Are changes in cerebrovascular autoregulation following cardiac arrest associated with neurological outcome? Results of a pilot study

Pham, Paul; Bindra, Jessica; Chuan, Alwin; Jaeger, M.; Åneman, Anders

doi:10.1016/j.resuscitation.2015.08.007

Cited by 67 publications

(58 citation statements)

References 29 publications

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“…Recently, Ameloot et al retrospectively calculated COx using MAP and rSO 2 to indicate that autoregulation was intact in 33 of 51 subjects with HIBI. Thereafter, Pham et al showed that COx was significantly higher in nonsurvivors of HIBI than in survivors [54]. Although higher COx was associated with nonsurvivors, there was no association between rSO 2 and mortality.…”

Section: Secondary Injurymentioning

confidence: 99%

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

2017

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Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Thereafter, the secondary injury of HIBI takes place in the hours and days following the initial CA and reperfusion. Among factors that may be implicated in this secondary injury include reperfusion injury, microcirculatory dysfunction, impaired cerebral autoregulation, hypoxemia, hyperoxia, hyperthermia, fluctuations in arterial carbon dioxide, and concomitant anemia.Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research to identify therapeutic targets. Most notably, targeted temperature management has been studied rigorously in preventing secondary injury after HIBI and is associated with improved outcome compared with hyperthermia. Recent advances point to important roles of anemia, carbon dioxide perturbations, hypoxemia, hyperoxia, and cerebral edema as contributing to secondary injury after HIBI and adverse outcomes. Furthermore, breakthroughs in the individualization of perfusion targets for patients with HIBI using cerebral autoregulation monitoring represent an attractive area of future work with therapeutic implications.We provide an in-depth review of the pathophysiology of HIBI to critically evaluate current approaches for the early treatment of HIBI secondary to CA. Potential therapeutic targets and future research directions are summarized.

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Section: Secondary Injurymentioning

confidence: 99%

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

2017

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“…If rSO 2 is measured in patients with a normal or mildly injured brain, rSO 2 should be correlated with SaO 2 , Hb, and PaCO 2 and not with MAP. This could explain Fick's formula (Nakashima et al, 2017) and display normal CVAR (Sundgreen et al, 2001;Brady et al, 2007;Pham et al, 2015). In this study, only patients in the favorable group at 24 hours were followed with this hypothesis.…”

Section: Discussionmentioning

confidence: 81%

“…It was reported that in the majority of PCAS patients in their acute phase after cardiac arrest, the CVAR and CBF were either absent or right shifted (Sundgreen et al, 2001). In addition, during the evaluation of rSO 2 for PCAS patients after ROSC, the impairment of CVAR following CA is associated with poor outcome (Brady et al, 2007;Ameloot et al, 2015;Pham et al, 2015). If CVAR is sustained because of mild brain injury in PCAS patients, rSO 2 may not change depending on MAP and may change on SaO 2 , Hb, and PaCO 2 as per the Fick's principle.…”

Section: Discussionmentioning

confidence: 99%

“…Although we could not explain this phenomenon exactly, it may be due to the following reasons: (1) the number of patients may be too small; (2) each parameter was managed within a narrow range, causing the variation range to be narrow; and (3) an unstable brain situation immediately after resuscitation at the start of monitoring and due to change in brain metabolism during the rewarming stage at 48 hours. Pham et al (2015) reported that early impairment of CVAR following cardiac arrest is independently associated with mortality. Our results suggest that rSO 2 was moderately correlated with MAP and CVAR and could be impaired in PCAS patients with unfavorable outcome.…”

Section: Discussionmentioning

confidence: 99%

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Parameters Influencing Brain Oxygen Measurement by Regional Oxygen Saturation in Postcardiac Arrest Patients with Targeted Temperature Management

Sakurai

Ihara

Tagami

et al. 2020

Therapeutic Hypothermia and Temperature Management

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In several studies, regional cerebral oxygen saturation (rSO 2 ) has been measured in patients with postcardiac arrest syndrome (PCAS) to analyze the brain's metabolic status. However, the significance of rSO 2 in PCAS patients remains unclear. In the present study, we investigated the relationship between rSO 2 and physiological parameters. Comatose survivors of out-of-hospital PCAS with targeted temperature management (TTM) at 34°C for 24 hours were included. All patients were monitored for their rSO 2 and additional parameters (arterial oxygen saturation [SaO 2 ], hemoglobin [Hb], mean arterial pressure [MAP], arterial carbon dioxide pressure [PaCO 2 ], and body temperature]) measured at the start of monitoring and 24 and 48 hours after return of spontaneous circulation (ROSC). Patients were divided into favorable and unfavorable groups, and the correlation between rSO 2 and these physiological parameters was evaluated by multiple regression analysis. Forty-nine patients were included in the study, with 15 in the favorable group and 34 in the unfavorable group. There was no significant difference in the rSO 2 value between the two groups at any time point. The multiple regression analysis of the favorable group revealed a moderate correlation between rSO 2 and SaO 2 , Hb, and PaCO 2 only at 24 hours (coefficients: 0.482, 0.422, and 0.531, respectively), whereas that of the unfavorable group revealed moderate correlations between rSO 2 and Hb values at all time points, PaCO 2 at 24 hours and MAP at 24 and 48 hours. rSO 2 was moderately correlated to MAP in unfavorable patients. To optimize brain oxygen metabolic balance for PCAS patients with TTM measuring rSO 2 , we suggest total evaluation of each parameters of SaO 2 , Hb, MAP, and PaCO 2 .

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“…This is an important pragmatic study that demonstrates the feasibility to monitor cerebrovascular autoregulation at the bedside using minimally invasive techniques and follows similar previous reports. [9][10][11] The moving correlation coefficient between arterial pressure and regional cerebral oxygen saturation, the cerebral oximetry index, COx, as a measure of cerebrovascular autoregulation could be derived in all patients during at least one monitoring period of 6 h along with the mean arterial pressure associated with the optimal autoregulatory capacity (MAP OPT ).…”

mentioning

confidence: 99%

The heart of the matter is brain: Monitoring cerebrovascular autoregulation after cardiac arrest

Åneman

2016

Resuscitation

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Are changes in cerebrovascular autoregulation following cardiac arrest associated with neurological outcome? Results of a pilot study

Cited by 67 publications

References 29 publications

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

Parameters Influencing Brain Oxygen Measurement by Regional Oxygen Saturation in Postcardiac Arrest Patients with Targeted Temperature Management

The heart of the matter is brain: Monitoring cerebrovascular autoregulation after cardiac arrest

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