Intensive Care Medicine

, Volume 29, Issue 6, pp 1016–1019 | Cite as

Cerebral perfusion pressure and cerebral tissue oxygen tension in a patient during cardiopulmonary resuscitation

  • Roberto Imberti
  • Guido Bellinzona
  • Francesca Riccardi
  • Michele Pagani
  • Martin Langer
Brief Report


Objective: To report on the effects of cardiopulmonary resuscitation (CPR) instituted immediately after a cardiac arrest on cerebral perfusion pressure (CPP) and cerebral tissue oxygen tension (PbrO2).

Design: Case report.

Setting: ICU of a university hospital.

Patient: A head-injured 17-year-old man submitted to multimodal neurological monitoring underwent sudden cardiac arrest and successful CPR.

Interventions: External chest compression, 100% oxygen ventilation, volume expansion and standard ACLS protocols.

Measurements and results: Heart rate, ECG, mean arterial blood pressure (MABP), ETCO2,PaO2, intracranial pressure (ICP), CPP and PbrO2 were continuously monitored during CPR and data recorded at 15-s intervals by a dedicated personal computer. At the onset of the cardiac arrest, PbrO2 decreased to zero. The institution of CPR resulted in a progressive increase of MABP, CPP and PbrO2. Assuming, on the basis of previous experimental and clinical reports, 8 mmHg PbrO2 as a possible ischaemic/hypoxic threshold value, during the first 6.5 min of CPR, PbrO2 values were below this threshold (range 0–7 mmHg) and CPP values were <25 mmHg for 81.5% of the time. In the following 5.5 min, more efficient CPR generated CPP values >25 mmHg for 77.3% of the time. These values were associated with a PbrO2 >8 mmHg (range 8–28 mmHg) at all times.

Conclusions: In the clinical setting of a witnessed cardiac arrest, immediate institution of CPR can be effective in generating PbrO2 values above a supposed ischaemic/hypoxic threshold when CPP is >25 mmHg. PbrO2 monitoring by the Licox system is sensitive and reliable, even at low values, and can be suitable for evaluating cerebral oxygenation during experimental CPR.


Cardiac arrest Cardiopulmonary resuscitation Brain tissue partial pressure of oxygen Intracranial pressure Cerebral perfusion pressure Cerebral oxygen metabolism 


  1. 1.
    Safar P (1986) Cerebral resuscitation after cardiac arrest: a review. Circulation 74 (Suppl IV):138–153Google Scholar
  2. 2.
    International Guidelines 2000 for CPR and ECC (2000) A consensus on science. Resuscitation 46:1–448CrossRefPubMedGoogle Scholar
  3. 3.
    Nozari A, Rubertsson S, Gedeborg R, Nordgren A, Wiklund L (1999) Maximization of cerebral blood flow during experimental cardiopulmonary resuscitation does not ameliorate post-resuscitation hypoperfusion. Resuscitation 40:27–35CrossRefPubMedGoogle Scholar
  4. 4.
    Farrar JK (1991) Tissue PO2 threshold of ischemic cell damage following MCA occlusion in cats. J Cereb Blood Flow Metab 11 (Suppl 2):S553Google Scholar
  5. 5.
    Kariman K, Hempel FG, Jobsis FF (1983) In vivo comparison of cytochrome a/a3 redox state and tissue PO2 in transient anoxia. J Appl Physiol 55:1057–1063PubMedGoogle Scholar
  6. 6.
    Kiening KL, Unterberg AW, Bardt TF, Schneider G-H, Lanksch WR (1996) Monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue PO2 versus jugular vein oxygen saturation. J Neurosurg 85:751–757PubMedGoogle Scholar
  7. 7.
    Dings J, Meixensberger J, Amschler J, Hamelbeck B, Roosen K (1996) Brain tissue PO2 in relation to cerebral perfusion pressure, TCD findings and TCD–CO2 reactivity after severe head injury. Acta Neurochir 138:425–434Google Scholar
  8. 8.
    Gopinath SP, Valadka AB, Uzura M, Robertson CS (1999) Comparison of jugular venous oxygen saturation and brain tissue PO2 as monitors of cerebral ischemia. Crit Care Med 27:2337–2345PubMedGoogle Scholar
  9. 9.
    Imberti R, Bellinzona G, Langer M (2002) Cerebral tissue PO2 and SjvO2 changes during moderate hyperventilation in patients with severe traumatic brain injury. J Neurosurg 96:97–102PubMedGoogle Scholar
  10. 10.
    Bruzzone P, Dionigi R, Bellinzona G, Imberti R, Stocchetti N (1998) Effects of cerebral perfusion pressure on brain tissue PO2 in patients with severe head injury. Acta Neurochir 71 (Suppl):111–113Google Scholar
  11. 11.
    Lang EW, Czosnyka M, Mehdorn M (2003) Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain injury. Crit Care Med 31:267–271PubMedGoogle Scholar
  12. 12.
    Shaffner DH, Eleff SM, Brambrink AM, Sugimoto H, Izuta M, Koehler RC, Traystman J (1999) Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs. Crit Care Med 27:1335–1342PubMedGoogle Scholar

Copyright information

© Springer-Verlag 2003

Authors and Affiliations

  • Roberto Imberti
    • 1
  • Guido Bellinzona
    • 1
  • Francesca Riccardi
    • 1
  • Michele Pagani
    • 1
  • Martin Langer
    • 1
  1. 1.Servizio di Anestesia e Rianimazione IIIRCCS Policlinico S. MatteoPaviaItaly

Personalised recommendations