stimulation of the hypoglossal nerve is a possible option. This multicenter, prospective, single-group, cohort trial and a follow-up randomized therapy-withdrawal trial were performed to evaluate the clinical safety and effectiveness of upper-airway stimulation for treating moderate to severe OSA.Patients who had difficulty accepting or adhering to CPAP treatment were included and served as their own controls. After initial screening, including polysomnography, qualified patients underwent surgery to implant the upper-airway stimulation system in which a stimulation electrode was placed on the hypoglossal nerve to recruit tongue-protrusion function. The sensing lead was placed between the internal and external intercostal muscles to detect ventilatory effort, and the neurostimulator was implanted in the right ipsilateral midinfraclavicular region. A month after implantation, patients had a second baseline diagnostic polysomnographic exam before the device was activated. Patients used a controller to initiate and stop therapy each night and then were assessed at 2, 3, 6, 9, and 12 months. The primary outcome was the change in the severity of OSA as determined by the apneahypopnea index (AHI; number of apnea or hypopnea events per hour; score ≥15 indicates moderate to severe OSA) and the O 2 desaturation index (ODI; number of times per hour of sleep that the blood O 2 level drops by ≥4 percentage points from baseline). At the 12-month assessment, a response to treatment was defined as an AHI reduction of 50% or greater from baseline and a score of less than 20 events per hour along with an ODI reduction of 25% or greater from baseline. The primary efficacy objectives were response rates of 50% or greater as assessed in the AHI and ODI. Secondary outcomes were the Epworth Sleepiness Scale, the Functional Outcomes of Sleep Questionnaire (FOSQ), and the percentage of sleep time with the O 2 saturation of less than 90%. Consecutive patients with a response were included in a randomized controlled therapywithdrawal trial in which they were assigned in a 1:1 ratio to either the therapy-maintenance or therapy-withdrawal group. The withdrawal group had the device turned off for 7 days; the maintenance group continued using the device. Polysomnography was done to measure the effects of withdrawal compared with continued use of therapy. Serious adverse events were those that led to death, lifethreatening illness, permanent impairment, or new or prolonged hospitalization with serious health impairment.Of the 126 participants, 83% were men; mean age was 54.5 years, and mean body mass index was 28.4 kg/m 2 . The mean AHI score on the initial screening polysomnography was 32.0 events per hour, and the mean ODI score was ...

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Regional cerebrovascular oxygen saturation, a quantitative measure of hemoglobin saturation in the combined arterial, venous, and microcirculatory compartments of the brain, can be measured noninvasively with near infrared spectroscopy. We assessed the sensitivity of this aggregate saturation to cerebral hypoxia during transient cerebral hypoxic hypoxia in seven human subjects. Regional cerebrovascular oxygen saturation measured over the middle frontal gyms and analog electroencephalogram were recorded. We compared the time to achieve two end points: the earliest paroxysmal burst of theta-delta background slowing and a cerebrovascular oxygen saturation of <55%. Saturation fell below 55% prior to the electroencephalographic change (/?<0.05). In a related effort, we also compared spectroscopically measured regional cerebrovascular oxygen saturation with an estimate of this value calculated from arterial and cerebral mixed venous saturation in nine patients. A positive linear relation (n=68, /f=0.55, s=4.2) was noted. (Stroke 1991^2:596-602)

Pressure gradients across and between the head and chest were studied during mechanical cardiopulmonary resuscitation (CPR) in 22 humans. Patients in medical cardiac arrest, managed by ACLS guidelines, underwent placement of aortic arch (Ao), jugular venous bulb (JVB), and right atrial (RA) catheters. Simultaneous pressures were measured, and intercatheter gradients were calculated. The JVB to RA pressure dilference is the gradient between the cervical and central venous circulations. It was negative when averaged throughout the CPR cycle and was more negative during compression than relaxation, -19±12 and -2±6 mm Hg, respectively. This indicates that the intrathoracic pressure rise was not transmitted to the jugular venous system, supporting the concept of a competent jugular valve mechanism during CPR. It is consistent with the thoracic pump model of cerebral perfusion. JVB to RA was positive only during early relaxation, allowing blood return from the head. The Ao to JVB gradient, although not equal to cerebral perfusion pressure, is the maximum potential pressure gradient for blood flow across the cerebral vasculature. It was positive throughout CPR, 25 + 17 during compression, and 9±10 mm Hg during relaxation. The Ao to RA gradient during the relaxation phase is CPR coronary perfusion pressure. In most patients, it was minimally positive in both phases of the CPR cycle: 7±14 in compression and 7±9 mm Hg during relaxation. This appears to be inadequate in providing sufficient blood flow to meet the metabolic needs of the myocardium. Four patients had larger gradients during compression suggestive of cardiac compression. We conclude that in most patients there are functional venous valves at the thoracic inlet and the potential for a thoracic pump mechanism for cerebral perfusion. A subset of patients may have direct cardiac compression. Thoracic and cardiac pump models of CPR are not mutually exclusive. (Circulation 1989:80:361-368) A fter the description of standard external cardiopulmonary resuscitation (CPR) by Kouwenhoven and associates,' forward flow was theorized to result from compression of the heart between the sternum and thoracic spine. More recent work by Rudikoff et al,2 Werner et al,3 Niemann et al,4'5 and others6 suggests that the thorax itself is the pump and that cerebral perfusion results from differential transmission of intrathoracic pressure to the carotid arterial and jugular venous systems. The lower peripheral venous pressure is thought to result from a valve located between the intrathoracic and extrathoracic veins.2 4 7 8 Because both sides of the coronary circulation are within the chest, this cannot be the basis of myocardial perfusion.9 Other work in animal models has indicated that blood flow across the heart is the result of cardiac compression and appropriate valve function,10'1' a cardiac pump mechanism, but this has not been the case in the few patients evaluated by echocardiography during CPR.3 Most studies into the mechanisms of blood flow and the magnitude of perfusion...