Elsevier

Resuscitation

Volume 76, Issue 1, January 2008, Pages 17-24
Resuscitation

Clinical paper
Changes in cerebral blood flow and oxygen extraction during post-resuscitation syndrome

https://doi.org/10.1016/j.resuscitation.2007.06.028Get rights and content

Summary

Introduction

Most survivors of out-of-hospital cardiac arrest (OHCA) will die subsequently from post-anoxic encephalopathy. In animals, the severity of brain damage is mainly influenced by the duration of cardiac arrest and also by the cerebral blood flow (CBF) and oxygen extraction (CEO2) abnormalities observed during the post-resuscitation period. The aim of our study was to describe CBF and CEO2 modifications during the first 72 h in OHCA patients treated by induced mild hypothermia.

Methods

Consecutive OHCA patients were studied every 12 h over 72 h. Diastolic flow velocities (dFV), mean flow velocities (mFV) and pulsatility index (PI) were assessed by transcranial doppler (TCD) as an estimate of CBF changes. Simultaneous measurements of CEO2 were obtained using retrograde jugular catheterisation.

Results

Eighteen patients (61 [47–74] years) were studied (12 non-survivors and 6 survivors). At admission, mFV values were low (27.3 [21.5–33.6] cm/s) but reached normal values after 72 h (50.5 [36.7–58.1] cm/s). Initial PI values were high (1.6 [1.3–1.9]) but reached normal values after 72 h (1.04 [0.82–1.2]). No differences were found between survivors and non-survivors regarding these CBF estimates. CEO2 values were quite normal at admission (20.4 [11–27%]) but decreased over time in non-survivors until H72 (25.8% [19.3–31.1] versus 5.7% [5.1–11.5], p = 0.02).

Conclusion

Cerebral haemodynamic and oxygenation values are altered considerably but evolve during the first 72 h following resuscitation after cardiac arrest. In particular, these changes may lead to a mismatch between CBF and CEO2 leading to a “luxurous perfusion” in non-survivors.

Introduction

Out-of-hospital cardiac arrest (OHCA) is a leading cause of death in Western countries. In the United States, approximately 275,000 persons annually experience a cardiac arrest with attempt at resuscitation, leading to only 29,000 persons surviving to hospital discharge.1 Despite recent advances in the management of cardiopulmonary resuscitation (CPR), survival rate of OHCA patients still remains very low. The vast majority of OHCA patients subsequently suffer from a post-anoxic encephalopathy leading to a post-resuscitation neurological deficiency that is either transient or permanent and represents the major cause of death in these patients.2 Currently, apart from mild hypothermia, no other treatment has shown any ability to decrease the consequences of cerebral ischaemia due to cardiac arrest.3, 4, 5

The severity of brain damage is of course mainly influenced by the length of the interruption of cerebral blood flow (CBF) that can be at best estimated by the duration of resuscitation maneouvers.6 However, the return of spontaneous circulation (ROSC) is frequently followed by a post-resuscitation syndrome which itself could lead to secondary neurological damages and to other organ dysfunctions.7 Animal experiments show that the mechanisms involved in the worsening of initial cerebral insults following reperfusion may be multiple.8 It has been suggested that these post-resuscitation cerebral damages are mostly related to an inadequacy between CBF and cerebral metabolic rate, a physiological variable that is itself mainly related to cerebral oxygen extraction (CEO2). The adequacy or inadequacy of these two variables during the post-resuscitation period is still discussed.9 A better understanding of haemodynamic and metabolic disturbances may have an impact on management and may also carry a prognostic value. However, to date these post-resuscitation haemodynamic disturbances have essentially been investigated in animal models and remain poorly studied in humans. When available, human data are limited to the first hours after cardiac arrest, leading to numerous residual questions regarding the following period and the potential influence of therapeutic interventions such as hypothermia.10 The main goal of our study was to describe CBF and CEO2 modifications during the first 72 h in OHCA patients treated by mild induced hypothermia, using transcranial Doppler (TCD) and jugular venous oxygen saturation (SjvO2). We also assessed the relationship between these changes and patients outcome. Some of the results of this study have been previously reported in the form of an abstract at the 19th meeting of the European Society of Intensive Care Medicine in 2006.11

Section snippets

Study design

This was a monocentric and observational study performed between February and August 2005 in the 24-bed medical intensive care unit (ICU) of the Cochin University Hospital (Paris, France). Protocol and consent procedures were approved by the Ethics Review Committee of the Cochin University Hospital, in accordance with the European Guidelines for Good Clinical Practice. Informed consent was obtained from all patients’ next of kin. Furthermore, written consent was obtained from all survivors.

Patients

The

Results

During the study period, 18 patients were analysed: 14 men and four women, with a median age of 61 years [47–74], a median SAPS 2 of 68 [55–77], and a mortality rate of 66% at day 28. In non-survivors, causes of death were post-resuscitation shock for two patients, severe brain damage in nine patients and brain death in one patient.

Pre-hospital resuscitation characteristics, demographic and clinical data at admission are summarised in Table 1 that also shows the characteristics of survivors and

Discussion

This study confirms that cerebral haemodynamic and oxygenation values are considerably altered following resuscitation after cardiac arrest. We show for the first time in humans that these changes are evolved during the first 72 h that follow resuscitation.

In normal subjects, CBF is independent of perfusion pressure through the principle of autoregulation. After cardiac arrest, cerebrovascular autoregulation is known to be impaired but not completely abolished.19, 20 In our patients, we found

Conclusion

In conclusion, cerebral haemodynamic and oxygenation values are considerably altered following resuscitation after cardiac arrest but these variables are evolve during the first 72 h. In survivors, both CBF and CEO2 equally improve over time whereas in non-survivors, CEO2 decreased in spite of TCD parameters improvement, leading to a “luxurious perfusion”. Since we believe that a better knowledge of cerebral haemodynamic changes during the post-resuscitation period is essential to treat patients

Conflict of interest

No potential conflict of interest has occurred since this work was initiated. The study was financially supported by a grant from the French Society of Anesthesiology and Intensive Care (SFAR) and the French Speaking Society of Intensive Care (SRLF).

Acknowledgements

Contributors. A. Cariou, O. Huet, B. Vigué and J. Duranteau designed the study. V. Lemiale, O. Huet, J.P. Mira and A. Cariou produced the manuscript. All authors contributed to the collection and analysis of data and approved the manuscript. J. Duranteau, B. Vigué, A. Mathonnet, C. Spaulding, and P. Carli participated to its critical revision. A. Cariou had full access to all the data in the study and endorsed final responsibility for the decision to submit for publication.

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    A Spanish translated version of the summary of this article appears as Appendix in the online version at 10.1016/j.resuscitation.2007.06.028.

    1

    These authors equally contributed to this work.

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