Blood flow velocity waveforms of the middle cerebral artery and abnormal neurological evaluations in live-born fetuses with absent or reverse end-diastolic flow velocities of the umbilical arteries

Author(s):  
Erich Weiss ◽  
Stefan Ulrich ◽  
Peter Berle
1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.


Stroke ◽  
2000 ◽  
Vol 31 (8) ◽  
pp. 1897-1903 ◽  
Author(s):  
Lewis A. Lipsitz ◽  
Seiji Mukai ◽  
Jason Hamner ◽  
Margaret Gagnon ◽  
Viken Babikian

Medicina ◽  
2020 ◽  
Vol 56 (6) ◽  
pp. 288
Author(s):  
Rasa Bukauskienė ◽  
Edmundas Širvinskas ◽  
Tadas Lenkutis ◽  
Rimantas Benetis ◽  
Rasa Steponavičiūtė

Background and Objectives: The aim of this study is to identify risk factors for the development of delayed neurocognitive recovery (dNCR). Materials and Methods: 140 patients underwent neurocognitive evaluations (Adenbrooke, MoCa, trial making, and CAM test) and middle cerebral artery (MCA) blood flow velocity (BFV) measurements, one day before cardiac surgery. BFV was re-evaluated after anesthesia induction, before the beginning, middle, end, and after cardiopulmonary bypass (CPB) and postsurgery. To measure glial fibrillary acidic protein (GFAP) and neurofilament heavy chain (Nf-H), blood samples were collected after anesthesia induction, 24 and 48 h after the surgery. Neurocognitive evaluation was repeated 7–10 days after surgery. According to the results, patients were divided into two groups: with dNCR (dNCR group) and without dNCR (non-dNCR group). Results: 101 patients completed participation in this research. GFAP increased in both the non-dNCR group (p < 0.01) and in the dNCR group (p < 0.01), but there was no difference between the groups (after 24 h, p 0.342; after 48 h, p 0.273). Nf-H increased in both groups (p < 0.01), but there was no difference between them (after 24 h, p = 0.240; after 48 h, p = 0.597). MCA BFV was significantly lower in the dNCR group during the bypass (37.13 cm/s SD 7.70 versus 43.40 cm/s SD 9.56; p = 0.001) and after surgery (40.54 cm/s SD 11.21 versus 47.6 cm/s SD 12.01; p = 0.003). Results of neurocognitive tests correlated with CO2 concentration (Pearson’s r 0.40, p < 0.01), hematocrit (r 0.42, p < 0.01), MCA BFV during bypass (r 0.41, p < 0.01), and age (r −0.533, p < 0.01). The probability of developing dNCR increases 1.21 times with every one year of increased age (p < 0.01). The probability of developing dNCR increases 1.07 times with a decrease of BFV within 1 cm/s during bypass (p = 0.02). Conclusion: Risk factors contributing to dNCR among the tested patients were older age and middle cerebral artery blood flow velocity decrease during bypass.


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