Changes in respiratory control during and after 48 h of isocapnic and poikilocapnic hypoxia in humans.

Ventilatory acclimatization to hypoxia is associated with an increase in ventilation under conditions of acute hyperoxia (VEhyperoxia) and an increase in acute hypoxic ventilatory response (AHVR). This study compares 48-h exposures to isocapnic hypoxia (protocol I) with 48-h exposures to poikilocapnic hypoxia (protocol P) in 10 subjects to assess the importance of hypocapnic alkalosis in generating the changes observed in ventilatory acclimatization to hypoxia. During both hypoxic exposures, end-tidal PO2 was maintained at 60 Torr, with end-tidal PCO2 held at the subject's prehypoxic level (protocol I) or uncontrolled (protocol P). VEhyperoxia and AHVR were assessed regularly throughout the exposures. VEhyperoxia (P < 0.001, ANOVA) and AHVR (P < 0.001) increased during the hypoxic exposures, with no significant differences between protocols I and P. The increase in VEhyperoxia was associated with an increase in slope of the ventilation-end-tidal PCO2 response (P < 0.001) with no significant change in intercept. These results suggest that changes in respiratory control early in ventilatory acclimatization to hypoxia result from the effects of hypoxia per se and not the alkalosis normally accompanying hypoxia.

Human ventilatory response to 8 h of euoxic hypercapnia.

Ventilation (VE) rises throughout 40 min of constant elevated end-tidal PCO2 without reaching steady state (S. Khamnei and P. A. Robbins. Respir. Physiol. 81: 117-134, 1990). The present study investigates 8 h of euoxic hypercapnia to determine whether VE reaches steady state within this time. Two protocols were employed: 1) 8-h euoxic hypercapnia (end-tidal PCO2 = 6.5 Torr above prestudy value, end-tidal PO2 = 100 Torr) followed by 8-h poikilocapnic euoxia; and 2) control, where the inspired gas was air. VE was measured over a 5-min period before the experiment and then hourly over a 16-h period. In the hypercapnia protocol, VE had not reached a steady state by the first hour (P < 0.001, analysis of variance), but there were no further significant differences in VE over hours 2-8 (analysis of variance). VE fell promptly on return to eucapnic conditions. We conclude that, whereas there is a component of the VE response to hypercapnia that is slow, there is no progressive rise in VE throughout the 8-h period.

Time course of the human pulmonary vascular response to 8 hours of isocapnic hypoxia.

To examine the hypothesis that the human pulmonary vascular response to hypoxia has a component with a slow time course, we measured pulmonary vascular resistance (PVR) in six healthy adult males during 8 h of isocapnic hypoxia. A balloon-tipped pulmonary artery catheter with thermistor was introduced via a forearm vein and used to derive PVR. The subjects were seated in a chamber in which the oxygen and carbon dioxide concentrations were adjusted to maintain an end-tidal Po2 of 50 Torr and an end-tidal Pco2 equal to the subject's normal prehypoxic value. PVR was measured before and at 0.5-h intervals during 8 h of hypoxia, the following 3 h of isocapnic euoxia (end-tidal Po2 100 Torr), and a subsequent 1-h reexposure to hypoxia. PVR rose from 1.23 +/- 0.26 (SE) Torr-min.1(-1) under euoxia [time (t) = 0] to 1.77 +/- 0.21 Torr.min.1(-1) at t = 0.5 h, reached a maximum at 2 h (2.91 +/- 0.33 Torr.min.1(-1)), and remained fairly constant between 2 and 8 h. Restoration of euoxia at 8 h led to a reduction in PVR with a slow component. Reexposure to hypoxia at 11 h resulted in a greater increase in PVR than at 1 h. Systemic vascular resistance had a similar slow component to its response, falling from 18.6 +/- 1.3 Torr.min.1(-1) at t = 0 to 17.3 +/- 1.4 Torr.min.1(-1) at t = 0.5 h, 14.4 +/- 0.6 Torr.min.1(-1) at t = 4 h, and 13.8 +/- 0.8 Torr.min.1(-1) at t = 8 h. The human pulmonary and systemic vascular responses to hypoxia extend over at least several hours.

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans.

This study examines the effects of prolonged hypoxia, with and without control of end-tidal CO2 partial pressure (PET,CO2), on the intensity-weighted mean velocity of blood flow in the middle cerebral artery (VIWM) and on heart rate (HR). Specifically, the time course of the responses, their reversibility with brief periods of hyperoxia and the recovery phase following prolonged hypoxia were all investigated. Twelve subjects were studied, of whom nine provided satisfactory data. A purpose-built chamber was used for the prolonged control of the end-tidal gases, and an end-tidal forcing system was used for generating the brief variations in end-tidal gases. Three 16 h protocols were employed: (1) 8 h eucapnic (average PET,CO2 = 39 mmHg) hypoxia (end-tidal O2 partial pressure, PET,O2 = 55 mmHg) followed by 8 h eucapnic euoxia (PET,O2 = 100 mmHg); (2) 8 h poikilocapnic (average PET,CO2 4 mmHg below eucapnia) hypoxia (PET,O2 = 55 mmHg) followed by 8 h poikilocapnic euoxia (PET,O2 = 100 mmHg); and (3) control (air inspired throughout). VIWM (using Doppler ultrasound) and HR were measured during brief exposures to hypoxic/euoxic and hyperoxic conditions with PET,CO2 held 1-2 mmHg above eucapnia, at 0, 20, 240 and 480 min in the first 8 h, and at the same times in the second 8 h. There were no significant trends in VIWM under hypoxic conditions for either hypoxic protocol (ANOVA) and no significant differences between the three protocols for VIWM in hyperoxia (ANOVA). In contrast to VIWM, there was a significant increase in HR over time during both hypoxic exposures (P < 0.01, ANOVA). HR increased to a similar extent for the two types of hypoxia, and there was some suggestion that HR remained elevated after the relief of hypoxia. The results suggest that, with the level of hypoxia employed, progressive changes in HR occur, but that this level and duration of hypoxia has little sustained effect on VIWM.

Human ventilatory response to acute hyperoxia during and after 8 h of both isocapnic and poikilocapnic hypoxia.

During 8 h of either isocapnic or poikilocapnic hypoxia, there may be a rise in ventilation (VE) that cannot be rapidly reversed with a return to higher PO2 (L. S. G. E. Howard and P. A. Robbins. J. Appl. Physiol. 78:1098-1107, 1995). To investigate this further, three protocols were compared: 1) 8-h isocapnic hypoxia [end-tidal PCO2 (PETCO2) held at prestudy value, end-tidal PO2 (PETO2) = 55 Torr], followed by 8-h isocapnic euoxia (PETO2 = 100 Torr); 2) 8-h poikilocapnic hypoxia followed by 8-h poikilocapnic euoxia; and 3) 16-h air-breathing control. Before and at intervals throughout each protocol, the VE response to eucapnic hyperoxia (PETCO2 held 1-2 Torr above prestudy value, PETO2 = 300 Torr) was determined. There was a significant rise in hyperoxic VE over 8 h during both forms of hypoxia (P < 0.05, analysis of variance) that persisted during the subsequent 8-h euoxic period (P < 0.05, analysis of variance). These results support the notion that an 8-h period of hypoxia increases subsequent hyperoxic VE, even if acid-base changes have been minimized through maintenance of isocapnia during the hypoxic period.

The WISECARE Project and the impact of information technology on nursing knowledge.

The European Union retained the WISECARE project "Work flow Information Systems for European nursing CARE" for funding. The project focuses on the use of telematics technology for clinical and resource management in oncology care in hospitals. This paper outlines the impact of introducing this kind of advanced nursing informatics application on the management of nursing knowledge. Three shift in knowledge management that will get high attention in WISECARE, are identified. The first is the shift from knowledge dissemination to knowledge sharing. The second is the shift from individual knowledge to organisational knowledge. The third is the shift from deductive, prescriptive knowledge as seen in guidelines, protocols to more inductive, experience based knowledge. The paper emphasizes that the real impact of information technology is not in the automation of existing processes but on the discovery of new ways of organisation and living.