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  • intracranial pressure  (4)
  • barbiturate reactivity  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 98 (1989), S. 153-163 
    ISSN: 0942-0940
    Keywords: Acute head injury ; barbiturate reactivity ; cerebral blood flow ; cerebral metabolism ; CO2 reactivity ; hyperventilation ; intracranial pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In nine patients with severe head injury subjected to continuous hyperventilation and barbiturate coma treatment with pentobarbitone, the regional cerebral blood flow was measured as initial slope index (ISI) with a 32 channel Cerebrograph, and cerebral metabolic rate of oxygen (CMRO2) was calculated as the product of mean global CBF and the arterio-venous oxygen content difference. CBF was measured at strategic intervals either to follow the treatment (hyperventilation and/or pentobarbitone), or to determine whether these principles of treatment should be intensified or reduced. During the flow measurements the CO2 reactivity and the reactivity to a bolus injection of thiopentone 5 mg/kg were calculated globally and regionally. The global CO2 reactivity was calculated as relative (%change CBF/ΔPaCO2 mmHg) and absolute (ΔCBF/ ΔPaCO2 mmHg), and the reactivity to barbiturate was calculated globally as Δ CMRO2, and regionally as %change rCBF. The absolute and relative global CO2 reactivities correlated positively with the mean. CBF values before hyperventilation, and the global barbiturate reactivity was dependent on the CMRO2 value obtained before hyperventilation. However, at low levels of CMRO2 ranging between 1.0 and 1.1 ml O2 the barbiturate reactivity was abolished. The regional studies of CBF, CMRO2, CO2 reactivity and barbiturate reactivity gave important information, when decisions concerning therapeutic regimes with special reference to hyperventilation and sedation with pentobarbitone were necessary.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 96 (1989), S. 100-106 
    ISSN: 0942-0940
    Keywords: Acute head injury ; CO2 reactivity ; cerebral blood flow ; cerebral ischaemia ; ischaemic threshold ; hyperventilation ; intracranial pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In 27 comatose patients with acute head injury, 45 paired studies of regional cerebral blood flow (rCBF) were performed before and after hyperventilation. In total 676 regions were studied, and rCBF was calculated as initial slope index using the intracarotid washout technique of 133 Xe. The tests were applied from one day to three weeks after the acute trauma. In total hyperventilation from PaCO2 averaging 4.8 to 3.5 kPa increased the frequency of regions with oligaemia defined CBF〈20ml/100g/min from 5 to 16%. Before hyperventilation oligaemia was observed in 11 of 45 studies (9 of 27 patients); after hyperventilation the frequency increased to 21 studies (15 patients). The frequency of severe oligaemia (CBF〈15 ml) increased from 0.1 to 3% of all regions, or from 2 to 8 of all studies (from 2 to 9 patients). The increased frequency of oligaemia after hyperventilation was correlated to a poor outcome (dementia, vegetative survival or death), where it was observed in 21% of all regions, in 16 of 26 studies and 11 of 15 patients, whereas the frequency in patients with a good recovery was found to be 7% of all regions and observed in 5 of 19 studies (4 of 12 patients). The high frequency of oligaemia after hyperventilation was associated to a low hemispheric CBF before hyperventilation, but not to the level of PaCO2, the level of intracranial pressure, cerebral perfusion pressure or CSF-pH or lactate. These findings strongly suggest that acute hyperventilation might be controversial as it provokes a decrease in rCBF close to ischaemic threshold, especially in patients with reduced rCBF prior to acute hyperventilation. Furthermore, it suggest that rCBF〈20 ml indicate a poor outcome.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0942-0940
    Keywords: Acute head injury ; barbiturate coma ; cerebral blood flow ; cerebral metabolism ; hyperventilation ; indomethacin ; intracranial pressure ; intracranial hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control intracranial pressure (ICP) (ICP〉20 mmHg) by artificial hyperventilation (PaCO2 level 3.5–4.0 kPa) and barbiturate sedation, indomethacin was used as a vasoconstrictor drug. In all patients, indomethacin (a bolus injection of 30 mg, followed by 30 mg/h for seven hours) reduced ICP below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in CBF at 2h. After 7h, ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In the other patients a return of ICP and CBF to pretreatment levels was observed. In all patients indomethacin treatment was followed by a fall in rectal temperature. These results suggest that indomethacin due to its cerebral vasoconstrictor and antipyretic effect should be considered as an alternative for treatment of ICP-hypertension in head-injured patients.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0942-0940
    Keywords: Head injury ; indomethacin reactivity ; hyperventilation ; intracranial pressure ; cerebral blood flow ; cerebral ischaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of this study was to compare the effect of hyper-ventilation and indomethacin on cerebral circulation, metabolism and pressures in patients with acute severe head injury in order to see if indomethacin may act supplementary to hyperventilation. Fourteen severely head injured patients entered the study. Intracranial pressure (ICP), mean arterial blood pressure (MABP) and cerebral perfusion pressure (CPP) were monitored continuously. Within the first four days after the trauma the CO2 and indomethacin vasoreactivities were studied by measurements of cerebral blood flow (CBF) (Cerebrograph 10a, intravenous133Xe technique) and arterio-venous difference of oxygen (AVdO2). Ischaemia was evaluated from changes in CBF, saturation of oxygen in the jugular bulb (SvjO2), lactate and lactate/oxygen index (LOI). Data are presented as medians and ranges, results are significant unless otherwise indicated. Before intervention ICP was well controlled (14.8 (9–24) mmHg) and basic CBF level was 39.1 (21.6–75.0) ml/100 g/min). The arterio-venous oxygen differences were generally decreased (AVdO2 = 4.3 (1.8–8.1) ml/100 ml) indicating moderate luxury perfusion. Levels of CMRO2 were decreased (1.54 (0.7–3.2) ml/100 g/min) as well. Duringhyperventilation (ΔAPaCO2 = 0.88 (0.62–1.55) kPa) CBF decreased with 11.8 (−33.4−29.7) %/kPa and ICP decreased with 3.8 (0–10) mmHg. AVdO2 increased 34.0 (4.0–139.2) %/kPa, MABP was unchanged, CMRO2 and CPP increased (ΔCPP = 3.9 (−10−20) mmHg). AVD (lactate) and LOI were unchanged. No correlations between CBF responses to hypocapnia and outcomes were observed. An i.v. bolus dose ofindomethacin (30 mg) decreased CBF 14.7 (−16.7−57.4) % and ICP decreased 4.3 (−1−17) mmHg. AVdO2 increased 27.8 (−40.0−66.7)%, MABP (ΔMABP = 4.9 (−2−21) mmHg) and CPP (ΔCPP = 8.7 (3–29) mmHg) increased while CMRO2 was unchanged. No changes in AVd (lactate) and LOI indicating cerebral ischaemia were found. Compared to hyperventilation (changes per 1 kPa, at PaCO2 level = 4.05 kPa) the changes in MABP, CPP and CBF were significantly greater after indomethacin, while the changes in AVdO2, ICP, SvjO2, and LOI were of the same order of magnitude. Nocorrelation between relative reactivities to indomethacin and CO2, evaluated from changes in CBF and AVdO2, or between the decrease in ICP after the two procedures were found. Thus, some patients reacted to indomethacin but not to hyperventilation, and vice versa. These results suggest that indomethacin and hyperventilation might act independently, or in a complementary fashion in the treatment of patients with severe head injury.
    Type of Medium: Electronic Resource
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