Ward Eertmans

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.

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.

Mean arterial pressure of 65 mm Hg versus 85-100 mm Hg in comatose survivors after cardiac arrest: Rationale and study design of the Neuroprotect post–cardiac arrest trial

Background Post–cardiac arrest (CA) patients admitted to the intensive care unit (ICU) have a poor prognosis, with estimated survival rates of around 30%‐50%. On admission, these patients have a large cerebral penumbra at risk for additional damage in case of suboptimal brain oxygenation during their stay in the ICU. The aim of the Neuroprotect post‐CA trial is to investigate whether forcing mean arterial blood pressure (MAP) and mixed venous oxygen saturation (SVO2) in a specific range (MAP 85–100 mm Hg, SVO2 65%‐75%) with additional pharmacological support (goal‐directed hemodynamic optimization) may better salvage the penumbra, reduce cerebral ischemia, and improve functional outcome when compared with current standard of care (MAP 65 mm Hg). Design The Neuroprotect post‐CA trial (NCT02541591) is a multicenter, randomized, parallel‐group, open‐label, assessor‐blinded, monitored, and investigator‐driven clinical trial. The trial will be conducted in 2 tertiary care hospitals in Belgium (UZ Leuven and ZOL‐Genk). A total of 112 eligible patients will be randomly assigned in a 1:1 ratio to goal‐directed hemodynamic optimization or standard care strategy by an interactive voice response system. Patients will be stratified according to the presence of an initial shockable rhythm. Adult patients (≥18 years) resuscitated from out‐of‐hospital CA of a presumed cardiac cause who are unconscious upon hospital admission are eligible for inclusion. Patients can be included irrespective of their presenting heart rhythm but need to have a sustained return of spontaneous circulation. Trial interventions will take 36 hours starting from ICU admission. The primary outcome is the extent of cerebral ischemia as quantified by the apparent diffusion coefficient on diffusion‐weighted magnetic resonance imaging to be performed at day 4–5 post‐CA. Secondary outcomes include surrogate biomarkers of brain injury (neuron specific enolase) at day 1–5, neuropsychological and functional testing at hospital discharge, a Short Form–36 health questionnaire at 180 days, and outcome as assessed with cerebral performance category scores at ICU discharge and at 180 days. Conclusions The Neuroprotect post‐CA trial will investigate whether a more aggressive hemodynamic strategy to obtain a MAP 85–100 mm Hg and SVO2 65%‐75% reduces brain ischemia and improves outcome when compared with standard treatment (MAP 65 mm Hg) in comatose post‐CA survivors.

The validation of simplified EEG derived from the bispectral index monitor in post-cardiac arrest patients

AIMS We aimed to validate retrospectively the accuracy of simplified electroencephalography (EEG) monitoring derived from the bispectral index (BIS) monitor in post-cardiac arrest (CA) patients. METHODS Successfully resuscitated CA patients were transferred to the Catherization Lab followed by percutaneous coronary intervention when indicated. On arrival at the coronary care unit, bilateral BIS monitoring was started and continued up to 72 h. Raw simplified EEG tracings were extracted from the BIS monitor at a time point coinciding with the registration of standard EEG monitoring. BIS EEG tracings were reviewed by two neurophysiologists, who were asked to indicate the presence of following patterns: diffuse slowing rhythm, burst suppression pattern, cerebral inactivity, periodic epileptiform discharges and status epilepticus (SE). Additionally, these simplified BIS EEG tracings were analysed by two inexperienced investigators, who were asked to indicate the presence of SE only. RESULTS Thirty-two simplified BIS EEG samples were analysed. Compared to standard EEG, neurophysiologists interpreted all simplified EEG samples with a sensitivity of 86%, a specificity of 100% and an interobserver variability of 0.843. Furthermore, SE was identified with a sensitivity of 80% and a specificity of 94% by two unexperienced physicians. CONCLUSION Using a simple classification system, raw simplified EEG derived from a BIS monitoring device is comparable to standard EEG monitoring. Moreover, investigators without EEG experience were capable to identify SE in post-CA patients. Future studies will be warranted to confirm our results and to determine the added value of using simplified BIS EEG in terms of prognostic and therapeutic implications.

The impact of global hemodynamics, oxygen and carbon dioxide on epileptiform EEG activity in comatose survivors of out-of-hospital cardiac arrest

AIM To study the association between global hemodynamics, blood gases, epileptiform EEG activity and survival after out-of-hospital CA (0HCA). METHODS We retrospectively analyzed 195 comatose post-CA patients. At least one EEG recording per patient was evaluated to diagnose epileptiform EEG activity. Refractory epileptiform EEG activity was defined as persisting epileptic activity on EEG despite the use of 2 or more anti-epileptics. The time weighted average mean arterial pressure 48h (TWA-MAP48), the percentage of time with a MAP below 65 and above 85mmHg and the percentage of time with normoxia, hypoxia (<70mmHg), hyperoxia (>150mmHg), normocapnia, hypocapnia (<35mmHg) and hypercapnia (>45mmHg) were calculated. RESULTS We observed epileptiform EEG activity in 57 patients (29%). A shockable rhythm was associated with a decreased likelihood of epileptic activity on the EEG (OR: 0.41, 95%CI 0.22-0.79). We did not identify an association between the TWA-MAP48, the percentage of time with MAP below 65mmHg or above 85mmHg, blood gas variables and the risk of post-CA epileptiform EEG activity. The presence of epileptiform activity decreased the likelihood of survival independently (OR: 0.10, 95% CI: 0.04-0.24). Interestingly, survival rates of patients in whom the epileptiform EEG resolved (n=20), were similar compared to patients without epileptiform activity on EEG (60% vs 67%,p=0.617). Other independent predictors of survival were presence of basic life support (BLS) (OR:5.08, 95% CI 1.98-13.98), presence of a shockable rhythm (OR: 7.03, 95% CI: 3.18-16.55), average PaO2 (OR=0.93, CI 95% 0.90-0.96) and% time MAP<65mmHg (OR: 0.96, CI 95% 0.94-0.98). CONCLUSION Epileptiform EEG activity in post-CA patients is independently and inversely associated with survival and this effect is mainly driven by patients in whom this pattern is refractory over time despite treatment with anti-epileptic drugs. We did not identify an association between hemodynamic factors, blood gas variables and epileptiform EEG activity after CA, although both hypotension, hypoxia and epileptic EEG activity were predictors of survival.

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.