Willem Boer

Cerebral tissue oxygen saturation during therapeutic hypothermia in post-cardiac arrest patients

AIM OF THE STUDY This observational study was performed to assess the cerebral tissue oxygen saturation during and after therapeutic hypothermia in comatose patients after out-of-hospital cardiac arrest. METHODS We performed a prospective observational study on the cerebral tissue oxygen saturation (SctO(2)) in post-cardiac arrest patients treated with therapeutic hypothermia (TH) between March 2011 and April 2012. SctO(2) (measured by near-infrared spectroscopy) was non-invasively and continuously measured in 28 post-cardiac arrest patients during hypothermia and active rewarming. RESULTS At the start of mechanically induced TH, SctO(2) was 68% (65-72) and PaCO(2) was 47.2 mmHg (36.9-51.4). SctO(2) and PaCO(2) significantly decreased to 59% (57-64; p=0.006) and 36.6 mmHg (33.9-44.7; p=0.002), respectively, within the first 3h of mechanically induced TH. Cerebral tissue oxygen saturation was significantly lower in non-survivors (n=10) compared with survivors (n=18) at 3h after induction of hypothermia (p=0.02) while the decrease in PaCO(2) was similar in both groups. During TH maintenance, SctO(2) gradually returned to baseline values (69% (63-72)) at 24h, with no differences between survivors and non-survivors (p=0.65). Carbon dioxide remained within the range of mild hypocapnia (32-38 mmHg) throughout the hypothermic period. During rewarming, SctO(2) further increased to 71% (67-78). CONCLUSIONS Induction of TH in comatose post-CA patients changes the balance between oxygen delivery and supply. The decrease in SctO(2) was less pronounced in patients surviving to hospital discharge.

Feasibility of absolute cerebral tissue oxygen saturation during cardiopulmonary resuscitation

IntroductionCurrent monitoring during cardiopulmonary resuscitation (CPR) is limited to clinical observation of consciousness, breathing pattern and presence of a pulse. At the same time, the adequacy of cerebral oxygenation during CPR is critical for neurological outcome and thus survival. Cerebral oximetry, based on near-infrared spectroscopy (NIRS), provides a measure of brain oxygen saturation. Therefore, we examined the feasibility of using NIRS during CPR.MethodsRecent technologies (FORE-SIGHT™ and EQUANOX™) enable the monitoring of absolute cerebral tissue oxygen saturation (SctO2) values without the need for pre-calibration. We tested both FORE-SIGHT™ (five patients) and EQUANOX Advance™ (nine patients) technologies in the in-hospital as well as the out-of-hospital CPR setting. In this observational study, values were not utilized in any treatment protocol or therapeutic decision. An independent t-test was used for statistical analysis.ResultsOur data demonstrate the feasibility of both technologies to measure cerebral oxygen saturation during CPR. With the continuous, pulseless near-infrared wave analysis of both FORE-SIGHT™ and EQUANOX™ technology, we obtained SctO2 values in the absence of spontaneous circulation. Both technologies were able to assess the efficacy of CPR efforts: improved resuscitation efforts (improved quality of chest compressions with switch of caregivers) resulted in higher SctO2 values. Until now, the ability of CPR to provide adequate tissue oxygenation was difficult to quantify or to assess clinically due to a lack of specific technology. With both technologies, any change in hemodynamics (for example, ventricular fibrillation) results in a reciprocal change in SctO2. In some patients, a sudden drop in SctO2 was the first warning sign of reoccurring ventricular fibrillation.ConclusionsBoth the FORE-SIGHT™ and EQUANOX™ technology allow non-invasive monitoring of the cerebral oxygen saturation during CPR. Moreover, changes in SctO2 values might be used to monitor the efficacy of CPR efforts.

An observational near-infrared spectroscopy study on cerebral autoregulation in post-cardiac arrest patients: Time to drop ‘one-size-fits-all’ hemodynamic targets?

AIMS A subgroup of patients with ROSC after cardiac arrest (CA) with disturbed cerebral autoregulation might benefit from higher mean arterial pressures (MAP). We aimed to (1) phenotype patients with disturbed autoregulation, (2) investigate whether these patients have a worse prognosis, (3) define an individual optimal MAP per patient and (4) investigate whether time under this individual optimal MAP is associated with outcome. METHODS Prospective observational study in 51 post-CA patients monitored with near infrared spectroscopy. RESULTS (1) 18/51 patients (35%) had disturbed autoregulation. Phenotypically, a higher proportion of patients with disturbed autoregulation had pre-CA hypertension (31±47 vs. 65±49%, p=0.02) suggesting that right shifting of autoregulation is caused by chronic adaptation of cerebral blood flow to higher blood pressures. (2) In multivariate analysis, patients with preserved autoregulation (n=33, 65%) had a significant higher 180-days survival rate (OR 4.62, 95% CI [1.06:20.06], p=0.04]. Based on an index of autoregulation (COX), the average COX-predicted optimal MAP was 85 mmHg in patients with preserved and 100 mmHg in patients with disturbed autoregulation. (3) An individual optimal MAP could be determined in 33/51 patients. (4) The time under the individual optimal MAP was negatively associated with survival (OR 0.97, 95% CI [0.96:0.99], p=0.02). The time under previously proposed fixed targets (65, 70, 75, 80 mmHg) was not associated with a differential survival rate. CONCLUSION Cerebral autoregulation showed to be disturbed in 35% of post-CA patients of which a majority had pre-CA hypertension. Disturbed cerebral autoregulation within the first 24h after CA is associated with a worse outcome. In contrast to uniform MAP goals, the time spent under a patient tailored optimal MAP, based on an index of autoregulation, was negatively associated with survival.

Hemodynamic targets during therapeutic hypothermia after cardiac arrest: A prospective observational study ☆

AIM In analogy with sepsis, current post-cardiac arrest (CA) guidelines recommend to target mean arterial pressure (MAP) above 65 mmHg and SVO2 above 70%. This is unsupported by mortality or cerebral perfusion data. The aim of this study was to explore the associations between MAP, SVO2, cerebral oxygenation and survival. METHODS Prospective, observational study during therapeutic hypothermia (24h - 33 °C) in 82 post-CA patients monitored with near-infrared spectroscopy. RESULTS Forty-three patients (52%) survived in CPC 1-2 until 180 days post-CA. The mean MAP range associated with maximal survival was 76-86 mmHg (OR 2.63, 95%CI [1.01; 6.88], p = 0.04). The mean SVO2 range associated with maximal survival was 67-72% (OR 8.23, 95%CI [2.07; 32.68], p = 0.001). In two separate multivariate models, a mean MAP (OR 3.72, 95% CI [1.11; 12.50], p=0.03) and a mean SVO2 (OR 10.32, 95% CI [2.03; 52.60], p = 0.001) in the optimal range persisted as independently associated with increased survival. Based on more than 1625000 data points, we found a strong linear relation between SVO2 (range 40-90%) and average cerebral saturation (R(2) 0.86) and between MAP and average cerebral saturation for MAPs between 45 and 101 mmHg (R(2) 0.83). Based on our hemodynamic model, the MAP and SVO2 ranges associated with optimal cerebral oxygenation were determined to be 87-101 mmHg and 70-75%. CONCLUSION we showed that a MAP range between 76-86 mmHg and SVO2 range between 67% and 72% were associated with maximal survival. Optimal cerebral saturation was achieved with a MAP between 87-101 mmHg and a SVO2 between 70% and 75%. Prospective interventional studies are needed to investigate whether forcing MAP and SVO2 in the suggested range with additional pharmacological support would improve outcome.

Increase in cerebral oxygenation during advanced life support in out-of-hospital patients is associated with return of spontaneous circulation

IntroductionBy maintaining sufficient cerebral blood flow and oxygenation, the goal of cardiopulmonary resuscitation (CPR) is to preserve the pre-arrest neurological state. To date, cerebral monitoring abilities during CPR have been limited. Therefore, we investigated the time-course of cerebral oxygen saturation values (rSO2) during advanced life support in out-of-hospital cardiac arrest. Our primary aim was to compare rSO2 values during advanced life support from patients with return of spontaneous circulation (ROSC) to patients who did not achieve ROSC.MethodsWe performed an observational study to measure rSO2 using Equanox™ (Nonin, Plymouth, MI) from the start of advanced life support in the pre-hospital setting.ResultsrSO2 of 49 consecutive out-of-hospital cardiac arrest patients were analyzed. The total increase from initial rSO2 value until two minutes before ROSC or end of advanced life support efforts was significantly larger in the group with ROSC 16% (9 to 36) compared to the patients without ROSC 10% (4 to 15) (P = 0.02). Mean rSO2 from the start of measurement until two minutes before ROSC or until termination of advanced life support was higher in patients with ROSC than in those without, namely 39% ± 7 and 31% ± 4 (P = 0.05) respectively.ConclusionsDuring pre-hospital advanced life support, higher increases in rSO2 are observed in patients attaining ROSC, even before ROSC was clinically determined. Our findings suggest that rSO2 could be used in the future to guide patient tailored treatment during cardiac arrest and could therefore be a surrogate marker of the systemic oxygenation state of the patient.

Regional cerebral oximetry during cardiopulmonary resuscitation: useful or useless?

BACKGROUND Approximately 375,000 people annually experience sudden cardiac arrest (CA) in Europe. Most patients who survive the initial hours and days after CA die of postanoxic brain damage. Current monitors, such as electrocardiography and end-tidal capnography, provide only indirect information about the condition of the brain during cardiopulmonary resuscitation (CPR). In contrast, cerebral near-infrared spectroscopy provides continuous, noninvasive, real-time information about brain oxygenation without the need for a pulsatile blood flow. It measures transcutaneous cerebral tissue oxygen saturation (rSO2). This information could supplement currently used monitors. Moreover, an evolution in rSO2 monitoring technology has made it easier to assess rSO2 in CA conditions. OBJECTIVE We give an overview of the literature regarding rSO2 measurements during CPR and the current commercially available devices. We highlight the feasibility of cerebral saturation measurement during CPR, its role as a quality parameter of CPR, predictor of return of spontaneous circulation (ROSC) and neurologic outcome, and its monitoring function during transport. DISCUSSION rSO2 is feasible in the setting of CA and has the potential to measure the quality of CPR, predict ROSC and neurologic outcome, and monitor post-CA patients during transport. CONCLUSION The literature shows that rSO2 has the potential to serve multiple roles as a neuromonitoring tool during CPR and also to guide neuroprotective therapeutic strategies.

Low hemoglobin levels are associated with lower cerebral saturations and poor outcome after cardiac arrest

PURPOSE Post-cardiac arrest (CA) patients have a large cerebral penumbra at risk for secondary ischemic damage in case of suboptimal brain oxygenation during ICU stay. The aims of this study were to investigate the association between hemoglobin, cerebral oxygenation (SctO2) and outcome in post-CA patients. METHODS Prospective observational study in 82 post-CA patients. Hemoglobin, a corresponding SctO2 measured by NIRS and SVO2 in patients with a pulmonary artery catheter (n=62) were determined hourly during hypothermia in the first 24h of ICU stay. RESULTS We found a strong linear relationship between hemoglobin and mean SctO2 (SctO2=0.70×hemoglobin+56 (R(2) 0.84, p=10(-6))). Hemoglobin levels below 10g/dl generally resulted in lower brain oxygenation. There was a significant association between good neurological outcome (43/82 patients in CPC 1-2 at 180 days post-CA) and admission hemoglobin above 13g/dl (OR 2.76, 95% CI 1.09:7.00, p=0.03) or mean hemoglobin above 12.3g/dl (OR 2.88, 95%CI 1.02:8.16, p=0.04). This association was entirely driven by results obtained in patients with a mean SVO2 below 70% (OR 6.25, 95%CI 1.33:29.43, p=0.01) and a mean SctO2 below 62.5% (OR 5.87, 95%CI 1.08:32.00, p=0.03). CONCLUSION Hemoglobin levels below 10g/dl generally resulted in lower cerebral oxygenation. Average hemoglobin levels below 12.3g/dl were associated with worse outcome in patients with suboptimal SVO2 or SctO2. The safety of a universal restrictive transfusion threshold of 7g/dl can be questioned in post-CA patients.

The Effect of Deep Versus Moderate Neuromuscular Block on Surgical Conditions and Postoperative Respiratory Function in Bariatric Laparoscopic Surgery: A Randomized, Double Blind Clinical Trial.

BACKGROUND: In recent literature, it has been suggested that deep neuromuscular block (NMB) improves surgical conditions during laparoscopy; however, the evidence supporting this statement is limited, and this was not investigated in laparoscopic bariatric surgery. Moreover, residual NMB could impair postoperative respiratory function. We tested the hypotheses that deep NMB could improve the quality of surgical conditions for laparoscopic bariatric surgery compared with moderate NMB and investigated whether deep NMB puts patients at risk for postoperative respiratory impairment compared with moderate NMB. METHODS: Sixty patients were evenly randomized over a deep NMB group (rocuronium bolus and infusion maintaining a posttetanic count of 1–2) and a moderate NMB group (rocuronium bolus and top-ups maintaining a train-of-four count of 1–2). Anesthesia was induced and maintained with propofol and remifentanil. The primary outcome measures were the quality of surgical conditions assessed by a single surgeon using a 5-point rating scale (1 = extremely poor, 5 = optimal), the number of intra-abdominal pressure increases >18 cmH2O and the duration of surgery. Secondary outcome measure was the postoperative pulmonary function assessed by peak expiratory flow, forced expiratory volume in 1 second, and forced vital capacity, and by the need for postoperative respiratory support. Data are presented as mean ± standard deviation with estimated treatment effect (ETE: mean difference [95% confidence interval]) for group comparisons. RESULTS: There was no statistically significant difference in the surgeon’s rating regarding the quality of the surgical field between the deep and moderate NMB group (4.2 ± 1.0 vs 3.9 ± 1.1; P = .16, respectively; ETE: 0.4 [−0.1, 0.9]). There was no difference in the proportional rating of surgical conditions over the 5-point rating scale between both groups (P = .91). The number of intra-abdominal pressure increases >18 cmH2O and the duration of surgery were not statistically different between the deep and moderate NMB group (0.2 ± 0.9 vs 0.3 ± 1.0; P = .69; ETE: −0.1 [−0.5, 0.4] and 61.3 ± 15.1 minutes vs 70.6 ± 20.8 minutes; P = .07, ETE: −9.3 [−18.8, 0.1], respectively). All the pulmonary function tests were considerably impaired in both groups when compared with baseline (P < .001). There was no statistically significant difference in the decrease in peak expiratory flow, forced expiratory volume in 1 second, and forced vital capacity (expressed as % change from baseline) between the deep and the moderate NMB group. CONCLUSIONS: Compared with a moderate NMB, there was insufficient evidence to conclude that deep NMB improves surgical conditions during laparoscopic bariatric surgery. Postoperative pulmonary function was substantially decreased after laparoscopic bariatric surgery independently of the NMB regime that was used. The study is limited by a small sample size.

Cerebral saturation monitoring during cardiopulmonary resuscitation should be used as dynamic, rather than static, information

With great interest we read the paper of Parnia et al.1 The uthors report a significantly higher overall mean rSO2 in patients ith return of spontaneous circulation (ROSC) in comparison with on-survivors (respectively 35 ± 5 vs 18 ± 0.4). First of all, both hese values are extremely low, despite the fact that all patients ad in-hospital cardiac arrest, and shorter delays to treatment (and igher overall mean rSO2) are expected compared to patients with ut of hospital arrest.2 The reason for these low values might be elated to the used near-infrared spectroscopy (NIRS) technology INVOS® is a relative O2 saturation monitoring). Secondly, the difference in rSO2 between survivors and nonurvivors is the highest during the final 5 min of resuscitation. This s not a surprising observation, since increasing rSO2 is a precuror of the onset of ROSC and at ROSC, the difference in rSO2 is or sure the greatest compared to rSO2 values in patients who ever had ROSC (and therefore worse hemodynamics without any ncrease in rSO2 during the whole cardiopulmonary resuscitation CPR)). We are not sure whether the slow increase in rSO2 observed efore ROSC might not be explained by the use of a “relative” NIRS echnology (with a proprietary averaging algorithm), not providing absolute” saturation values. The authors confirmed that their findings indicate that rSO2 in ardiac arrest is a dynamic measurement and that any decrease or

Regional cerebral saturation monitoring during withdrawal of life support until death

AIMS The aim of this pilot study was to explore the regional cerebral oxygen saturation (rSO2) during the process of dying in Intensive Care Unit (ICU) patients in whom it was decided to withdraw life support. METHODS Regional cerebral saturation was measured from the moment active treatment was stopped until the moment of death, defined as the onset of asystole. Simultaneously, heart rate and arterial blood pressure were recorded using a radial arterial catheter. Baseline rSO2 values were calculated as mean values over one hour in stable haemodynamic conditions immediately after the decision to withdraw life support. RESULTS Cerebral saturation was measured in six dying ICU patients. The mean age of patients was 64year. The median baseline rSO2 value was 64% (58%-68%). At time of death, median rSO2 was 33% (7%-40%). The median decrease in rSO2 from baseline until death was 31% (25%-45%). The median decrease in rSO2 observed during the last hour before time of death was 20% (12%-31%). CONCLUSION A continuous and patient specific decrease in rSO2 was observed in all patients with a simultaneous decrease in MAP. However, the absolute rSO2 value at moment death was clinically determined, had a broad range, indicating that there is no clear cut-off rSO2 value for death probably due to the heterogeneity of the studied population. Taken together, these observations highlight the importance of following trends and comparing rSO2 values in the cardiac arrest setting.