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Background The relationship between low oxygen delivery (DO2) on cardiopulmonary bypass and morbidity and mortality following cardiac surgery remains unexamined. Methods We reviewed patients undergoing Society of Thoracic Surgeons index procedures from March 2019 to July 2020, coincident with implementation of a new electronic perfusion record that provides for continuous recording of DO2 and flow parameters. Continuous perfusion variables were analyzed using area-over-the-curve (AOC) calculations below predefined thresholds (DO2 24 hours, stroke, sternal wound infection, and reoperation). Results Eight hundred thirty-four patients were included; 42.7% (356) underwent isolated coronary artery bypass grafting (CABG), whereas 57.3% underwent nonisolated CABG (eg, valvular or combined CABG/valvular operations). DO2 24 hours (P = .04), an effect again most pronounced in nonisolated-CABG cases (P = .002), as well as acute kidney injury Conclusions Low DO2 on bypass may be associated with morbidity/mortality following cardiac surgery, particularly in patients undergoing nonisolated CABG. These results underscore the importance of goal-directed perfusion strategies.

Intraoperative hypotension (IOH) is a major concern to the anesthesiologist. Its appropriate identification and management require an understanding of the physiology of blood pressure regulation, prudent blood pressure monitoring, and treatment. Even short durations of low mean arterial pressure have been associated with adverse postoperative clinical outcomes. The challenge is for the clinician to respond proactively, address the specific etiology of IOH, and keep in mind any changes to the patient's physiology. Predictive technology, such as the Hypotension Prediction Index, offers the clinician new insight into IOH. It has been shown to predict hypotension up to 15 minutes before occurrence. It also calculates stroke volume variation, dynamic arterial elastance, and left ventricular contractility, which can inform the anesthesiologist of the etiology of IOH to direct management. This new technology has the potential to reduce duration or even prevent IOH. In the authors' opinion, it is an example of how human-machine interaction will contribute to future advances in medicine. Additional studies should evaluate the effects of its use on postoperative outcomes.

Background and objective: Fluid overload is an important factor of morbidity and mortality in hemodialysis patients. Today correct determination of dry weight (DW) remains an important issue of hemodialysis practice. Within this context, it is subjected to new method searching. The objective of this study was to calculate estimated pulmonary capillary wedge pressure (ePCWP) with Tissue Doppler Imaging (TDI) in hemodialysis patients and to evaluate its correlation with the other volume markers and to evaluate whether it can be a new method for detection of DW. Materials and methods: Echocardiographic, hemodynamic, and biochemical volume markers of 41 hemodialysis patients were evaluated in the pre- and post-dialysis periods. Patients were divided into two groups based on ePCWP values (Group 1 ePCWP 20 mmHg). Results: In the pre-dialysis period; parameters related to volume load including ePCWP, systolic blood pressure, mean arterial pressure, pulse pressure, left atrial diameter, left atrial volume, E/e, ratio and E/V-p ratio were statistically significantly higher in Gmup2 compared to Group1. On the other hand, strong correlations were found between pre-dialysis ePCWP and systolic blood pressure, mean arterial pressure, pulse pressure, NT-ProBNP, left atrial diameter, E/e ratio and E/V-p ratio. Conclusions: Strong correlations found between ePCWP which was calculated with TDI and the other volume markers both in pre-dialysis and post-dialysis periods. These findings can provide a significant contribution to routine evaluating of DW in hemodialysis patients. From this aspect, the prediction of ePCWP with TDI can be a new practical and reproducible method for the determination of DW. (C) 2021 Sociedad Espanola de Nefrologia. Published by Elsevier Espana, S.L.U.

Introduction Intra- and postoperative nausea, vomiting and shivering are mentioned as the most common problem following spinal anesthesia. The aim of this study is to compare two different doses of granisetron to control the shivering, nausea, and vomiting caused by spinal anesthesia in women undergoing cesarean section (C/S). Method This study is a randomized, triple-blind clinical trial. The participants received 1-mg or 3-mg granisetron. Women who underwent elective C/S were enrolled. Inclusion criteria were ASA (American Society of Anesthesiologists) physical status grade I or II and age range of 18–40 years. Primary outcome was changes in the score of shivering, and nausea and vomiting. Secondary outcomes were Apgar score, mean arterial pressure, systolic blood pressure, diastolic blood pressure, temperature and heart rate. Results According to binary logistic regression, the incidence of shivering (6.9% vs. 1.5%; p-value = 0.049), and nausea and vomiting (19.2% vs. 9.2%; p-value = 0.024) was significantly higher in patients received 1-mg granisetron in comparison with 3-mg granisetron. Multinomial logistic regression showed that the occurrence of shivering, and nausea and vomiting were not associated with the dose of granisetron. There was no significant difference between the age and Apgar score of 1 (p = 0.908) and 5 (p = 0.843) minute(s) between the two groups. Conclusion This study showed that although 3-mg of granisetron reduces the incidence of intra- and postoperative shivering, nausea and vomiting after spinal anesthesia in comparison with 1-mg of granisetron, the difference was not statistically significant.

Introduction: It has been extensively highlighted that SARS-CoV-2 affects the RAS (renin-angiotensin system) and the angiotensinconverting enzyme-2 receptors play the most important role in the presentation of the COVID-19 disease 2-5 The ACE2 is type I membrane protein expressed on endothelial cells in the kidney, heart, gastrointestinal tract, blood vessels, and, importantly, lung AT2 alveolar epithelial cells, which are particularly prone to SARS-CoV-2 infection As SARS-CoV-2 is a new coronavirus, and its cardiovascular complications and the underlying pathology is still emerging However, it is accepted that the virus affects the total vasculature in the human body and this infection becomes a highly accelerated process for the target organ damage In the case of acute cardiological manifestation, it is termed as Acute COVID-19 Cardiovascular Syndrome (ACovCS) by the American Heart Association's white paper 6 European Society of Cardiology (ESC) has published a detailed review paper 7 on the involvement of various cardiovascular target organs in COVID-19 disease This review clearly establishes a close two-way relationship between COVID-19 disease and all cardiovascular diseases (CVD) The prognosis is even worse in patients with preexisting cardiovascular system involvement Cardiovascular involvement in COVID-19 is seen as a key manifestation The best way to assess endothelial dysfunction is an assessment of its clinical manifestation, i e , an increase in arterial stiffness There have been multiple in vitro and in vivo studies that have shown that the vascular endothelium is an important factor in setting the vascular tone and endothelial dysfunction leads to arterial stiffness 8 Arterial stiffness and enhanced wave reflections are markers of cardiovascular disease and independent predictors of cardiovascular risk 9-12 Stiffening of the large arteries and enhanced wave reflections lead to increased left ventricular (LV) afterload, disturbed coronary perfusion, and mechanical fatigue of the arterial wall 13 The relationship between systemic inflammation and arterial stiffness is well established in the literature 14 The cause-and-effect relationship that acute systemic inflammation leads to deterioration of large-artery stiffness Findings in study15 on induced inflammation have shown that an acute inflammation caused a temporary increase in central blood pressure and arterial stiffness in terms of pulse wave velocity This implies the increased risk of cardiovascular events associated with acute systemic inflammation in the COVID-19 COVID-19 diseaserelated worldwide research and proposed mechanisms pointed to pathophysiological involvement of endothelial dysfunction and arterial wall compromise However, there was no empirical evidence of the functional compromise of arterial walls Hence, a study was urgently needed to study an increase in arterial stiffness in COVID-19 patients due to systemic inflammation to stratify the risk and mitigate further cardiovascular damage with guided therapeutic treatment based on the severity of arterial stiffness This pressing need is justified by a comprehensive review article16 published after the present study was envisaged We hope that the findings from our study will fulfill the need to a large extent Objectives: Primary objective: To study if the measurement of arterial stiffness using pulse wave velocity in mild-moderate and a severe group of COVID-19 patients can stratify cardiovascular risk Secondary objective: To determine if initial measurements and subsequent changes in arterial stiffness can project the future course of the COVID-19 patient and hence predict the grade of clinical management a confirmed COVID-19 patient would require Materials and methods: The present prospective nonrandomized observational study {titled - “To study the relationship of COVID-19 severity with arterial stiffness: A prospective cross-sectional study” (“COSEVAST study”)} was conducted in the COVID-19 ICU, medical ICU, and various wards of dedicated COVID hospital at AIIMS, Patna, Bihar, India The study protocol, informed consents, and other trial-related documents received the written approval of the Institutional Ethics Committee (IEC No AIIMS/Pat/IEC/2020/595) The study design was registered with the Clinical Trials Registry of India (CTRI No CTRI/2020/10/028489) All COVID-19 patients were subject to RT-PCR test and had a confirmed infection of the SARS-CoV-2 virus Participants, after understanding the study protocol and procedures, gave their written informed consent for the study The exclusion criteria were known history of any of these diseases - diabetes mellitus (DM), hypertension (HTN), CAD, stroke, neuropathy, PAD, nephropathy, MI, pregnancy, peripheral edema or inflammation, cardiac arrhythmia, and any preexisting cardiovascular disorder Patient categorization: The selected patients after fulfilling the inclusion criteria were grouped into three categories - mild, moderate, and severe category based on the latest NIH Guidelines 27 as follows: •Mild category: Individuals with mild signs and symptoms like fever, cough, sore throat, malaise, headache, muscle pain, nausea, vomiting, diarrhea, loss of taste and smell but who do not have shortness of breath, dyspnea, or abnormal chest imaging •Moderate category: Individuals who show evidence of lower respiratory disease during clinical assessment or imaging and who have a saturation of oxygen (SpO2) ≥ 94% on room air at sea level •Severe category: Individuals who have a saturation of oxygen (SpO2) 30 breaths/minute, PaO2/FiO2

BACKGROUND: Increasing iron bioavailability attenuates hypoxic pulmonary vasoconstriction in both lowlanders and Sherpas at high altitude. In contrast, the pulmonary vasculature of Andeans with chronic mountain sickness (CMS) is resistant to iron administration. Although pulmonary vascular remodeling and hypertension are characteristic features of CMS, the effect of iron administration in healthy Andeans, to our knowledge, has not been investigated. If the interplay between iron status and pulmonary vascular tone in healthy Andeans remains intact, this could provide valuable clinical insight into the role of iron regulation at high altitude. RESEARCH QUESTION: Is the pulmonary vasculature in healthy Andeans responsive to iron infusion? STUDY DESIGN AND METHODS: In a double-blinded, block-randomized design, 24 healthy high-altitude Andeans and 22 partially acclimatized lowlanders at 4,300 m (Cerro de Pasco, Peru) received an IV infusion of either 200 mg of iron (III)-hydroxide sucrose or saline. Markers of iron status were collected at baseline and 4 h after infusion. Echocardiography was performed in participants during room air breathing (partial pressure of inspired oxygen [PIO(2)] of approximately 96 mm Hg) and during exaggerated hypoxia (PIO(2) of approximately 73 mm Hg) at baseline and at 2 and 4 h after the infusion. RESULTS: Iron infusion reduced pulmonary artery systolic pressure (PASP) by approximately 2.5 mm Hg in room air (main effect, P < .001) and by approximately 7 mm Hg during exaggerated hypoxia (main effect, P < .001) in both lowlanders and healthy Andean highlanders. There was no change in PASP after the infusion of saline. Iron metrics were comparable between groups, except for serum ferritin, which was 1.8-fold higher at baseline in the Andeans than in the lowlanders (95% CI, 74-121 ng/mL vs 37-70 ng/mL, respectively; P = .003). INTERPRETATION: The pulmonary vasculature of healthy Andeans and lowlanders remains sensitive to iron infusion, and this response seems to differ from the pathologic characteristics of CMS

Introduction and objectives Prevalence of hypertension increases as glomerular filtration rate (GFR) declines. Renalase metabolizes catecholamines and have an important role in blood pressure (BP) regulation. The purpose of the study was to evaluate the effect of kidney transplantation on renalase levels and BP in kidney donors and recipients. Materials and methods Twenty kidney transplant recipients and their donors were included in the study. Serum renalase levels and ambulatory BP values were measured in both donors and recipients before and after transplantation. Factor associated with change in renalase and BP levels were also evaluated. Results In donors; mean GFR and hemoglobin levels decreased while night-time systolic blood pressure (SBP) and diastolic blood pressure (DBP) levels and serum renalase levels increased simultaneously after nephrectomy. Day-time SBP and DBP levels did not changed and the night/day ratio of mean arterial pressure (MAP) increased significantly. In recipients, mean GFR increased, while mean serum renalase levels, creatinine and BP levels decreased after transplantation. Correlation analysis revealed that changes in MAP correlated with alteration in serum renalase levels and GFR. Conclusions After transplantation, serum renalase levels increased in donors and decreased in recipients. The renalase levels are associated with change in MAP and circadian rhythm of BP in donors and recipients.

Postmenopausal women (PMW) display exaggerated increases in blood pressure (BP) during exercise, yet the mechanism(s) involved remain unclear. Moreover, research on the impact of menopausal changes in estradiol on cardiovascular control during exercise are limited. Herein, we tested the hypothesis that sympathetic responses during exercise are augmented in PMWcompared with young women (YW), and estradiol administration attenuates these responses.Muscle sympathetic nerve activity (MSNA) and mean arterial pressure (MAP) were measured in 13 PMW (58 ± 1 yr) and 17 YW (22 ± 1 yr) during 2 min of isometric handgrip. Separately, MSNA and BP responses were measured during isometric handgrip in six PMW (53 ± 1 yr) before and after 1 month of transdermal estradiol (100 μg·d-1). A period of postexercise ischemia (PEI) to isolate muscle metaboreflex activation followed all handgrip bouts.Resting MAP was similar between PMW and YW, whereas MSNA was greater in PMW (23 ± 3 vs 8 ± 1 bursts per minute; P0.05). During handgrip, the increases in MSNA (PMW Δ16 ± 2 vs YW Δ6 ± 1 bursts per minute; P0.05) and MAP (PMW Δ18 ± 2 vs YW Δ12 ± 2 mm Hg; P0.05) were greater in PMW and remained augmented during PEI. Estradiol administration decreased resting MAP but not MSNA in PMW. Moreover, MSNA (PMW (-E2) Δ27 ± 8 bursts per minute versus PMW (+E2) Δ12 ± 5 bursts per minute; P0.05) and MAP (Δ31 ± 8 mm Hg vs Δ20 ± 6 mm Hg; P0.05) responses during handgrip were attenuated in PMW after estradiol administration. Likewise, MAP responses during PEI were lower after estradiol.These data suggest that PMW exhibit an exaggerated MSNA and BP response to isometric exercise, due in part to heightened metaboreflex activation. Furthermore, estradiol administration attenuated BP and MSNA responses to exercise in PMW.

Acute spinal cord injury (ASCI) is a devastating event that can have severe hemodynamic consequences, depending on location and severity of the lesion. Knowledge of hyperacute hemodynamic changes is important for researchers using porcine models of thoracic ASCI. The goal of this study was to determine the hyperacute hemodynamic changes observed after ASCI when using pigs as their own controls. Five Yucatan gilts were anesthetized, and a dorsal laminectomy performed at T10-T12. Standardized blunt trauma was applied for 5 consecutive min, and hemodynamic variables were collected 5 min before ASCI, and at 2, 4, 6, 8, 10, 20, 30, 60, 80 and 120 min after ASCI. Arterial blood gas samples were collected at 60 min and 10 min before, and at 30 min and between 120 and 240 min after ASCI. Parametric data were analyzed using a mixed effects model with time point as the fixed factor and subject as the random factor. We found no effect on heart rate, pulse pressure, SpO2, EtCO2, and respiratory rate between baseline and timepoints after ASCI. Diastolic arterial pressure, mean arterial pressure, and systolic arterial pressure fell significantly by 18%, 16%, and 15%, respectively, at 2 min after ASCI. However, none of the decrements in arterial pressures resulted in hypotension at any time point. Heart rate did not change significantly after ASCI. Blood glucose progressively increased to 50% above baseline between 120 and 240 minutes after ASCI. Low thoracic ASCI caused a consistent and statistically significant but clinically minor hyperacute decrease in arterial pressures (-15%) that did not produce hypotension or metabolic changes suggestive of tissue hypoperfusion. Our findings using this model suggest that mean arterial pressures should be maintained above 85 mm Hg prior to spinal trauma in order to avoid hypotensive states after ASCI.

The study aimed to investigate whether serum sFlt-1 (soluble fms-like tyrosine kinase-1) at 11-13 weeks’ gestation in pregnancies that subsequently developed preeclampsia was different from those without preeclampsia and compare screening performance of the International Prediction of Pregnancy Complications (IPPIC) reported models, which include various combinations of maternal factors, systolic blood pressure, diastolic blood pressure, PlGF (placental growth factor) and sFlt-1 and the competing risk (CR) models, which include various combinations of maternal factors, mean arterial pressure (MAP) and PlGF for predicting any-onset, early-onset, and late-onset preeclampsia. This was a prospective multicenter study in 7877 singleton pregnancies. The differences of the predictive performance between the IPPIC and CR models were compared. There were 141 women (1.79%) who developed preeclampsia, including 13 cases (0.17%) of early-onset preeclampsia and 128 cases (1.62%) of late-onset preeclampsia. In pregnancies that developed preeclampsia compared to unaffected pregnancies, median serum sFlt-1 levels and its MoMs were not significantly different ( p >0.05). There was no significant association between gestational age at delivery and log 10 sFlt-1 and log 10 sFlt-1 MoM ( p >0.05). The areas under the curve of CR models were significantly higher than the IPPIC models for the prediction of any-onset and late-onset preeclampsia but not for early-onset preeclampsia. In conclusion, there are no significant differences in the maternal serum sFlt-1 levels at 11-13 weeks’ gestation between women who subsequently develop preeclampsia and those who do not. Moreover, the CR models for the prediction of any-onset and late-onset preeclampsia perform better than the IPPIC reported model.

Background We examined the link between increased intra-abdominal pressure, intracranial pressure, and vasopressin release as a potential mechanism. Intra-abdominal pressure, produced by abdominal-cavity insufflation with carbon dioxide (CO2) during laparoscopic abdominal procedures to facilitate visualization, is associated with various complications, including arterial hypertension and oliguria. Methods Mean arterial pressure, optic nerve sheath diameter, measured as a proxy for intracranial pressure, plasma vasopressin, serum and urine osmolarity, and urine output were measured 4 times during laparoscopic sleeve gastrectomy in 42 patients: before insufflation with CO2 (T0); after insufflation to 15 cm water (H2O) pressure, with 5 cm H2O positive end-expiratory pressure (T1); after positive end-expiratory pressure was raised to 10 cm H2O (T2); and after a return to the baseline state (T3). Mean values at T0 to T3 and the directional consistency of changes (increase/decrease/ unchanged) were compared among the 4 data-collection points. Results Statistically significant elevations (all P ≤ .001) were noted from T0 to T1 and from T0 to T2 in mean arterial pressure, optic nerve sheath diameter, and vasopressin, followed by decreases at T3. For optic nerve sheath diameter and vasopressin, the increases at T1 and T2 occurred in 98% and 100% of patients, ultimately exceeding normal levels in 88 and 97%, respectively. Conversely, urine output fell from T0 to T1 and T2 by 60.9 and 73.4%, decreasing in 88.1% of patients (all P Conclusion Increased mean arterial pressure, intracranial pressure, and vasopressin release appear to be intermediary steps between increased intra-abdominal pressure and oliguria. Further research is necessary to determine any causative links between these physiological changes.

Mean systemic filling pressure (Pms) is a promising parameter in determining intravascular fluid status. Pms derived from venous return curves during inspiratory holds with incremental airway pressures (Pms-Insp) estimates Pms reliably but is labor-intensive. A computerized algorithm to calculate Pms (Pmsa) at the bedside has been proposed. In previous studies Pmsa and Pms-Insp correlated well but with considerable bias. This observational study was performed to validate Pmsa with Pms-Insp in cardiac surgery patients. Cardiac output, right atrial pressure and mean arterial pressure were prospectively recorded to calculate Pmsa using a bedside monitor. Pms-Insp was calculated offline after performing inspiratory holds. Intraclass-correlation coefficient (ICC) and assessment of agreement were used to compare Pmsa with Pms-Insp. Bias, coefficient of variance (COV), precision and limits of agreement (LOA) were calculated. Proportional bias was assessed with linear regression. A high degree of inter-method reliability was found between Pmsa and Pms-Insp (ICC 0.89; 95%CI 0.72–0.96, p = 0.01) in 18 patients. Pmsa and Pms-Insp differed not significantly (11.9 mmHg, IQR 9.8–13.4 vs. 12.7 mmHg, IQR 10.5–14.4, p = 0.38). Bias was −0.502 ± 1.90 mmHg (p = 0.277). COV was 4% with LOA –4.22 − 3.22 mmHg without proportional bias. Conversion coefficient Pmsa ➔ Pms-Insp was 0.94. This assessment of agreement demonstrates that the measures Pms-Insp and the computerized Pmsa-algorithm are interchangeable (bias −0.502 ± 1.90 mmHg with conversion coefficient 0.94). The choice of Pmsa is straightforward, it is non-interventional and available continuously at the bedside in contrast to Pms-Insp which is interventional and calculated off-line. Further studies should be performed to determine the place of Pmsa in the circulatory management of critically ill patients. (www.clinicaltrials.gov; TRN NCT04202432, release date 16-12-2019; retrospectively registered).Clinical Trial Registrationwww.ClinicalTrials.gov, TRN: NCT04202432, initial release date 16-12-2019 (retrospectively registered).

Purpose Hydroxocobalamin has been observed to cause transient hypertension in healthy subjects, but rigorous studies examining its efficacy are lacking. Materials and methods Adults in shock who received hydroxocobalamin from 2017 to 2021 were analyzed retrospectively. Hourly hemodynamics from 24 h before and after treatment were collected, and the difference and hourly change of mean arterial pressure (MAP), systolic blood pressure (SBP), diastolic blood pressure (DBP), and norepinephrine-equivalent dose (NED) were examined in mixed-effects models. Results This study included 3992 hemodynamic data points from 35 patients and is the largest case series to date. In the mixed effects model, there was no difference in MAP 24-h after hydroxocobalamin administration (estimated fixed effect [EFE] −0.2 mmHg, p = 0.89). A two-piecewise mixed model found that the hourly change in MAP was not different from zero in either the pre-administration (EFE 0.0 mmHg/h, p = 0.80) or post-administration segments (EFE 0.0 mmHg/h, p = 0.55). Analysis of the SBP, DBP, and NED also found similar insignificant results. Conclusions Although hydroxocobalamin has been observed to cause hypertension in healthy subjects, our results suggest that in patients with shock, hydroxocobalamin may not be effective in improving hemodynamics at 24 h after administration.

In this study, we have examined patients who seek help for hypertensive crisis. The patients received the treatment using intravenous introduction of antihypertensive agents: nitroglycerin or urapidil. At the admission to the hospital and after stabilization of blood pressure, ultrasound examination of blood flow velocity in the aorta, the renal artery, at the exit from the aorta and at the site of entry into the kidney were carried out. On the background of treatment, there has been indicated the same decline in systolic blood pressure and mean arterial pressure. The blood flow velocity decreased in the aorta and renal artery at the site of exit from the aorta. During urapidil administration, flow velocity in the renal artery, at the site of entry into the kidney, improved, indicating the maintenance or even improvement of renal blood flow. When administered nitroglycerin, renal blood flow rate was significantly reduced.

Background. Accidental hypothermia is one of the most difficult problems of modern intensive care of critical states. The aim of the work was to study the efficiency of the developed method for the intensive care of accidental hypothermia, to assess its impact on the rate of the correction of pathophysiological changes and the level of mortality of patients in critical or terminal states. The aim of this study was to evaluate the effectiveness of the developed method for the intensive care of accidental hypothermia, the assessment of its impact on the speed of the correction of pathophysiological changes on the level of morta­lity of patients in critical states. Materials and methods. The study included 50 critically ill patients (mean age 43.00 ± 3.62 years) with accidental hypothermia, who were treated in the intensive care unit for polytrauma patients of I.I. Mechnikov Dnipro­petrovsk Regional Clinical Hospital. In all patients, the general classification of the stages of accidental hypothermia of the Swiss Society for Mountain Medicine has been used. Patients were divided into 2 groups. Group I (n = 25) — active warming using convection heating system WarmAir 135 (CSZ, USA) and infusion of crystalloid solutions (37 °C) in the following doses: for mild — 20–30 ml/kg; moderate and severe — 50–70 ml/kg. In patients with severe accidental hypothermia first 1–1.5 liters fell on colloidal plasma expanders (low molecular weight hydroxyethyl starch and gelatin). Group II (n = 25) — the passive war­ming and standard intensive care including crystalloid and colloid infusion solutions with indoor temperature at a dose of 20–30 ml/kg. We studied the esophageal (the core of the body — Tco (CSZ, USA)) and tympanic temperature (Tt (Omron, Japan)), hemodynamic parameters (blood pressure, heart rate, mean arterial pressure (MAP)), neurologic impairment according to the Glasgow Coma Scale, the rate of warming. Results. Initial Tco in group I was 29.03 ± 2.76 °C, in group II — 31.50 ± 1.97 °C. Minimum and maximum Tco: in group I — 24.3 and 33.6 °C, in group II — 27.2 and 34.5 °C, respectively. At the baseline, MAP in group I was 49.86 ± 20.71 mmHg, in group II — 70.45 ± 11.72 mmHg; after 48 hours — 76.65 ± 12.27 mmHg and 60.82 ± 36.39 mmHg, respectively. Rate of attaining normothermia (36.0 °C) in the first and second groups was: 6.48 ± 3.47 hours and 9.20 ± 6.52 hours, respectively. Mortality in group I was 12 %, in group II — 48 %, these differences were significant. More indicative mortality rates were in subgroups of patients with severe accidental hypothermia, since in group I it was 25 %, while in the group II — 100 %. It should be noted that the analysis of the three deceased patients in group I with a severe accidental hypothermia has shown that two of them had not acute hypothermia, but gradual cooling during a long time (from 12 to 24 h). The third patient had died with Tco 24.5 °C, and the death occurred in the first hours after admission to the hospital due to the significant hemodynamic instability, and failure of cardiopulmonary resuscitation. Conclusions. The most effective method of war­ming the patient with accidental hypothermia is active warming using convection hea­ting system. After securing the venous access, it is necessary to conduct infusion therapy with 37°C crystalloid solutions. In patients with mild accidental hypothermia, the total volume of infusion therapy should be 20–30 ml/kg; in patients with moderate to severe accidental hypothermia — 50–70 ml/kg. Thus, in patients with severe accidental hypothermia, the first 1–1.5 liters must account for colloidal plasma expanders (based on low molecular weight hydroxyethyl starch and/or ge­latin). Use of the method of intensive care is not indicated in the slow development of the accidental hypothermia du­ring a long time. Our preliminary data indicate that forced air rewarming and infusion of 37°C crystalloid solutions are efficient and safe met­hods of managing patients with accidental hypothermia and reduce mortality to 25 %.

The Hypotension Prediction Index (HPI) is a commercially available machine-learning algorithm that provides warnings for impending hypotension, based on real-time arterial waveform analysis. The HPI was developed with arterial waveform data of surgical and intensive care unit (ICU) patients, but has never been externally validated in the latter group. In this study, we evaluated diagnostic ability of the HPI with invasively collected arterial blood pressure data in 41 patients with COVID-19 admitted to the ICU for mechanical ventilation. Predictive ability was evaluated at HPI thresholds from 0 to 100, at incremental intervals of 5. After exceeding the studied threshold, the next 20 min were screened for positive (mean arterial pressure (MAP)

Objective To determine the effect of fentanyl on the minimum alveolar concentration of isoflurane (MACISO) and cardiovascular variables in dogs, and how the treatment of bradycardia affects them. Study design Prospective, randomized crossover-controlled trial. Animals A total of six male Beagle dogs weighing 9.9 ± 0.7 kg (mean ± standard deviation) and aged 13 months. Methods To each dog, two treatments were assigned on different days: fentanyl (FENTA) or fentanyl plus glycopyrrolate (FENTAglyco) to maintain heart rate (HR) between 100 and 132 beats minute−1. Determinations of MACISO were performed with 10 plasma fentanyl target concentrations ([Fenta]Target (0, 0.16, 0.32, 0.64, 1.25, 2.5, 5.0, 10.0, 20.0 and 40.0 ng mL−1) for FENTA and 5 [Fenta]Target (0, 1.25, 2.5, 5.0, 10.0 ng mL−1)) for FENTAglyco. During each MACISO determination, cardiovascular variables [mean arterial pressure (MAP), HR and cardiac index (CI)] were measured, and systemic vascular resistance index (SVRI) calculated. Pharmacodynamic models were used to describe the plasma fentanyl concentration [Fenta]–response relationship for the effect on MACISO and cardiovascular variables. A mixed-model analysis of variance followed by Dunnett’s or Tukey’s test, and the Bonferroni adjustment were used for comparisons within and between each treatment, respectively. Significance was set as p Results Fentanyl decreased MACISO by a maximum of 84%. The [Fenta] producing 50% decrease in MAC, HR and CI were 2.64, 3.65 and 4.30 ng mL−1 (typical values of population model), respectively. The prevention of fentanyl-mediated bradycardia caused no significant effect on MACISO, but increased HR, MAP and CI, and decreased SVRI when compared with isoflurane alone. Conclusions and clinical relevance Fentanyl caused a plasma concentration-dependent decrease in MACISO, HR and CI and an increase in SVRI. Cardiovascular improvements associated with fentanyl in isoflurane-anesthetized dogs only occurred when the fentanyl-mediated bradycardia was prevented.

Supplemental Digital Content is available in the text., It remains debated whether pulse pressure is associated with left ventricular traits and adverse outcomes over and beyond mean arterial pressure (MAP) in patients with heart failure (HF) with preserved ejection fraction. We investigated these associations in 3428 patients with HF with preserved ejection fraction (51.5% women; mean age, 68.6 years) enrolled in the TOPCAT trial (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist). We computed association sizes and hazards ratios with 1-SD increase in MAP and pulse pressure. In multivariable-adjusted analyses, association sizes (P≤0.039) for MAP were 0.016 cm and 0.014 cm for septal and posterior wall thickness, −0.15 for E/A ratio, −0.66 for E/e′, and −0.64% for ejection fraction, independent of pulse pressure. With adjustment additionally applied for MAP, E/A ratio and longitudinal strain increased with higher pulse pressure with association sizes amounting to 0.067 (P=0.026) and 0.40% (P=0.023). In multivariable-adjusted analyses of both placebo and spironolactone groups, lower MAP and higher pulse pressure predicted the primary composite end point (P≤0.028) and hospitalized HF (P≤0.002), whereas MAP was also significantly associated with total mortality (P≤0.007). Sensitivity analyses stratified by sex, median age, and region generated confirmatory results with exception for the association of adverse outcomes with pulse pressure in patients with age ≥69 years. In conclusion, the clinical application of MAP and pulse pressure may refine risk estimates in patients with HF with preserved ejection fraction. This finding may help further investigation for the development of HF with preserved ejection fraction preventive strategies targeting pulsatility and blood pressure control.

Objective To investigate the safety and effectiveness of extraluminal placement of a bronchial blocker compared with carbon dioxide (CO2) artificial pneumothorax in infants undergoing video-assisted thoracoscopic surgery (VATS). Methods The study involved 33 infants (group A) who underwent one-lung ventilation (OLV) with extraluminal placement of a bronchial blocker and 35 other infants (group B) who underwent CO2 artificial pneumothorax. Clinical characteristics, the degree of lung collapse, and complications were compared. Results The degree of lung collapse in group A was significantly higher than that in group B at T2 and T3. The mean arterial pressure (MAP) of group B was significantly lower than that of group A at 10 min and 30 min after OLV. The partial pressure of carbon dioxide (PaCO2) of group B was significantly higher than that of group A at 30 min after OLV. The incidence of hypotension in group B was higher than that in group A. Conclusion Compared with CO2 artificial pneumothorax, extraluminal placement of a bronchial blocker is associated with a better degree of lung collapse, fewer episodes of hypotension, and lower PaCO2 accumulation during OLV in infants undergoing VATS.

Changes in the gravitational vector by postural changes or weightlessness induce fluid shifts impacting ocular hemodynamics and regional pressures. This investigation explores the impact of changes in direction of the gravitational vector on intraocular pressure (IOP), mean arterial pressure at eyelevel (MAPeye), and ocular perfusion pressure (OPP), which is critical for ocular health. Thirteen subjects underwent 360° of tilt (including both prone and supine positions) at 15o increments. At each angle, steady-state IOP and MAPeye were measured and OPP calculated as MAPeye-IOP. Experimental data were compared to a 6-compartment lumped parameter model of the eye. Mean IOP, MAPeye, and OPP significantly increased from 0o supine to 90o head down tilt (HDT) by 20.7±1.7 mmHg (ᵅD; < 0.001), 38.5±4.1 mmHg (ᵅD; < 0.001), and 17.4±3.2 mmHg (ᵅD

Background and objectives Laryngoscopy and tracheal intubation lead to a sympathoadrenal response. We compared the efficacy of dexmedetomidine with fentanyl bolus to attenuate this response. Methods One hundred patients admitted for routine surgical procedures under general anesthesia were enrolled in this double blind, randomized, controlled study. Patients were randomly assigned to two groups: Group F received injection of fentanyl 2 μg.kg-1 and Group D received injection of dexmedetomidine 0.5 μg.kg-1 diluted up to 5 mL by adding normal saline intravenously over 60 seconds. Five minutes thereafter, following induction with propofol and vecuronium, tracheal intubation was performed after 3 minutes of mask ventilation. Hemodynamic parameters were observed at an interval of 2 minutes before tracheal intubation and at an interval of 1 minute for 5 minutes after tracheal tube cuff inflation. Continuous variables are presented as mean with 95% confidence interval, and t-test was applied for comparing the difference of means between two groups after checking the normality condition. Chi-square test was applied to test the independence of attributes of categorical variables. Repeated measures two-way ANOVA was performed to compare the outcome variables between the two groups. Results The difference in heart rate and mean arterial pressure of patients in two groups after laryngoscopy and intubation was not statistically significant at any point of time. The hemodynamic changes did not require any intervention in the form of administration of rescue medication. Conclusions Dexmedetomidine 0.5 μg.kg-1 is as effective as fentanyl 2 μg.kg-1 in attenuating the hemodynamic response accompanying laryngoscopy and tracheal intubation. Clinical trial number & registry URL CTRI/2017/09/009857 [ctri.nic.in]

The prevalence of sleep-disordered breathing (SDB) is higher in older adults compared with younger individuals. The increased propensity for ventilatory control instability in older adults may contribute to the increased prevalence of central apneas. Reductions in the cerebral vascular response to CO(2) may exacerbate ventilatory overshoots and undershoots during sleep. Thus, we hypothesized that hypercapnia-induced cerebral vasodilation (HCVD) will be reduced in older compared with younger adults. In 11 older and 10 younger adults with SDB, blood flow velocity in the middle cerebral artery (MCAV) was measured using Doppler transcranial ultrasonography during multiple steady-state hyperoxic hypercapnic breathing trials while awake, interspersed with room air breathing. Changes in ventilation, MCAV, and mean arterial pressure (MAP) via finger plethysmography during the trials were compared with baseline eupneic values. For each hyperoxic hypercapnic trial, the change (Δ) in MCAV for a corresponding change in end-tidal CO(2) and the HCVD or the change in cerebral vascular conductance (MCAV divided by MAP) for a corresponding change in end-tidal CO(2) was determined. The hypercapnic ventilatory response was similar between the age groups, as was ΔMCAV/Δ [Formula: see text]. However, compared with young, older adults had a significantly smaller HCVD (1.3 ± 0.7 vs. 2.1 ± 0.6 units/mmHg, P = 0.004). Multivariable analyses demonstrated that age and nadir oxygen saturation during nocturnal polysomnography were significant predictors of HCVD. Thus, our data indicate that older age and SDB-related hypoxia are associated with diminished HCVD. We hypothesize that this impairment in vascular function may contribute to breathing instability during sleep in these individuals. NEW & NOTEWORTHY This study demonstrates, for the first time, in individuals with sleep-disordered breathing (SDB) that aging is associated with decreased hypercapnia-induced cerebral vasodilation (HCVD). In addition to advanced age, the magnitude of nocturnal oxygen desaturation due to SDB is an equal independent predictor of HCVD.

The cerebral pressure-flow relationship has directional sensitivity, meaning the augmentation in cerebral blood flow is attenuated when mean arterial pressure (MAP) increases vs MAP decreases. We employed repeated squat-stands (RSS) to quantify it using a novel metric. However, its within-day reproducibility and the impacts of diurnal variation and biological sex are unknown. Study aims were to evaluate this metric for: 1) within-day reproducibility and diurnal variation in middle (MCA; ∆MCAvT/∆MAPT) and posterior cerebral arteries (PCA; ∆PCAvT/∆MAPT); 2) sex differences. ∆MCAvT/∆MAPT and ∆PCAvT/∆MAPT were calculated at seven time-points (08:00-17:00) in 18 participants (8 women; 24 ± 3 yrs) using the minimum-to-maximum MCAv or PCAv and MAP for each RSS at 0.05 Hz and 0.10 Hz. Relative metric values were also calculated (%MCAvT/%MAPT, %PCAvT/%MAPT). Intraclass correlation coefficient (ICC) evaluated reproducibility, which was good (0.75-0.90) to excellent (>0.90). Time-of-day impacted ∆MCAvT/∆MAPT (0.05 Hz: p = 0.002; 0.10 Hz: p = 0.001), %MCAvT/%MAPT (0.05 Hz: p = 0.035; 0.10 Hz: p = 0.009), and ∆PCAvT/∆MAPT (0.05 Hz: p = 0.024), albeit with small/negligible effect sizes. MAP direction impacted both arteries' metric at 0.10 Hz (all p < 0.024). Sex differences in the MCA only (p = 0.003) vanished when reported in relative terms. These findings demonstrate this metric is reproducible throughout the day in the MCA and PCA and is not impacted by biological sex.

Sepsis is the leading cause of acute respiratory distress syndrome (ARDS) in adults and carries a high mortality. Utilizing a previously validated porcine model of sepsis-induced ARDS, we sought to refine our novel therapeutic technique of in vivo lung perfusion (IVLP). We hypothesized that 2 hours of IVLP would provide non-inferior lung rehabilitation compared to 4 hours of treatment. Adult swine (n = 8) received lipopolysaccharide to develop ARDS and were placed on central venoarterial extracorporeal membrane oxygenation. Animals were randomized to 2 vs 4 hours of IVLP. The left pulmonary vessels were cannulated to IVLP using antegrade Steen solution. After IVLP treatment, the left lung was decannulated and reperfused for 4 hours. Total lung compliance and pulmonary venous gases from the right lung (control) and left lung (treatment) were sampled hourly. Biochemical analysis of tissue and bronchioalveolar lavage was performed along with tissue histologic assessment. Throughout IVLP and reperfusion, treated left lung PaO2/FiO2 ratio was significantly higher than the right lung control in the 2-hour group (332.2 ± 58.9 vs 264.4 ± 46.5, P = 0.01). In the 4-hour group, there was no difference between treatment and control lung PaO2/FiO2 ratio (258.5 ± 72.4 vs 253.2 ± 90.3, P = 0.58). Wet-to-dry weight ratios demonstrated reduced edema in the treated left lungs of the 2-hour group (6.23 ± 0.73 vs 7.28 ± 0.61, P = 0.03). Total lung compliance was also significantly improved in the 2-hour group. Two hours of IVLP demonstrated superior lung function in this preclinical model of sepsis-induced ARDS. Clinical translation of IVLP may shorten duration of mechanical support and improve outcomes.

OBJECTIVE To evaluate the level of agreement (LOA) between direct and oscillometric blood pressure (BP) measurements and the ability of oscillometric measurements to accurately detect hypotension in anesthetized chimpanzees (Pan troglodytes). ANIMALS 8 captive, adult chimpanzees. PROCEDURES During prescheduled annual examinations, each chimpanzee underwent general anesthesia and patient monitoring for their examination, echocardiography for a concurrent study, and measurement of direct BP with the use of tibial artery catheterization and oscillometry with the use of a cuff placed around a brachium and a cuff placed around the second digit of the contralateral forelimb for the present study. Bland-Altman plots were generated to compare results for direct and oscillometric BP measurements. Mean bias and 95% LOAs were calculated for oscillometric measurements of systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and mean arterial pressure (MAP) for each cuff site. Sensitivity and specificity in detecting hypotension were also determined for each cuff site. RESULTS There were 74 paired direct and brachial oscillometric measurements of each, SAP, MAP, and DAP and 66 paired direct and digit oscillometric measurements of each, SAP, MAP, and DAP. Only brachial oscillometric measurements of MAP had adequate sensitivity (78%) and specificity (95%) to accurately detect hypotension, and this technique also had the least mean bias (0.8 mm Hg; 95% LOA, –29 to 31 mm Hg). CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that brachial oscillometric measurement of MAP provided reasonable agreement with tibial arterial direct MAP measurement and performed well in diagnosing hypotension in anesthetized chimpanzees.

A radial-to-femoral pressure gradient (RFPG) can occur in roughly one-third of cardiac surgical patients. Such a gradient has been associated with smaller stature and potentially smaller radial artery diameter. We hypothesized that preoperative radial artery diameter could be a predictor of RFPG. We also investigated the clinical impact of using a femoral versus a radial arterial catheter in terms of vasoactive support.Using ultrasound, we measured the bilateral radial artery diameters of 160 cardiac surgical patients. All arterial pressure values were continuously recorded. Significant RFPG was defined as ≥25 mm Hg in systolic and/or ≥10 mm Hg in mean arterial pressure. One hundred and forty-nine additional patients were used to validate the impact of our observations.Using 78,013 pressure datapoints in 129 patients, 34.8% of patients had an RFPG with a mean duration of 54 ± 48 minutes. Patients with a radial artery diameter1.8 mm were more likely to have an RFPG (n = 14 [48.3%] vs 12 [22.2%];A significant RFPG occurs in one-third of cardiac surgical patients and in 48% of those with a radial artery diameter1.8 mm. The use of a single radial arterial catheter instead of dual radial and femoral catheters was associated with greater vasopressor requirements in the operating room and in the intensive care unit. We do not recommend the use of a single radial artery catheter in cardiac surgery.

Background The effect of intravenous (IV) fluid administration type on cerebral perfusion pressure (CePP) during cardiopulmonary resuscitation (CPR) is controversial. The purpose of this study was to evaluate the association between IV fluid type and CePP in a porcine cardiac arrest model. Methods We randomly assigned 12 pigs to the hypertonic crystalloid, isotonic crystalloid and no-fluid groups. After 4 min of untreated ventricular fibrillation (VF), chest compression was conducted for 2 cycles (CC only). Chest compression with IV fluid infusion (CC + IV) was followed for 2 cycles. Advanced life support, including defibrillation and epinephrine, was added for 8 cycles (ALS phase). Mean arterial pressure (MAP), intracranial pressure (ICP) and CePP were measured. A paired t-test was used to measure the mean difference in CePP. Results Twelve pigs underwent the experiment. The hypertonic crystalloid group showed higher CePP values than those demonstrated by the isotonic crystalloid group from ALS cycles 2 to 8. The MAP values in the hypertonic group were higher than those in the isotonic group starting at ALS cycle 2. The ICP values in the hypertonic group were lower than those in the isotonic group starting at ALS cycle 4. From ALS cycles 2 to 8, the reduction in the mean difference in the isotonic group was larger than that in the other groups. Conclusion In a VF cardiac arrest porcine study, the hypertonic crystalloid group showed higher CePP values by maintaining higher MAP values and lower ICP values than those of the isotonic crystalloid group.

Aim: The cardio-ankle vascular index (CAVI) consists of intrinsic and functional arterial stiffness mainly regulated by vasoactive compounds. A new stiffness index of the aorta (aBeta) and iliac-femoral arteries (ifBeta) was determined by applying the CAVI theory to the whole aorta and iliac-femoral arteries. We investigated the changes in aBeta and ifBeta in response to decreased blood pressure (BP) induced by the Ca 2＋ channel blocker nicardipine to elucidate the involvement of Ca 2＋ in aBeta and ifBeta. Methods: Pressure waves at the origin of the aorta (oA), distal end of the abdominal aorta (dA), and left femoral artery (fA) as well as flow waves at the oA were simultaneously recorded before and after the infusion of nicardipine (50 µg/kg/min) for 2 min in 12 male rabbits under pentobarbital anesthesia. Beta was calculated using the following formula: Beta=2ρ / PP×ln (SBP / DBP)×PWV 2 , where ρ, SBP, DBP, and PP denote blood density and systolic, diastolic, and pulse pressures, respectively. aBeta, ifBeta, and aortic-iliac-femoral Beta (aifBeta) were calculated using aPWV, ifPWV, and aifPWV, respectively. Results: SBP, mean arterial pressure (MAP), DBP, and total peripheral vascular resistance significantly decreased during the administration of nicardipine, whereas cardiac output significantly increased. aBeta and ifBeta significantly increased and decreased, respectively, whereas aifBeta did not change despite the decrease in BP. ifBeta and aBeta positively and negatively correlated with BP, respectively, whereas aifBeta did not correlate with SBP. Conclusions: There were contradictory arterial responses to nicardipine between the elastic and muscular arteries. Unknown vasoconstriction mechanisms that are not involved in Ca 2＋ influx may function in the aorta in response to decreased BP.

Background In middle-aged adults with depression, cerebral vasodilatory reactivity is blunted; however, this has not been examined in treatment-naive young adults with major depressive disorder (MDD). We tested the hypothesis that cerebrovascular reactivity would be blunted in young adults (18–30 yrs) with MDD compared to healthy non-depressed adults (HA) and would be attenuated to a greater extent in adults with symptomatic MDD (sMDD) compared to adults with MDD in remission (euthymic MDD; eMDD). Methods Sixteen adults with MDD [21±3yrs; n = 8 sMDD (6 women); n = 8 eMDD (5 women)] and 14 HA (22±3yrs; 9 women) participated. End-tidal carbon dioxide concentration (PETCO2; capnograph), beat-to-beat mean arterial pressure (MAP; finger photoplethysmography), middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound), and internal carotid artery (ICA) diameter and blood velocity (Doppler ultrasound) were continuously measured during baseline and rebreathing-induced hypercapnia. Cerebrovascular reactivity was calculated as the relative increase in vascular conductance during hypercapnia. Results In adults with MDD, cerebrovascular reactivity in the MCA (∆39±9 HA vs. ∆31±13% MDD, p = 0.04), but not the ICA (∆36±24 HA vs. ∆34±18% MDD, p = 0.84), was blunted compared to HA. In the MCA, cerebrovascular reactivity was reduced in adults with sMDD compared to adults with eMDD (∆36±11 eMDD vs. ∆25±13% sMDD, p = 0.02). Limitations The cross-sectional nature approach limits conclusions regarding the temporal nature of this link. Conclusion These data indicate that MCA cerebrovascular reactivity is blunted in young adults with MDD and further modulated by current depressive symptomology, suggesting that the management of depressive symptomology may secondarily improve cerebrovascular health.

Nalfurafine is a G-protein–biased KOR (kappa opioid receptor) agonist that produces analgesia and lacks central nervous system adverse effects. Here, we examined the cardiovascular and renal responses to intravenous and oral nalfurafine alone and in combination with furosemide, hydrochlorothiazide, or amiloride. We hypothesized that nalfurafine, given its distinct mechanism of vasopressin inhibition, would increase urine output to these diuretics and limit electrolyte loss. Following catheterization, conscious Sprague-Dawley rats received an isotonic saline infusion and were then administered an intravenous bolus of nalfurafine, a diuretic, or a combination. Mean arterial pressure, heart rate, and urine output were recorded for 90 minutes. In another study, rats were placed in metabolic cages and administered drug in an oral volume load. Hourly urine samples were then collected for 5 hours. Intravenous and oral nalfurafine produced a marked diuresis, antinatriuresis, antikaliuresis, and a decrease in mean arterial pressure. Compared with diuretic treatment alone, intravenous coadministration with nalfurafine significantly increased urine output to furosemide and hydrochlorothiazide and decreased sodium and potassium excretion. Notably, mean arterial pressure was reduced with nalfurafine/diuretic combination therapy compared to diuretics alone. Similarly, oral coadministration of nalfurafine significantly increased urine output to hydrochlorothiazide and decreased sodium and potassium excretion, whereas combination with furosemide only limited the amount of sodium excreted. Further, both intravenous and oral coadministration of nalfurafine enhanced the diuresis to amiloride and decreased sodium excretion. Together, these findings demonstrate that nalfurafine enhances the diuresis to standard-of-care diuretics without causing an excessive loss of electrolytes, offering a new approach to treat several cardiovascular conditions.

BackgroundObesity can cause hypertension and exacerbates sleep-disordered breathing (SDB). Leptin is an adipocyte-produced hormone, which increases metabolic rate, suppresses appetite, modulates control of breathing, and increases blood pressure. Obese individuals with high circulating levels of leptin are resistant to metabolic and respiratory effects of leptin, but they appear to be sensitive to hypertensive effects of this hormone. Obesity-induced hypertension has been associated with hyperleptinemia. New Zealand obese (NZO) mice, a model of polygenic obesity, have high levels of circulating leptin and hypertension, and are prone to develop SDB, similarly to human obesity. We hypothesize that systemic leptin receptor blocker Allo-aca will treat hypertension in NZO mice without any effect on body weight, food intake, or breathing.MethodsMale NZO mice, 12–13 weeks of age, were treated with Allo-aca (n = 6) or a control peptide Gly11 (n = 12) for 8 consecutive days. Doses of 0.2 mg/kg were administered subcutaneously 2×/day, at 10 AM and 6 PM. Blood pressure was measured by telemetry for 48 h before and during peptide infusion. Ventilation was assessed by whole-body barometric plethysmography, control of breathing was examined by assessing the hypoxic ventilatory response (HVR), and polysomnography was performed during light-phase at baseline and during treatment. Heart rate variability analyses were performed to estimate the cardiac autonomic balance.ResultsSystemic leptin receptor blockade with Allo-aca did not affect body weight, body temperature, and food intake in NZO mice. Plasma levels of leptin did not change after the treatment with either Allo-aca or the control peptide Gy11. NZO mice were hypertensive at baseline and leptin receptor blocker Allo-aca significantly reduced the mean arterial pressure from 134.9 ± 3.1 to 124.9 ± 5.7 mmHg during the light phase (P < 0.05), whereas the control peptide had no effect. Leptin receptor blockade did not change the heart rate or cardiac autonomic balance. Allo-aca did not affect minute ventilation under normoxic or hypoxic conditions and HVR. Ventilation, apnea index, and oxygen desaturation during NREM and REM sleep did not change with leptin receptor blockade.ConclusionSystemic leptin receptor blockade attenuates hypertension in NZO mice, but does not exacerbate obesity and SDB. Thus, leptin receptor blockade represents a potential pharmacotherapy for obesity-associated hypertension.

Background: Monitoring of vascular access outflow (VAO) in dialysis is based on the indicator dilution method by ultrasound (UD). The role of arterial needle orientation in VAO measurement is not clear. We compared the impact of the retrograde (RET) versus the antegrade orientation (ANT) in terms of (a) VAO (UD) and (b) dialysis adequacy. Moreover, we compared VAO (UD ANT and RET orientation) with VAO measured by Doppler ultrasound. Methods: 22 patients participated in the study. Inclusion criteria: Dialysis > 6 months with a functioning AVF, no stenosis, no active infection, EF > 45% and informed consent. 4 flow measurements were taken on the same dialysis day (4 consecutive weeks). To account for blood pressure variation, we “corrected” VAO for a mean arterial pressure of 100 mmHg. Doppler VAO was measured just before dialysis. Means were compared by the paired t-test. For correlation and agreement, linear regression and Bland-Altman analysis were performed respectively. Results: Mean VAO (UD) was higher in the (ANT) versus the (RET) orientation: 1286.17 mL/min (SD = 455.78, 95%CI = 1084–1488) versus 1189.96 mL/min (SD = 401.05, 95%CI = 1012–1368) (p = 0.013) with a mean difference of 96.21 mL/min (5.66%). Mean Kt/V (RET orientation) was 1.57 (SD = 0.10, 95%CI = 1.52–1.61) versus 1,55 (SD = 0.10, 95%CI = 1.50–1.60) (ANT) orientation (p = 0.062). Recirculation was always 0%. The mean VAO (Doppler) was 1079.54 mL/min (SD = 356.04, 95%CI = 922–1237), 16% lower than VAO measured by UD with (ANT) orientation (p = 0.009) and 9.3% lower than the VAO in the (RET) orientation (p = 0.113). Linear regression analysis showed that VA flows (ANT versus RET) orientation of the needle correlates well between them (r = 0.93, p < 0.001) but show poor agreement (Bland–Altman analysis). Conclusion: VAO (UD) in the RET orientation was significantly lower than VAO in the ANT orientation and more consistent with VAO assessed by Doppler without influencing dialysis adequacy. Therefore, when using UD for VAO surveillance, the RET orientation should be used.

BACKGROUND Acute cervical spinal cord injury (ACSCI) is commonly complicated by spinal shock, resulting in hemodynamic instability characterized by bradycardia and hypotension that can have fatal consequences. Current guidelines recommend the use of intravenous beta and dopamine agonists, such as norepinephrine and dopamine, respectively. We sought to determine whether enteral albuterol would be a safe and feasible treatment for bradycardia without an increase in the occurrence of known side effects of albuterol in patients with ACSCI. METHODS A retrospective review of patients with ACSCI admitted to an intensive care unit at a level I trauma center and treated with enteral albuterol was conducted. Patients were excluded for the following reasons: pure beta blocker use prior to injury, concurrent use of pacemaker, age of less than 18 years, or age more than 75 years. As part of the standard of care, all patients underwent mean arterial pressure (MAP) augmentation to reach a goal of greater than 85 mm Hg during the first 7 days post injury. All eligible patient charts were reviewed for demographic characteristics, daily minimum and maximum heart rate and MAP, and concomitant vasoactive medication use. Bradycardia and tachycardia were defined as heart rate less than 60 beats per minute (bpm) and greater than 100 bpm, respectively. Factors found to be associated with bradycardia on univariate analysis were entered into a multivariable generalized estimating equation analysis to determine factors independently associated with bradycardia during the study period. RESULTS There were 58 patients with cervical ASCI (age 45 ± 18 years, 76% men) admitted between January 1, 2016, and December 31, 2017, that met the study criteria. The mean time to initiation of albuterol was 1.5 ± 1.7 days post injury, with a duration of 9.3 ± 4.5 days and a mean daily dosage of 7.8 ± 4.5 mg. Bradycardia was observed in 136 of 766 patient days (17%). There were a few episodes of hyperglycemia (1%) and tachycardia (3%), but no episodes of hypokalemia. In a multivariable analysis, female sex (P = 0.006) and American Spinal Cord Injury Association grade A, B, or C (P

OBJECTIVES The effect of ischaemic postconditioning (IPost) on postcardioplegic cardiac function is not known. We hypothesized that IPost was cardioprotective in adult patients undergoing elective aortic valve replacement. METHODS In a multicentre, prospective, randomized trial, patients (n = 209) were randomized to either a standard operation (controls) or postconditioning. Immediately before the cross-clamp was released, patients in the postconditioning group underwent 3 cycles of flow/non-flow (2 min each) of normothermic blood via the antegrade cardioplegia line. The primary end point was cardiac index. Secondary end points included additional haemodynamic measurements, biomarkers of cardiomyocyte injury, renal function parameters, intra- and postoperative arrhythmias and use of inotropic agents. RESULTS There was no significant difference between the groups regarding cardiac index [mean between-group difference, 95% confidence interval (CI), 0.11 (−0.1 to 0.3), P = 0.27]. Postconditioning had no effect on other haemodynamic parametres. There was no between-group difference regarding troponin T or creatine kinase MB. Postconditioning reduced the relative risk for arrhythmias by 45% (P = 0.03) when postoperative atrial fibrillation and intraoperative ventricular fibrillation were combined. There were no differences in patients with/without diabetes, patients above/below 70 years of age or between the centres. However, after postconditioning, the cardiac index [95% CI, 0.46 (0.2–0.7), P = 0.001], cardiac output (P CONCLUSIONS IPost had no overall cardioprotective effects in patients undergoing aortic valve replacement but improved postoperative cardiac performance in men compared to women.

New findings What is the central question of this study? During a steady-state cerebrovascular CO2 reactivity test, do different data extraction time points change the outcome for cerebrovascular CO2 reactivity? What is the main finding and its importance? Once steady-state end-tidal pressure of CO2 and haemodynamics were achieved, cerebral blood flow was stable, and so cerebrovascular CO2 reactivity values remained unchanged regardless of data extraction length (30 vs. 60 s) and time point (at 2-5 min). Abstract This study assessed cerebrovascular CO2 reactivity (CVR) and examined data extraction time points and durations with the hypotheses that: (1) there would be no difference in CVR values when calculated with cerebral blood flow (CBF) measures at different time points following the attainment of physiological steady-state, (2) once steady-state was achieved there would be no difference in CVR values derived from 60 to 30 s extracted means, and (3) that changes in V E would not be associated with any changes in CVR. We conducted a single step iso-oxic hypercapnic CVR test using dynamic end-tidal forcing (end-tidal P C O 2 , +9.4 ± 0.7 mmHg), and transcranial Doppler and Duplex ultrasound of middle cerebral artery (MCA) and internal carotid artery (ICA), respectively. From the second minute of hypercapnia onwards, physiological steady-state was apparent, with no subsequent changes in end-tidal P C O 2 , P O 2 or mean arterial pressure. Therefore, CVR measured in the ICA and MCA was stable following the second minute of hypercapnia onwards. Data extraction durations of 30 or 60 s did not give statistically different CVR values. No differences in CVR were detected following the second minute of hypercapnia after accounting for mean arterial pressure via calculated conductance or covariation of mean arterial pressure. These findings demonstrate that, provided the P C O 2 stimulus remains in a steady-state, data extracted from any minute of a CVR test during physiological steady-state conditions produce equivalent CVR values; any change in the CVR value would represent a failure of CVR mechanisms, a change in the magnitude of the stimulus, or measurement error.

BACKGROUND Vaping, the use of an electronic device to deliver a drug-infused aerosol has become an increasingly popular way to consume nicotine since its introduction to the market in the early 2000s. Despite the differences in consumption patterns relative to combustible tobacco, the impact of ad libitum nicotine vaping on cardiovascular response has not been thoroughly studied. SUBJECT AND METHODS This research was conducted on vapers (n = 17) and smokers (n = 14) who represent a subsample of a larger study that explored the relationship among nicotine use, activities of daily living and 24-hour cardiovascular response using Spacelabs ambulatory blood pressure monitors. These data were analysed via ANOVA models and t-tests using SPSS 25.0 for Macintosh. RESULTS Vapers consumed nicotine significantly more frequently than did smokers, at 48.2% and 18.1% of every 15-minute waking measurements, respectively (p = 0.000). The act of nicotine consumption, rather than the mode of delivery, was significantly associated with increases in systolic, diastolic, mean arterial pressure, and heart rate readings. There was no difference in mean amplitude of response to nicotine between vapers and smokers. CONCLUSIONS This study's strong statistical findings, visually evident on ambulatory blood pressure monitor reports, demonstrated that ad libitum nicotine consumption has an acute, dose-dependent effect on cardiovascular response regardless of whether it is smoked or vaped. However, since vapers consumed nicotine more frequently, future studies should be conducted with a larger sample size, and controlled for age and comorbidities to improve statistical strength.

Objective: The aim of this study was to investigate the effect of oral supplementation with L-arginine on serum biochemical profile, blood pressure, microcirculation, and vasoreactivity/endothelial function in young controls, and elderly women with and without type 2 diabetes mellitus (T2DM). Methods: Healthy young (n = 25), healthy elderly (n = 25), and elderly women with type 2 diabetes mellitus (T2DME, n = 23, glycated Hb ≥6.4% and mean of 7.7 years for duration of the disease), aged 18–30 and older than 65 years, respectively, were included in the study. All patients underwent biochemical analysis (fasting glycemia and lipidogram), arterial blood pressure, nailfold videocapillaroscopy (capillary diameters, functional capillary density [FCD], peak red blood cell velocity [RBCVmax] after 1 min ischemia, time to reach peak RBCV [TRBCVmax]), and venous occlusion plethysmography (vasoreactivity), before and after 14 days of oral supplementation with L-arginine (5 g/day). Results: L-Arginine did not change fasting glycemia and lipidogram, but it decreased systolic, diastolic, and mean arterial pressure in elderly women, increased RBCVmax in all groups, and did not decrease TRBCVmax in T2DME. Capillary diameters and FCD remained unchanged in all groups. L-Arginine improved vasoreactivity during reactive hyperemia and after sublingual nitroglycerin (0.4 mg) in all groups. Conclusion: L-Arginine supplementation (5g/day during 14 days) was able to improve vascular/microvascular health in the elderly women with or without T2DM.

BACKGROUND Acetaminophen is commonly used as part of multimodal analgesia for acute pain. The intravenous formulation offers a more predictable bioavailability compared to oral and rectal acetaminophen. There have been reports of hypotension with intravenous acetaminophen attributable to centrally mediated and vasodilatory effects. We tested the hypothesis that in adults having abdominal surgery the use of intravenous acetaminophen versus placebo for postoperative pain management is associated with a decrease in mean arterial pressure (MAP) after its administration. METHODS This is a substudy of eFfect of intravenous ACetaminophen on posToperative hypOxemia after abdominal surgeRy (FACTOR) trial (NCT02156154). FACTOR trial randomly assigned adults undergoing abdominal surgery to either 1 g of acetaminophen or placebo every 6 hours during the first postoperative 48 hours. Continuous monitoring of blood pressure was obtained by noninvasive ViSi Mobile device (Sotera Wireless, Inc, San Diego, CA) at 15-second intervals during initial 48 hours postoperatively. We excluded patients without continuous monitoring data available. The primary outcome was the MAP difference between MAP 5 minutes before study drug administration (baseline) and MAP 30 minutes poststudy drug administration initiation. We used a linear mixed effects model to assess the treatment effect on MAP change. The secondary outcome was MAP area under baseline (AUB) during the 30 minutes after treatment. In a sensitivity analysis of change in MAP from predrug to postdrug administration, we instead used postdrug MAP as the outcome adjusting for the baseline MAP in the model. RESULTS Among 358 patients analyzed, 182 received acetaminophen and 176 placebo. The mean (standard deviation [SD]) of average MAP change was -0.75 (5.9) mm Hg for the treatment and 0.32 (6.3) mm Hg for the placebo. Acetaminophen was found to decrease the MAP from baseline more than placebo after drug administration. The estimated difference in mean change of MAP was -1.03 (95% confidence interval [CI] -1.60 to -0.47) mm Hg; P < .001. The sensitivity analysis showed postoperative MAP in the acetaminophen group was 1.33 (95% CI, 0.76-1.90) mm Hg lower than in the placebo group (P < .001). The median of MAP AUB was 33 [Q1 = 3.3, Q3 = 109] mm Hg × minutes for the treatment and 23 [1.6, 79] mm Hg × minutes for the placebo. Acetaminophen was found to increase the AUB with an estimated median difference of 15 (95% CI, 5-25) mm Hg × minutes (P = .003). CONCLUSIONS Intravenous acetaminophen decreases MAP after its administration. However, this decrease does not appear to be clinically meaningful. Clinicians should not refrain to use intravenous acetaminophen for acute pain management because of worries of hypotension.

BACKGROUND Traumatic brain injury (TBI) is a major cause of death and disability. Episodes of hypotension are associated with worse TBI outcomes. Our aim was to model the real-time risk of intraoperative hypotension in TBI patients, compare machine learning and traditional modeling techniques, and identify key contributory features from the patient monitor and medical record for the prediction of intraoperative hypotension. METHODS The data included neurosurgical procedures in 1005 TBI patients at an academic level 1 trauma center. The clinical event was intraoperative hypotension, defined as mean arterial pressure

Objective To characterize the safety of sildenafil in premature infants. Study design A phase I, open-label trial of sildenafil in premature infants receiving sildenafil per usual clinical care (cohort 1) or receiving a single IV dose of sildenafil (cohort 2). Safety was evaluated based on adverse events (AEs), transaminase levels, and mean arterial pressure monitoring. Results Twenty-four infants in cohort 1 (n = 25) received enteral sildenafil. In cohort 2, infants received a single IV sildenafil dose of 0.25 mg/kg (n = 7) or 0.125 mg/kg (n = 2). In cohort 2, there was one serious AE related to study drug involving hypotension associated with a faster infusion rate than specified by the protocol. There were no AEs related to elevated transaminases. Conclusion Sildenafil was well tolerated by the study population. Drug administration times and flush rates require careful attention to prevent infusion-related hypotension associated with faster infusions of IV sildenafil in premature infants. Clinical trial ClinicalTrials.gov Identifier: NCT01670136.

Background and Aims: During Cesarean section, hypotension occurs in the most of parturients, following spinal anesthesia. This prospective observational study was undertaken to determine the efficacy of two different Bolus Doses of Phenylephrine for Prevention of Spinal-Induced Hypotension during Cesarean Section. Materials and Methods: A total of 120 parturients undergoing cesarean section were divided into two groups of group A and group B with sixty in each group. Group A received phenylephrine 75 mcg IV bolus, while Group B received phenylephrine 100 mcg IV bolus, immediately after giving spinal anesthesia. For the next 20 minutes, systolic blood pressure (SBP), diastolic blood pressure (DSP), mean arterial pressure (MAP), and heart rate (HR) were recorded every 2 minutes, and APGAR scores at 1 and 5 minutes were recorded. Results: There was no difference between the two groups in terms of preventing hypotension, with 16.6% in Group A and 16.6% in Group B. In the first 2–6 minutes, however, the rise in systolic pressure in Group B was higher than in Group A. Group B (46.66 %) had a higher rate of bradycardia than Group A (25 %). Conclusion: Both phenylephrine dosages were equally effective in preventing hypotension following spinal anesthesia. However, Prophylactic bolus dose of phenylephrine 75 mcg was found to be effective for the management of spinal-induced hypotension and should be preferred over 100 mcg which causes significant bradycardia and reactive hypertension.

Introduction: Paramedic duties include assessing, treating, and maneuvering patients in physically challenging environments. Whether clinical skills and patient care are affected by these occupational demands is unknown. High-fidelity simulation affords the opportunity to study this in a controlled setting. Methods: Using a randomized crossover design, 11 regional paramedicine students and graduates (mean ± SD age = 23 ± 2 years) completed two, 20-minute high-fidelity simulations that included cardiopulmonary resuscitation (CPR) immediately after either an acute bout of occupational physical activity (OPA) or a rest period (REST). Heart rate, respiratory rate, and mean arterial pressure were measured throughout. Clinical performance was scored using the Global Rating Score and a patient care record. Measures of CPR efficacy were recorded in the manikin. Results: There were no significant differences in Global Rating Score (P = 0.07, ES = 0.03) or CPR efficacy between conditions. Patient care record accuracy was higher after the OPA versus REST simulations (mean ± SD = 61.8 ± 12.6% vs. 55.5 ± 12.0%, P = 0.03, ES = 0.5). Mean heart rate was higher during OPA simulations versus REST simulations (121 ± 14 vs. 84 ± 9 beats per minute, P < 0.01, ES = 3.1), as was mean respiratory rate (19 ± 3 vs. 16 ± 3 breaths per minute, P < 0.01, ES = 1.0). Mean arterial pressure was higher for OPA versus REST at simulation start (105 ± 11.3 vs. 95.8 ± 11.8 mm Hg, P = 0.01, Effect Size = 0.8), although not different after simulation. Conclusions: Paramedicine students including recent graduates performed as well, or better, in a simulated clinical scenario immediately after occupation-specific acute physical exertion compared with a REST, despite higher physiological exertion. Whether this is the case for more experienced but potentially less physically fit paramedics in the workforce warrants investigation.

Background In patient requiring vasopressors, the radial artery pressure may underestimate the true central aortic pressure leading to unnecessary interventions. When using a femoral and a radial arterial line, this femoral-to-radial arterial pressure gradient (FR-APG) can be detected. Our main objective was to assess the accuracy of non-invasive blood pressure (NIBP) measures; specifically, measuring the gradient between the NIBP obtained at the brachial artery and the radial artery pressure and calculating the non-invasive brachial-to-radial arterial pressure gradient (NIBR-APG) to detect an FR-APG. The secondary objective was to assess the prevalence of the FR-APG in a targeted sample of critically ill patients. Methods Adult patients in an intensive care unit requiring vasopressors and instrumented with a femoral and a radial artery line were selected. We recorded invasive radial and femoral arterial pressure, and brachial NIBP. Measurements were repeated each hour for 2 h. A significant FR-APG (our reference standard) was defined by either a mean arterial pressure (MAP) difference of more than 10 mmHg or a systolic arterial pressure (SAP) difference of more than 25 mmHg. The diagnostic accuracy of the NIBR-APG (our index test) to detect a significant FR-APG was estimated and the prevalence of an FR-APG was measured and correlated with the NIBR-APG. Results Eighty-one patients aged 68 [IQR 58–75] years and an SAPS2 score of 35 (SD 7) were included from which 228 measurements were obtained. A significant FR-APG occurred in 15 patients with a prevalence of 18.5% [95%CI 10.8–28.7%]. Diabetes was significantly associated with a significant FR-APG. The use of a 11 mmHg difference in MAP between the NIBP at the brachial artery and the MAP of the radial artery led to a specificity of 92% [67; 100], a sensitivity of 100% [95%CI 83; 100] and an AUC ROC of 0.93 [95%CI 0.81–0.99] to detect a significant FR-APG. SAP and MAP FR-APG correlated with SAP (r2 = 0.36; p, Key messages A significant radial-to-femoral pressure gradient occurs in nearly one-fifth of patients in ICU. Repeated non-invasive assessment of the radial-to-brachial pressure gradient was significantly correlated with the invasive radio-femoral arterial pressure gradient.

Purpose Fluid boluses (FB) are often used in post-cardiac arrest (CA) patients with haemodynamic instability. Although FB may improve cardiac output (CO) and mean arterial pressure (MAP), FB may also increase central venous pressure (CVP), reduce arterial PaO2, dilute haemoglobin and cause interstitial oedema. The aim of the present study was to investigate the net effect of FB administration on cerebral tissue oxygenation saturation (SctO2) in post-CA patients. Methods Pre-planned sub-study of the Neuroprotect post-CA trial (NCT02541591). Patients with anticipated fluid responsiveness based on stroke volume variation (SVV) or passive leg raising test were administered a FB of 500 ml plasma-lyte A (Baxter Healthcare) and underwent pre- and post-FB assessments of stroke volume, CO, MAP, CVP, haemoglobin, PaO2 and SctO2. Results 52 patients (mean age 64 ± 12 years, 75% male) received a total of 115 FB. Although administration of a FB resulted in a significant increase of stroke volume (63 ± 22 vs 67 ± 23 mL, p = 0.001), CO (4,2 ± 1,6 vs 4,4 ± 1,7 L/min, p = 0.001) and MAP (74,8 ± 13,2 vs 79,2 ± 12,9 mmHg, p = 0.004), it did not improve SctO2 (68.54 ± 6.99 vs 68.70 ± 6.80%, p = 0.49). Fluid bolus administration also resulted in a significant increase of CVP (10,0 ± 4,5 vs 10,7 ± 4,9 mmHg, p = 0.02), but did not affect PaO2 (99 ± 31 vs 94 ± 31 mmHg, p = 0.15) or haemoglobin concentrations (12,9 ± 2,1 vs 12,8 ± 2,2 g/dL, p = 0.10). In a multivariate model, FB-induced changes in CO (beta 0,77; p = 0.004) and in CVP (beta −0,23; p = 0.02) but not in MAP (beta 0,02; p = 0.18) predicted post-FB ΔSctO2. Conclusions Despite improvements in CO and MAP, FB administration did not improve SctO2 in post-cardiac arrest patients.

We aimed to investigate the resuscitative efficacy of hemoglobin vesicles (HbVs) as a red blood cell (RBC) substitute for the initial treatment of severe postpartum hemorrhage (PPH). Twenty-five pregnant rabbits underwent cesarean section; uncontrolled hemorrhage was induced by transecting the right uterine artery to establish a severe PPH model. During the first 30 min, all rabbits were administered 6% hydroxyethyl starch (HES) of an equivalent volume to the hemorrhage every 5 min. Thereafter, they received any of the following three isovolemic fluids for resuscitation every 5 min: RBCs with platelet-poor plasma (RBC/PPP) (n = 8), 6% HES (n = 7), or HbVs with 25% human serum albumin (n = 10). After surgical hemostasis at 60 min, survival was monitored until 12 h. No rabbits receiving only HES infusion survived beyond 6 h, whereas all rabbits receiving RBC/PPP transfusion survived. The rabbits receiving HbV infusion showed significantly higher mean arterial pressure and hemoglobin levels than the HES-receiving rabbits, and 8 of 10 rabbits survived for 6 h. The HbV group showed significantly higher survival than the HES group but worse survival than the RBC/PPP group. In conclusion, HbV infusion for severe PPH effectively prevents lethal hemorrhagic shock in a pregnant rabbit model.

BACKGROUND The effects of adrenaline on cerebral blood vessels during cardiopulmonary resuscitation (CPR) are not well understood. We developed an extracorporeal CPR model that maintains constant low systemic blood flow while allowing adrenaline-associated effects on cerebral vasculature to be assessed at different mean arterial pressure (MAP) levels independently of the effects on systemic blood flow. METHODS After eight minutes of cardiac arrest, low-flow extracorporeal life support (ECLS) (30 ml/kg/min) was started in fourteen pigs. After ten minutes, continuous adrenaline administration was started to achieve MAP values of 40 (n = 7) or 60 mmHg (n = 7). Measurements included intracranial pressure (ICP), cerebral perfusion pressure (CePP), laser-Doppler-derived regional cerebral blood flow (CBF), cerebral regional oxygen saturation (rSO2), brain tissue oxygen tension (PbtO2) and extracellular cerebral metabolites assessed by cerebral microdialysis. RESULTS During ECLS without adrenaline, regional CBF increased by only 5% (25th to 75th percentile: -3 to 14; p = 0.2642) and PbtO2 by 6% (0-15; p = 0.0073) despite a significant increase in MAP to 28 mmHg (25-30; p

Objectives The purpose of the present study was to describe how the perioperative hemodynamic profile before and after cardiopulmonary bypass during cardiac surgery is influenced by age and to describe the association between postoperative hemodynamics and one-year mortality. Design A retrospective registry-based study. Setting University Hospital of Aarhus, Denmark. Participants The study comprised 6,595 patients undergoing elective on-pump cardiac surgery from 2006 to 2016. Measurements and Main Results Perioperative hemodynamic values were derived from computerized anesthesia and intensive care reports, including mean arterial pressure, cardiac index, and oxygenation saturation from mixed venous blood in the pulmonary artery, during the perioperative period. Perioperative hemodynamic values were stratified according to age. Logistic regression was applied to predict the crude probability of death within one year from surgery according to hemodynamic values at six hours after surgery, stratified by age and use of inotropic agents, respectively. Lower values for cardiac index and mixed venous blood in the pulmonary artery with increasing age, across all points in time in the perioperative course, were observed. Higher probability of death was associated with lower hemodynamic values in the postoperative phase, and the probability of death was modified by age and the need for inotropic agents. Discussion This is a large registry based study describing the perioperative hemodynamic profile of patients undergoing cardiac surgery and the results enhance our understanding of age-differentiated values of CI and SvO2 in this specific population.

Background Colloids are thought to sustain blood pressure and cardiac index better than crystalloids. However, the relative effects of intraoperative hydroxyethyl starch and crystalloid administration on the cardiac index and blood pressure remain unclear. This study therefore tested in this subanalysis of a previously published large randomized trial the hypothesis that intraoperative goal-directed colloid administration increases the cardiac index more than goal-directed crystalloid administration. Further, the effects of crystalloid and colloid boluses on blood pressure were evaluated. Methods This planned subanalysis of a previous trial analyzed data from 973 patients, of whom 480 were randomized to colloids and 493 were randomized to crystalloids. Fluid administration was guided by esophageal Doppler. The primary outcome was the time-weighted average cardiac index during surgery between the colloid and crystalloid group. The secondary outcomes were the cardiac index just after bolus administration, time elapsed between boluses, and the average real variability during surgery. The study recorded cardiac index, corrected flow time, and blood pressure at 10-min intervals, as well as before and after each bolus. Results Time-weighted average of cardiac index over the duration of anesthesia was only slightly greater in patients given colloid than crystalloid, with the difference being just 0.20 l · min–1 · m–2 (95% CI, 0.11 to 0.29; P < 0.001). However, the hazard for needing additional boluses was lower after colloid administration (hazard ratio [95% CI], 0.60 [0.55 to 0.66]; P < 0.001) in a frailty time-to-event model accounting for within-subject correlation. The median [quartiles] number of boluses per patient was 4 [2, 6] for colloids and 6 [3, 8] for crystalloids, with a median difference (95% CI) of –1.5 (–2 to –1; P < 0.001). The average real mean arterial pressure variability did not differ significantly between the groups (difference in means [95% CI] of –0.03 (–0.07 to 0.02) mmHg, P = 0.229). Conclusions There were not clinically meaningful differences in the cardiac index or mean pressure variability in patients given goal-directed colloid and crystalloids. As might be expected from longer intravascular dwell time, the interval between boluses was longer with colloids. However, on a case basis, the number of boluses differed only slightly. Colloids do not appear to provide substantial hemodynamic benefit. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Aim Evaluate cerebrovascular autoregulation (CAR) using near-infrared spectroscopy (NIRS) after pediatric cardiac arrest and determine if deviations from CAR-derived optimal mean arterial pressure (MAPopt) are associated with outcomes. Methods CAR was quantified by a moving, linear correlation between time-synchronized mean arterial pressure (MAP) and regional cerebral oxygenation, called cerebral oximetry index (COx). MAPopt was calculated using a multi-window weighted algorithm. We calculated burden (magnitude and duration) of MAP less than 5 mmHg below MAPopt (MAPopt - 5), as the area between MAP and MAPopt - 5 curves using numerical integration and normalized as percentage of monitoring duration. Unfavorable outcome was defined as death or pediatric cerebral performance category (PCPC) at hospital discharge ≥3 with ≥1 change from baseline. Univariate logistic regression tested association between burden of MAP less than MAPopt - 5 and outcome. Results Thirty-four children (median age 2.9 [IQR 1.5,13.4] years) were evaluated. Median COx in the first 24 h post-cardiac arrest was 0.06 [0,0.20]; patients spent 27% [19,43] of monitored time with COx ≥ 0.3. Patients with an unfavorable outcome (n = 24) had a greater difference between MAP and MAPopt - 5 (13 [11,19] vs. 9 [8,10] mmHg, p = 0.01) and spent more time with MAP below MAPopt - 5 (38% [26,61] vs. 24% [14,28], p = 0.03). Patients with unfavorable outcome had a higher burden of MAP less than MAPopt - 5 than patients with favorable outcome in the first 24 h post-arrest (187 [107,316] vs. 62 [43,102] mmHg × Min/Hr; OR 4.93 [95% CI 1.16–51.78]). Conclusions Greater burden of MAP below NIRS-derived MAPopt - 5 during the first 24 h after cardiac arrest was associated with unfavorable outcomes.

Objective: To compare levobupivacaine based caudal epidural anesthesia and spinal anesthesia in terms of Intraoperative hemodynamic changes and postoperative pain and patient comfort in subjects undergoing perianal surgery in outpatient setting. Material and methods: All consecutive patients who were scheduled for perianal surgery. The difference in intraoperative hemodynamic changes, sensory and motor block level, postoperative pain and patient comfort was the primary outcome measure of this study. Results: There were no significant differences between the groups in terms of mean arterial pressure and heart rate recorded. Subjects randomized to spinal anesthesia had a significantl extensive motor and sensory block compared to those randomized to caudal epidural anesthesia. Visual analogue scale scores for surgical pain at postoperative 12 hours was significantly higher in subjects receiving spinal anesthesia compared to those receiving caudal epidural anesthesia (p< 0.05). Time to first analgesic administration was significantly lower in subjects randomized to spinal anesthesia compared to those receiving caudal epidural anesthesia (p< 0.01). Conclusion: Spinal anesthesia is associated with more extensive sensory and motor block compared to caudal epidural anesthesia in patients undergoing perianal surgery. Both techniques lead to similar hemodynamic changes. Postoperative pain control is more favorable with caudal block than the spinal anesthesia.