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 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of oxygen inhalation at atmospheric pressure (1 ATA.O2) on CBF were studied in subarachnoid hemorrhage (SAH) patients due to ruptured intracranial aneurysms to prove the usefulness of the "O2 response" test for the evaluation of the cerebral vascular response. "O2 response" means the CBF (or ICP) decrease during hyperoxemia. CBF was measured by 10 m Ci 133Xe intravenous injection method using rCBF analyzer BI-1400 (Valmet). Two-compartmental analysis was used for the calculation of initial slope index (ISI). Studied cases were 53 postoperative SAH patients and 100 times examinations were done under the condition of Rest-1 ATA.O2. The incidence of global disturbance of the O2 response was 33% from day 0 to 3, 31% during day 4 to 7, 30% during day 8 to 14, and 23% at day 15 to 30. But, after day 31, there was no case which revealed an impaired O2 response. It was not possible to detect focal or hemispheric abnormalities of the O2 response because of the limitation of noninvasive two-dimensional CBF measurement method employed. The causes of O2 response abnormality, within a month after the onset, were increased ICP, hydrocephalus and diffuse brain damage. Multiple regression analysis proved that elevated PaO2 is the major factor in reducing CBF. CBF and ICP correlation study showed that the higher the Rest ICP, the fewer the CBF decreases during pure O2 inhalation. This may indicate that the increase in ICP in the acute stage changes the O2 response according to the level of increased ICP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effects of hyperoxemia on cerebral blood flow in subarachnoid hemorrhage patients]. 311 11

Both metabolic rate and protein catabolism are known to increase following severe head trauma, but the etiology of this hypermetabolism is unknown. To further investigate the problem, we studied the metabolism of 17 patients with indirect calorimetry who had severe craniocerebral trauma only and who required ICP monitoring for management. Patients were studied daily and immediately after ICP spikes greater than 20 mm Hg, prior to treatment with hyperventilation, osmotic diuretics, or barbiturates. Oxygen consumption (VO2) was correlated with ICP. Two groups of patients were identified. Group I patients were treated with hyperventilation and osmotic diuretics while Group II patients additionally received cerebral metabolic depressants. Group I had a significant correlation coefficient between VO2 and ICP. Significant hypercatabolism early in the post trauma period was demonstrated by increased urine urea nitrogen. Our observations suggest that in patients with craniocerebral trauma, elevated ICP is associated with increased oxygen consumption, protein catabolism and systemic hypermetabolism. Cerebral metabolic depressants blunted increases in VO2 which were seen with elevated ICP.
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PMID:Elevated intracranial pressure associated with hypermetabolism in isolated head trauma. 317 29

Ten patients with cerebral tumours were anaesthetized with thiopentone, 70% nitrous oxide in oxygen and fentanyl. Ventilation was controlled to give mean PaCO2 4.8 (range 3.6-6.7) kPa. Enflurane 2% was administered and ICP and MAP were recorded continuously for 10-15 min. The changes in ICP were not significant and ranged from -18.5 to 5.5 mm Hg. There were significant decreases in MAP (P less than 0.001) and CPP (P less than 0.001) during the administration of enflurane. In four patients the administration of enflurane had to be terminated prematurely because of a low CPP. Thus, enflurane has very little effect on ICP in patients with cerebral tumours and low concentrations of enflurane can safely be used during anaesthesia for intracranial operations, provided that the arterial pressure is monitored carefully.
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PMID:Effects of 2% enflurane on intracranial pressure and cerebral perfusion pressure. 641 82

In nine patients, with preoperative ICP monitoring, anaesthesia was induced with thiopentone 5 mg kg-1 given over 1 min, followed by pancuronium 0.1 mg kg-1. After manual hyperventilation with nitrous oxide and oxygen for 3 min they were given thiopentone 2.5 mg kg-1 over 30 s (phase 1); 30 s later laryngoscopy was performed and topical analgesia administered to the larynx. Endotracheal intubation was performed 1 min after spraying the cords (phase 2). The measurements continued for a further 5 min during which the patients were mechanically ventilated (phase 3). ICP and intra-arterial pressure were recorded. Although there was a significant decrease (P less than 0.05) in MAP at the end of the second dose of thiopentone, there were no other significant changes in ICP, MAP or PaCO2 throughout the study. In two patients there were transient decreases in cerebral perfusion pressure to less than 60 mm Hg. Although MAP increased in five of the patients during laryngoscopy and intubation, there was no increase in ICP, showing that the MAP was still within the autoregulatory limits.
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PMID:Prevention of intracranial hypertension during laryngoscopy and endotracheal intubation. Use of a second dose of thiopentone. 643 51

Twelve dogs were anesthetized and instrumental for determination of CVP, arterial pressure, intracranial pressure, left atrial pressure, and frontal cerebral cortical blood flow (CCBF) by the thermal method. A catheter was introduced into the venous return of the cerebral confluence to allow determination of cerebral A-V oxygen saturation differences. The animals were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery and a second circuit from the left ventricular apex to the left femoral artery. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left side bypass circuit. All animals were heparinized during bypass. Ventricular fibrillation was induced after completion of the bypass surgery. Two dogs served as controls. Pre-arrest determinations of hemoglobin, glucose, CCBF, and cerebral A-V oxygen differences were taken. Full circulatory arrest was carried out for 20 minutes by shutting off the cardiac bypass. Resuscitation was achieved by resumption of bypass perfusion. Acid-base balance was corrected quickly, and pre-arrest perfusion pressure was achieved and maintained for 90 minutes. All pressure parameters were monitored continuously. All pre-arrest determinations were repeated at 20, 40, 60, and 90 minutes post resuscitation. Five dogs were treated with 6 microgram/kg flunarizine administered IV drip over 10 minutes immediately post reperfusion. Five dogs were not treated post arrest. Treated animals had a prompt return of CCBF rates equal to or greater than pre-arrest flow, which persisted throughout the period of post-arrest observation. Untreated animals had markedly reduced CCBF and increased resistance. CCBF uniformly proceeded to near zero flow by 90 minutes. The ICP was not significantly altered by treatment.
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PMID:Effect of flunarizine on canine cerebral cortical blood flow and vascular resistance post cardiac arrest. 706 84

A prospective observational study was performed to assess the reliability of fibreoptic oximetric catheters and to identify the incidence and causes of jugular bulb oxygen desaturation in patients with acute closed head injury. There were twenty-five patients (30 +/- 16 years) with GCS < or = 8 in this study. Jugular bulb oximetry, mean arterial pressure, intracranial pressure, end-tidal CO2 and pulse oximetry were monitored continuously. Catheter calibration against a laboratory oximeter was performed post insertion and thereafter eight-hourly. Cerebral venous desaturation was defined as a jugular bulb oxygen saturation < 55% of > 10 minutes duration. There was a poor correlation for the first in vivo calibration (r2 = 0.602, P < 0.001, n = 25). Thereafter a close correlation between jugular bulb catheter and oximetry values was demonstrated (r2 = 0.868, P < 0.001, n = 205). Forty-two episodes of jugular bulb oxygen desaturation of 88 minutes mean duration (range 10 to 555) were observed. 83% occurred within 48 hours following injury. Hypocapnia was associated in 45% of episodes; hypoperfusion in 22%; raised ICP in 9% and a combination of the above in 24%. Validation with a laboratory oximeter is essential prior to continuous jugular bulb oximetry. Sustained episodes of cerebral venous desaturation are frequent within the first 48 hours following acute head injury. Factors such as hypocapnia and cerebral hypoperfusion that primarily reduce cerebral blood flow are predominant.
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PMID:Detection of cerebral venous desaturation by continuous jugular bulb oximetry following acute neurotrauma. 866 39

The administration of an intravenous anaesthetic agent before experimental cerebral ischaemia in animals improves the functional and histological outcome. Cerebral ischaemia may be global or focal, complete or incomplete. Intravenous anaesthetic agents reduce the cerebral metabolic demand for oxygen (CMRO2) and abolish electrophysiological activity. This reflects a discontinuation of the functional neuronal activity with maintenance of its basic metabolic activity. The oxygen spared by the decrease in consumption, while reducing the functional activity, might be used by the neurons to sustain longer periods of ischaemia. This protective effect is also observed after pretreatment with either lidocaine or volatile agents, but their potentially deleterious vasodilating effect must be considered. Ketamine has recently been shown to antagonize NMDA receptors. The protective effect of barbiturates was experimentally demonstrated more than 30 years ago. They are still used as a reference. They reduce CMRO2, optimise the ratio between oxygen consumption and oxygen delivery and thus reduce cerebral blood flow and cerebral blood volume, as a result of the decrease of the metabolic demand. This might explain why a protective effect is seen in case of global or focal hypoxia with increased intracranial pressure, while no protection is documented in case of global cerebral ischaemia, such as after cardiac arrest, where EEG is immediately flat and ICP low. However, at doses required to obtain a protective effect, barbiturates induce deleterious side effects such as severe arterial hypotension, which limits their use. Cerebrovascular and cardiac surgery or surgery of the carotids are characterised by potentially ischaemic episodes which can be predicted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral protection: contribution of intravenous anesthetic agents]. 767 77

Monitoring plays an essential role in the management of critically ill children, although continuous observation along with frequent clinical examination remains the best readily available monitor. Unfortunately, human beings do not have the capability of a prolonged, uninterrupted attention span and nurses often have multiple tasks assigned that limit their ability for continuous observation. Furthermore, some information cannot be obtained accurately by clinical examination alone, e.g. oxygen saturation, ICP, etc. Therefore, it is important to understand the principles and practical points to be able to use these monitors, and first rule out malfunction, disconnection, or improper electrode placement when abnormal reading appear on these monitors before initiating clinical intervention on a patient.
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PMID:Monitoring in pediatric intensive care. 824 87

Ischaemic brain lesions still have a high prevalence in fatally head injured patients and are the single most important cause of secondary brain damage. The present study was undertaken to explore the acute phase of severely head injured patients in order to detect early ischaemia using Robertson's approach of estimating cerebral blood flow (CBF) from calculated arterio-jugular differences of oxygen (AVDO2), lactates (AVDL), and the lactate-oxygen index (LOI). Twenty-eight cases with severe head injury were included (Glasgow Coma Scale Score below or equal to 8). All patients but one had a non-missile head injury. All the patients had a diffuse brain injury according to the admission CT scan. ICP measured at the time of admission was below 20 mmHg in 17 cases (61%). All patients were evaluated with the ischaemia score (IS) devised in our center to evaluate risk factors for developing ischaemia. Mean time from injury to the first AVDO2/AVDL study was 23.9 +/- 9.9 hours. According to Robertson's criteria, 13 patients (46%) had a calculated LOI (-AVDL/AVDO2) value above or equal to 0.08 and therefore an ischaemia/infarction pattern in the first 24 hours after the accident. Of the 15 patients without the ischaemia/infarction pattern, in three cases the CBF was below the metabolic demands and therefore in a situation of compensated hypoperfusion. No patient in our series had hyperaemia. Comparing different variables in ischaemic and non-ischaemic patients, only arterial haemoglobin and ischaemia score (IS) was significantly different in both groups. The ischaemia score had mean of 4.3 +/- 1.7 in the ischaemic group and 2.7 +/- 1.4 in non-ischaemic patients (p = 0.01). It is concluded that ischaemia is highly prevalent in the early period after severe head injury. Factors potentially responsible of early ischaemia are discussed.
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PMID:Early ischaemia after severe head injury. Preliminary results in patients with diffuse brain injuries. 837 9

To evaluate the effects of deflation timing of an intraaortic balloon (IAB) on ventriculoarterial (VA) coupling and left ventricular (LV) mechanics, we assessed contractility: Emax (mmHg/ml); VA coupling: Ea/Ees; myocardial oxygen consumption: LV pressure-volume area (PVA); and energy efficiency: external work (EW)/PVA during IAB pumping, using four different timing intervals of IAB deflation in eight dogs weighing 19.8 +/- 3.8 kg. In the conventional timing group (G-conv), the IAB was deflated before LV systole. In the real time group (G-1, 2, 3), the IAB was deflated during isovolumic contraction (ICP), and the group was subdivided into three groups based on time of deflation: G-1 at the onset of ICP, G-2 at the midpoint of ICP, and G-3 at the end of ICP. Percent changes in values with IAB compared to those without assist were calculated. Based on the results, IAB deflation during ICP reduces LV end-systolic pressure and significantly optimizes VA coupling and LV efficiency during IAB support, compared with conventional timing.
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PMID:Effects of timing on ventriculoarterial coupling and mechanical efficiency during intraaortic balloon pumping. 857 71


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