Low cerebral blood flow after cardiac arrest is not associated with anaerobic cerebral metabolism

C.W.E. Hoedemaekers, Philip N. Ainslie, S. Hinssen, M.J. Aries, Laurens L. Bisschops, Jeannette Hofmeijer, J.G. van der Hoeven

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Abstract

Aim of the study Estimation of cerebral anaerobic metabolism in survivors and non-survivors after cardiac arrest. Methods We performed an observational study in twenty comatose patients after cardiac arrest and 19 healthy control subjects. We measured mean flow velocity in the middle cerebral artery (MFVMCA) by transcranial Doppler. Arterial and jugular blood samples were used for calculation of the jugular venous-to-arterial CO2/arterial to-jugular venous O2 content difference ratio. Results After cardiac arrest, MFVMCA increased from 26.0[18.6–40.4] cm/sec on admission to 63.9[48.3–73.1] cm/sec after 72 h (p < 0.0001), with no significant differences between survivors and non-survivors (p = 0.4853). The MFVMCA in controls was 59.1[52.8–69.0] cm/sec. The oxygen extraction fraction (O2EF) was 38.9[24.4–47.7]% on admission and decreased significantly to 17.3[12.1–26.2]% at 72 h (p < 0.0001). The decrease in O2EF was more pronounced in non-survivors (p = 0.0173). O2EF in the control group was 35.4[32.4–38.7]%. The jugular bulb-arterial CO2 to arterial-jugular bulb O2 content difference ratio was >1 at all time points after cardiac arrest and did not change during admission, with no differences between survivors and non-survivors. Values in cardiac arrest patients were similar to those in normal subjects. Conclusions In this study, low CBF after cardiac arrest is not associated with anaerobic metabolism. Hypoperfusion appears to be the consequence of a decrease of neuronal functioning and metabolic needs. Alternatively, hypoperfusion may decrease cerebral metabolism. Subsequently, metabolism increases in survivors, consistent with resumption of neuronal activity, whereas in non-survivors lasting low metabolism reflects irreversible neuronal damage.
Original languageEnglish
Pages (from-to)45-50
JournalResuscitation
Volume120
DOIs
Publication statusPublished - Nov 2017

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Cerebrovascular Circulation
Anaerobiosis
Heart Arrest
Survivors
Neck
Middle Cerebral Artery
Coma
Observational Studies
Healthy Volunteers

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Hoedemaekers, C. W. E., Ainslie, P. N., Hinssen, S., Aries, M. J., Bisschops, L. L., Hofmeijer, J., & van der Hoeven, J. G. (2017). Low cerebral blood flow after cardiac arrest is not associated with anaerobic cerebral metabolism. Resuscitation, 120, 45-50. https://doi.org/10.1016/j.resuscitation.2017.08.218
Hoedemaekers, C.W.E. ; Ainslie, Philip N. ; Hinssen, S. ; Aries, M.J. ; Bisschops, Laurens L. ; Hofmeijer, Jeannette ; van der Hoeven, J.G. / Low cerebral blood flow after cardiac arrest is not associated with anaerobic cerebral metabolism. In: Resuscitation. 2017 ; Vol. 120. pp. 45-50.
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title = "Low cerebral blood flow after cardiac arrest is not associated with anaerobic cerebral metabolism",
abstract = "Aim of the study Estimation of cerebral anaerobic metabolism in survivors and non-survivors after cardiac arrest. Methods We performed an observational study in twenty comatose patients after cardiac arrest and 19 healthy control subjects. We measured mean flow velocity in the middle cerebral artery (MFVMCA) by transcranial Doppler. Arterial and jugular blood samples were used for calculation of the jugular venous-to-arterial CO2/arterial to-jugular venous O2 content difference ratio. Results After cardiac arrest, MFVMCA increased from 26.0[18.6–40.4] cm/sec on admission to 63.9[48.3–73.1] cm/sec after 72 h (p < 0.0001), with no significant differences between survivors and non-survivors (p = 0.4853). The MFVMCA in controls was 59.1[52.8–69.0] cm/sec. The oxygen extraction fraction (O2EF) was 38.9[24.4–47.7]{\%} on admission and decreased significantly to 17.3[12.1–26.2]{\%} at 72 h (p < 0.0001). The decrease in O2EF was more pronounced in non-survivors (p = 0.0173). O2EF in the control group was 35.4[32.4–38.7]{\%}. The jugular bulb-arterial CO2 to arterial-jugular bulb O2 content difference ratio was >1 at all time points after cardiac arrest and did not change during admission, with no differences between survivors and non-survivors. Values in cardiac arrest patients were similar to those in normal subjects. Conclusions In this study, low CBF after cardiac arrest is not associated with anaerobic metabolism. Hypoperfusion appears to be the consequence of a decrease of neuronal functioning and metabolic needs. Alternatively, hypoperfusion may decrease cerebral metabolism. Subsequently, metabolism increases in survivors, consistent with resumption of neuronal activity, whereas in non-survivors lasting low metabolism reflects irreversible neuronal damage.",
author = "C.W.E. Hoedemaekers and Ainslie, {Philip N.} and S. Hinssen and M.J. Aries and Bisschops, {Laurens L.} and Jeannette Hofmeijer and {van der Hoeven}, J.G.",
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Hoedemaekers, CWE, Ainslie, PN, Hinssen, S, Aries, MJ, Bisschops, LL, Hofmeijer, J & van der Hoeven, JG 2017, 'Low cerebral blood flow after cardiac arrest is not associated with anaerobic cerebral metabolism' Resuscitation, vol. 120, pp. 45-50. https://doi.org/10.1016/j.resuscitation.2017.08.218

Low cerebral blood flow after cardiac arrest is not associated with anaerobic cerebral metabolism. / Hoedemaekers, C.W.E.; Ainslie, Philip N.; Hinssen, S. ; Aries, M.J.; Bisschops, Laurens L.; Hofmeijer, Jeannette ; van der Hoeven, J.G.

In: Resuscitation, Vol. 120, 11.2017, p. 45-50.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Low cerebral blood flow after cardiac arrest is not associated with anaerobic cerebral metabolism

AU - Hoedemaekers, C.W.E.

AU - Ainslie, Philip N.

AU - Hinssen, S.

AU - Aries, M.J.

AU - Bisschops, Laurens L.

AU - Hofmeijer, Jeannette

AU - van der Hoeven, J.G.

PY - 2017/11

Y1 - 2017/11

N2 - Aim of the study Estimation of cerebral anaerobic metabolism in survivors and non-survivors after cardiac arrest. Methods We performed an observational study in twenty comatose patients after cardiac arrest and 19 healthy control subjects. We measured mean flow velocity in the middle cerebral artery (MFVMCA) by transcranial Doppler. Arterial and jugular blood samples were used for calculation of the jugular venous-to-arterial CO2/arterial to-jugular venous O2 content difference ratio. Results After cardiac arrest, MFVMCA increased from 26.0[18.6–40.4] cm/sec on admission to 63.9[48.3–73.1] cm/sec after 72 h (p < 0.0001), with no significant differences between survivors and non-survivors (p = 0.4853). The MFVMCA in controls was 59.1[52.8–69.0] cm/sec. The oxygen extraction fraction (O2EF) was 38.9[24.4–47.7]% on admission and decreased significantly to 17.3[12.1–26.2]% at 72 h (p < 0.0001). The decrease in O2EF was more pronounced in non-survivors (p = 0.0173). O2EF in the control group was 35.4[32.4–38.7]%. The jugular bulb-arterial CO2 to arterial-jugular bulb O2 content difference ratio was >1 at all time points after cardiac arrest and did not change during admission, with no differences between survivors and non-survivors. Values in cardiac arrest patients were similar to those in normal subjects. Conclusions In this study, low CBF after cardiac arrest is not associated with anaerobic metabolism. Hypoperfusion appears to be the consequence of a decrease of neuronal functioning and metabolic needs. Alternatively, hypoperfusion may decrease cerebral metabolism. Subsequently, metabolism increases in survivors, consistent with resumption of neuronal activity, whereas in non-survivors lasting low metabolism reflects irreversible neuronal damage.

AB - Aim of the study Estimation of cerebral anaerobic metabolism in survivors and non-survivors after cardiac arrest. Methods We performed an observational study in twenty comatose patients after cardiac arrest and 19 healthy control subjects. We measured mean flow velocity in the middle cerebral artery (MFVMCA) by transcranial Doppler. Arterial and jugular blood samples were used for calculation of the jugular venous-to-arterial CO2/arterial to-jugular venous O2 content difference ratio. Results After cardiac arrest, MFVMCA increased from 26.0[18.6–40.4] cm/sec on admission to 63.9[48.3–73.1] cm/sec after 72 h (p < 0.0001), with no significant differences between survivors and non-survivors (p = 0.4853). The MFVMCA in controls was 59.1[52.8–69.0] cm/sec. The oxygen extraction fraction (O2EF) was 38.9[24.4–47.7]% on admission and decreased significantly to 17.3[12.1–26.2]% at 72 h (p < 0.0001). The decrease in O2EF was more pronounced in non-survivors (p = 0.0173). O2EF in the control group was 35.4[32.4–38.7]%. The jugular bulb-arterial CO2 to arterial-jugular bulb O2 content difference ratio was >1 at all time points after cardiac arrest and did not change during admission, with no differences between survivors and non-survivors. Values in cardiac arrest patients were similar to those in normal subjects. Conclusions In this study, low CBF after cardiac arrest is not associated with anaerobic metabolism. Hypoperfusion appears to be the consequence of a decrease of neuronal functioning and metabolic needs. Alternatively, hypoperfusion may decrease cerebral metabolism. Subsequently, metabolism increases in survivors, consistent with resumption of neuronal activity, whereas in non-survivors lasting low metabolism reflects irreversible neuronal damage.

U2 - 10.1016/j.resuscitation.2017.08.218

DO - 10.1016/j.resuscitation.2017.08.218

M3 - Article

VL - 120

SP - 45

EP - 50

JO - Resuscitation

JF - Resuscitation

SN - 0300-9572

ER -