Nitrous oxide reduces inspired oxygen fraction but does not compromise circulation and oxygenation during hemodilution in pigs

Background: The use of nitrous oxide (N₂O) during hemodilution has been questioned. Nitrous oxide reduces the inspired oxygen fraction (F₁O₂), depresses myocardial function and may reduce cardiac output (CO) and systemic oxygen delivery (DO_2SY). The aim of this study was to evaluate the importance of the effects of nitrous oxide on systemic and myocardial circulation and oxygenation during extreme, acute, normovolemic hemodilution. Methods: Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to 65% N₂O before and after extreme isovole-mic hemodilution (hematocrit 33±1% and 10±1%, respectively). Systemic and myocardial hemodynamics, oxygen delivery and consumption and blood lactate were measured before (at FrO₂ 1.0 and 0.35) and during N₂O exposure. Results: Hemodilution caused an increase in CO from 137±43 to 229±32 ml kg^-1 min^-1 (P< 0.01), a decrease in systemic vascular resistance (from 42±14 to 20±4 mmHg L^-1 min^-1, P < 0.05), a decrease in mean arterial blood pressure (from 119±19 to 100±26 mmHg, P<0.05) and a decrease in DO_2SY from 21.1 ±6.9 to 13.7±2.1 ml kg^-1 min^-1 (P < 0.01). Cardiac venous blood flow increased by 135% (P < 0.01) and cardiac venous saturation from 25±6 to 41±5% (P < 0.05). After hemodilution, changing F_IO₂ from 1.0 to 0.35 reduced arterial blood oxygen content from 59.4±3.7 to 52.3±5.1 ml L^-1 (P < 0.01), mixed venous saturation (SvO₂) from 75±9 to 47±7% (P < 0.05) and DO_2SY from 13.7±2.1 to 11.9+2.3 ml kg^-1 - min^-1 (P < 0.05). Dissolved oxygen at F₁O₂=1.0 and F₁O₂=0.35 constituted 25.4±3.1% and 10.1 ±1.5%, respectively, of systemic oxygen delivery after hemodilution, compared with 10.7±1.2% and 3.9±0.5% before hemodilution (P < 0.01). Left ventricular oxygen delivery and consumption were unchanged. Exposure to N₂O did not affect mean arterial blood pressure or systemic vascular resistance before or after hemodilution. After hemodilution during N₂O-exposure, CO and DO_2SY decreased by 9% (P < 0.01 and P < 0.05, respectively), but no changes in SvO₂, systemic oxygen uptake or arterial lactate were observed. The effect of N₂O on myocardial oxygenation was similar before and after hemodilution; cardiac venous blood flow, left ventricular oxygen delivery and uptake decreased, but no animals showed left ventricular lactate production. Conclusion: Nitrous oxide did not compromise systemic and myocardial circulation and oxygenation during acute normovolemic hemodilution in pigs. Possible adverse effects from the use of nitrous oxide during hemodilution seem to be related to a reduced F_IO₂, reducing the safety margin for systemic oxygen delivery.     

Norepinephrine causes a pressure‐dependent plasma volume decrease in clinical vasodilatory shock

Background: Recent experimental studies have shown that a norepinephrine‐induced increase in blood pressure induces a loss of plasma volume, particularly under increased microvascular permeability. We studied the effects of norepinephrine‐induced variations in the mean arterial pressure (MAP) on plasma volume changes and systemic haemodynamics in patients with vasodilatory shock. Methods: Twenty‐one mechanically ventilated patients who required norepinephrine to maintain MAP ≥70 mmHg because of septic/postcardiotomy vasodilatory shock were included. The norepinephrine dose was randomly titrated to target MAPs of 60, 75 and 90 mmHg. At each target MAP, data on systemic haemodynamics, haematocrit, arterial and mixed venous oxygen content and urine flow urine were measured. Changes in the plasma volume were calculated as 100 × (Hct_pre/Hct_post?1)/ (1?Hct_pre), where Hct_pre and Hct_post are haematocrits before and after intervention. Results: Norepinephrine doses to obtain target MAPs of 60, 75 and 90 mmHg were 0.20±0.18, 0.29±0.18 and 0.42±0.31 μg/kg/min, respectively. From 60 to 90 mmHg, increases in the cardiac index (15%), systemic oxygen delivery index (25%), central venous pressure (CVP) (20%) and pulmonary artery occlusion pressure (33%) were seen, while the intrapulmonary shunt fraction was unaffected by norepinehrine. Plasma volume decreased by 6.5% and 9.4% (P<0.0001) when blood pressure was increased from 60 to 75 and 90 mmHg, respectively. MAP (P<0.02) independently predicted the decrease in plasma volume with norepinephrine but not CVP (P=0.19), cardiac index (P=0.73), norepinephrine dose (P=0.58) or urine flow (P=0.64). Conclusions: Norepinephrine causes a pressure‐dependent decrease in the plasma volume in patients with vasodilatory shock most likely caused by transcapillary fluid extravasation.     

Correlação entre saturação venosa central de oxigênio perioperatória e mortalidade em cirurgia cardíaca: estudo prospectivo observacional

BackgroundCardiac surgery can produce persistent deficit in the ratio of Oxygen Delivery (DO₂) to Oxygen Consumption (VO₂). Central venous oxygen Saturation (ScvO₂) is an accessible and indirect measure of DO₂/VO₂ ratio.ObjectiveTo monitor perioperative ScvO₂ and assess its correlation with mortality during cardiac surgery.MethodsThis prospective observational study evaluated 273 patients undergoing cardiac surgery. Blood gas samples were collected to measure ScvO₂ at three time points: T0 (after anesthetic induction), T1 (end of surgery), and T2 (24 hours after surgery). The patients were divided into two groups (survivors and nonsurvivors). The following outcomes were analyzed: intrahospital mortality, length of Intensive Care Unit (ICU) and hospital stay (LOS), and variation in ScvO₂.ResultsOf the 273 patients, 251 (92%) survived and 22 (8%) did not. There was a significant perioperative reduction of ScvO₂ in both survivors (T0 = 78% ± 8.1%, T1 = 75.4% ± 7.5%, and T2 = 68.5% ± 9%; p < 0.001) and nonsurvivors (T0 = 74.4% ± 8.7%, T1 = 75.4% ± 7.7%, and T2 = 66.7% ± 13.1%; p < 0.001). At T0, the percentage of patients with ScvO₂ < 70% was greater in the nonsurvivor group (31.8% vs. 13.1%; p = 0.046) and the multiple logistic regression showed that ScvO₂ is an independent risk factor associated with death, OR = 2.94 (95% CI 1.10 − 7.89) (p = 0.032). The length of ICU and LOS were 3.6 ± 3.1 and 7.4 ± 6.0 days respectively and was not significantly associated with ScvO₂.ConclusionsEarly intraoperative ScvO₂ < 70% indicated a higher risk of death. A perioperative reduction of ScvO₂ was observed in patients undergoing cardiac surgery, with high intraoperative and lower postoperative levels.     

Low central venous oxygen saturation in haemodynamically stabilized trauma patients is associated with poor outcome

Background: Central venous oxygen saturation (ScvO₂) is suggested to reflect the adequacy of oxygen delivery, and the main objective of the present study was to determine whether ScvO₂ is associated with outcome in haemodynamically stabilized trauma patients. Methods: Haemodynamically unstable trauma patients receiving a central venous line within 1 h of admission were eligible for inclusion in this prospective observational study. The mean arterial pressure (MAP), lactate and ScvO₂ were recorded at inclusion and every 6 h for 36 h or until lactate was <2.0 mmol/l and ScvO₂ was >75% in two consecutive measurements. Patients with a MAP of ≥70 mmHg were considered to be haemodynamically stabilized. The outcome measure was complications defined as infections, delta sequential organ failure assessment score of >0, and mortality. Results: Fifty patients with a median new injury severity score of 27 (17–34) were analysed. Complications occurred in 33 patients. An association between ScvO₂ following resuscitation to MAP ≥70 mmHg and complications was detected with an odds ratio of 0.94 (95% confidence interval; 0.89–0.99). This association was also significant when adjusted for injury severity. The result implies that a low ScvO₂ value is associated with more complications. The optimal cut‐off for ScvO₂ to discriminate between patients who did or did not develop complications was found to be 66.5% (56–86%). Conclusions: These data suggest that low ScvO₂ in haemodynamically stabilized patients is associated with a poor outcome and that ScvO₂ represents a potential endpoint of resuscitation in trauma patients.     

Normal Values and Incidence of Cardiorespiratory Complications in Dogs During General Anaesthesia. A Review of 1281 Cases

This paper describes the cardiorespiratory variables and the incidence of anaesthetic complications in dogs. For this, a retrospective study of 1281 anaesthesias was performed. Heart rate (HR), non‐invasive mean arterial (MAP), systolic (SP) and diastolic pressures (DP), invasive mean arterial (IMAP), systolic (ISP) and diastolic pressures (IDP), central venous pressure (CVP), respiratory rate (RR), tidal volume (V_T), minute volume (V_M), end‐tidal CO₂ (EtCO₂), arterial oxygen saturation (SpO₂), temperature (T) and death are reported. Data were described both globally and separately for each ASA (American Society of Anaesthesiologists classification) status. An anova and a Tukey’s test were used for comparing the different ASA status’ values (α = 0.05). During anaesthetic maintenance, the mean ± SD of the studied variables were: HR: 91 ± 27 bpm. MAP: 86 ± 24 mmHg. IMAP: 80 ± 22 mmHg. SP: 114 ± 25 mmHg. ISP: 109 ± 26 mmHg. DP: 67 ± 23 mmHg. IDP: 66 ± 22 mmHg. CVP: 5 ±3 mmHg. RR: 19 ± 11 rpm. V_T: 14 ± 7 ml/kg. V_M: 191 ± 93 ml/kg/min. EtCO₂: 40 ± 8 mmHg. T: 37.1 ± 1.7°C. ASA III and ASA IV patients, compared with those with ASA I, showed higher values of HR, RR, V_T and V_M and lower in IMAP, CVP, EtCO₂, SpO₂ and T. The most frequent complications were bradycardia (36.3% of the patients), hypotension (37.9%), hypoventilation (63.4%), hypoxia (16.4%), hypothermia (4.8%) and death (0.9%). Cardiorespiratory complications frequently occur in dogs during general anaesthesia.     

Hypertonic saline and dextran in normovolaemic and hypovolaemic healthy volunteers increases interstitial and intravascular fluid volumes

Background : Hypertonic saline (HS) is increasingly used for fluid resuscitation in hypovolaemic patients. Although the effects of HS have been investigated in animal models, controlled studies in healthy human individuals are few. Aim : The effects of iv. hypertonic saline 75 mg . ml^-1 in dextran 70, 60 mg . ml^-1 (HSD) infusion on fluid shifts between the interstitial and intravascular fluid spaces, diuresis and haemodynamics were studied in normovolaemic and moderately hypovolaemic healthy volunteers. Material and methods : Nine fasting subjects received 4 ml . kg^-1 HSD as a 10-min infusion in a normovolaemic situation. Seven days later they served as their own controls in a hypovolaemic situation after 10% of the calculated blood volume had been withdrawn during a 15-min period. Before and after the HSD infusion, interstitial colloid osmotic pressure (COP_i) and interstitial fluid hydrostatic pressure (P_i) were measured on the lateral part of the thorax. During the study, blood sampling and pressure measurements were performed through a radial artery cannula, and central venous pressure measured through a catheter in the cubital vein. Results : In these awake and normovolaemic healthy volunteers, HSD infusion caused a transitory unpleasant sensation of headache and heat in the thorax up to the throat. A transitory haemodynamic effect was found with increased heart rate (HR), increased mean arterial pressure (MAP) from 77 ± 5 mmHg to 92 ± 13 mmHg (P<0.05) and CVP increase from 5 ± 1 mmHg to 8 ± 1 mmHg (P<0.05) after end of infusion. A haemodilution with increase in calculated blood volume lasting longer than the MAP increase was observed, with decreased COP_i from 14.4 ± 2.2 mmHg to 12.1 ± 2.0 mmHg (P<0.05). The diuresis measured at 180 min was higher in the normovolaemic than in the hypovolaemic situation. More pronounced effects of the infused fluid (HSD) on calculated blood volume, interstitial compartment and CVP were observed during moderate hypovolaemia. Conclusions : HSD infusion resulted in increased calculated blood volume with increased HR, MAP, and CVP. These effects were greater in a hypovolaemic situation. The haemodilution was most likely caused by fluid shifts from the intracellular compartment to the interstitial and vascular fluid spaces, eventually increasing diuresis.     

Global and right ventricular end‐diastolic volumes correlate better with preload after correction for ejection fraction

Background: Volumetric monitoring with right ventricular end‐diastolic volume indexed (RVEDVi) and global end‐diastolic volume indexed (GEDVi) is increasingly being suggested as a superior preload indicator compared with the filling pressures central venous pressure (CVP) or the pulmonary capillary wedge pressure (PCWP). However, static monitoring of these volumetric parameters has not consistently been shown to be able to predict changes in cardiac index (CI). The aim of this study was to evaluate whether a correction of RVEDVi and GEDVi with a measure of the individual contractile reserve, assessed by right ventricular ejection fraction (RVEF) and global ejection fraction, improves the ability of RVEDVi and GEDVi to monitor changes in preload over time in critically ill patients. Methods: Hemodynamic measurements, both by pulmonary artery and by transcardiopulmonary thermodilution, were performed in 11 mechanically ventilated medical ICU patients. Correction of volumes was achieved by normalization to EF deviation from normal EF values in an exponential fashion. Data before and after fluid administration were obtained in eight patients, while data before and after diuretics were obtained in seven patients. Results: No correlation was found between the change in cardiac filling pressures (ΔCVP, ΔPCWP) and ΔCI (R² 0.01 and 0.00, respectively). Further, no correlation was found between ΔRVEDVi or ΔGEDVi and ΔCI (R² 0.10 and 0.13, respectively). In contrast, a significant correlation was found between ΔRVEDVi corrected to RVEF (ΔcRVEDVi) and ΔCI (R² 0.64), as well as between ΔcGEDVi and ΔCI (R² 0.59). An increase in the net fluid balance with +844 ± 495 ml/m² resulted in a significant increase in CI of 0.5 ± 0.3 l/min/m²; however, only ΔcRVEDVi (R² 0.58) and ΔcGEDVi (R² 0.36) correlated significantly with ΔCI. Administration of diuretics resulting in a net fluid balance of ?942 ± 658 ml/m² caused a significant decrease in CI with 0.7 ± 0.5 l/min/m²; however, only ΔcRVEDVi (R² 0.80) and ΔcGEDVi (R² 0.61) correlated significantly with ΔCI. Conclusion: Correction of volumetric preload parameters by measures of ejection fraction improved the ability of these parameters to assess changes in preload over time in this heterogeneous group of critically ill patients.     

Effects of buffering in hypercapnia and hypercapnic hypoxemia

Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (Paco_2-20 kPa) at Fio₂ 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 ±0.01 vs 7.01±0.01 (mean ± s.e.mean, P < 0.01). Serum osmolality and Paco₂ did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 ± 6 vs 189±12 min^-1 (P < 0.01), mean arterial pressure (MAP) 109 ± 4 vs 124 ± 4 mmHg (14.5 ± 0.5 vs 16.5 ± 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16±1 vs 23 ± 1 mmHg (2.1 ±0.1 vs 3.1 ±0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 ± 21 vs 343 ± 20 dyn s-cm^-5 (2490±210 vs 3430±200 μN-s-cm^-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in Fio₂ (0.15, 0.10, 0.05) at 30-min intervals, while Fico₂ was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At Fio₂ 0.15, buffered animals had higher arterial oxygen saturation (73 ± 5%) than the controls (55 ± 5%), (P < 0.05). The control animals died after 1–29 min (mean 14 min) at Fio₂ 0.10, while all buffered animals survived Fio₂ 0.10 with stable MAP (122 ± 14 mmHg (16.3 ± 1.9 kPa). The buffered animals died after 4–22 min (mean 15 min) at Fio₂ 0.05. We conclude that buffering to a pH of 7.21 attenuates the observed hemodynamic response in extreme hypercapnia and improves survival in hypercapnic hypoxemia.     

Evaluation of mechanism of increased intracranial pressure with insufflation

Background: Previous studies have documented an increase in intracranial pressure with abdominal insufflation, but the mechanism has not been explained. Methods: Nine 30–35-kg domestic pigs underwent carbon dioxide insufflation at 1.5 l/min. Intracranial pressure (ICP), lumbar spinal pressure (LP), central venous pressure (CVP), inferior vena cava pressure (IVCP), heart rate, systemic arterial blood pressure, pulmonary arterial pressure, cardiac output, heart rate, respiratory rate, temperature, and end-tidal CO₂ were continuously measured. Mechanical ventilation was used to maintain a constant pCO₂. Measurements were recorded at 0, 5, 10, and 15 mmHg of abdominal pressure with animals in supine, Trendelenburg (T), and reverse Trendelenburg (RT) positions. Prior to recording measurements, the animals were allowed to stabilize for 40 min after each increase in abdominal pressure and for 20 min after each position change. Results: The animals showed a significant increase in ICP (mmHg) with each 5-mmHg increase in abdominal pressure (0 mmHg: 14 ± 1.7; 5 mmHg: 19.8 ± 2.3, p < 0.001; 10 mmHg: 24.8 ± 2.5, p < 0.001; 15 mmHg: 29.8 ± 4.7, p < 0.01). The ICP at 15 mmHg abdominal pressure increased further in the T position (39 ± 4, p < 0.01). Insufflating in the RT position did not significantly reduce the increase in ICP. The IVCP (mmHg) increased with increased abdominal pressure (0 mmHg: 11.5 ± 6.2, 15 mmHg: 22.1 ± 3.5, p < 0.01). This increase correlated with the increase in ICP and LP (r of mean pressures ≥0.95). There was no significant change in CVP. Conclusions: This study suggests that care may be needed with laparoscopy in patients at risk for increased ICP due to head injury or a space occupying lesion. The mechanism of increased ICP associated with insufflation is most likely impaired venous drainage of the lumbar venous plexus at increased intraabdominal pressure. Further studies of cerebral spinal fluid movement during insufflation are currently underway to confirm this hypothesis. Received: 28 March 1997/Accepted: 5 August 1997     

The effects of cardiopulmonary bypass on postoperative oxygen metabolism

The relationships between oxygen delivery (DO₂), oxygen consumption (VO₂), and the extraction rate (ER=VO₂/DO₂x100) in patients undergoing cardiopulmonary bypass (CPB) may differ from the normal physiologic state due to the oxygen debt acquired during CPB. Blood gas analysis and hemodynamic parameters were repeatedly measured for the determination of DO₂ and VO₂ in 40 patients undergoing CPB, every 8h during the first 48h postoperatively. As a control, 20 patients who had suffered acute myocardial infarction (AMI) were also studied using the same protocol. In the CPB group, a regression analysis showed that VO₂ was significantly dependent on DO₂, even within the physiologic range of DO₂ (>500 ml/min per m²); VO₂=121.4+0.0844×DO₂ (r=0.254,P=0.023). Conversely, in the AMI group, no such supply-dependent consumption was observed within the same range of DO₂. At an ER of 30%, which is the optimal value in general, the DO₂ of the CPB group was 575 ml/min per m² and that of the AMI group was 493 ml/min per m². All these results suggest that patients undergoing CPB need a much higher oxygen supply to recover from the oxygen debt acquired during open heart surgery.     

Nitric oxide inhalation increases oxygen delivery after cardiovascular surgery in adult patients whether or not they have pulmonary hypertension

Purpose The purpose of this study was to quantify the increase in oxygen delivery (DO₂) produced by nitric oxide (NO) inhalation, and to clarify whether NO inhalation might be effective in adult patients after cardiovascular surgery whether or not they have pulmonary hypertension (PH). Methods The study was done on 26 adult patients after cardiovascular surgery. The indications for NO inhalation were postoperative hypoxic respiratory failure (POHRF) with or without PH. NO was administered via a premixing system or via a side-stream system. The dose was adjusted to between 1 and 10 (5.7±2.0) (mean±SD) ppm. Data were obtained just before and within 120 min after the initiation of NO inhalation. We initially analyzed the data from all the patients together and then compared data from two groups made up from just 22 of the 26 patients: 14 patients without PH whose PaO₂/FiO₂ before NO inhalation was less than 200 mmHg (simple POHRF group), and 8 patients who had both POHRF and PH (systolic pulmonary arterial pressure higher than 40 mmHg) (POHRF with PH group). Results In the original group of 26 patients, significant improvements were observed in PaO₂, PaO₂/FiO₂, CI, SPAP, CaO₂, DO₂I, and SvO₂ during NO inhalation. The increase in DO₂I was 68 ml·min⁻¹·m⁻² (+19.5%). PaO₂, PaO₂/FiO₂, CaO₂, DO₂I, and SvO₂ increased significantly in both groups. The increase in DO₂I was 60 ml·min⁻¹·m⁻² (+18.9%) in the simple POPHRF group and 79ml·min⁻¹·m⁻² (+18.0%) in the POHRF with PH group. Conclusion NO inhalation increases DO₂ by approximately 20% in adult patients after cardiovascular surgery, irrespective of whether or not they have pulmonary hypertension.     

Sodium nitroprusside after cardiac surgery: systemic and splanchnic blood flow and oxygen transport

Background: Vasoactive drugs may interfere with splanchnic blood flow and tissue oxygenation. Sodium nitroprusside (SNP) is widely used in the treatment of postoperative hypertension after cardiac surgery, but the effects of SNP and other vasodilators on splanchnic blood flow have not been well documented. Methods: The effects of SNP on systemic blood flow, oxygen transport and gastric intramucosal pH (pH_i) were studied in 12 patients with arterial hypertension after coronary artery bypass grafting. In 9 of these patients, the effect on regional (splanchnic and leg) blood flow and oxygen transport was also measured. Hemodynamic and regional blood flow responses were measured before and during SNP infusion (mean 2.8±1.7 μg/kg/min, range 0.6-6.3 μg/kg/min), when the goal of the vasodilator treatment, mean arterial pressure 70–80 mmHg, had been reached. Results: SNP increased splanchnic (0.65±0.22 vs. 0.87±0.37 L·min^-1·m^-2, P<0.01) and femoral blood flow (0.15±0.04 vs. 0.21±0.06 L·min^-1·m^-2, P<0.05) in parallel with cardiac index (2.6±0.6 vs. 3.3±0.7 L·min^-1·m^-2, P<0.01). Fractional regional blood flows did not change. Mean gastric intramucosal pH decreased slightly (7.40±0.07 vs. 7.37±0.06, P<0.05). Both systemic (420±85 vs. 495±90 mL·min^-1·m^-2, P<0.05) and femoral oxygen delivery (25±5 vs. 32±10 mL·min^-1·m^-2, P<0.05) increased, but neither systemic nor regional oxygen consumption changed. Conclusions: These results suggest that vasoregulation is well preserved during treatment of early postoperative hypertension with SNP, and that SNP has no adverse effects on splanchnic tissue oxygenation.     

Regional cerebral oxygenation by NIRS does not correlate with central or jugular venous oxygen saturation during interventional catheterisation in children

Purpose: To evaluate whether regional cerebral oxygenation (rSO₂) by near‐infrared spectroscopy correlates with central venous (SvO₂) or internal jugular (SjO₂) oxygen saturation, and whether changes over time (Δ) in rSO₂ (ΔrSO₂) predict changes in SvO₂ (ΔSvO₂) and SjO₂ (ΔSjO₂). Methods: The rSO₂ values were measured using the INVOS 5100 cerebral oximeter in children undergoing interventional cardiac catheterization and were compared with the oxygen saturation of analysed central venous and internal jugular blood samples. Changes over time (Δ) were calculated as the difference between the values before and after catheter intervention for rSO₂·(ΔrSO₂), SvO₂·(ΔSvO₂) and SjO₂·(ΔSjO₂). Simple regression and Bland–Altman analysis were performed. Data are presented as median (range). Results: Sixty patients aged 4.3 (0.2–16.0) years were investigated. A closer correlation was found between rSO₂ and SvO₂ (r=0.728, P<0.0001) than between rSO₂ and SjO₂ (r=0.665, P<0.0001). The bias between rSO₂ and SvO₂·(SjO₂) was 0.17% (?0.60%), with limits of agreement from ?15.5% to 15. 9% (?18.6–17.4%). The sensitivity/specificity for ΔrSO₂ to indicate a fall in SvO₂ or in SjO₂ was 70.3%/65.2% and 68.6%/60.0%, respectively. Conclusion: Neither absolute values nor changes in rSO₂ using the INVOS 5100 allowed reliable estimation of SvO₂ or SjO₂ and their trends.     

Reliability of the sit-up test in individuals with spinal cord injury

Abstract

Objective

To determine the day-to-day reliability of blood pressure responses during a sit-up test in individuals with a traumatic spinal cord injury (SCI).

Design

Within-subject, repeated measures design.

Setting

Community outpatient assessments at a research laboratory at the University of British Columbia.

Participants

Five men and three women with traumatic SCI (age: 31 ± 6 years; C4-T11; American Spinal Injury Association Impairment Scale A-B; 1–17 years post-injury).

Outcome measure

Maximum change in systolic (ΔSBP) and diastolic (ΔDBP) blood pressure upon passively moving from a supine to seated position.

Results

The average values for ΔSBP were –11 ± 13 mmHg (range –38 to 3 mmHg) for visit 1, and ?12 ± 8 mmHg (range ?26 to ?1 mmHg) for visit 2. The average values for ΔDBP were ?9 ± 8 mmHg (range -21 to 0 mmHg) for visit 1, and –13 ± 8 mmHg (range –29 to –3 mmHg) for visit 2. The ΔSBP demonstrated substantial reliability with an intraclass correlation coefficient of 0.79 (P = 0.006; 95% CI 0.250–0.953), while the ΔDBP demonstrated almost perfect reliability with an intraclass correlation coefficient of 0.92 (P < 0.001; 95% CI 0.645–0.983). The smallest detectable differences in ΔSBP and ΔDBP were 7 mmHg and 6 mmHg, respectively.

Conclusion

Blood pressure responses to the sit-up test are reliable in individuals with SCI, which supports its implementation as a practical bedside assessment for orthostatic hypotension in this at risk population.     

Effect of high-frequency jet ventilation on oxygenation during one-lung ventilation in patients undergoing thoracic aneurysm surgery

Purpose To evaluate the effect of high-frequency jet ventilation (HFJV) and continuous positive airway pressure (CPAP) on oxygenation and the shunt fraction (Qs/Qt) during one-lung ventilation (OLV). Methods Twenty-five patients who were undergoing resection of a descending aortic aneurysm were studied. Arterial oxygenation, Qs/Qt, and hemodynamics were evaluated just before the initiation of OLV (T₁), 15 min after OLV (T₂), and 15 min (T₃) and 30 min (T₄) after the application of HFJV or CPAP to the nondependent lung. Results There were no significant changes in the mean arterial blood pressure (MAP), heart rate (HR), central venous pressure (CVP), or mixed venous partial pressure of oxygen throughout this study. The arterial partial pressure of oxygen (Pa_O2) values after the application of HFJV or CPAP increased significantly, from 173.8 ± 39.6 mmHg (T₂) to 344.1 ± 87.9 mmHg (T₃) and 359.9 ± 82.4 mmHg (T₄) in the HFJV group (P < 0.05), and from 153 ± 38.5 mmHg (T₂) to 243 ± 48.5 mmHg (T₃) and 249.7 ± 55.0 mmHg (T₄) in the CPAP group (P < 0.05). The shunt fraction decreased significantly after the initiation of HFJV or CPAP, from 38.7% ± 8.9% (T₂) to 27.0% ± 8.0% (T₃) and 25.9% ± 8.7% (T₄) in the HFJV group (P < 0.05), and from 44.6% ± 8.6% (T₂) to 34.3% ± 10.2% (T₃) and 32.6% ± 8.5% (T₄) in the CPAP group (P < 0.05). The arterial saturation of oxygen (Sa_O2) increased significantly after the application of either HFJV or CPAP (P < 0.05). Conclusions Both HFJV and CPAP can improve oxygenation during OLV.     

Continuous measurement of oxygen consumption using the reversed fick method

We developed a continuous oxygen consumption (Vo₂) measurement system employed the reversed Fick method, in which Vo₂ in computed from continuously measured sured arterial and mixed venous oxygen saturation assed by pulse oximetry and mixed venous oximetry, respectively, and cardiac output by the heat deprivation technique. This system was compared with the conventional intermittent reversed fick method in 7 patients during surgery and with indirect calorimetry in 4 intensive care unit (ICU) patients. The Vo₂ measured by the continuous reversed Fick method showed a high correlation with those simultaneously measured by the intermittent Fick method (r=0.97,P<0.01) and by indirect calorimetry (r=0.74,P<0.01). The 95% confidence limits (bias±2 SD) of the continuous reversed Fick method were −0.6±45 ml·min⁻¹ with the intermittent Fick method and −31±56 ml·min⁻¹ with indirect calorimetry. The continuous Fick method is in satisfactory agreement with the conventional methods for the measured of Vo₂ and potentially allows for convenient assessment of Vo₂ in critically ill patients. This study was supported in part by Grants-in-Aid for the Encouragement of Young Scientists 01771185 and 04857171 from the Ministry of Education, Science and Culture of Japan     

Dexmedetomidine Alters the Cardiovascular Response During Infra-Renal Aortic Cross-Clamping in Sevoflurane-Anesthetized Dogs

Some properties of the volatile anesthetics, such as vasodilatation and myocardial depression, combined with the sympathetic inhibition that α2-agonists can produce, may determine hemodynamic alterations during aortic surgery. The interaction between dexmedetomidine (DEX), an α2-agonist, and sevoflurane during aortic surgery is unknown. We studied the effects of DEX on hemodynamics and systemic oxygenation during aortic cross-clamping (Aox) and unclamping (UAox) in sevoflurane-anesthetized dogs. Twenty dogs were anesthetized with sevoflurane and were randomly assigned to two groups prior to Aox and UAox: control, n = 10, received saline infusion only, and DEX (1 μg.kg^?1 load followed by 1 μg.kg^?1.h^?1 infusion), n = 10. Hemodynamic and oxygenation variables were measured at baseline, after saline or DEX loading dose, 20 and 40 min after Aox, and 20 and 40 min after UAox. After DEX administration, heart rate, cardiac index (CI) and systemic oxygen transport index (DO₂I) were lower than in control group. Aox increased mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) in both groups, but the effects were greater with DEX. CI, heart rate, and DO₂I were lower, while central venous pressure (CVP) and pulmonary artery occlusion pressure were higher in DEX compared to control. After UAox, MAP, CVP and SVRI were maintained higher in DEX in relation to control. We conclude that in sevoflurane-anesthetized dogs DEX alters the cardiovascular response during aortic surgery.     

Central and mixed venous blood oxygen correlate well during acute normovolemic hemodilution in anesthetized pigs

Background : Central venous oxygen saturation (S_cvO₂) and oxygen tension (p_cvO₂), obtained from the superior vena cava, correlate well with mixed venous (pulmonary arterial) oxygen saturation (S_vO₂) and tension (p_vO₂) when the hematocrit is normal. The present study was undertaken to assess whether extreme hemodilution affects this relation. Methods : We compared mixed and central venous blood during graded arterial desaturation (inspired fraction of oxygen (F_IO₂) between 1.0 and 0.10) in 10 hemodiluted pigs, and in 10 pigs with normal hematocrit (control), during fentanyl-ketamine-pancuronium anesthesia and mechanical ventilation. Results : Arterial oxygen saturation decreased from 100% at F_IO₂=1.0 to 44 ± 12% at F_IO₂=0.10 (mean ± SD). Venous oxygen saturation ranged from 3.5% to 97.3%. The regression coefficient between S_vO₂ and S_cvO₂ was 0.97 (R²= 0.93, bias -2.4 ± 5.8%) in the hemodiluted and 0.99 (R²= 0.97, bias -3.0 ± 5.0%) in the control group. Venous oxygen tension values ranged from 0.5 kPa to 9.5 kPa, and the regression coefficient for oxygen tension was 0.94 (R²= 0.89, bias -0.20 ± 0.47 kPa) in the hemodiluted and 0.99 (R²= 0.97, bias -0.43 ± 0.48 kPa) in the control group. The regression coefficient for pH was 0.95 in the hemodiluted and 0.98 in the control animals. Conclusion : The findings indicate that also during hemodilution monitoring of central venous blood oxygen may be as useful as monitoring of mixed venous blood oxygen.     

临时性腔门静脉半转位术在门静脉栓塞患者肝移植术中作用

摘要：目的:探讨临时性腔门静脉半转位术(TCPHT)在门静脉栓塞(PVT)患者经典非转流肝移植(OLT)中的应用价值。 方法:总结5年间32例肝移植术前合并Yerdel Ⅲ~Ⅳ级PVT患者中11例施行TCPHT术（TCPHT组）、21例未施行TCPHT术(对照组)者的临床资料。比较两组患者的手术时间和无肝期时间、再灌注期平均动脉压（MAP）、中心静脉压（CVP）和肺动脉楔压（PAWP）等循环参数以及无肝期尿量、再灌注期尿量等肾功能参数。结果:TCPHT组和对照组手术时间和无肝期时间均无显著性差异（P>0.05）。两组比较，虽然术后第1天肾功能指标差异无显著性，但TCPHT组无肝期尿量明显增加，两者分别为（64.09±20.79）mL和（25.90±12.17）mL （P=0.033)；再灌注期尿量分别是(1254.56±311.81) mL和（800.00±375.83）mL,（P=0.002)，且TCPHT组术后需要透析的病例数较对照组显著减少(P<0.05)。体循环血流动力学显示，TCPHT组较对照组开放后具有更加稳定的MAP，两组分别为(76.45±12.67)mmHg和（66.52±7.48）mmHg（P=0.032)；CVP分别为（13.96±1.74）cm H2O和（12.44±1.07）cm H2O （P=0.005)；PAWP分别为（24.04±1.48）mmHg和（22.81±1.23）mmHg （P=0.018)。结论:TCPHT能有效地稳定门静脉栓塞患者肝移植再灌注期血流动力学，减少术后肾功能不全的发生率，而不增加手术难度。