Effect of surfactant on pharyngeal mechanics in sleeping humans: implications for sleep apnoea.

Instillation of surfactant into the pharyngeal lumen reduces the pressure required to reopen an occluded airway, and decreases the apnoea/hypopnoea index (AHI). The authors hypothesised that surfactant also reduces the sleep-related increase in pharyngeal resistance. To test this hypothesis two single blind, crossover, placebo-controlled studies were performed. In protocol A seven male, asymptomatic snoring subjects were studied during sleep. Inspiratory pharyngeal resistance was calculated from plots of airflow versus supraglottic pressure (seven breaths) before and after surfactant or saline instillation. In protocol B, in a different group of seven male subjects with sleep apnoea (AHI 15.2 (12) events x h(-1)) the effect of surfactant or saline on sleep disordered breathing was measured, for 1 h immediately before and after surfactant or saline instillation. Surfactant decreased pharyngeal resistance calculated at peak pressure (group mean (SD): pre versus post 83.7 (76.4) versus 49.4 (71.1) cmH2O x L(-1) x s(-1)) and significantly reduced the respiratory disturbance index (RDI pre versus post 79.7 (58.7) versus 59.6 (56.9) events x h(-1)). Saline did not decrease resistance (pre versus post 58.6 (31.1) versus 72.5 (73.4) cmH2O x L(-1) x s(-1)) or RDI (pre versus post 75.3 (42.4) versus 79.9 (46.1) events x h(-1)). Surfactant reduced the collapsibility of the pharynx and led to a modest reduction in respiratory disturbance index. The authors speculate that surfactant may delay occlusion by reducing the liquid "bridging" within the folded pharyngeal lining.

Exposure to hypoxia produces long-lasting sympathetic activation in humans.

The relative contributions of hypoxia and hypercapnia in causing persistent sympathoexcitation after exposure to the combined stimuli were assessed in nine healthy human subjects during wakefulness. Subjects were exposed to 20 min of isocapnic hypoxia (arterial O(2) saturation, 77-87%) and 20 min of normoxic hypercapnia (end-tidal P(CO)(2), +5.3-8.6 Torr above eupnea) in random order on 2 separate days. The intensities of the chemical stimuli were manipulated in such a way that the two exposures increased sympathetic burst frequency by the same amount (hypoxia: 167 +/- 29% of baseline; hypercapnia: 171 +/- 23% of baseline). Minute ventilation increased to the same extent during the first 5 min of the exposures (hypoxia: +4.4 +/- 1.5 l/min; hypercapnia: +5.8 +/- 1.7 l/min) but declined with continued exposure to hypoxia and increased progressively during exposure to hypercapnia. Sympathetic activity returned to baseline soon after cessation of the hypercapnic stimulus. In contrast, sympathetic activity remained above baseline after withdrawal of the hypoxic stimulus, even though blood gases had normalized and ventilation returned to baseline levels. Consequently, during the recovery period, sympathetic burst frequency was higher in the hypoxia vs. the hypercapnia trial (166 +/- 21 vs. 104 +/- 15% of baseline in the last 5 min of a 20-min recovery period). We conclude that both hypoxia and hypercapnia cause substantial increases in sympathetic outflow to skeletal muscle. Hypercapnia-evoked sympathetic activation is short-lived, whereas hypoxia-induced sympathetic activation outlasts the chemical stimulus.

Effect of hypoxia on the hypopnoeic and apnoeic threshold for CO(2) in sleeping humans.

1. Rhythmic breathing during sleep requires that P(CO2) be maintained above a sensitive hypocapnic apnoeic threshold. Hypoxia causes periodic breathing during sleep that can be prevented or eliminated with supplemental CO(2). The purpose of this study was to determine the effect of hypoxia in changing the difference between the eupnoeic P(CO2) and the P(CO2) required to produce hypopnoea or apnoea (hypopnoea/apnoeic threshold) in sleeping humans. 2. The effect of hypoxia on eupnoeic end-tidal partial pressure of CO(2) (P(ET,CO2)) and hypopnoea/apnoeic threshold P(ET,CO2) was examined in seven healthy, sleeping human subjects. A bilevel pressure support ventilator in a spontaneous mode was used to reduce P(ET,CO2) in small decrements by increasing the inspiratory pressure level by 2 cmH2O every 2 min until hypopnoea (failure to trigger the ventilator) or apnoea (no breathing effort) occurred. Multiple trials were performed during both normoxia and hypoxia (arterial O(2) saturation, S(a,O2) = 80 %) in a random order. The hypopnoea/apnoeic threshold was determined by averaging P(ET,CO2) of the last three breaths prior to each hypopnoea or apnoea. 3. Hypopnoeas and apnoeas were induced in all subjects during both normoxia and hypoxia. Hypoxia reduced the eupnoeic P(ET,CO2) compared to normoxia (42.4 +/- 1.3 vs. 45.0 +/- 1.1 mmHg, P < 0.001). However, no change was observed in either the hypopnoeic threshold P(ET,CO2) (42.1 +/- 1.4 vs. 43.0 +/- 1.2 mmHg, P > 0.05) or the apnoeic threshold P(ET,CO2) (41.3 +/- 1.2 vs. 41.6 +/- 1.0 mmHg, P > 0.05). Thus, the difference in P(ET,CO2) between the eupnoeic and threshold levels was much smaller during hypoxia than during normoxia (-0.2 +/- 0.2 vs. -2.0 +/- 0.3 mmHg, P < 0.01 for the hypopnoea threshold and -1.1 +/- 0.2 vs. -3.4 +/- 0.3 mmHg, P < 0.01 for the apnoeic threshold). We concluded that hypoxia causes a narrowing of the difference between the baseline P(ET,CO2) and the hypopnoea/apnoeic threshold P(ET,CO2), which could increase the likelihood of ventilatory instability.

Longitudinal study of moderate weight change and sleep-disordered breathing.

CONTEXT: Excess body weight is positively associated with sleep-disordered breathing (SDB), a prevalent condition in the US general population. No large study has been conducted of the longitudinal association between SDB and change in weight. OBJECTIVE: To measure the independent longitudinal association between weight change and change in SDB severity. DESIGN: Population-based, prospective cohort study conducted from July 1989 to January 2000. SETTING AND PARTICIPANTS: Six hundred ninety randomly selected employed Wisconsin residents (mean age at baseline, 46 years; 56% male) who were evaluated twice at 4-year intervals for SDB. MAIN OUTCOME MEASURES: Percentage change in the apnea-hypopnea index (AHI; apnea events + hypopnea events per hour of sleep) and odds of developing moderate-to-severe SDB (defined by an AHI > or =15 events per hour of sleep), with respect to change in weight. RESULTS: Relative to stable weight, a 10% weight gain predicted an approximate 32% (95% confidence interval [CI], 20%-45%) increase in the AHI. A 10% weight loss predicted a 26% (95% CI, 18%-34%) decrease in the AHI. A 10% increase in weight predicted a 6-fold (95% CI, 2.2-17.0) increase in the odds of developing moderate-to-severe SDB. CONCLUSIONS: Our data indicate that clinical and public health programs that result in even modest weight control are likely to be effective in managing SDB and reducing new occurrence of SDB.

Neurocirculatory consequences of intermittent asphyxia in humans.

We examined the neurocirculatory and ventilatory responses to intermittent asphyxia (arterial O(2) saturation = 79-85%, end-tidal PCO(2) =3-5 Torr above eupnea) in seven healthy humans during wakefulness. The intermittent asphyxia intervention consisted of 20-s asphyxic exposures alternating with 40-s periods of room-air breathing for a total of 20 min. Minute ventilation increased during the intermittent asphyxia period (14.2 +/- 2.0 l/min in the final 5 min of asphyxia vs. 7.5 +/- 0.4 l/min in baseline) but returned to the baseline level within 2 min after completion of the series of asphyxic exposures. Muscle sympathetic nerve activity increased progressively, reaching 175 +/- 12% of baseline in the final 5 min of the intervention. Unlike ventilation, sympathetic activity remained elevated for at least 20 min after removal of the chemical stimuli (150 +/- 10% of baseline in the last 5 min of the recovery period). Intermittent asphyxia caused a small, but statistically significant, increase in heart rate (64 +/- 4 beats/min in the final 5 min of asphyxia vs. 61 +/- 4 beats/min in baseline); however, this increase was not sustained after the return to room-air breathing. These data demonstrate that relatively short-term exposure to intermittent asphyxia causes sympathetic activation that persists after removal of the chemical stimuli. This carryover effect provides a potential mechanism whereby intermittent asphyxia during sleep could lead to chronic sympathetic activation in patients with sleep apnea syndrome.

Prospective study of the association between sleep-disordered breathing and hypertension.

BACKGROUND: Sleep-disordered breathing is prevalent in the general population and has been linked to chronically elevated blood pressure in cross-sectional epidemiologic studies. We performed a prospective, population-based study of the association between objectively measured sleep-disordered breathing and hypertension (defined as a laboratory-measured blood pressure of at least 140/90 mm Hg or the use of antihypertensive medications). METHODS: We analyzed data on sleep-disordered breathing, blood pressure, habitus, and health history at base line and after four years of follow-up in 709 participants of the Wisconsin Sleep Cohort Study (and after eight years of follow-up in the case of 184 of these participants). Participants were assessed overnight by 18-channel polysomnography for sleep-disordered breathing, as defined by the apnea-hypopnea index (the number of episodes of apnea and hypopnea per hour of sleep). The odds ratios for the presence of hypertension at the four-year follow-up study according to the apnea-hypopnea index at base line were estimated after adjustment for base-line hypertension status, body-mass index, neck and waist circumference, age, sex, and weekly use of alcohol and cigarettes. RESULTS: Relative to the reference category of an apnea-hypopnea index of 0 events per hour at base line, the odds ratios for the presence of hypertension at follow-up were 1.42 (95 percent confidence interval, 1.13 to 1.78) with an apnea-hypopnea index of 0.1 to 4.9 events per hour at base line as compared with none, 2.03 (95 percent confidence interval, 1.29 to 3.17) with an apnea-hypopnea index of 5.0 to 14.9 events per hour, and 2.89 (95 percent confidence interval, 1.46 to 5.64) with an apnea-hypopnea index of 15.0 or more events per hour. CONCLUSIONS: We found a dose-response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors. The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population.

Role of respiratory motor output in within-breath modulation of muscle sympathetic nerve activity in humans.

We measured muscle sympathetic nerve activity (MSNA, peroneal microneurography) in 5 healthy humans under conditions of matched tidal volume, breathing frequency, and end-tidal CO(2), but varying respiratory motor output as follows: (1) passive positive pressure mechanical ventilation, (2) voluntary hyperventilation, (3) assisted mechanical ventilation that required the subject to generate -2.5 cm H(2)O to trigger each positive pressure breath, and (4) added inspiratory resistance. Spectral analyses showed marked respiratory periodicities in MSNA; however, the amplitude of the peak power was not changed with changing inspiratory effort. Time domain analyses showed that maximum MSNA always occurred at end expiration (25% to 30% of total activity) and minimum activity at end inspiration (2% to 3% of total activity), and the amplitude of the variation was not different among conditions despite marked changes in respiratory motor output. Furthermore, qualitative changes in intrathoracic pressure were without influence on the respiratory modulation of MSNA. In all conditions, within-breath changes in MSNA were inversely related to small changes in diastolic pressure (1 to 3 mm Hg), suggesting that respiratory rhythmicity in MSNA was secondary to loading/unloading of carotid sinus baroreceptors. Furthermore, at any given diastolic pressure, within-breath MSNA varied inversely with lung volume, demonstrating an additional influence of lung inflation feedback on sympathetic discharge. Our data provide evidence against a significant effect of respiratory motor output on the within-breath modulation of MSNA and suggest that feedback from baroreceptors and pulmonary stretch receptors are the dominant determinants of the respiratory modulation of MSNA in the intact human.

Daytime blood pressure elevation after nocturnal hypoxia.

The purpose of this study was to investigate whether nocturnal hypoxia causes daytime blood pressure (BP) elevation. We hypothesized that overnight exposure to hypoxia leads the next morning to elevation in BP that outlasts the hypoxia stimulus. We studied the effect on BP of two consecutive night exposures to hypobaric hypoxia in 10 healthy normotensive subjects. During the hypoxia nights, subjects slept for 8 h in a hypobaric chamber at a simulated altitude of 4,000 m (barometric pressure = 462 mmHg). Arterial O(2) saturation and electrocardiogram were monitored throughout the night. For 30 min before the nocturnal simulated ascent and for 4 h after return to baseline altitude the next morning, BP was measured every 5 min while the subject was awake. The same measurements were made before and after 2 normoxic nights of sleep in the hypobaric chamber at ambient barometric pressure (745 mmHg). Principal components analysis was applied to evaluate patterns of BP response after the second night of hypoxia and normoxia. A distinct pattern of diastolic BP (DBP) elevation was observed after the hypoxia night in 9 of the 10 subjects but in none after the normoxia night. This pattern showed a mean increase of 4 mmHg in DBP compared with the presleep-awake baseline in the first 60 min and a return to baseline by 90 min. We conclude that nocturnal hypoxia leads to a carryover elevation of daytime DBP.

Non-chemical inhibition of respiratory motor output during mechanical ventilation in sleeping humans.

1. To determine the magnitude and time course of changes in respiratory motor output caused by non-chemical influences, six sleeping subjects underwent assist-control mechanical ventilation (ACMV) at increased tidal volume (VT). During ACMV, end-tidal PCO2 (PET,CO2) was either held at normocapnic levels (PET,CO2, 0.6-1.1 mmHg > control) by adding CO2 to the inspirate, or it was allowed to fall (hypocapnia). 2. Each sleeping subject underwent several repeat trials of twenty-five ACMV breaths (VT, 1.3 or 2.1 times control; peak flow rate, 30-40 l min-1; inspiratory time, +/- 0.3 s of control). The end-tidal to arterial PCO2 difference throughout normocapnic ACMV at raised VT was unchanged from eupnoeic levels during studies in wakefulness. 3. Normocapnic ACMV at both the smaller and larger increases in VT decreased the amplitude of respiratory motor output, as judged by decreased maximum rate of rise of mask pressure (Pm) (mean dPm/dtmax, 46-68% of control), reduced diaphragmatic EMG (to 55% of control) and reduced VT on the first spontaneous breath after ACMV (to 70% of control). Expiratory time (TE) was slightly prolonged (13-32% > control). This inhibition of amplitude of respiratory motor output progressed over the first five to seven ventilator cycles, was maintained over the remaining 18-20 cycles and persisted for three to five spontaneous breaths immediately following cessation of ACMV. 4. Hypocapnia did not further inhibit respiratory motor output amplitude beyond the effect of normocapnic ACMV at high VT, but did cause highly variable prolongation of TE when PET,CO2 was reduced by greater than 3 mmHg for at least five ventilator cycles. 5. These data in sleeping humans support the existence of a significant, non-chemical inhibitory influence of ACMV at increased VT and positive pressure upon the amplitude of respiratory motor output; this effect is manifested both during and following normocapnic mechanical ventilation.

Arousal from sleep shortens sympathetic burst latency in humans.

1. Bursts of sympathetic activity in muscle nerves are phase-locked to the cardiac cycle by the sinoaortic baroreflexes. Acoustic arousal from non-rapid eye movement (NREM) sleep reduces the normally invariant interval between the R-wave of the electrocardiogram (ECG) and the peak of the corresponding sympathetic burst; however, the effects of other forms of sleep disruption (i.e. spontaneous arousals and apnoea-induced arousals) on this temporal relationship are unknown. 2. We simultaneously recorded muscle sympathetic nerve activity in the peroneal nerve (intraneural electrodes) and the ECG (surface electrodes) in seven healthy humans and three patients with sleep apnoea syndrome during NREM sleep. 3. In seven subjects, burst latencies were shortened subsequent to spontaneous K complexes (1.297 +/- 0.024 s, mean +/- s. e.m.) and spontaneous arousals (1.268 +/- 0.044 s) compared with latencies during periods of stable NREM sleep (1.369 +/- 0.023 s). In six subjects who demonstrated spontaneous apnoeas during sleep, apnoea per se did not alter burst latency relative to sleep with stable electroencephalogram (EEG) and breathing (1.313 +/- 0.038 vs. 1.342 +/- 0.026 s); however, following apnoea-induced EEG perturbations, burst latencies were reduced (1.214 +/- 0.034 s). 4. Arousal-induced reduction in sympathetic burst latency may reflect a temporary diminution of baroreflex buffering of sympathetic outflow. If so, the magnitude of arterial pressure perturbations during sleep (e.g. those caused by sleep disordered breathing and periodic leg movements) may be augmented by arousal.

An induced blood pressure rise does not alter upper airway resistance in sleeping humans.

Sleep apnea is associated with episodic increases in systemic blood pressure. We investigated whether transient increases in arterial pressure altered upper airway resistance and/or breathing pattern in nine sleeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nose or face mask. During non-rapid-eye-movement sleep, we injected 40- to 200-microgram i.v. boluses of phenylephrine. Parasympathetic blockade was used if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 +/- 5 (mean +/- SD) mmHg (range 12-37 mmHg) within 12 s and remained elevated for 105 s. There were no significant changes in inspiratory or expiratory pharyngeal resistance (measured at peak flow, peak pressure, 0.2 l/s or by evaluating the dynamic pressure-flow relationship). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20-25 s. At 26 s after peak MAP, tidal volume fell by 19%, consistent with hypocapnic ventilatory inhibition. We conclude that transient increases in MAP of a magnitude commonly observed during non-rapid-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.

Blood pressure perturbations caused by subclinical sleep-disordered breathing.

We studied the acute effects of apneas and hypopneas on blood pressure in a nonclinic population of middle-aged adults. Arterial pressure was measured noninvasively (photoelectric plethysmography) during an overnight, in-laboratory polysomnographic study in 72 men and 23 women enrolled in the Wisconsin Sleep Cohort Study, a population-based study of sleep-disordered breathing. Sleep-disordered breathing events (272 apneas and 1469 hypopneas) were observed in 92% of subjects. The across-subject mean decreases in arterial O2 saturation were 9+/-8% (SD) for apneas (17+/-8 seconds duration) and 4+/-3% for hypopneas (21+/-6 seconds duration; 41+/-17% of baseline ventilation). In both apneas and hypopneas, even those with only 1% to 3% O2 desaturations, blood pressure decreased during the event, followed by an abrupt increase in the postevent recovery period. Mean values for peak changes in blood pressure (difference between the maximum during the recovery period and the minimum during the event) were 23+/-10 mm Hg for systolic and 13+/-6 mm Hg for diastolic pressure. The strongest predictors of the pressor responses to apneas and hypopneas were (in order of importance): magnitude of the ventilatory overshoot, length of the event, magnitude of changes in heart rate and arterial O2 saturation, and presence or absence of electroencephalographic arousal. We speculate that these fluctuations may play a role in the pathogenesis of hypertension in individuals with subclinical sleep-disordered breathing.

Ventilatory response to induced auditory arousals during NREM sleep.

Sleep state instability is a potential mechanism of central apnea/hypopnea during non-rapid eye movement (NREM) sleep. To investigate this postulate, we induced brief arousals by delivering transient (0.5 second) auditory stimuli during stable NREM sleep in eight normal subjects. Arousal was determined according to American Sleep Disorders Association (ASDA) criteria. A total of 96 trials were conducted; 59 resulted in cortical arousal and 37 did not result in arousal. In trials associated with arousal, minute ventilation (VE) increased from 5.1 +/- 1.24 minutes to 7.5 +/- 2.24 minutes on the first posttone breath (p = 0.001). However, no subsequent hypopnea or apnea occurred as VE decreased gradually to 4.8 +/- 1.5 l/minute (p > 0.05) on the fifth posttone breath. Trials without arousal did not result in hyperpnea on the first breath nor subsequent hypopnea. We conclude that 1) auditory stimulation resulted in transient hyperpnea only if associated with cortical arousal; 2) hypopnea or apnea did not occur following arousal-induced hyperpnea in normal subjects; 3) interaction with fluctuating chemical stimuli or upper airway resistance may be required for arousals to cause sleep-disordered breathing.

Effect of induced hypocapnic hypopnea on upper airway patency in humans during NREM sleep.

We wished to determine the effect of reduced ventilatory drive (hypopnea) on upper airway patency in humans during non-rapid-eye-movement (NREM) sleep. We studied nine subjects (58 trials) spanning the spectrum of susceptibility to upper airway collapse including normals, snorers and patients with mild sleep apnea. Hypocapnic hypopnea was induced by abrupt cessation of brief (1 min) nasal mechanical hyperventilation. Surface inspiratory EMG (EMGinsp) was used as an index of drive. Upper airway resistance and supraglottic pressure-flow plots were used as indexes of upper airway patency. Termination of nasal mechanical ventilation resulted in reduced VE to 4904 of pre-mechanical ventilation eupneic control. Upper airway resistance at a fixed flow did not change significantly in inspiration or expiration. Likewise, pressure-flow plots showed no increase in upper airway resistance except in one subject. However, maximum flow (Vmax) decreased during hypopnea in four subjects who demonstrated inspiratory flow-limitation (IFL) during eupneic control. In contrast, no IFL was noted in subjects who showed no evidence of IFL during eupnea. We concluded: (1) Reduced ventilatory drive does not compromise upper airway patency in normal subjects during NREM sleep; (2) the reduction in Vmax during hypopnea in subjects with IFL during eupneic control, suggests that reduced drive is associated with increased upper airway compliance in these subjects; and (3) upper airway susceptibility to narrowing/closure is an important determinant of the response to induced hypopnea during NREM sleep.

Programs and services to prevent pregnancy, childbearing, and poor birth outcomes among adolescents in rural areas of the southeastern United States.

PURPOSE: To illustrate how rural adolescents' needs for pregnancy prevention and improved birth outcomes are currently being addressed, and to suggest strategies for future programs. METHODS: Local and state-level informants knowledgeable about services to adolescents in the Southeastern United States were identified. Semistructured interviews were used to determine the program start date and time frame, funding sources, target population, participating counties, implementing agency or organization, specific program services, and status of program activities. These programs were categorized by the type of services offered and the population targeted. RESULTS: The most common adolescent services in the rural Southeast attempt either to improve life options of youth, reduce sexual activity, or provide prenatal and postnatal care. Unlike urban areas where there are a variety of family planning providers, in the rural Southeast, health departments are the primary source of family planning for adolescents. There are no abortion providers in most rural areas of the Southeast. The majority of rural programs that include adolescents among the population served are developed for all women rather than specifically for adolescents. Programs specific to rural adolescents are described. CONCLUSIONS: The majority of programs in the rural Southeast address only selected adolescent health issues. Successful interventions require locally supported, multipronged, intensive approaches with consistent messages targeted to high-risk populations. Evaluation tools are needed to determine the effectiveness of each component of prevention programs.

The impact of Mississippi's mandatory delay law on abortions and births.

CONTEXT: Beginning August 8, 1992, a woman in the state of Mississippi had to wait 24 hours after in-person receipt of state-mandated information regarding abortion and birth complications, fetal development, and alternatives to abortion before an abortion could be performed. OBJECTIVE: To analyze the effect of the law on the abortion and birth rates of Mississippi residents. DESIGN: A retrospective analysis of abortion and birth rates before and after the law in Mississippi as contrasted with abortion and birth rates in 2 comparison states, Georgia and South Carolina. Neither Georgia nor South Carolina enforced a mandatory delay law, but both states began enforcement of parental notification statutes during the study period. PATIENTS: Female residents of reproductive age in Mississippi, Georgia, and South Carolina between 1989 and 1994. MAIN OUTCOME MEASURES: We compared birth rates, abortion rates, the percentage of late abortions, and the percentage of abortions performed outside the state of residence for all women and then by age and race before and after August 1992 among women of Mississippi, Georgia, and South Carolina. RESULTS: We found that rate ratios (RRs) of resident abortion rates (rate after law implementation/rate before law implementation) declined 12% more in Mississippi than in South Carolina (95% confidence interval [CI], 8%-15%) and 14% more in Mississippi than in Georgia (95% CI, 10%-17%) in the 12 months after the law went into effect. Rate ratios for white adults declined 22% more in Mississippi than in South Carolina (95% CI, 17%-27%) and 20% more in Mississippi than in Georgia (95% CI, 15%-25%). Changes among nonwhite adults and white teens were more modest but also statistically significant (P<.05). For all women, RRs of the percentage of abortions performed after 12 weeks' gestation increased 39% more in Mississippi than in either South Carolina or Georgia (P<.05); the increase in the percentage of abortions after 12 weeks' gestation was observed for white and non-white adults (P<.05). We also show that the percentage of abortions performed out of state increased 42% more among women in Mississippi relative to women in South Carolina after the law (95% CI, 34%-50%). CONCLUSION: The timing of the decline in abortion rates in Mississippi, the lack of similar declines in comparison states, the rise in percentage of late abortions and abortions performed out of state and the apparent completeness of abortion reports suggest that Mississippi's mandatory delay statute was responsible for a decline in abortion rates and an increase in abortions performed later in pregnancy among residents of Mississippi. The effect of delay laws in other states will likely depend on whether statutes require 2 separate visits to the abortion provider (ie, clinics, hospitals, or physicians' offices where abortions are performed) and the availability of abortion services.

Population-based study of sleep-disordered breathing as a risk factor for hypertension.

BACKGROUND: Clinical observations have linked sleep-disordered breathing, a condition of repeated apneas and hypopneas during sleep, with hypertension but evidence for an independent association has been lacking. Understanding this relationship is important because the prevalence of sleep-disordered breathing is high in adults. OBJECTIVE: To test the hypothesis that sleep-disordered breathing is related to elevated blood pressure independent of confounding factors. METHODS: The sample included 1060 employed women and men aged 30 through 60 years who had completed an overnight protocol as part of the Wisconsin Sleep Cohort Study. In-laboratory polysomnography was used to determine sleep-disordered breathing status, quantified as the number of apneas and hypopneas per hour of sleep (apnea-hypopnea index). Blood pressure was measured on the night polysomnography was performed. RESULTS: Blood pressure increased linearly with increasing apnea-hypopnea index (P = .003 for systolic, P = .01 for diastolic, adjusted for confounding factors). The magnitude of the linear association increased with decreasing obesity. At a body mass index (weight in kilograms divided by the square of the height in meters) of 30 kg/m2, an apnea-hypopnea index of 15 (vs 0) was associated with blood pressure increases of 3.6 mm Hg for systolic (95% confidence interval, 1.3-6.0) and 1.8 mm Hg for diastolic (95% confidence interval, 0.3-3.3). The odds ratio for hypertension associated with an apnea-hypopnea index of 15 (vs 0) was 1.8 (95% confidence interval, 1.3-2.4). CONCLUSIONS: There is a dose-response relationship between sleep-disordered breathing and blood pressure, independent of known confounding factors. If causal, the high prevalence of sleep-disordered breathing could account for hypertension in a substantial number of adults in the United States.

Automated detection and classification of sleep-disordered breathing from conventional polysomnography data.

Efficient automated detection of sleep-disordered breathing (SDB) from routine polysomnography (PSG) data is made difficult by the availability of only indirect measurements of breathing. The approach we used to overcome this limitation was to incorporate pulse oximetry into the definitions of apnea and hypopnea. In our algorithm, 1) we begin with the detection of desaturation as a fall in oxyhemoglobin saturation level of 2% or greater once a rate of descent greater than 0.1% per second (but less than 4% per second) has been achieved and then ask if an apnea or hypopnea was responsible; 2) an apnea is detected if there is a period of no breathing, as indicated by sum respiratory inductive plethysmography (RIP), lasting at least 10 seconds and coincident with the desaturation event; and 3) if there is breathing, a hypopnea is defined as a minimum of three breaths showing at least 20% reduction in sum RIP magnitude from the immediately preceding breath followed by a return to at least 90% of that "baseline" breath. Our evaluation of this algorithm using 10 PSG records containing 1,938 SDB events showed strong event-by-event agreement with manual scoring by an experienced polysomnographer. On the basis of manually verified computer desaturations, detection sensitivity and specificity percentages were, respectively, 73.6 and 90.8% for apneas and 84.1 and 86.1% for hypopneas. Overall, 93.1% of the manually detected events were detected by the algorithm. We have designed an efficient algorithm for detecting and classifying SDB events that emulates manual scoring with high accuracy.