Jo Dens

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.

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.

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.

Cerebral tissue saturation, the next step in cardiopulmonary resuscitation management?

No abstract

Post-cooling controlled normothermia and pyrexia after therapeutic hypothermia.

With interest we read the manuscript of Leary et al., on pyrexia nd neurologic outcome after therapeutic hypothermia for cariac arrest.1 The main conclusion of the authors is that 41% of he post-arrest patients with therapeutic hypothermia developed yrexia 24 h following re-warming and most importantly, was not ssociated with worse neurological outcomes among survivors to ospital discharge. This study is a multicenter retrospective report. Patient data rom 11 institutes were collected. Unfortunately, different coolng and re-warming protocols with diverse techniques (e.g. cold aline or external cooling pads and invasive devices) were used n the different centers. Some of these methods hamper the fineuning of both cooling and re-warming.2,3 Most remarkably, in 2 f the institutes, there was an active normothermia phase, induced or 48 h after rewarming. The authors defined post-cooling fever s a temperature exceeding 38◦ within the first 24 h following rearming. It is unclear whether patients that were managed with 8 h active normothermia (following rewarming) were excluded rom this analysis. In their paper, the authors mention that of “those atients who had pyrexia, all were treated at institutions that did ot have controlled normothermia protocols”. Did this imply that o patient that was treated with active normothermia did actully develop fever? As far as today, no hard scientific data promote he use of an active normothermia phase after rewarming. Refering to this paper, outcome in their patients was not related to he occurrence of post-cooling fever, providing no arguments in avor of the use of controlled normothermia? We suggest that the uthors should clarify the number of patients that were treated ith controlled normothermia and should indicate the occurrence f post-controlled normothermia fever in these patients and its ossible influence on final neurologic outcome. Mild hypothermia after cardiac arrest in non-conscious surivors became the standard of treatment. Hyperthermia after e-warming occurs frequently (according to our data in 89% of ooled post-arrest patients)4 and future careful research needs to e done to reveal its possible causes (thermoregulatory dysfuncion, infection, SIRS. . .), to assess the possible harmfulness and to earch for therapeutic measures (like active normothermia), resultng in improved outcome.

Association of serum lactate and survival outcomes after cardiac arrest.

With great interest we read the paper by Starodub et al. on he association of serum lactate and survival outcomes in patients ndergoing therapeutic hypothermia after cardiac arrest. 1 The uthors concluded that serum lactate levels at 12 h and 24 h, but ot initially following cardiac arrest, are associated with survival o hospital discharge after resuscitation from CA. The goal of this study was to confirm and extend the findings f Cocchi et al., who find an association between initial lactate levls (and vasopressor treatment at any time point during the ER anagement) and mortality after CA.2 In the discussion of Staroub et al., the authors refer to the differences between both patient opulations as one of the reasons for the discrepancy in the prognotic value of initial lactate levels, between their results and those ublished earlier by Cocchi et al. Less than 50% of the patients in he paper of Cocchi et al. underwent therapeutic hypothermia (TH) nd 63% of the non-survivors had asystole as initial rhythm, while tarodub et al. included only patients receiving TH with a higher roportion of patients with initial shockable rhythms. Although nitial rhythm and the use of TH could have played an important ole, there is another difference in both patient populations. Cocchi t al., as well as most of the other studies analyzing the prognotic value of initial lactate levels, only included patients suffering rom out-of-hospital CA (OHCA),3,4 while Starodub et al. included A patients regardless of the location of arrest. One can assume that n-hospital CA arrest patients have shorter no-flow and low flow ime,5 but more extensive comorbidities. Therefore, it would be nteresting to know if the authors analyzed the possible influence f the inclusion of the high number of patients suffering from inospital CA (21.4%) on their observed relationship between initial actate and survival. Patients suffering from IHCA are expected to resent with lower initial lactate levels and worse outcome. Thereore, these characteristics might have interfered with the overall elationship between initial lactate and final outcome in this paper.

Cerebral saturation in cardiac arrest patients measured with near-infrared technology during pre-hospital advanced life support. Results from Copernicus I cohort study

AIM To date, monitoring options during pre-hospital advanced life support (ALS) are limited. Regional cerebral saturation (rSO2) may provide more information concerning the brain during ALS. We hypothesized that an increase in rSO2 during ALS in out-of hospital cardiac arrest (OHCA) patients is associated with return of spontaneous circulation (ROSC). METHODS A prospective, non-randomized multicenter study was conducted in the pre-hospital setting of six hospitals in Belgium. Cerebral saturation was measured during pre-hospital ALS by a medical emergency team in OHCA patients. Cerebral saturation was continuously measured until ALS efforts were terminated or until the patient with sustained ROSC (>20 min) arrived at the emergency department. To take the longitudinal nature of the data into account, a linear mixed model was used. The correlation between the repeated measures of a patient was handled by means of ​a random intercept and a random slope. Our primary analysis tested the association of rSO2 with ROSC. RESULTS Of the 329 patients 110 (33%) achieved ROSC. First measured rSO2 was 30% ± 18 in the ROSC group and 24% ± 15 in the no-ROSC group (p = .004; mean ± SD). Higher mean rSO2 values were observed in the ROSC group compared to the no-ROSC group (41% ± 13 versus 33% ± 13 respectively; p < 0.001). The median increase in rSO2, measured from start until two minutes before ROSC, was higher in the ROSC group (ROSC group 17% (IQR 6-29)) than in the no-ROSC group (8% (IQR 2-13); p < 0.001). An increase in rSO2 above 15% was associated with ROSC (OR 4.5; 95%CI 2.747-7.415; p < 0.001). CONCLUSION Regional cerebral saturation measurements can be used during pre-hospital ALS as an additional marker to predict ROSC. An increase of at least 15% in rSO2 during ALS is associated with a higher probability of ROSC.

Influence of continuously evolving transcatheter aortic valve implantation technology on cerebral oxygenation

This study assessed the influence of the evolution in Transcatheter Aortic Valve Implantation technology on cerebral oxygenation. Cerebral oxygenation was measured continuously with Near-Infrared Spectroscopy and compared retrospectively between balloon-expandable, self-expandable and differential deployment valves which were implanted in 12 (34%), 17 (49%) and 6 patients (17%), respectively. Left and right SctO2 values were averaged at four time points and used for analysis (i.e. at baseline, balloon-aortic valvuloplasty, valve deployment, and at the end of the procedure). During balloon-aortic valvuloplasty and valve deployment, cerebral oxygenation decreased in patients treated with balloon or self-expandable valves (balloon-expandable: p = 0.003 and p = 0.002; self-expandable: p < 0.001 and p = 0.003, respectively). The incidence of cerebral desaturations below 80% of baseline was significantly larger in patients treated with balloon-expandable valves (p = 0.001). In contrast, patients who received differential deployment valves never experienced a cerebral desaturation below 80% of baseline. Furthermore, both the incidence and duration below a cerebral oxygenation of 55% was significantly different between balloon and self-expandable valves (p = 0.038 and p = 0.018, respectively). This study demonstrated that Transcatheter Aortic Valve Implantation procedures are associated with significant cerebral desaturations, especially during balloon-aortic valvuloplasty and valve deployment. Moreover, our results showed that latest innovations in Transcatheter Aortic Valve Implantation technology beneficially influenced the adequacy of cerebral perfusion.