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Cardio-respiratory reanimation: The brain is the target organ

Refers to article:

Cardiac arrest – Midway between two guidelines: From an anaesthesiologist's point of view
Jacob Steinmetz
Current Anaesthesia & Critical Care
June 2009 (Vol. 20, Issue 3, Pages 113-119)
Abstract | Full Text | Full-Text PDF (274 KB)

Article Outline

• Conflict of interest

• References

• Copyright

Steinmetz1 has published a very good review updating current information on cardiac arrest, related to actual recommendations and guidelines on this subject, and possible cognitive impairment after surgery.2, 3, 4, 5

We will focus our commentaries about the effects of hypoxia and ischemia on the brain after cardiac arrest. The human brain uses approximately 20% of the cardiac output in such a way that cerebral blood flow (CBF) is tightly regulated to meet the brain's metabolic demands. The CBF dropping to less than 20mL/100gm/min produces ischemic neuronal activity reduction, but still reversible neuronal changes. CBF values less than 10mL/100gm/min result in irreversible ischemic neuronal damage within minutes, as reflected by membrane failure. That's why the CBF values between 10 and 20mL/100gm/min are considered the ischemic penumbra, and represent neuronal tissue which may potentially be rescued.6, 7, 8, 9, 10, 11, 12

Therefore, even when resuscitation attempts in cardiac arrest are successful, recovery is too often limited by anoxic encephalopathy. The potential danger of this complication increases with the delay in resuscitation, and then the prognosis for comatose survivors of cardiac arrest is frequently13, 14, 15, 16, 17, 18 poor.

Several research groups have run protocols for lowering body temperature in comatose survivors of cardiac arrest, resulting in a notable improvement in the neurologic outcome.15, 19, 20, 21, 22 Safar et al. have documented in dog experimental models of prolonged exsanguination brain and organ preservation during cardiac arrest (no-flow) durations of up to 90 or 120min.23, 24, 25, 26 Circumstantial evidence for the protective effects of hypothermia is provided by is supported by reports of patients who having suffered accidental hypothermia (immersion/submersion in cold water, snow avalanche or prolonged exposure to cold surroundings) combined with circulatory arrest or severe circulatory failure, were then rewarmed to normothermia by use of extracorporeal circulation, with good outcome in several cases.15, 19, 22, 27, 28 But the key point in these cases is that the neuroprotective effect of accidental hypothermia occurred very early, even before a complete cardiac arrest had occurred.13

Hence we conclude that any actual of future developed neuroprotective treatment for preventing brain damage to anoxia and ischemia, should be initiated as soon as possible after cardiac arrest, and maintained during the application of cardiopulmonary resuscitation.16, 29, 30, 31, 32, 33

Of course, this has technical limitations, because in out-of hospital settings this treatment is usually applied by paramedics at the site of accident and inside ambulances, in subjects with a slow and unstable blood flow supported or provided by CPR. There are clear technical difficulties. Nonetheless, this may be the only way to achieve a neuroprotective effect for preventing brain damage after cardiac arrest.34

Conflict of interest

None.

References

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2. 2Steinmetz J, Barnung S, Nielsen SL, Risom M, Rasmussen LS. Improved survival after an out-of-hospital cardiac arrest using new guidelines. Acta Anaesthesiologica Scandinavica. 2008;52:908–913.

3. 3Steinmetz J, Christensen KB, Lund T, Lohse N, Rasmussen LS, ISPOCD Group. Long-term consequences of postoperative cognitive dysfunction. Anesthesiology. 2009;110:548–555. CrossRef

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34. 34Landau WM, Schneider S, Machado M, Longstreth WT, Fahrenbruch CE, Olsufka E, et al. Randomized clinical trial of magnesium, diazepam, or both after out-of-hospital cardiac arrest. Neurology. 2003;60:1868–1869.

Institute of Neurology and Neurosurgery, Department of Clinical Neurophysiology, 29 y D, Vedado, La Habana 10400, Havana, Cuba

Hermanos Ameijeiras Hospital, Service of Neurology, Havana, Cuba

Institute of Neurology and Neurosurgery, Department of Clinical Neurophysiology, Havana, Cuba

New York University Medical Center, New York, USA

Corresponding author.

PII: S0953-7112(09)00116-1

doi:10.1016/j.cacc.2009.09.001

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