Showing papers by "James B. Skatrud published in 2003"
TL;DR: It is concluded that apnoea‐induced fluctuations in CFV were caused primarily by increases and decreases in arterial partial pressure of CO2 (Pa,CO2) and that sympathetic nervous system activity was not required for either the initiation or the maintenance of the cerebrovascular response to hyper‐ and hypocapnia.
Abstract: We measured ventilation, arterial O2 saturation, end-tidal CO2 (PET,CO2), blood pressure (intra-arterial catheter or photoelectric plethysmograph), and flow velocity in the middle cerebral artery (CFV) (pulsed Doppler ultrasound) in 17 healthy awake subjects while they performed 20 s breath holds under control conditions and during ganglionic blockade (intravenous trimethaphan, 4.4 ± 1.1 mg min−1 (mean ±s.d.)). Under control conditions, breath holding caused increases in PET,CO2 (7 ± 1 mmHg) and in mean arterial pressure (MAP) (15 ± 2 mmHg). A transient hyperventilation (PET,CO2−7 ± 1 mmHg vs. baseline) occurred post-apnoea. CFV increased during apnoeas (by 42 ± 3 %) and decreased below baseline (by 20 ± 2 %) during post-apnoea hyperventilation. In the post-apnoea recovery period, CFV returned to baseline in 45 ± 4 s. The post-apnoea decrease in CFV did not occur when hyperventilation was prevented. During ganglionic blockade, which abolished the increase in MAP, apnoea-induced increases in CFV were partially attenuated (by 26 ± 2 %). Increases in PET,CO2 and decreases in oxyhaemoglobin saturation (Sa,O2) (by 2 ± 1 %) during breath holds were identical in the intact and blocked conditions. Ganglionic blockade had no effect on the slope of the CFV response to hypocapnia but it reduced the CFV response to hypercapnia (by 17 ± 5 %). We attribute this effect to abolition of the hypercapnia-induced increase in MAP. Peak increases in CFV during 20 s Mueller manoeuvres (40 ± 3 %) were the same as control breath holds, despite a 15 mmHg initial, transient decrease in MAP. Hyperoxia also had no effect on the apnoea-induced increase in CFV (40 ± 4 %). We conclude that apnoea-induced fluctuations in CFV were caused primarily by increases and decreases in arterial partial pressure of CO2 (Pa,CO2) and that sympathetic nervous system activity was not required for either the initiation or the maintenance of the cerebrovascular response to hyper- and hypocapnia. Increased MAP or other unknown influences of autonomic activation on the cerebral circulation played a smaller but significant role in the apnoea-induced increase in CFV; however, negative intrathoracic pressure and the small amount of oxyhaemoglobin desaturation caused by 20 s apnoea did not affect CFV.
103 citations
TL;DR: The findings suggest that 1) arousal-induced changes in parasympathetic activity are strongly coupled to respiratory pattern and 2) the sympathoexcitatory cardiovascular effects of arousal are relatively long lasting and may accumulate if repetitive arousals occur in close succession.
Abstract: We performed time-varying spectral analyses of heart rate variability (HRV) and blood pressure variability (BPV) recorded from 16 normal humans during acoustically induced arousals from sleep. Time...
91 citations
TL;DR: DS stabilized CSA and improved sleep quality in patients with CHF without significant acute adverse effects on the cardiovascular function.
85 citations
TL;DR: It is concluded that, during non-rapid eye movement sleep, carotid chemoreceptors are required to produce apneas that normally occur after a transient ventilatory overshoot and for PB.
Abstract: We determined the effects on breathing of transient ventilatory overshoots and concomitant hypocapnia, as produced by pressure support mechanical ventilation (PSV), in intact and carotid body chemoreceptor denervated (CBX) sleeping dogs. In the intact dog, PSV-induced transient increases in tidal volume and hypocapnia caused apnea within 10–11 s, followed by repetitive two-breath clusters separated by apneas, i.e., periodic breathing (PB). After CBX, significant expiratory time prolongation did not occur until after 30 s of PSV-induced hypocapnia, and PB never occurred. Average apneas of 8.4 ± 1-s duration after a ventilatory overshoot required a decrease below eupnea of end-tidal Pco 2 5.1 ± 0.4 Torr below eupnea in the intact animal and 10.1 ± 2 Torr in the CBX dog, where the former reflected peripheral and the latter central dynamic CO2 chemoresponsiveness, as tested in the absence of peripheral chemoreceptor input. Hyperoxia when the dogs were intact shortened PSV-induced apneas and reduced PB but did...
78 citations
TL;DR: Cerebrovascular CO2 responsiveness was not altered by baroreflex‐induced sympathetic activation, challenging the concept that sympathetic activation restrains cerebrov vascular responses to alterations in CO2 pressure.
Abstract: We investigated the effect of baroreflex-induced sympathetic activation, produced by lower body negative pressure (LBNP) at −40 mmHg, on cerebrovascular responsiveness to hyper- and hypocapnia in healthy humans. Transcranial Doppler ultrasound was used to measure blood flow velocity (CFV) in the middle cerebral artery during variations in end-tidal carbon dioxide pressure (PET,CO2) of +10, +5, 0, −5, and −10 mmHg relative to eupnoea. The slopes of the linear relationships between PET,CO2 and CFV were computed separately for hyper- and hypocapnia during the LBNP and no-LBNP conditions. LBNP decreased pulse pressure, but did not change mean arterial pressure. LBNP evoked an increase in ventilation that resulted in a 9 ± 2 mmHg decrease in PET,CO2, which was corrected by CO2 supplementation of the inspired air. LBNP did not affect cerebrovascular CO2 response slopes during steady-state hypercapnia (3.14 ± 0.24 vs. 2.96 ± 0.26 cm s−1 mmHg−1) or hypocapnia (1.31 ± 0.18 vs. 1.32 ± 0.19 cm s−1 mmHg−1), or the CFV responses to voluntary apnoea (+51 ± 19 vs.+50 ± 18 %). Thus, cerebrovascular CO2 responsiveness was not altered by baroreflex-induced sympathetic activation. Our data challenge the concept that sympathetic activation restrains cerebrovascular responses to alterations in CO2 pressure.
66 citations
TL;DR: The core competencies can be designed to improve physician knowledge and skills in recognizing and intervening in sleep problems and disorders and serve as an important bridge across multiple medical content areas and disciplines and between undergraduate and postgraduate training.
Abstract: Study Objectives: Sleep and circadian rhythms are biologic processes operative in health and disease, but as yet there is no articulated curriculum for undergraduate medical education. Design: A multidisciplinary expert-opinion approach was utilized to assess and define education objectives and the potential for implementation. Setting: N/A Patients or Participants: National Institutes of Health Sleep Academic Awardees Interventions: N/A Results: Four competencies with examples of instruction objectives were identified relating to sleep processes and sleep need, the impact of sleep and sleep disorders on human illness, the sleep history, and the application of sleep physiology and pathophysiology to patient care. Various strategies and tools are currently available for implementation and assessment of learning objectives for these knowledge and skills. Conclusion: The core competencies can be designed to improve physician knowledge and skills in recognizing and intervening in sleep problems and disorders. Learning objectives can be immediately incorporated into most medical school curricula. At the same time, these competencies serve as an important bridge across multiple medical content areas and disciplines and between undergraduate and postgraduate training.
21 citations
TL;DR: Control mechanical ventilation at increased frequency plus moderate elevations in VT reset respiratory rhythm and inhibited respiratory motor output to a much greater extent than did increased VT alone.
Abstract: Central apneas occur after cessation of mechanical ventilation despite normocapnic conditions. We asked whether this was due to ventilator-induced increases in respiratory rate or VT. Accordingly, we compared the effects of increased VT (135 to 220% of eupneic VT) with and without increased respiratory rate, using controlled and assist control mechanical ventilation, respectively, upon transdiaphragmatic pressure in sleeping humans. Increasing ventilator frequency +1 per minute and VT to 165-200% of baseline eupnea eliminated transdiaphragmatic pressure during controlled mechanical ventilation and prolonged expiratory time (two to four times control) after mechanical ventilation. During and after assist control mechanical ventilation at 135-220% of eupneic VT, transdiaphragmatic pressure was reduced in proportion to the increase in ventilator volume. However, every ventilator cycle was triggered by an active inspiration, and immediately after mechanical ventilation, expiratory time during spontaneous breathing was prolonged less than 20% of that observed after controlled mechanical ventilation at similar VT. We conclude that both increased frequency and VT during mechanical ventilation significantly inhibited respiratory motor output via nonchemical mechanisms. Controlled mechanical ventilation at increased frequency plus moderate elevations in VT reset respiratory rhythm and inhibited respiratory motor output to a much greater extent than did increased VT alone.
17 citations
01 Jan 2003
TL;DR: In this article, the core competencies can be designed to improve physi- cian knowledge and skills in recognizing and intervening in sleep prob- lems and disorders, and serve as an important bridge across multiple medical content areas and disciplines and between undergraduate and postgraduate training.
Abstract: tion of sleep physiology and pathophysiology to patient care. Various strategies and tools are currently available for implementation and assessment of learning objectives for these knowledge and skills. Conclusion: The core competencies can be designed to improve physi- cian knowledge and skills in recognizing and intervening in sleep prob- lems and disorders. Learning objectives can be immediately incorporated into most medical school curricula. At the same time, these competencies serve as an important bridge across multiple medical content areas and disciplines and between undergraduate and postgraduate training.
16 citations