Central venous oxygen saturation and carbon dioxide gap as resuscitation targets in a hemorrhagic shock.

BACKGROUND: Fluid resuscitation is still a major challenge. We aimed to describe changes in central venous oxygen saturation (ScvO2 ) and venous-to-arterial carbon dioxide gap (dCO2 ) during an experimental stroke volume (SV) index (SVI)-guided hemorrhage and fluid resuscitation model in pigs. METHODS: Twelve anesthetized, mechanically ventilated pigs were bled till baseline SVI (Tbsl ) dropped by 50% (T0 ), thereafter fluid resuscitation was performed with balanced crystalloid in four steps until initial SVI was reached (T4 ). Statistical analysis was performed with Statistical Program for Social Sciences version 18.0; data are expressed as mean ± standard deviation. RESULTS: After bleeding, ScvO2 dropped (Tbsl = 78 ± 7 vs. T0 = 61 ± 5% P < 0.05) and oxygen extraction ratio increased (Tbsl = 0.20 ± 0.07 vs. T0 = 0.36 ± 0.05, P < 0.05). By T4 the ScvO2 normalized, but on average it remained 5% lower than at Tbsl (T4 = 73 ± 9% P < 0.05) and oxygen extraction also remained higher as compared with Tbsl (T4 = 0.24 ± 0.09 P = 0.001). ScvO2 showed significant correlation with SVI (r = 0.564, P < 0.001). dCO2 increased during hypovolemia (Tbsl :5.3 ± 2.0 vs. T0 :9.6 ± 2.3 mmHg, P = 0.001), then returned to normal by T4 = 5.1 ± 2.6 mmHg, and it also showed significant correlation with SVI (R = -0.591, P < 0.001) and oxygen extraction (R = 0.735, P < 0.001). CONCLUSIONS: In this SV-guided bleeding and fluid resuscitation model, both ScvO2 and dCO2 correlated well with changes in SV, but only the dCO2 returned to its baseline, normal value, while ScvO2 remained significantly lower than at baseline. These results suggest that dCO2 may be a good hemodynamic endpoint of resuscitation, while ScvO2 is not strictly a hemodynamic parameter, but rather an indicator of the balance between oxygen delivery and consumption.

Inflammatory activation after experimental cardiac tamponade.

BACKGROUND/PURPOSE: Cardiac tamponade is a medical emergency situation associated with a high rate of life-threatening complications, even after immediate interventions. Our aim was to characterize the acute inflammatory consequences of this event in a clinically relevant large animal model. METHODS: Cardiac tamponade was induced for 60 min in anesthetized, ventilated and thoracotomized minipigs by intrapericardial fluid administration, the mean arterial pressure (MAP) being maintained in the interval of 40-45 mm Hg (n = 8). A further group (n = 7) served as sham-operated control. The global macrohemodynamics, including the right- and left-heart end-diastolic volumes (RHEDV and LHEDV), the pulmonary vascular resistance index (PVRI) and the superior mesenteric artery (SMA) flow, were monitored for 240 min, and the intestinal microcirculatory changes (pCO2 gap) were evaluated by indirect tonometry. Blood samples were taken for the determination of cardiac troponin T and vasoactive inflammatory mediators, including histamine, nitrite/nitrate, big-endothelin, superoxide and high-mobility group box protein-1 levels in association with intestinal leukocyte and complement activation. RESULTS: The cardiac tamponade induced significant decreases in MAP, cardiac output, LHEDV and SMA flow, while the PVRI and the pCO2 gap increased significantly. After the removal of fluid from the pericardial sac, the MAP and the LHEDV were decreased, while the PVRI and the pCO2 gap remained elevated when compared with those in the sham-operated group. In the posttamponade period, the abrupt release of inflammatory mediators was accompanied by a significant splanchnic leukocyte accumulation and complement activation. CONCLUSIONS: The macrocirculatory and splanchnic microcirculatory disturbances were accompanied by a significant proinflammatory reaction; endothelin and the complement system may be significant components of the inflammatory cascade that is activated in this porcine model of pericardial tamponade.

Central venous oxygen saturation is a good indicator of altered oxygen balance in isovolemic anemia.

BACKGROUND: Red blood cell transfusion is done primarily as a means to improve oxygen delivery (DO2). Current transfusion guidelines are based solely on hemoglobin levels, regardless of actual DO2 need. As central venous oxygen saturation (ScvO2) may reflect imbalances in DO2 and consumption (VO2) the aim of this study was to investigate the value of ScvO2 as an indicator of oxygen balance in isovolemic anemia. METHODS: After splenectomy, anesthetized Vietnamese mini pigs (n = 13, weight range: 18-30 kg) underwent controlled bleeding in five stages (T0-T5). During each stage approximately 10% of the estimated starting total blood volume was removed and immediately replaced with an equal volume of colloid. Hemodynamic measurements and blood gas analysis were then performed. RESULTS: Each stage of bleeding resulted in a significant fall in hemoglobin, T0 : 125 (113-134) to T(5) : 49 (43-55) g/l [T0 : 7.7 (6.9-8.2) to T5 : 3.0 (2.6-3.4) mmol/l]. The O2-extraction (VO2/DO2) increased significantly only from T3 : 35 (21-40) %, P < 0.05. The change of ScvO2 showed a similar pattern and dropped below the physiological threshold of 70% at T4 : 68 (61-76) %. At this point, hemoglobin was below the recommended transfusion trigger value, 59 (53-67) g/l [3.6 (3.3-4.1) mmol/l]. There was a strong significant association between ScvO2< 70%) and VO2/DO2 > 30%): r = -0.71, r² = 0.50, P < 0.001. CONCLUSION: The results of this study show that ScvO2 reflects changes of VO2/DO2 in isovolemic anemia better than Hb alone, therefore it may be used as an additional indicator of blood transfusion in clinical practice.

N-Methyl-D-aspartate receptor antagonism decreases motility and inflammatory activation in the early phase of acute experimental colitis in the rat.

BACKGROUND: Inflammatory bowel diseases are accompanied by severe motility disorders. The aim of our study was to investigate whether the blockade of peripheral N-methyl-D-aspartate (NMDA)-sensitive glutamate receptors (NMDA-Rs) alters motility changes in chemically induced acute colitis and how this modulation is accomplished. METHODS: The inflammatory and motility changes in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis were studied in anaesthetized Wistar rats following treatment with the natural NMDA-R antagonist kynurenic acid (KynA) or SZR-72, a blood-brain barrier-permeable synthetic KynA analogue. The macrohaemodynamics, serosal microcirculation (visualized by intravital videomicroscopy), plasma levels of tumour necrosis factor alpha (TNF-alpha), inflammatory enzyme activities (xanthine oxidoreductase (XOR), myeloperoxidase (MPO) and nitric oxide synthase (NOS)), and colonic motility (with a strain-gauge technique) were evaluated 17 h after colitis induction and compared with the control conditions. KEY RESULTS: The TNBS enema induced a systemic hyperdynamic circulatory reaction, increased the serosal capillary blood flow, significantly elevated the mucosal XOR, MPO and NOS activities and augmented the colonic motility relative to the controls. The NMDA-R antagonist treatment with KynA or SZR-72 significantly reduced the XOR, NOS and MPO activities, decreased the motility and increased the tone of the colon. CONCLUSIONS & INFERENCES: These data demonstrate a potential modulatory mechanism of NMDA-R in altered colonic motility in TNBS colitis. Inhibition of the enteric NMDA-Rs may provide a therapeutic option via which to influence intestinal hypermotility, microcirculatory changes and inflammatory activation simultaneously.