Ketamine Induced Anesthesia in Hemorrhagic Shock and Increased Intracranial Pressure

1985 ◽  
Vol 1 (S1) ◽  
pp. 284-286
Author(s):  
Hans-Joachim Hartung ◽  
Roderich Klose ◽  
R. Kotsch ◽  
Th. Walz

In a considerable number of cases, many polytraumatized patients in a state of hemorrhagic shock, who require immediate surgical treatment, there is craniocerebral trauma. Ketamine is viewed, on one hand, as an appropriate induction anesthetic, due to its circulatory stimulating effect in treating shock victims, and, on the other hand, it is rejected for treating patients with craniocerebral injuries, because of the danger of possible increase in intracranial pressure (ICP). Therefore, we examined the effects of ketamine on ICP and calculated the cerebral perfusion pressure, using test animals in a state of hemorrhagic shock and a space occupying intracranial process.

1978 ◽  
Vol 44 (1) ◽  
pp. 25-27 ◽  
Author(s):  
J. S. Huseby ◽  
E. G. Pavlin ◽  
J. Butler

Application of positive end-expiratory pressure to dogs with noncardiogenic pulmonary edema increased intracranial pressure (measured as cerebrospinal fluid pressure) and decreased cerebral perfusion pressure. The magnitude of these changes depended on the amount of end-expiratory pressure applied and the lung compliance.


1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski

✓ 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.


PEDIATRICS ◽  
1987 ◽  
Vol 79 (4) ◽  
pp. 538-543
Author(s):  
Sergio Fanconi ◽  
Gabriel Duc

In a prospective nonrandomized study, using each baby as his or her own control, we compared intracranial pressure (anterior fontanel pressure as measured with the Digilab pneumotonometer), cerebral perfusion pressure, BP, heart rate, transcutaneous Po2, and transcutaneous Pco2 before, during, and after endotracheal suctioning, with and without muscle paralysis, in 28 critically ill preterm infants with respiratory distress syndrome. With suctioning, there was a small but significant increase in intracranial pressure in paralyzed patients (from 13.7 [mean] ± 4.4 mm Hg [SD] to 15.8 ± 5.2 mm Hg) but a significantly larger (P < .001) increase when they were not paralyzed (from 12.5 ± 3.6 to 28.5 ± 8.3 mm Hg). Suctioning led to a slight increase in BP with (from 45.3 ± 9.1 to 48.0 ± 8.7 mm Hg) and without muscle paralysis (from 45.1 ± 9.4 to 50.0 ± 11.7 mm Hg); but there was no significant difference between the two groups. The cerebral perfusion pressure in paralyzed infants did not show any significant change before, during, and after suctioning (31.5 ± 9.1 mm Hg before v 32.0 ± 8.7 mm Hg during suctioning), but without muscle paralysis cerebral perfusion pressure decreased (P < .001) from 32.8 ± 9.7 to 21.3 ± 13.1 mm Hg. Suctioning induced a slight decrease in mean heart rate and transcutaneous Po2, but pancuronium did not alter these changes. There was no statistical difference in transcutaneous Pco2, before, during, and after suctioning with and without muscle paralysis. Our data demonstrate that muscle paralysis in sick preterm infants can significantly minimize the increase in intracranial pressure and can stabilize the cerebral perfusion pressure without having any effect on the BP increase during suctioning.


2020 ◽  
pp. 3892-3897
Author(s):  
David K. Menon

Normal intracranial pressure is between 5 and 15 mm Hg in supine subjects. Intracranial hypertension (ICP >20 mm Hg) is common in many central nervous system diseases and in fatal cases is often the immediate cause of death. Increases in intracranial volume and hence—given the rigid skull—intracranial pressure may be the consequence of brain oedema, increased cerebral blood volume, hydrocephalus, and space-occupying lesions. Brain perfusion depends on the cerebral perfusion pressure which is mean arterial pressure minus intracranial pressure. The normal brain autoregulates cerebral blood flow down to a lower limit of cerebral perfusion pressure of about 50 mm Hg in healthy subjects, and perhaps 60–70 mm Hg in disease. Cerebral perfusion pressure reduction to below these values results in cerebral ischaemia.


Sign in / Sign up

Export Citation Format

Share Document