Isoflurane in contrast to propofol promotes fluid extravasation during cardiopulmonary bypass in pigs.

BACKGROUND: A highly positive intraoperative fluid balance should be prevented as it negatively impacts patient outcome. Analysis of volume-kinetics has identified an increase in interstitial fluid volume after crystalloid fluid loading during isoflurane anesthesia. Isoflurane has also been associated with postoperative hypoxemia and may be associated with an increase in alveolar epithelial permeability, edema formation, and hindered oxygen exchange. In this article, the authors compare fluid extravasation rates before and during cardiopulmonary bypass (CPB) with isoflurane- versus propofol-based anesthesia. METHODS: Fourteen pigs underwent 2 h of tepid CPB with propofol (P-group; n = 7) or isoflurane anesthesia (I-group; n = 7). Fluid requirements, plasma volume, colloid osmotic pressures in plasma and interstitial fluid, hematocrit levels, and total tissue water content were recorded, and fluid extravasation rates calculated. RESULTS: Fluid extravasation rates increased in the I-group from the pre-CPB level of 0.27 (0.13) to 0.92 (0.36) ml·kg·min, but remained essentially unchanged in the P-group with significant between-group differences during CPB (pb = 0.002). The results are supported by corresponding changes in interstitial colloid osmotic pressure and total tissue water content. CONCLUSIONS: During CPB, isoflurane, in contrast to propofol, significantly contributes to a general increase in fluid shifts from the intravascular to the interstitial space with edema formation and a possible negative impact on postoperative organ function.

Repeated magnetic resonance imaging and cerebral performance after cardiac arrest--a pilot study.

AIM OF THE STUDY: Prognostication may be difficult in comatose cardiac arrest survivors. Magnetic resonance imaging (MRI) is potentially useful in the prediction of neurological outcome, and it may detect acute ischemia at an early stage. In a pilot setting we determined the prevalence and development of cerebral ischemia using serial MRI examinations and neurological assessment. METHODS: Ten witnessed out-of-hospital cardiac arrest patients were included. MRI was carried out approximately 2h after admission to the hospital, repeated after 24h of therapeutic hypothermia and 96 h after the arrest. The images were assessed for development of acute ischemic lesions. Neurophysiological and cognitive tests as well as a self-reported quality-of-life questionnaire, Short Form-36 (SF-36), were administered minimum 12 months after discharge. RESULTS: None of the patients had acute cerebral ischemia on MRI at admission. Three patients developed ischemic lesions after therapeutic hypothermia. There was a change in the apparent diffusion coefficient, which significantly correlated with the temperature (p < 0.001). The neurophysiological tests appeared normal. The patients scored significantly better on SF 36 than the controls as regards both bodily pain (p = 0.023) and mental health (p = 0.016). CONCLUSIONS: MRI performed in an early phase after cardiac arrest has limitations, as MRI performed after 24 and 96 h revealed ischemic lesions not detectable on admission. ADC was related to the core temperature, and not to the volume distributed intravenously. Follow-up neurophysiologic tests and self-reported quality of life were good.

Capillary leakage in post-cardiac arrest survivors during therapeutic hypothermia - a prospective, randomised study.

BACKGROUND: Fluids are often given liberally after the return of spontaneous circulation. However, the optimal fluid regimen in survivors of cardiac arrest is unknown. Recent studies indicate an increased fluid requirement in post-cardiac arrest patients. During hypothermia, animal studies report extravasation in several organs, including the brain. We investigated two fluid strategies to determine whether the choice of fluid would influence fluid requirements, capillary leakage and oedema formation. METHODS: 19 survivors with witnessed cardiac arrest of primary cardiac origin were allocated to either 7.2% hypertonic saline with 6% poly (O-2-hydroxyethyl) starch solution (HH) or standard fluid therapy (Ringer's Acetate and saline 9 mg/ml) (control). The patients were treated with the randomised fluid immediately after admission and continued for 24 hours of therapeutic hypothermia. RESULTS: During the first 24 hours, the HH patients required significantly less i.v. fluid than the control patients (4750 ml versus 8010 ml, p = 0.019) with comparable use of vasopressors. Systemic vascular resistance was significantly reduced from 0 to 24 hours (p = 0.014), with no difference between the groups. Colloid osmotic pressure (COP) in serum and interstitial fluid (p < 0.001 and p = 0.014 respectively) decreased as a function of time in both groups, with a more pronounced reduction in interstitial COP in the crystalloid group. Magnetic resonance imaging of the brain did not reveal vasogenic oedema. CONCLUSIONS: Post-cardiac arrest patients have high fluid requirements during therapeutic hypothermia, probably due to increased extravasation. The use of HH reduced the fluid requirement significantly. However, the lack of brain oedema in both groups suggests no superior fluid regimen. Cardiac index was significantly improved in the group treated with crystalloids. Although we do not associate HH with the renal failures that developed, caution should be taken when using hypertonic starch solutions in these patients. TRIAL REGISTRATION: NCT00347477.

Surface cooling versus core cooling: comparative studies of microvascular fluid- and protein-shifts in a porcine model.

OBJECTIVE: To describe how surface cooling compared with core cooling influences fluid and protein distribution, vascular capacity and hemodynamic variables. METHODS: 14 anesthetized piglets were, following 60 min normothermic stabilization, randomly cooled by surface cooling (ice-sludge) (n=7) or core cooling (endovascular cooling) (n=7) to about 28 degrees C. Fluid balance, hemodynamic variables, colloid osmotic pressures (plasma/interstitial fluid), hematocrit, serum-albumin and -protein concentrations, intracranial pressure (ICP) and cerebral metabolic markers of ischemia were measured. Fluid shifts and changes in albumin and protein masses were calculated. At the end total tissue water content was assessed and compared with a normothermic control group. RESULTS: Both cooling modes induced an increase in fluid extravasation rate from 33.9 (31.9) and 27.8 (28.0) to 109.0 (16.5) (P=0.006) and 95.6 (29.1) ml/kg/min x 10(-3) (P=0.024) in the surface-cooled and core-cooled groups, respectively. Albumin extravasation was reflected by a significant drop in the albumin mass from 148.8 (11.7) to 111.4 (10.3) (P=0.000) and from 163.4 (27.8) to 136.8 (19.0) g/kg x 10(-2) (P=0.001) in the surface-cooled and core-cooled animals, respectively. Similar findings were obtained concerning serum-protein masses. The total tissue water content increased in most organs including brain in both study groups compared with a control. ICP and cerebral metabolic markers remained normal in both groups. CONCLUSION: Rapid lowering of body core temperature results in extravasation of water and proteins. The amount of extravated fluid and proteins is similar either cooling is a result of surface cooling or core cooling. Cold-induced fluid extravasation is associated with edema in most tissues including brain.

Time course variations of haemodynamics, plasma volume and microvascular fluid exchange following surface cooling: an experimental approach to accidental hypothermia.

OBJECTIVE: To describe how surface cooling influences fluid distribution, vascular capacity and haemodynamic variables. METHODS: Seven anaesthetised pigs, following normothermic stabilization for 60 min, were cooled to 27.8+/-1.6 degrees C. Fluid balance, haemodynamics, colloid osmotic pressures (plasma/interstitial fluid), haematocrit [s-albumin/protein] were recorded and plasma volume measured together with tissue perfusion during normothermia, cooling and stable hypothermia (coloured microspheres). Fluid shifts and changes in albumin and protein masses were calculated. At the end tissue water content was assessed. RESULTS: Haemodynamic variables changed with the start of cooling in parallel with a decreasing cardiac output. During hypothermia the haematocrit increased from 0.31+/-0.01 to 0.35+/-0.01 (P < 0.01). Plasma volume decreased from 1139.0+/-65.4 ml at start of cooling to 882.0+/-67.5 ml 3 h later (P < 0.05). In parallel the plasma albumin and protein masses decreased from 37.8+/-2.5 g and 54.6+/-4.0 g to 28.0+/-2.7 g (P < 0.05) and 41.2+/-4.1 g (P > 0.05), respectively. The main changes occurred 120-180 min after start of each experiment. In this period the fluid extravasation rate was elevated (P < 0.05) without influencing the colloid osmotic pressure of plasma/interstitial fluid. The increased fluid filtration was reflected by an increase in tissue water content. CONCLUSION: Our results are in favour of a shift of plasma from circulation to the interstitial space during surface cooling. This conclusion is based on the parallel losses of fluid and proteins from circulation with unchanged colloid osmotic pressures (plasma/interstitial fluid). Inflammation may be involved.