We present a narrative review focusing on the new role of nociception monitor in intraoperative anesthetic management. Higher invasiveness of surgery elicits a higher degree of surgical stress responses including neuroendocrine-metabolic and inflammatory-immune responses, which are associated with the occurrence of major postoperative complications. Conversely, anesthetic management mitigates these responses. Furthermore, improper attenuation of nociceptive input and related autonomic effects may induce increased stress response that may adversely influence outcome even in minimally invasive surgeries. The original role of nociception monitor, which is to assess a balance between nociception caused by surgical trauma and anti-nociception due to anesthesia, may allow an assessment of surgical stress response. The goal of this review is to inform healthcare professionals providing anesthetic management that nociception monitors may provide intraoperative data associated with surgical stress responses, and to inspire new research into the effects of nociception monitor-guided anesthesia on postoperative complications.

Microcirculatory alterations are frequently observed in critically ill patients undergoing major surgery and those who suffer from trauma or sepsis. Despite the need for adequate fluid administration to restore microcirculation, there is no consensus regarding optimal fluid therapy for these patients. The recent recognition of the importance of the endothelial glycocalyx layer in capillary fluid and solute exchange has largely changed our views on fluid therapy in critical illness. Given that disease status largely differs among critically ill patients, fluid therapy must not be considered generally, but rather tailored to the clinical condition of each patient. This review outlines the current understanding of context-sensitive volume expansion by fluid solutions and considers its clinical implications for critically ill patients. The modulation of capillary hydrostatic pressure through the appropriate use of vasopressors may increase the effectiveness of fluid infusion and thereby reduce detrimental effects resulting from excessive fluid administration.

Information is lacking concerning optimal infusion rates of crystalloid during resuscitation from acute haemorrhage. In this study, a mathematical model was used to predict infusion volume of crystalloid needed to restore and maintain blood volume after acute haemorrhage. The scenario was a haemorrhage of 15 ml kg⁻¹ over 30 min in a 70 kg man. A bolus of crystalloid was administered at a rate of 40, 60, 80, 100, or 120 ml kg⁻¹ h⁻¹ until blood volume was restored. Fluid infusion rate needed to maintain blood volume for a further 1 h was computed. Blood volume was restored earlier at high bolus infusion rates compared with low bolus infusion rates (6 min at 120 ml kg⁻¹ h⁻¹vs 63 min at 40 ml kg⁻¹ h⁻¹). Fluid infusion rates for blood volume maintenance approached 33 ml kg⁻¹ h⁻¹ irrespective of bolus infusion rates. The restoration fluid volume at 40 ml kg⁻¹ h⁻¹ was 2.9 litre, three times that at 80–120 ml kg⁻¹ h⁻¹. The maintenance fluid volume at 80–120 ml kg⁻¹ h⁻¹ was 2.9 litre, 0.6 litre more than that at 40 ml kg⁻¹ h⁻¹. During the blood volume maintenance, the interstitial volume increased to 3.8 litre above normal at 40 ml kg⁻¹ h⁻¹ and to 2.5 litre at 80–120 ml kg⁻¹ h⁻¹. Bolus crystalloid infusion exceeding 80 ml kg⁻¹ h⁻¹ may not increase effectiveness of fluid resuscitation. Crystalloid resuscitation for more than 2 h may be detrimental in view of an excessive net fluid retention.

BACKGROUND Fluid responsiveness is an important factor to consider for fluid volume loading during major surgery. The effect of continuous vasopressor infusion on fluid responsiveness during prolonged major surgery is a concern. OBJECTIVE We hypothesised that continuous vasopressor infusion during major surgery might not exert significant effects on changes in stroke volume variation (SVV) following fluid bolus infusion, and thereby on fluid responsiveness. DESIGN Randomised controlled trial. SETTING University hospital from April 2014 to August 2016. PATIENTS Patients undergoing liver resection who were randomised to receive continuous intravenous infusion of phenylephrine (P group), norepinephrine (N group), or no vasopressor (C group) (n=17/group). Exclusion criteria were cardiac arrhythmia and severe cardiac, pulmonary or renal dysfunction. INTERVENTION Patients received 4 ml kg⁻¹ fluid boluses of 6% hydroxyethyl starch solution when SVV was at least 12%. Vasopressors were administered continuously to maintain the systemic vascular resistance index at more than 1900 dyn s cm⁻⁵ m⁻². MAIN OUTCOME MEASURES Cardiac index and SVV were measured using the FloTrac^™/Vigileo^™ system (Version 4.00). The number of fluid boluses with fluid responsiveness (i.e. >15% increase in cardiac index) was compared between groups using multilevel logistic regression analysis. RESULTS Numbers of fluid responsive boluses in the C, P and N groups were 12 (14%), 22 (34%) and 19 (27%), respectively. Odds ratios on fluid responsiveness for phenylephrine and norepinephrine compared with the control were 3.65 (97.5% confidence interval, 1.15 to 11.6; P = 0.012) and 2.56 (97.5% confidence interval, 0.82 to 8.00; P = 0.064), respectively. Decreases in SVV after fluid bolus infusion for the P and N groups were comparable with the C group (P = 0.23 and 0.53, respectively). CONCLUSION Continuous administration of phenylephrine increased fluid responsiveness during liver resection, suggesting complex effects of continuous vasopressor infusion involving changes in cardiac preload and afterload. TRIAL REGISTRATION UMIN000011024.

Surgical injury causes acute sequestration of interstitial fluid in injured tissue. Fluid sequestration treated with IV fluid administration can lead to postoperative complications related to excessive intravascular volume. Quantitative prediction of interstitial fluid sequestration may foster a better understanding of the relationship between fluid administered and the resulting balance between intra- and extravascular fluid. We developed a mathematical model describing the dynamic distribution and transport of fluid and proteins with the goal of quantifying the balance of fluid between intra- and extravascular compartments. Fluid volume changes in the plasma, interstitial and urine compartments were calculated for a simulated 4 h abdominal surgery in a 70 kg male. To validate the model, we compared the results obtained with those measured by segmental bioelectrical impedance on 30 patients undergoing elective abdominal surgery. The model predicted that, compared to the normal state, surgical injury would result in the sequestration of 705 mL of interstitial fluid in injured tissue, whereas plasma volume would undergo a 356 mL decrease. During surgery, it was not possible to obtain a normal plasma volume, even with fluid replacement at a rate of almost 20 mL x kg(-1) x h(-1). Bias and limit of agreement on interstitial fluid volume changes in body segments between bioelectrical impedance and model prediction were -131 and 325 mL, respectively for limbs, and -157 and 834 mL for the trunk. The model shows that increasing the fluid replacement rate above 10 mL x kg(-1) x h(-1) does not have the desired effect on plasma volume but instead increases the interstitial volume.

We demonstrated that acoustic waves could induce nucleation of both a ${}^4\mathrm{He}$ crystal in superfluid and a superfluid droplet in the crystal in the same temperature range depending on whether an acoustic transducer was covered by the superfluid or the crystal. The temperature dependences of crystal nucleation at and above the melting pressure and that of superfluid droplet nucleation at the melting pressure were investigated systematically by changing the acoustic wave powers. The nucleation processes were monitored by a high-speed camera. Crystals were nucleated above the melting pressure in a metastable superfluid when the sum of the overpressure and the effective overpressure by the acoustic wave reached a threshold value. Crystal nucleation above the melting pressure was effectively induced by acoustic waves at low temperatures and was not induced at all above $800\mathrm{mK}$. Crystal nucleation at the melting pressure was induced when the acoustic wave power exceeded a threshold value. The threshold was temperature independent below $300\mathrm{mK}$ and increased divergently approaching $600\mathrm{mK}$. We saw no sign of nucleation above $600\mathrm{mK}$ even in our maximum acoustic wave power. Superfluid droplet nucleation at the melting pressure was also induced above a threshold power. The threshold was temperature independent at low temperatures with a small maximum at $600\mathrm{mK}$ and decreased with warming at high temperatures. All the behaviors cannot be explained by mere heating, and a possible effect of acoustic radiation pressure on the nucleation is discussed.