Effect of neuromonitor-guided titrated care on brain tissue hypoxia after opioid overdose cardiac arrest

Elmer, Jonathan; Flickinger, Katharyn L; Anderson, Maighdlin; Koller, Allison C; Sundermann, Matthew L; Dezfulian, Cameron; Okonkwo, David O.; Shutter, Lori; Salcido, David D; Callaway, Clifton W.; Menegazzi, James J.

doi:10.1016/j.resuscitation.2018.04.013

Cited by 21 publications

(26 citation statements)

References 29 publications

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“…Delineating the significance of brain tissue hypoxia as a modifiable factor, as opposed to an expected epiphenomenon in the natural history of HIBI, is essential. In animal models, MAP augmentation using exogenous vasopressors has demonstrated improved PbtO2 in thalamic and cortical tissue, structures which are exquisitely susceptible to secondary injury (9,11). We also observed a relationship between MAP and PbtO2 in individual patients over time.…”

Section: Discussionsupporting

confidence: 58%

“…Observational studies demonstrate that perturbations in CDO2 from hypotension (6,7) and hypocapnia (8) after ROSC during no-reflow are associated with worse neurological outcome. Animal models have confirmed the no-reflow phenomenon (9) and demonstrate that increasing CDO2 with mean arterial pressure (MAP) augmentation results in improved thalamic and subcortical brain tissue oxygenation (PbtO2) (10,11). A recent systematic review suggests increased MAP is associated with improved neurologic outcome following cardiac arrest (12).…”

Section: Introductionmentioning

confidence: 95%

See 1 more Smart Citation

The Burden of Brain Hypoxia and Optimal Mean Arterial Pressure in Patients With Hypoxic Ischemic Brain Injury After Cardiac Arrest*

Sekhon

Gooderham

Menon

et al. 2019

Critical Care Medicine

111

110

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Objectives: In patients at risk of hypoxic ischemic brain injury following cardiac arrest, we sought to (i) characterize brain oxygenation and determine the prevalence of brain hypoxia, (ii) characterize autoregulation using the pressure reactivity index (PRx) and identify the optimal mean arterial pressure (MAPOPT), and (iii) assess the relationship between MAPOPT and brain tissue oxygenation (PbtO2). Design: Prospective interventional study. Setting: Quaternary intensive care unit. Patients: Adult patients with return to spontaneous circulation (ROSC) greater than 10 minutes and a post-resuscitation Glasgow Coma Score under 9 within 72 hours of cardiac arrest. Interventions: All patients underwent multimodal neuromonitoring which included: (i) PbtO2, (ii) intracranial pressure; (iii) jugular venous continuous oximetry (SjvO2); (iv) regional saturation of oxygen (rSO2) using near-infrared spectroscopy, and (iv) PRx based determination of MAPOPT, lower and upper limit of autoregulation. We additionally collected MAP, end tidal carbon dioxide (ETCO2) and temperature. All data were captured at 300 Hz using ICM+® brain monitoring software. Measurements and Main Results: Ten patients (7 males) were included with a median age 47 (range 20-71) and ROSC 22 minutes (12-36). The median duration of monitoring was 47 hours (15-88) and median duration from cardiac arrest to inclusion was 15 hours (6-44). The mean PbtO2 was 23 mmHg (SD 8) and the mean percentage of time with a PbtO2 below 20 mmHg was 38% (6-100). The mean PRx was 0.23 (0.27) and the percentage of time with a PRx greater than 0.3 was 50% (12-91). The mean MAPOPT, lower and upper of autoregulation were 89 mmHg (11), 82mmHg (8) and 96 mmHg (9), respectively. There was marked betweenpatient variability in the relationship between MAP and indices of brain oxygenation. As the patients' actual MAP approached MAPOPT, PbtO2 increased (p<0.001). This positive relationship did not persist when the actual MAP was above MAPOPT. Conclusions: Episodes of brain hypoxia in HIBI are frequent and perfusion within proximity of MAPOPT is associated with increased PbtO2. PRx can yield MAPOPT, lower and upper limit of autoregulation in patients following cardiac arrest.

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Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 95%

The Burden of Brain Hypoxia and Optimal Mean Arterial Pressure in Patients With Hypoxic Ischemic Brain Injury After Cardiac Arrest*

Sekhon

Gooderham

Menon

et al. 2019

Critical Care Medicine

111

110

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“…Hyperoxemia may exacerbate oxygen free radical-mediated damage in the brain and promote pulmonary inflammation [4,30]. In contrast, a recent porcine model of CA demonstrated a reduced incidence of low brain tissue oxygenation in swine treated with a FiO 2 of 1.0 and a 20-mmHg increase in mean arterial pressure (MAP) from baseline compared to those treated with a SpO2 target of 94-98% and a MAP target of > 65 mmHg [31]. This may help explain our finding of a lower mortality associated with hyperoxia.…”

Section: Discussionmentioning

confidence: 99%

The interaction between arterial oxygenation and carbon dioxide and hospital mortality following out of hospital cardiac arrest: a cohort study

et al. 2020

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Background: Outcomes following out of hospital cardiac arrest (OHCA) are poor. The optimal arterial oxygen and carbon dioxide (PaCO 2) levels for managing patients following OHCA are unknown. We hypothesized that abnormalities in arterial oxygenation (PaO 2 /FiO 2 ratio or PaO 2) and PaCO 2 would be associated with hospital mortality following OHCA. We hypothesized that PaCO 2 would significantly modify the oxygenation-mortality relationship. Methods: This was an observational cohort study using data from OHCA survivors admitted to adult critical care units in England, Wales and Northern Ireland from 2011 to 2018. Logistic regression analyses were performed to assess the relationship between hospital mortality and oxygenation and PaCO 2. Results: The analysis included 23,625 patients. In comparison with patients with a PaO 2 /FiO 2 > 300 mmHg, those with a PaO 2 /FiO 2 ≤ 100 mmHg had higher mortality (adjusted OR, 1.79; 95% CI, 1.48 to 2.15; P < 0.001). In comparison to hyperoxemia (PaO 2 > 100 mmHg), patients with hypoxemia (PaO 2 < 60 mmHg) had higher mortality (adjusted OR, 1.34; 95% CI, 1.10 to 1.65; P = 0.004). In comparison with normocapnia, hypercapnia was associated with lower mortality. Hypocapnia (PaCO2 ≤ 35 mmHg) was associated with higher mortality (adjusted OR, 1.91; 95% CI, 1.63 to 2.24; P < 0.001). PaCO 2 modified the PaO 2 /FiO 2-mortality and PaO 2-mortality relationships, though these relationships were complex. Patients who were both hyperoxic and hypercapnic had the lowest mortality. Conclusions: Low PaO 2 /FiO 2 ratio, hypoxemia and hypocapnia are associated with higher mortality following OHCA. PaCO 2 modifies the relationship between oxygenation and mortality following OHCA; future studies examining this interaction are required.

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“…Although limited data are available on the relationship between PbtO 2 and neurologic injury after cardiac arrest [ 22 , 23 ], a number of studies have suggested that the depth and duration of low PbtO 2 values correlate with unfavorable outcomes in patients with severe traumatic brain injury [ 24 , 25 , 26 , 27 ]. Our findings, together with those of these studies [ 24 , 25 , 26 , 27 ], indicate a plausible link between PbtO 2 and neurologic outcome among the survivors of the epinephrine group in the PARAMEDIC2 trial.…”

Section: Discussionmentioning

confidence: 99%

“…The epinephrine-induced, persistent reduction of PbtO 2 in the present study, in contrast to the rapid reversal of epinephrine-induced reduction of PbtO 2 observed in the study by Ristagno et al [ 5 ], might be due to the prolonged duration before treatment of cardiac arrest in the present study. No studies, to the best of our knowledge, have evaluated the effects of the duration of untreated cardiac arrest on the epinephrine-induced reduction of PbtO 2 , but several experimental studies using a model with relatively prolonged duration of untreated cardiac arrest reported findings suggestive of sustained reduction in PbtO 2 after ROSC [ 9 , 23 ]. In a study in which rats underwent 9 min or 12 min of asphyxial cardiac arrest followed by CPR including epinephrine administration [ 9 ], cortical PbtO 2 was similar to baseline until 15 min after ROSC but was lower than baseline from 30 min to 120 min after ROSC.…”

Section: Discussionmentioning

confidence: 99%

Effect of Epinephrine Administered during Cardiopulmonary Resuscitation on Cerebral Oxygenation after Restoration of Spontaneous Circulation in a Swine Model with a Clinically Relevant Duration of Untreated Cardiac Arrest

Lee

Shamsiev

Mamadjonov

et al. 2021

IJERPH

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Severe neurological impairment was more prevalent in cardiac arrest survivors who were administered epinephrine than in those administered placebo in a randomized clinical trial; short-term reduction of brain tissue O2 tension (PbtO2) after epinephrine administration in swine following a short duration of untreated cardiac arrest has also been reported. We investigated the effects of epinephrine administered during cardiopulmonary resuscitation (CPR) on cerebral oxygenation after restoration of spontaneous circulation (ROSC) in a swine model with a clinically relevant duration of untreated cardiac arrest. After 7 min of ventricular fibrillation, 24 pigs randomly received either epinephrine or saline placebo during CPR. Parietal cortex measurements during 60-min post-resuscitation period showed that the area under the curve (AUC) for PbtO2 was smaller in the epinephrine group than in the placebo group during the initial 10-min period and subsequent 50-min period (both p < 0.05). The AUC for number of perfused cerebral capillaries was smaller in the epinephrine group during the initial 10-min period (p = 0.005), but not during the subsequent 50-min period. In conclusion, epinephrine administered during CPR reduced PbtO2 for longer than 10 min following ROSC in a swine model with a clinically relevant duration of untreated cardiac arrest.

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Effect of neuromonitor-guided titrated care on brain tissue hypoxia after opioid overdose cardiac arrest

Abstract: In this model of opioid overdose cardiac arrest, brain tissue hypoxia is common and treatable. Further work will elucidate best strategies and impact of titrated care on functional outcomes.

Cited by 21 publications

References 29 publications

The Burden of Brain Hypoxia and Optimal Mean Arterial Pressure in Patients With Hypoxic Ischemic Brain Injury After Cardiac Arrest*

The Burden of Brain Hypoxia and Optimal Mean Arterial Pressure in Patients With Hypoxic Ischemic Brain Injury After Cardiac Arrest*

The interaction between arterial oxygenation and carbon dioxide and hospital mortality following out of hospital cardiac arrest: a cohort study

Effect of Epinephrine Administered during Cardiopulmonary Resuscitation on Cerebral Oxygenation after Restoration of Spontaneous Circulation in a Swine Model with a Clinically Relevant Duration of Untreated Cardiac Arrest

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