A. Benzer

Significance of working conditions on burnout in anesthetists

Background:  The influence of working conditions on the development of burnout syndrome was assessed in anesthetists working at a university hospital.

Effects of normo- and hypocapnic nitrous-oxide-inhalation on cerebral blood flow velocity in patients with brain tumors.

Nitrous oxide (N2O) use during anesthesia for intracranial procedures has been a subject of controversy in the past. To date, the isolated influence of N2O on mean cerebral blood flow velocity in the middle cerebral artery (VMCA) has not been investigated during hypocapnia in patients with brain tumors. We compared VMCA during normocapnic (ETCO2: 40 mm Hg) and hypnocapnic (ETCO2: 25 mm Hg) inhalation of air and 50% nitrous oxide in oxygen N2O/O2 in eight patients with unilateral brain tumors on both the tumor side and the healthy side. Six patients completed the study. Mean VMCA increased during normocapnic inhalation of N2O/O2 (tumor side: 86 ± 16 cm sec-1; healthy side: 74 ± 17 cm sec-1) when compared with air (tumor side: 72 ± 18 cm sec-1; healthy side: 62 ± 14 cm sec-1, p < 0.01), whereas during hyperventilation VMCA decreased on both sides (p < 0.001). Mean VMCA values were quite similar during hypocapnic inhalation of 50% N2O/O2 (tumor side: 50 ± 12 cm sec-1; healthy side: 45 ± 13 cm sec-1) and air (tumor side: 51 ± 14 cm sec-1; healthy side: 45 ± 12 cm sec-1). The data of our study suggest that in patients with cerebral tumors the N,O-induced increase in mean VMCA can be completely reversed by hyperventilation.

Influence of urapidil on cerebrospinal fluid pressure in humans with uncompromised intracranial compliance

ObjectiveDetermine the influence of urapidil on mean lumbar cerebrospinal fluid pressure (CSFP), mean arterial pressure (MAP), mean central venous pressure (CVP) and heart rate (HR) in awake humans without any evidence of cerebral or cardiovascular disease.DesignOpen, single-dose volunteer study.InterventionsCSFP was measured via a spinal needle after i.v. injection of a single dose of 0.2 mg kg−1 urapidil in six volunteers (2 female, 4 male).Measurements and resultsAfter administration of urapidil, CSFP increased from 7±1 mmHg to 10±1 mmHg (p<0.05), MAP decreased from 88±7 mmHg to 74±5 mmHg (p<0.05), CPP decreased from 81±7 mmHg to 64±5 mmHg (p<0.05) and CVP decreased from 0±1 mmHg to −3±1 mmHg (p<0.05).ConclusionOur data suggest that in humans with presumed normal intracranial compliance the administration of urapidil causes a small but statistically significant increase in CSFP due to a parallel decrease in MAP.

Nitrous oxide and cerebral haemodynamics

Sir, The study by Strebel et al. (1) evaluates the influence of nitrous oxide on cerebral hemodynamics. Although they clearly showed that N,O is a potent cerebral vasodilator during normocapnia leading to an increase in cerebral blood flow velocity (CBFV), their conclusions and recommendations are somewhat misleading. When the authors write that “in patients with an elevated ICP or a reduced intracranial compliance, the possibility that nitrous oxide may be a potent cerebral vasodilator should be considered,” they forget that these patients, who were not the subject of their study, should be hyperventilated intraoperatively, while the cerebral healthy (!) patients examined by the authors were normoventilated. A recent study (2), however, was able to show in cerebral healthy volunteers that the increase in CBFV caused by 50% N,O in oxygen can be completely reversed by hyperventilation. In our opinion it is always problematic to attempt to draw direct conclusions for the treatment of patients from findings made in healthy individuals.