According to Guyton's model of circulation, mean systemic filling pressure (MSFP), right atrial pressure (RAP), and resistance to venous return (RVR) determine venous return. MSFP has been estimated from inspiratory hold-induced changes in RAP and blood flow. We studied the effect of positive end-expiratory pressure (PEEP) and blood volume on venous return and MSFP in pigs. MSFP was measured by balloon occlusion of the right atrium (MSFPRAO), and the MSFP obtained via extrapolation of pressure-flow relationships with airway occlusion (MSFPinsp_hold) was extrapolated from RAP/pulmonary artery flow (QPA) relationships during inspiratory holds at PEEP 5 and 10 cmH2O, after bleeding, and in hypervolemia. MSFPRAO increased with PEEP [PEEP 5, 12.9 (SD 2.5) mmHg; PEEP 10, 14.0 (SD 2.6) mmHg, P = 0.002] without change in QPA [2.75 (SD 0.43) vs. 2.56 (SD 0.45) l/min, P = 0.094]. MSFPRAO decreased after bleeding and increased in hypervolemia [10.8 (SD 2.2) and 16.4 (SD 3.0) mmHg, respectively, P < 0.001], with parallel changes in QPA Neither PEEP nor volume state altered RVR (P = 0.489). MSFPinsp_hold overestimated MSFPRAO [16.5 (SD 5.8) vs. 13.6 (SD 3.2) mmHg, P = 0.001; mean difference 3.0 (SD 5.1) mmHg]. Inspiratory holds shifted the RAP/QPA relationship rightward in euvolemia because inferior vena cava flow (QIVC) recovered early after an inspiratory hold nadir. The QIVC nadir was lowest after bleeding [36% (SD 24%) of preinspiratory hold at 15 cmH2O inspiratory pressure], and the QIVC recovery was most complete at the lowest inspiratory pressures independent of volume state [range from 80% (SD 7%) after bleeding to 103% (SD 8%) at PEEP 10 cmH2O of QIVC before inspiratory hold]. The QIVC recovery thus defends venous return, possibly via hepatosplanchnic vascular waterfall.

We developed a modified nitrogen washin/washout technique based on standard monitors using inspiratory and end-tidal gas concentration values for functional residual capacity (FRC) measurements in patients with acute respiratory failure (ARF). For validation we used an oxygen-consuming lung model ventilated with an inspiratory oxygen fraction (Fio(2)) between 0.3 and 1.0. The respiratory quotient of the lung model was varied between 0.7 and 1.0. Measurements were performed changing Fio(2) with fractions of 0.1, 0.2, and 0.3. In 28 patients with ARF, duplicate measurements were performed. In the lung model, an Fio(2) change of 0.1 resulted in a value of 103 +/- 5% of the reference FRC value of the lung model, and the precision was equally good up to an Fio(2) of 1.0 with a value of 103 +/- 7%. In the patients, duplicate measurements showed a bias of -5 mL with a 95% confidence interval [-38; 29 mL ]. A comparison of a change in Fio(2) of 0.1 with 0.3 showed a bias of -9 mL and limits of agreement of [-365; 347 mL]. This study shows good precision of FRC measurements with standard monitors using a change in Fio(2) of only 0.1. Measurements can be performed with equal precision up to an Fio(2) of 1.0.

Table of contentsP001 - Sepsis impairs the capillary response within hypoxic capillaries and decreases erythrocyte oxygen-dependent ATP effluxR. M. Bateman, M. D. Sharpe, J. E. Jagger, C. G. EllisP002 - Lower serum immunoglobulin G2 level does not predispose to severe flu.J. Solé-Violán, M. López-Rodríguez, E. Herrera-Ramos, J. Ruíz-Hernández, L. Borderías, J. Horcajada, N. González-Quevedo, O. Rajas, M. Briones, F. Rodríguez de Castro, C. Rodríguez GallegoP003 - Brain protective effects of intravenous immunoglobulin through inhibition of complement activation and apoptosis in a rat model of sepsisF. Esen, G. Orhun, P. Ergin Ozcan, E. Senturk, C. Ugur Yilmaz, N. Orhan, N. Arican, M. Kaya, M. Kucukerden, M. Giris, U. Akcan, S. Bilgic Gazioglu, E. TuzunP004 - Adenosine a1 receptor dysfunction is associated with leukopenia: A possible mechanism for sepsis-induced leukopeniaR. Riff, O. Naamani, A. DouvdevaniP005 - Analysis of neutrophil by hyper spectral imaging - A preliminary reportR. Takegawa, H. Yoshida, T. Hirose, N. Yamamoto, H. Hagiya, M. Ojima, Y. Akeda, O. Tasaki, K. Tomono, T. ShimazuP006 - Chemiluminescent intensity assessed by eaa predicts the incidence of postoperative infectious complications following gastrointestinal surgeryS. Ono, T. Kubo, S. Suda, T. Ueno, T. IkedaP007 - Serial change of c1 inhibitor in patients with sepsis – A prospective observational studyT. Hirose, H. Ogura, H. Takahashi, M. Ojima, J. Kang, Y. Nakamura, T. Kojima, T. ShimazuP008 - Comparison of bacteremia and sepsis on sepsis related biomarkersT. Ikeda, S. Suda, Y. Izutani, T. Ueno, S. OnoP009 - The changes of procalcitonin levels in critical patients with abdominal septic shock during blood purificationT. Taniguchi, M. OP010 - Validation of a new sensitive point of care device for rapid measurement of procalcitoninC. Dinter, J. Lotz, B. Eilers, C. Wissmann, R. LottP011 - Infection biomarkers in primary care patients with acute respiratory tract infections – Comparison of procalcitonin and C-reactive proteinM. M. Meili, P. S. SchuetzP012 - Do we need a lower procalcitonin cut off?H. Hawa, M. Sharshir, M. Aburageila, N. SalahuddinP013 - The predictive role of C-reactive protein and procalcitonin biomarkers in central nervous system infections with extensively drug resistant bacteriaV. Chantziara, S. Georgiou, A. Tsimogianni, P. Alexandropoulos, A. Vassi, F. Lagiou, M. Valta, G. Micha, E. Chinou, G. MichaloudisP014 - Changes in endotoxin activity assay and procalcitonin levels after direct hemoperfusion with polymyxin-b immobilized fiberA. Kodaira, T. Ikeda, S. Ono, T. Ueno, S. Suda, Y. Izutani, H. ImaizumiP015 - Diagnostic usefullness of combination biomarkers on ICU admissionM. V. De la Torre-Prados, A. Garcia-De la Torre, A. Enguix-Armada, A. Puerto-Morlan, V. Perez-Valero, A. Garcia-AlcantaraP016 - Platelet function analysis utilising the PFA-100 does not predict infection, bacteraemia, sepsis or outcome in critically ill patientsN. Bolton, J. Dudziak, S. Bonney, A. Tridente, P. NeeP017 - Extracellular histone H3 levels are in...

No abstract

ETT connections and secretions cause a variance in resistance. Tracheal pressure can be measured with high precision with an air- or liquid-filled catheter. An end hole catheter placed within 2 cm above or below the ETT tip will give sufficiently precise measurements for clinical purposes.

Using an algorithm to derive a mean systemic filling pressure analogue, cardiac power and dynamic measures of the venous return pressure gradient relative to the mean systemic filling pressure provided an assessment of the efficiency of volume expansion in post-surgical cardiac patients.

The relevance of right atrial pressure (RAP) as the backpressure for venous return (Q) and mean systemic filling pressure as upstream pressure is controversial during dynamic changes of circulation. To examine the immediate response of Q (sum of caval vein flows) to changes in RAP and pump function, we used a closed-chest, central cannulation, heart bypass porcine preparation ( = 10) with venoarterial extracorporeal membrane oxygenation. Mean systemic filling pressure was determined by clamping extracorporeal membrane oxygenation tubing with open or closed arteriovenous shunt at euvolemia, volume expansion (9.75 ml/kg hydroxyethyl starch), and hypovolemia (bleeding 19.5 ml/kg after volume expansion). The responses of RAP and Q were studied using variable pump speed at constant airway pressure (P) and constant pump speed at variable P Within each volume state, the immediate changes in Q and RAP could be described with a single linear regression, regardless of whether RAP was altered by pump speed or P ( = 0.586-0.984). RAP was inversely proportional to pump speed from zero to maximum flow ( = 0.859-0.999). Changing P caused immediate, transient, directionally opposite changes in RAP and Q (RAP: ≤ 0.002 and Q: ≤ 0.001), where the initial response was proportional to the change in Q driving pressure. Changes in P generated volume shifts into and out of the right atrium, but their effect on upstream pressure was negligible. Our findings support the concept that RAP acts as backpressure to Q and that Guyton's model of circulatory equilibrium qualitatively predicts the dynamic response from changing RAP. Venous return responds immediately to changes in right atrial pressure. Concomitant volume shifts within the systemic circulation due to an imbalance between cardiac output and venous return have negligible effects on mean systemic filling pressure. Guyton's model of circulatory equilibrium can qualitatively predict the resulting changes in dynamic conditions with right atrial pressure as backpressure to venous return.

We describe a method based on a Fabry-Perot interferometer at the tip of an optic fiber with a diameter of 0.25 mm for direct measurement of tracheal pressure in pediatric respiratory monitoring. The response time of the pressure transducer and its influence on the resistance of pediatric endotracheal tubes (internal diameter, 2.5 to 5 mm) during constant and dynamic flow at different ventilator settings in a lung model were measured. The transducer was positioned at Ϫ1.5 (inside), 0, and ϩ1.5 cm (outside) relative to the tip of the endotracheal tube and compared with a reference pressure inside the trachea. The clinical application of the transducer was tested in five pediatric patients. The response time of the transducer was 1.3 ms. The influence of the fiberoptic transducer on tube resistance was negligible during constant flow in inspiratory and expiratory directions for all endotracheal tubes tested. There was no difference in pressure measurements with the transducer positioned at or 1.5 cm below or above the tip of the endotracheal tube during dynamic measurements. During clinical circumstances insertion of the fiberoptic transducer was easy, recordings were stable, and the safety of the patient was not jeopardized. The fiberoptic transducer provided a reliable and promising way of monitoring tracheal pressure in intubated pediatric patients. The presence of the probe did not interfere with either pressure-flow relationship or patient care and safety. The technique is proposed for monitoring of respiratory mechanics and calculation of changes in tube resistance caused by kinking and secretions. Respiratory monitoring in pediatric intensive care is currently represented by proximal P/V loops obtained in ventilator software or intensive care monitors using flowmeters placed near the connection between the ventilator system and ETT. This is obviously insufficient as information gained from such P/V loops mainly stems from ETT resistance and performance of ventilator valves. We have previously demonstrated that monitoring respiratory mechanics by direct measurement of tracheal pressure offers considerable advantages compared with monitoring based on either measurements obtained proximal to the tube or tracheal pressures calculated by subtracting pressure needed to overcome flow-dependent tube resistance. In the adult setting tracheal pressure measurement is accomplished by introducing an air-or liquid-filled catheter into the ETT and connecting it to a conventional pressure transducer (1). In the pediatric setting it has generally been held to be impossible to use endotracheal catheters for continuous pressure measurement owing to the encroachment on cross-sectional area of the narrow pediatric tubes (2). Instead hydrodynamic models of varying complexity have been proposed for the calculation of tracheal pressure, i.e. the pressure fall across the ETT because of its resistance, based on measurements above the tube. Guttmann et al. (2)