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Arterial Partial Pressure (arterial + partial_pressure)
Selected AbstractsVentilatory control in humans: constraints and limitationsEXPERIMENTAL PHYSIOLOGY, Issue 2 2007Susan A. Ward Below the lactate threshold (,L), ventilation responds in close proportion to CO2 output to regulate arterial partial pressure of CO2. While ventilatory control models have traditionally included proportional feedback (central and carotid chemosensory) and feedforward (central and peripheral neurogenic) elements, the mechanisms involved remain unclear. Regardless, putative control schemes have to accommodate the close dynamic ,coupling' between and . Above ,L, is driven down to constrain the fall of arterial pH by a compensatory hyperventilation, probably of carotid body origin. When requirements are high (as in highly fit endurance athletes), can attain limiting proportions. Not only does this impair gas exchange at these work rates, but there may be an associated high metabolic cost for generation of respiratory muscle power, which may be sufficient to divert a fraction of the cardiac output away from the muscles of locomotion to the respiratory muscles, further compromising exercise tolerance. [source] The Contribution of Chemoreflex Drives to Resting Breathing in ManEXPERIMENTAL PHYSIOLOGY, Issue 1 2001Safraaz Mahamed The contribution of automatic drives to breathing at rest, relative to behavioural drives such as ,wakefulness', has been a subject of debate. We measured the combined central and peripheral chemoreflex contribution to resting ventilation using a modified rebreathing method that included a prior hyperventilation and addition of oxygen to maintain isoxia at a PET,O2 (end-tidal partial pressure of oxygen) of 100 mmHg. During rebreathing, ventilation was unrelated to PET,CO2 (end-tidal partial pressure of carbon dioxide) in the hypocapnic range, but after a threshold PET,CO2 was exceeded, ventilation increased linearly with PET,CO2. We considered the sub-threshold ventilation to be an estimate of the behavioural drives to breathe (mean ± S.E.M. = 3.1 ± 0.5 l min,1), and compared it to ventilation at rest (mean ± S.E.M. = 9.1 ± 0.7 l min,1). The difference was significant (Student's paired t test, P < 0.001). We also considered the threshold PCO2 observed during rebreathing to be an estimate of the chemoreflex threshold at rest (mean ± S.E.M. = 42.0 ± 0.5 mmHg). However, PET,CO2 during rebreathing estimates mixed venous or tissue PCO2, whereas the resting PET,CO2 during resting breathing estimates Pa,CO2 (arterial partial pressure of carbon dioxide). The chemoreflex threshold measured during rebreathing was therefore reduced by the difference in PET,CO2 at rest and at the start of rebreathing (the plateau estimates the mixed venous PCO2 at rest) in order to make comparisons. The corrected chemoreflex thresholds (mean ± S.E.M. = 26.0 ± 0.9 mmHg) were significantly less (paired Student's t test, P < 0.001) than the resting PET,CO2 values (mean ± S.E.M. = 34.3 ± 0.5 mmHg). We conclude that both the behavioural and chemoreflex drives contribute to resting ventilation. [source] Effect of intra-operative pressure support vs pressure controlled ventilation on oxygenation and lung function in moderately obese adults*ANAESTHESIA, Issue 2 2010M. Zoremba Summary Obesity impairs peri-operative lung function. To evaluate the impact of pressure support ventilation vs pressure controlled ventilation in moderately obese adults upon early postoperative lung function, we randomly assigned 68 moderately obese patients (body mass index 25,35 kg.m,2) undergoing minor surgery to receive intra-operative ventilation either with pressure support or pressure controlled ventilation. We performed intra-operative blood gas analysis and measured pulse oximetry saturation, spirometry values at pre-operative assessment (baseline) and at 10 min, 30 min, 2 h and 24 h after extubation. The intra-operative oxygenation index (arterial partial pressure of oxygen/fraction of inspired oxygen) in the pressure support ventilation group was significantly improved over time (p < 0.0001). Postoperatively, the pressure support ventilation group also had better lung function and oxygenation values than did the pressure controlled ventilation group (p < 0.005). We conclude that pressure support ventilation better maintains lung function than pressure controlled ventilation in moderately overweight patients scheduled for minor surgery. [source] Laparoscopic surgery impairs tissue oxygen tension more than open surgeryBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2007E. Fleischmann Background: Wound infection remains a common and serious complication after colonic surgery. Although many colonic operations are performed laparoscopically, it remains unclear whether this has any impact on the incidence of wound infection. Subcutaneous tissue oxygenation is an excellent predictor of surgical wound infection. The impact of open and laparoscopic colonic surgery on tissue oxygenation was compared. Methods: Fifty-two patients undergoing elective open and laparoscopic left-sided colonic resections were evaluated in a prospective observational study. Anaesthesia management was standardized and intraoperative arterial partial pressure of oxygen was kept at 150 mmHg in both groups. Oxygen tension was measured in the subcutaneous tissue of the right upper arm. Results: At the start of surgery subcutaneous tissue oxygen tension (PsqO2) was similar in both groups (mean(s.d.) 65·8(17·2) and 63·7(23·6) mmHg for open and laparoscopic operations respectively; P = 0·714). Tissue oxygen remained stable in the open group, but dropped significantly in the laparoscopic group during the course of surgery (PsqO2 after operation 53·4(12·9) and 45·5(11·6) mmHg, respectively; P = 0·012). Conclusion: Laparoscopic colonic surgery significantly decreases PsqO2, an effect that occurs early in the course of surgery. As tissue oxygen tension is a predictor of wound infection, these results may explain why the risk of wound infection after laparoscopic surgery remains higher than expected. Copyright © 2006 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] |