Carbon dioxide reactivity during prostaglandin E1 induced hypotension for cerebral aneurysm surgery
| Autor: | Akira Demizu, Ikuto Yoshiya, Takashi Mima, Kazuo Abe, Kitaro Kamada |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Adult
Male Time Factors Hemodynamics Blood Pressure Hypotension Controlled Group B chemistry.chemical_compound Aneurysm Heart Rate medicine Humans Reactivity (chemistry) Glasgow Coma Scale Alprostadil Prostaglandin E1 Aged Aged 80 and over Neurologic Examination Rupture Spontaneous business.industry Intracranial Aneurysm General Medicine Blood flow Carbon Dioxide Middle Aged Subarachnoid Hemorrhage medicine.disease Anesthesiology and Pain Medicine Treatment Outcome chemistry Cerebral blood flow Anesthesia Cerebrovascular Circulation Female business Respiratory minute volume |
| Zdroj: | Canadian journal of anaesthesia = Journal canadien d'anesthesie. 39(3) |
| ISSN: | 0832-610X |
| Popis: | The cerebral vasomotor reactivity to carbon dioxide was studied, using a thermal gradient blood flow meter in 43 patients with intracranial cerebral aneurysm under deliberate hypotension induced by prostaglandin E1 (PGE1) infusion. The patients were divided into three groups according to the neurological status. Patients in Groups A and B had subarachnoid haemorrhage due to ruptured cerebral aneurysms. Group A consisted of 23 patients with a neurological grade of I–II and Group B consisted of 11 patients with a grade of III–V. Nine patients with non-ruptured cerebral aneurysm served as controls (Group C). After the dura was opened, local cerebral blood flow (LCBF) was measured. The PGE1 was started with an initial dose of 0.1 μg · kg−1 · min−1 and the dose was adjusted to maintain MAP at about 70 mmHg. The LCBF and carbon dioxide (CO2) reactivity were estimated during and after PGE1 administration. The LCBF did not change among groups throughout the study period. Carbon dioxide reactivity was estimated as follows: absolute; ΔLCBF/ ΔPaCO2, and relative; %ΔLCBF/ΔPaCO2 after changing PaCO2 by increasing minute ventilation. Absolute and relative CO2 reactivity did not change within groups throughout the study. Absolute CO2 reactivity values before, during and after, hypotension were 1.07 ± 0.4, 1.13 ± 0.48, 1.18 ± 0.6 (ml · min−1 · 100 g−1 · mmHg−1) in Group A, 0.8 ± 0.28, 0.71 ± 0.25, 0.72 ± 0.3 in Group B and 2.13 ± 0.75, 2.17 ± 0.88, 2.06 ± 0.69 in Group C. Relative CO2 reactivity values before, during and after hypotension were 1.95 ± 0.72, 2.17 ± 0.83, 2.13 ± 0.61 (% · mmHg−1) in Group A, 1.29 ± 0.22, 1.37 ± 0.48, 1.37 ± 0.48 in Group B and 3.58 ± 0.91, 4.17 ± 1.81, 4.03 ± 1.91 in Group C. Carbon dioxide activity was less in Groups A and B than in Group C (P < 0.05) and there was a significant difference between Groups A and B (P < 0.05). There was a close correlation between presurgical neurological status and CO2 reactivity (before: rs = − 0.704, P < 0.01, during: rs = −0.625, P < 0.01, and after deliberate hypotension: rs = −0.618, P < 0.01). The LCBF and CO2 reactivity were well maintained during PGE1 infusion in all groups. Outcome was correlated with presurgical neurological status (rs = 0.646, P < 0.01), and the initial cerebral blood flow was correlated with presurgical neurological status (rs = − 0.402, P < 0.05). These results suggest that presurgical neurological status is closely correlated with CO2 reactivity and cerebral blood flow, and that PGE1 induced hypotension does not change significantly LCBF and CO2 reactivity. |
| Databáze: | OpenAIRE |
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