Oxygen and Carbon Dioxide in the Cerebral Circulation during Progression to Brain Death

2005 ◽  
Vol 103 (5) ◽  
pp. 957-961 ◽  
Author(s):  
Nino Stocchetti ◽  
Elisa Roncati Zanier ◽  
Rita Nicolini ◽  
Emelie Faegersten ◽  
Katia Canavesi ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Brain Death ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Brain Infarction ◽  
Carbon Dioxide Tension ◽  
Aerobic Metabolism ◽  
Compensatory Mechanisms ◽  
Oxygen Difference

Background The authors propose that for a moderate reduction of perfusion during progressive irreversible ischemia, oxygen extraction increases to maintain aerobic metabolism, and arteriojugular oxygen difference (AJDo2) increases. Because of reduced carbon dioxide washout, venoarterial difference in carbon dioxide tension (DPco2) increases, with no change in the DPco2/AJDo2 ratio. With further reduction of cerebral perfusion, the aerobic metabolism will begin to decrease, AJDo2 will decrease while DPco2 will continue to increase, and the ratio will increase. When brain infarction develops, the metabolism will be abated, no oxygen will be consumed, and no carbon dioxide will be produced. Methods The authors studied 12 patients with acute cerebral damage that evolved to brain death and collected intermittent arterial and jugular blood samples. Results Four patterns were observed: (1) AJDo2 of 4.1 +/- 0.7 vol%, DPco2 of 6.5 +/- 1.9 mmHg, and a ratio of 1.55 +/- 0.3 with cerebral perfusion pressure of 62.5 +/- 13.4 mmHg; (2) a coupled increase of AJDo2 (5.8 +/- 0.7 vol%) and DPco2 (10.1 +/- 1.0 mmHg) with no change in ratio (1.92 +/- 0.14) and cerebral perfusion pressure (57.9 +/- 5.8 mmHg); (3) AJDo2 of 4.7 +/- 0.4 vol% with an increase in DPco2 (11.8 +/- 1 mmHg) and correspondingly higher ratio (2.7 +/- 0.2); in this phase, cerebral perfusion pressure was 39.7 +/- 10.5 mmHg; (4) immediately before diagnosis of brain death (cerebral perfusion pressure, 17 +/- 10.4 mmHg), there was a decrease of AJDo2 (1.1 +/- 0.1 vol%) and of DPco2 (5.3 +/- 0.6 mmHg) with a further ratio increase (5.1 +/- 0.8). Conclusions Until compensatory mechanisms are effective, AJDo2 and DPco2 remain coupled. However, when the brain's ability to compensate for reduced oxygen delivery is exceeded, the ratio of DPco2 to AJDo2 starts to increase.

Transcranial Doppler ultrasonography in raised intra-cranial pressure and in intracranial circulatory arrest

1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski
Keyword(s):  
Intracranial Pressure ◽  
Brain Death ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Transcranial Doppler ◽  
Cerebral Perfusion ◽  
Doppler Ultrasonography ◽  
Perfusion Pressure ◽  
Circulatory Arrest ◽  
Transcranial Doppler Ultrasonography

✓ Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial. Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.

Cerebrovascular time constant: dependence on cerebral perfusion pressure and end-tidal carbon dioxide concentration

2012 ◽  
Vol 34 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Marek Czosnyka ◽  
Hugh K Richards ◽  
Matthias Reinhard2 ◽  
Luzius A Steiner3 ◽  
Karol Budohoski ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Cerebral Perfusion Pressure ◽  
Time Constant ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Carbon Dioxide Concentration ◽  
End Tidal Carbon Dioxide ◽  
End Tidal

Detection of Brain Death in Barbiturate Coma: The Dilemma of an Intracranial Pulse

Neurosurgery ◽  
1989 ◽  
Vol 25 (2) ◽  
pp. 275-278 ◽  
Author(s):  
Howard H. Kaufman ◽  
Fred H. Geisler ◽  
Thomas Kopitnik ◽  
William Higgins ◽  
Dan Stewart
Keyword(s):  
Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Brain Death ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Elevated Intracranial Pressure ◽  
Barbiturate Coma ◽  
The Face

Abstract Patients treated with barbiturate coma for elevated intracranial pressure after head injury may suffer brain death. Since such patients have an iatrogenically induced absence of neurological function, brain death cannot be diagnosed clinically. Furthermore, as demonstrated by two of our patients, monitoring of intracranial pressure, even in the face of brain death, may show a low intracranial pressure and an intracranial pulse, suggesting the presence of adequate cerebral perfusion pressure and, therefore, brain viability. Under these circumstances. however, significant intracranial blood flow may be absent. Therefore, we suggest that a patient in barbiturate coma should undergo serial blood flow studies. even when the intracranial pressure is low and an intracranial pulse is present. to determine whether brain death has occurred.

Intracranial pressure and cerebral perfusion pressure in patients developing brain death

2016 ◽  
Vol 34 ◽  
pp. 1-6 ◽  
Author(s):  
Farid Salih ◽  
Martin Holtkamp ◽  
Stephan A. Brandt ◽  
Olaf Hoffmann ◽  
Florian Masuhr ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Brain Death ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Developing Brain

Progress of intracranial pressure and cerebral perfusion pressure in patients during the development of brain death

2019 ◽  
Vol 398 ◽  
pp. 171-175 ◽  
Author(s):  
Christian Roth ◽  
Andreas Ferbert ◽  
Johannes Matthaei ◽  
Stefanie Kaestner ◽  
Holger Engel ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Brain Death ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure

scholarly journals Practical and comprehensive guidelines for bedside cerebral hemometabolic multitherapeutic optimization

2002 ◽  
Vol 60 (3A) ◽  
pp. 670-674 ◽  
Author(s):  
Julio Cruz
Keyword(s):  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Brain Injuries ◽  
Perfusion Pressure ◽  
Mortality Rates ◽  
Carbon Dioxide Tension ◽  
Controlled Study ◽  
Pertinent Literature ◽  
Cerebral Extraction Of Oxygen ◽  
Prospective Controlled Study

In recent years, noncomprehensive "guidelines" were proposed for the management of severe acute brain injuries, focusing strictly on two approaches: 1) to maintain cerebral perfusion pressure anywhere above 70 mm Hg; and 2) to maintain arterial carbon dioxide tension levels above 30 torr. Strictly following these propositions, a recently reported prospective controlled study addressed mortality rates of no less than 75-76%, far worse than mortality rates reported before those "guidelines" were published. As a humanitarian alternative, the present comprehensive guidelines are aimed at addressing practical bedside strategies to manage no only intracranial pressure and cerebral perfusion pressure but also cerebral extraction of oxygen, based on solid previously reported papers which revealed the lowest mortality rates (below 15%) in the pertinent literature, in recent years.

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