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Biomedical subjects

G E Cold

Publications and source records attributed to G E Cold.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Changes in PaO2, PaCO2 and pH during the apnea test].

Changes in PaCO2, PaO2 and arterial pH were monitored during a 10 min apnoea test in nine clinically brain dead subjects. The patients were preoxygenated for 15 min with 100% O2. During the apnoea test they were oxygenated by tracheal cannulation with 5 l O2 per min. PaCO2 rose 1.3-2.1 kPa during the first two minutes of apnoea. Patients with PaCO2 greater than or equal to 5.5 kPa at the beginning of apnoea all had PaCO2 greater than 8 kPa after 5 min of apnoea for five minutes. With one exception, all of the patients were sufficient oxygenated during the apnoea test. If patients are ventilated to a PaCO2 greater than or equal to 5.5 kPa then 5 min of apnoea testing will increase PaCO2 above 8 kPa. As a few patients may develop hypoxemia, patients should be monitored with pulseoximetry.

Adult↗
PubMed1990

The effects of midazolam on cerebral blood flow and oxygen consumption. Interaction with nitrous oxide in patients undergoing craniotomy for supratentorial cerebral tumours.

Cerebral blood flow and the cerebral metabolic rate of oxygen were measured in 30 patients during craniotomy for supratentorial cerebral tumours by a modification of the Kety-Schmidt technique using Xenon 133 intravenously. Anaesthesia was induced with midazolam 0.3 mg/kg, fentanyl and pancuronium, and maintained with midazolam as a continuous infusion, fentanyl, pancuronium and nitrous oxide in oxygen or oxygen in air. The concentration of midazolam in the blood of 10 patients was about 300 ng/litre during two measurements; the patients' lungs were ventilated with N2O in oxygen. The concentration of midazolam in the blood of another 10 patients was doubled to about 600 ng/litre during the second flow measurement; the patients' lungs were ventilated with N2O/O2. The concentration of midazolam in the blood of the third group of 10 patients was doubled to 600 ng/litre during the second flow measurement; the patients' lungs were ventilated with oxygen in air. No relationship was found between the dose of midazolam and cerebral blood flow or oxygen consumption. Nitrous oxide in combination with midazolam also had no effect on these variables.

Adult↗
PubMed1990

Changes of blood pressure and cerebral arterio-venous oxygen content differences (AVDO2) with and without bupivacaine scalp infiltration during craniotomy.

In 20 patients subjected to craniotomy for supratentorial cerebral tumours, the effect of scalp infiltration with bupivacaine before incision was evaluated by measuring mean arterial blood pressure (MABP) and cerebral arterio-venous oxygen content differences (AVDO2) repeatedly during the operation. All patients were given halothane 0.5% anaesthesia. Ten patients were given bupivacaine 0.25% and ten patients were given normal saline for scalp infiltration prior to incision. The study was performed in a double-blind randomized fashion. Significantly higher values of MABP (P less than 0.0005) after incision were found in the saline group compared to the bupivacaine group. Significantly lower values of AVDO2 (P less than 0.0005) after incision were seen in the saline group compared to the bupivacaine group. The results indicate that the increase in MABP associated with a decrease in AVDO2, suggesting an increase in CBF and cerebral hyperperfusion, is reduced by using bupivacaine scalp infiltration prior to incision.

Adult↗
PubMed1990

[Indomethacin in severe cerebral contusions with intracranial hypertension].

In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control ICP by hyperventilation and barbiturate sedation, indomethacin Confortid was used as a cerebral vasoconstrictor drug. In all patients indomethacin reduced ICP below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in cerebral blood flow (CBF) at 2 hours. After 7 hours. ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In two 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. Outcome scaling has not yet been performed, but all patients left hospital without neurological deficits. These results suggest that indomethacin is an alternative in the treatment of intracranial hypertension in head-injured patients.

Adult↗
PubMed1990

Cerebral blood flow in acute head injury. The regulation of cerebral blood flow and metabolism during the acute phase of head injury, and its significance for therapy.

During the last decade several studies of cerebral blood flow (CBF) and metabolism in the acute phase of head injury have been published. It is the aim of this review to describe the dynamic changes in CBF, cerebral metabolic rate of oxygen (CMRO2), cerebral autoregulation (CA), and reactivity to PaCO2 and barbiturate (metabolic reactivity) in the acute phase after severe head injury and to discuss the therapeutical consequences with reference to prolonged artificial hyperventilation, hypothermia, barbiturate sedation, and mannitol therapy. On the basis of present knowledge concerning cerebral circulation and its regulation, the author reviews the literature concerning methodology for experimental and clinical CBF measurements and regulation of CBF and cerebral oxygen uptake. Emphasis is placed on studies of the effect of body temperature (hypothermia) as a therapeutic tool in the control of cerebral metabolism, blood flow, and intracranial pressure. Although hypothermia significantly reduces cerebral metabolism and blood flow, the effect of hypothermia on cerebral blood flow, metabolism, ICP, and outcome after acute head injury has never been investigated in clinically controlled studies. Experimental and clinical studies concerning sensitivity of CBF for changes in PaCO2 are reviewed. The normal CO2 reactivity defined as absolute (delta CBF/delta PaCO2) and relative (% change CBF/delta PaCO2) or delta in CBF/PaCO2 mm Hg are mentioned. In awake normocapnic man the relative CO2 reactivity averages 4%/mm Hg and the absolute CO2 reactivity 2ml/mm Hg. Uncontrolled prospective studies show a therapeutic effect of artificially prolonged hyperventilation on outcome. Only one preliminary controlled study indicates that the outcome is poorer and recovery prolonged. Nevertheless, in the acute phase of HI, artificial hyperventilation is used routinely for control of intracranial hypertension and during the intensive care management of the patients. The steal and inverse steal phenomena are reviewed. Although of considerable theoretical interest these phenomena are without clinical significance in patients with head injury, unless clinical CBF measurements are performed. The frequency of the inverse steal phenomenon in studies of rCBF with a 16-channel Cerebrograph (intraarterial approach) is found to be about 10%. During prolonged hyperventilation experimental studies and clinical studies of apoplexy show an adaptation of CBF and CSF-pH and bicarbonate.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1989

[Use of controlled hyperventilation in the treatment of comatose patients with cranial injuries].

Controlled hyperventilation is a recognized method by which it is possible to reduce the intracerebral blood volume and thus the intracranial pressure (ICP). In the review, the physiological conditions involved in the regulation of ICP are illustrated, particularly in connection with acute cranial traumata and effect of controlled hyperventilation in these situations is discussed. Controlled hyperventilation is recommended in the hyperacute phase for all patients with cranial trauma prolonged impairment of consciousness (Glasgow Coma Scale less than 7 for more than 30 minutes) and other clinical evidence of expanding space-occupying intracranial process. Prolonged hyperventilation is recommended for younger patients as these have most frequently hyperaemia and retained CO2 reactivity and for patients with predominantly cortical lesions as assessed by CT scanning. Caution in the employment of hyperventilation is advised in elderly patients, severely traumatized patients and late in the course of cerebral trauma.

Adult↗
PubMed1989

Measurements of CO2 reactivity and barbiturate reactivity in patients with severe head injury.

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/delta PaCO2 mmHg) and absolute (deltaCBF/deltaPaCO2 mmHg), and the reactivity to barbiturate was calculated globally as delta 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.

Adolescent↗
PubMed1989

Does acute hyperventilation provoke cerebral oligaemia in comatose patients after acute head injury?

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 less than 20 ml/100 g/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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

The cerebral arterio-venous oxygen content differences (AVDO2) during halothane and neurolept anaesthesia in patients subjected to craniotomy.

In 20 patients subjected to craniotomy for supratentorial cerebral tumours, the haemodynamic changes during halothane and neurolept anaesthesia were evaluated by measuring mean arterial blood pressure (MABP) and cerebral arterio-venous oxygen content differences (AVDO2) repeatedly during the operation. Ten patients were given 0.5% halothane anaesthesia and ten patients neurolept anaesthesia. MABP, AVDO2 and PaCO2 were measured after induction of anaesthesia, before and after incision, after opening and closure of the dura, at the time of extubation and 1 h later. Concerning MABP and PaCO2, no significant difference between the two groups was found. In both groups an increase in MABP was observed after incision (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group) and in the neurolept group after extubation (P less than 0.01). In both groups a decrease in AVDO2 was observed after incision (P less than 0.01) and after extubation (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group). During the operation AVDO2 values were significantly higher in the neurolept group (P less than 0.05). The results indicate that even a moderate increase in MABP after incision during neuroanaesthesia affects AVDO2 values, suggesting an increase in cerebral blood flow. The study suggests that autoregulation of cerebral blood flow might be better preserved during neurolept anaesthesia. A state of hyperperfusion of the brain after extubation was unveiled in both groups.

Adult↗
PubMed1988

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2 reactivity during neurolept anaesthesia in patients subjected to craniotomy for supratentorial cerebral tumours.

In 10 patients subjected to craniotomy for supratentorial cerebral tumours in neurolept anaesthesia, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice peroperatively by a modification of the Kety & Schmidt technique, using 133Xe. The relative CO2 reactivity was assessed indirectly as the % change of the arteriovenous oxygen difference (AVDO2) per mm change in PaCO2. The patients were premedicated with diazepam 10-15 mg perorally. For induction, thiopentone 4-6 mg/kg, droperidol 0.2 mg/kg and fentanyl 5 micrograms/kg were used, and for maintenance N2O 67% and fentanyl 4 micrograms/kg/h. During the first flow measurement the median and range of CBF was 30 ml/100 g/min (range 17-45), of AVDO2 8.0 vol % (range 4.1-9.5), and of CMRO2 2.28 ml O2/100 g/min (range 1.57-2.84). During the second CBF study, AVDO2 increased to 9.3 vol % (range 3.4-11) (P less than 0.05), and CMRO2 increased to 2.51 ml O2/100 g/min (range 1.88-3.00) P less than 0.05, while CBF was unchanged. The CO2 reactivity was present in all studies, median 1.8%/mmHg (range 0.5-15.1). The correlation coefficients between jugular venous oxygen tension/saturation, respectively, and CBF were high at tensions/saturations exceeding 4.0 kPa and 55%, indicating that hyperperfusion is easily unveiled by venous samples from the jugular vein during this anaesthesia.

Adult↗
PubMed1987

Cerebral blood flow and metabolism during isoflurane-induced hypotension in patients subjected to surgery for cerebral aneurysms.

Cerebral blood flow and cerebral metabolic rate for oxygen were measured during isoflurane-induced hypotension in 10 patients subjected to craniotomy for clipping of a cerebral aneurysm. Flow and metabolism were measured 5-13 days after the subarachnoid haemorrhage by a modification of the classical Kety-Schmidt technique using xenon-133 i.v. Anaesthesia was maintained with an inspired isoflurane concentration of 0.75% (plus 67% nitrous oxide in oxygen), during which CBF and CMRO2 were 34.3 +/- 2.1 ml/100 g min-1 and 2.32 +/- 0.16 ml/100 g min-1 at PaCO2 4.1 +/- 0.1 kPa (mean +/- SEM). Controlled hypotension to an average MAP of 50-55 mm Hg was induced by increasing the dose of isoflurane, and maintained at an inspired concentration of 2.2 +/- 0.2%. This resulted in a significant decrease in CMRO2 (to 1.73 +/- 0.16 ml/100 g min-1), while CBF was unchanged. After the clipping of the aneurysm the isoflurane concentration was reduced to 0.75%. There was a significant increase in CBF, although CMRO2 was unchanged, compared with pre-hypotensive values. These changes might offer protection to brain tissue during periods of induced hypotension.

Adult↗
PubMed1987

The effect of isoflurane on cerebral blood flow and metabolism in humans during craniotomy for small supratentorial cerebral tumors.

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumors. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anesthesia was induced with thiopental 5-7 mg X kg-1, fentanyl 0.2 mg, and pancuronium, and maintained with 0.75% inspired isoflurane concentration in 67% nitrous oxide, and moderate hypocapnia. In one group of patients (n = 7), the inspired isoflurane concentration was maintained at 0.75% throughout anesthesia. One hour after induction of anesthesia, CBF and CMRO2 averaged 31 +/- 3 ml X 100 g-1 X min-1 and 2.1 +/- 0.2 ml O2 X 100 g-1 X min-1 (X +/- SEM), respectively. During repeat studies 1 h later, CBF and CMRO2 were unchanged. In a second group of patients (n = 7), an increase in the inspired isoflurane concentration from 0.75% to 1.5% was associated with a significant decrease in CMRO2 from 2.4 +/- 0.1 to 1.9 +/- 0.1 ml O2 X 100 g-1 X min-1, and no change in CBF. It is concluded that this anesthetic regimen is safe to use in patients with small supratentorial tumors in whom only a small midline shift has occurred.

Adult↗
PubMed1987

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2-reactivity during craniotomy for supratentorial cerebral tumours in halothane anaesthesia. A dose-response study.

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anaesthesia was induced with thiopental 4-6 mg kg-1, fentanyl and pancuronium, and maintained with an inspiratory halothane concentration of 0.45% in nitrous oxide 67% at a moderate hypocapnic level. In one group of patients (n = 7) the inspiratory halothane concentration was maintained at 0.45% throughout anaesthesia. About 1 h after induction of anaesthesia CBF and CMRO2 averaged 35 +/- 2 ml 100 g-1 min-1 and 2.7 +/- 0.3 ml O2 100 g-1 min-1 (mean +/- s.c. mean), respectively. During repeat studies 1 h later CBF and CMRO2 did not change. In another group of patients (n = 7) an increase in halothane concentration from 0.45% to 0.90% was associated with a significant decrease in CMRO2 from 2.3 +/- 0.1 to 2.0 +/- 0.1 ml O2 100 g-1 min-1. The CO2-reactivity measured after the second flow measurement was preserved. It is concluded that halothane in this study induces a dose-dependent decrease in cerebral metabolism, an increase in CBF while CO2-reactivity is maintained.

Adolescent↗
PubMed1986

Changes in CMRO2, EEG and concentration of etomidate in serum and brain tissue during craniotomy with continuous etomidate supplemented with N2O and fentanyl.

Fourteen patients with supratentorial cerebral tumours were anaesthetized with continuous etomidate infusion (30 or 60 micrograms kg-1 min-1) supplemented with N2O 67% and fentanyl. Peroperatively cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by the Kety and Schmidt method. Simultaneously with the CBF measurements, blood for serum etomidate was sampled and EEG was recorded in 2-min periods in 12 patients. In 10 patients a brain biopsy for etomidate was taken peroperatively and correlated with the other data. The results indicate a dose-dependant increase in serum etomidate and brain tissue etomidate, a decrease in CMRO2 and suppression of EEG activity. In individual studies an increase in serum etomidate or a decrease in CMRO2 correlated to a suppression of the EEG activity, and vice versa. However, the wide variations in these relationships within and between patients make any conclusion regarding CMRO2 impossible from the EEG recording, infusion rate of etomidate or serum concentration of etomidate.

Adult↗
PubMed1986

The relationship between cerebral metabolic rate of oxygen and cerebral blood flow in the acute phase of head injury.

In 20 comatose patients (Glasgow coma scale less than or equal to 6 at admission) with severe head injury, the cerebral metabolic rate of oxygen (CMRO2) was calculated as the product of the hemispheric cerebral blood flow (CBF) and the arterio-venous oxygen content difference (AVDO2). The hemispheric CBF was calculated by the intracarotid 133xenon washout method by stochastic analysis as the average of 16 regions, and the measurements were performed within 3 weeks after the acute trauma. Generally no significant correlation (P less than 0.05) between CMRO2 and CBF was found, either in the total number of paired observations, in studies of hyperaemia defined as CBF greater than or equal to 30 ml 100 g-1 min-1; or in studies with reduced flow (CBF less than 30 ml 100 g-1 min-1). However, in about 50% of patients subjected to repeated studies within days, CBF was positively correlated to CMRO2, and this correlation was observed independently of the CBF value. Hyperaemia was associated with a significant decrease in AVDO2, a significant increase in both absolute and relative CO2 reactivity, and a significant increase in ventricular fluid pH; but not to an increase in intraventricular pressure, mean arterial blood pressure or significant changes in ventricular fluid lactate or lactate/pyruvate ratio.

Acute Disease↗
PubMed1986

CBF and CMRO2 during craniotomy for small supratentorial cerebral tumours in enflurane anaesthesia. A dose-response study.

In 14 patients with supratentorial cerebral tumours with midline shift less than or equal to 10 mm, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice on the contralateral side of the craniotomy, using a modification of the Kety & Schmidt method. For induction of anaesthesia, thiopental, fentanyl and pancuronium were used. The anaesthesia was maintained with enflurane 1% in nitrous oxide 67%. Moderate hypocapnia to a level averaging 4.3 kPa was achieved. The patients were divided into two groups. In Group 1 (n = 7), 1% enflurane was used throughout the anaesthesia, and CBF and CMRO2 measured about 70 min after induction averaged 30.1 ml 100 g-1 min-1 and 1.98 ml O2 100 g-1 min-1, respectively. During the second CBF study 1 h later, CBF and CMRO2 were unchanged (P greater than 0.05). In Group 2 (n = 7), the inspiratory enflurane concentration was increased from 1 to 2% after the first CBF measurement. In this group a significant decrease in CMRO2 was observed, while CBF was unchanged. In six patients EEG was recorded simultaneously with the CBF measurements. In patients subjected to increasing enflurane concentration (Group 2), a suppression in the EEG activity was observed without spike waves. It is concluded that enflurane induces a dose-related decrease in CMRO2 and suppression in the EEG activity, whereas CBF was unchanged.

Adult↗