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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The amount of blood used in transfusions during certain neurosurgical operations was less in 1978-79 than in 1971-72 and in 1965-66. The operations investigated were for gliomas and meningiomas of the brain, pituitary adenomas, acoustic neurinomas, arteriovenous malformations, and arterial aneurysms. The major change in anaesthetic techniques between 1965-66 and 1971-72 was the introduction of hypocapnia by controlled artificial hyperventilation. We suggest that this was the main factor responsible for the reduction in the need for blood transfusions. The avoidance of halothane, the use of induced hypotension, and microsurgical technique may have been responsible for the smaller drop between 1971-72 and 1978-79. Good neurosurgical anaesthesia demands anaesthetic expertise, reliable apparatus, and instant laboratory service, but may also reduce costs by reducing the need for blood transfusions.
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PMID:Changes in the requirements for blood transfusion in brain surgery. 731 52

Blood solubilities of halothane and enflurane are in a favourable range and differ only for 21%. There are some pharmacokinetical advantages to enflurane compared to halothane, but more because of its lower tissue/blood partition coefficient than due to the difference in blood solubility. The differences in physical behaviour are of more practical significance during recovery than during induction. With the use of enflurane recovery will be more rapid and somewhat less influenced by the duration of anesthesia and by alterations of distribution capacity. With both agents induction can be made faster by adjusting to a higher inspiratory concentration, whereas the waking-up time is commonly reduced by starting recovery from a lower alveolar concentration immediately at the end of operation. Hyperventilation in this period is limited by the resulting hypocapnia with reduced brain perfusion.
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PMID:Current knowledge on pharmacokinetics of halothane and enflurane. 745 50

Cerebral protection combines techniques aimed 1) to avoid death of neurones which sustained primary ischemic of traumatic insults and 2) to prevent secondary insults to the brain. The chemical brain retractor concept includes the use of a total intravenous anesthesia technique, mild hypocapnia and mannitol with strict monitoring and maintenance of the global cerebral homeostasis. This contributes to decrease brain volume and intracranial pressure and allows the best possible access to the operating site, while avoiding excessive pressure under the surgical brain retractors. Neuronal protection is based on a better understanding of the biological basis of secondary brain damage; therapeutic or prophylactic techniques include the use of specific pharmacological agents, hypothermia, hemodilution and maintenance of an elevated cerebral perfusion pressure. In short, although the favourable effects of such techniques are nor easy to demonstrate in man, their use in today's clinical practice, in association with the concept of the chemical brain retractor, is an effective way to prevent ischemic cerebral insults during neurosurgical procedures.
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PMID:[Relaxation and protection of the brain on the operating table]. 759 56

Eight morbidly obese patients (body mass index [BMI] = 46) were studied during general anesthesia and controlled mechanical ventilation. To evaluate the effect of large tidal volume ventilation on oxygenation and ventilation, the baseline 13 mL/kg tidal volume (VT) (calculated by the ideal body weight) was increased in 3 mL/kg volume increments to 22 mL/kg, while ventilatory rate (RR) and inspiratory time (TI) were kept constant. Each volume increment was maintained for 15 min. Gas exchange was assessed by measuring the arterial blood oxygen tensions, and calculating the indices of alveolar-arterial oxygen tension difference [P(A-a)O2] and arterial/alveolar oxygen tension ratio (a/A). Peak inspiratory airway pressure (Ppeak), end-inspiratory airway pressure (Pplateau), and compliance of the respiratory system (CRS) were recorded using the Capnomac Ultima (Datex, Helsinki, Finland) on-line respiratory monitor. Increasing tidal volumes to 22 mL/kg increased the recorded Ppeak (26.3 +/- 4.1 vs 37.9 +/- 3.2 cm H2O, P < 0.008), Pplateau (21.5 +/- 3.6 vs 27.7 +/- 4.3 cm H2O, P < 0.01), and CRS (39.8 +/- 7.7 vs 48.5 +/- 8.3 mL/cm H2O) significantly without improving arterial oxygen tension and resulted in severe hypocapnia. Since changes in arterial oxygenation were small and not statistically significant, mechanical ventilation of morbidly obese patients with large VTS seems to offer no advantage to smaller (13 mL/kg ideal body weight) VTS.
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PMID:Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anesthesia. 761 32

Long-term tracheostomy-ventilated patients have better speech with a cuffless tracheostomy tube and a large tidal volume. Moderate day time hyperventilation from a pressure-limited ventilator is necessary in these patients to avoid hypoxia during sleep due to the variable insufflation leak. This study sought to confirm whether a dead space of 3 ml.kg-1 could help to provide normocapnic hyperventilation during waking time without causing hypercapnia and hypoxaemia during sleep. Transcutaneous blood gas studies were performed on 11 patients with high tetraplegia undergoing pressure-limited pulmonary ventilation with room air. Recordings were made for 120 min each when awake and asleep, with and without dead space. The mean derived arterial PCO2 without the dead space was 2.95 kPa awake and 3.21 kPa asleep, whilst the corresponding tensions with dead space were 3.39 kPa and 3.79 kPa. These small increases associated with the dead space, both awake and asleep, were statistically significant. There was a statistically, though not clinically significant decrease in oxygen tension when the patients without dead space went to sleep. The fact that the carbon dioxide tension was higher during sleep when dead space was in situ indicates that, despite the insufflation leak in these patients, there is significant rebreathing back through the dead space. Amelioration of hypocapnia during waking and sleeping is achievable using a dead space extension in these patients.
Anaesthesia 1995 Aug
PMID:Does dead space ventilation always alleviate hypocapnia? Long-term ventilation with plain tracheostomy tubes. 764 97

Deliberate hypocapnia during the anaesthetic management of the patient undergoing craniotomy has become an accepted standard of care. However there has been a resurgence of interest, in how hypocapnia should be applied in intra- and extra-operative settings. There are three possible therapeutic effects of hypocapnia, namely, (a) reduction of brain bulk through a reduction in cerebral blood volume, with a decrease cerebral blood flow; (b) developing an "inverse steal" by redistribution of blood from normal to ischaemic regions and (c) acting to offset cerebral acidosis by increasing pH in the extracellular space. In anaesthetic intraoperative practice, hypocapnia is used as a specific treatment of, or prophylaxis against, intracranial hypertension during induction of anaesthesia and the period before dural exposure. More commonly, hypocapnia is used for intraoperative brain relaxation (intracranial pressure = 0). Severe hypocapnia (< 20 mmHg) may result in cerebral production of lactate; however no studies have shown that a Paco2 in the range of 23-28 mmHg has deleterious effects. Recent studies in head-injured patients suggest that routine long-term hyperventilation, without an objective index of cerebral flow/metabolism coupling, may place the brain at risk for adverse outcome. The few data available for intraoperative management suggest that Paco2 figures of 30-35 mmHg result in acceptable operating conditions. Unless otherwise specifically indicated by surgical conditions or cerebral flow/metabolism coupling (e.g. jugular O2 saturation), routine application of profound (Paco2 < 28-30 mmHg) hyperventilation should probably be avoided and its use needs reevaluation.
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PMID:[Is there still a place for routine deep hypocapnia in intracranial surgery?]. 767 90

Because hypocapnia is routine during general anaesthesia for intracranial procedures, we have compared, in 13 healthy volunteers, the effect of normocapnia (PE'CO2 5.3 kPa) and hypocapnia (PE'CO2 3.3 kPa) on mean blood flow velocity in the middle cerebral artery (Vmca) during normoventilation and hyperventilation with air and with 50% nitrous oxide in oxygen. After replacement of air with 50% nitrous oxide in oxygen, there was an increase in mean Vmca during normoventilation (air: mean 68.23 (SD 16.98) cm s-1 vs nitrous oxide in oxygen: 90.69 (20.41) cm s-1; P < 0.01), whereas during hyperventilation mean Vmca values were similar regardless of the inhaled gas mixture (air: 43.46 (9.97) cm s-1 vs nitrous oxide in oxygen: 41.69 (8.08) cm s-1. Our data suggest that the nitrous oxide-induced increase in mean Vmca can be blocked by hyperventilation.
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PMID:Hyperventilation reverses the nitrous oxide-induced increase in cerebral blood flow velocity in human volunteers. 777 42

Although changes in cerebral blood flow (CBF) and the electroencephalogram (EEG) have been reported with nitrous oxide (N2O) administration, the interaction of these parameters is unclear. The purpose of this study was to measure CBF and EEG during N2O administration in eight patients. A craniotomy was performed and CBF was measured in major brain arteries using a transit time Doppler flowmeter. EEG was recorded bilaterally from frontooccipital leads. Power spectrum analysis was performed on the EEG and power for delta, theta, alpha, and beta frequency bands analyzed over time. Arterial blood pressure was recorded continuously. N2O (66%) was added to the inspired gases during isoflurane anesthesia (0.8% end tidal) under hypocapnic (Paco2 = 29 mm Hg) and normocapnic conditions (Paco2 = 39 mm Hg). During hypocapnia, N2O administration decreased alpha EEG activity and increased delta activity but did not change CBF. During normacapnia, N2O produced similar but greater changes in EEG and increased CBF 39%. In three patients, the isoflurane concentration was increased to 1.6% end tidal during normocapnia. N2O administration in these patients also enhanced delta EEG activity and increased CBF. The slowing of EEG activity with N2O is temporally related to increases in CBF during normocapnia. Hypocapnia abolished the increase in CBF during N2O and attenuated the shift of EEG to delta activity.
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PMID:Nitrous oxide added to isoflurane increases brain artery blood flow and low frequency brain electrical activity. 777 71

The aim of this study was to examine the influence of ketanserin, a 5-hydroxytryptamine antagonist antihypertensive agent, on the relationship between cerebral blood flow (CBF) and middle cerebral artery flow velocity (Vmean MCA) and to compare Doppler-sonographic indices of downstream resistance (pulsatility index, PI; resistance index, RI) with calculations of cerebrovascular resistance (CVR) in 17 male patients under fentanyl/midazolam anesthesia. CBF was measured with the Kety-Schmidt technique using argon as a tracer. Cerebral perfusion pressure (CPP) was calculated as the difference between mean arterial pressure (MAP) and jugular bulb pressure. Measurements of Vmean MCA and determinations of PI and RI were performed by use of a 2-MHz transcranial Doppler ultrasound device. All variables were measured at normo- and moderate hypocapnia before and after intravenous (i.v.) bolus administration of 0.3 mg/kg ketanserin followed by an infusion of 0.06 mg.kg-1.h-1. Ketanserin changed neither average CBF nor Vmean MCA. The CO2 reactivity of Vmean MCA was significantly lower than the CO2 reactivity of CBF (P < 0.01); however, ketanserin did not change the relationship between CBF and Vmean MCA. During hypocapnia, CVR as well as PI and RI significantly increased (P < or = 0.01), indicating consistent directional changes in arteriolar resistance and flow velocity pulsatility. In contrast, after i.v. administration of ketanserin, CVR decreased (P < 0.05), whereas both Doppler-derived indices increased (P < 0.01). These results suggest that ketanserin in a clinically relevant dose does not alter the validity of serial Vmean MCA measurements as an index of global CBF and that ketanserin does not change the diameter of middle cerebral arteries (MCAs). Doppler-derived indices of pulsatility and resistance, which are supposed to estimate changes in downstream resistance, reflect changes, after administration of ketanserin, in systemic hemodynamics rather than changes in CVR.
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PMID:Effect of ketanserin on global cerebral blood flow and middle cerebral artery flow velocity. 780 2

The purpose of this study is to investigate the mechanisms of the effect of hyperventilation on the spinal pain modulating system by using phentolamine. Under enflurane anaesthesia, cats received mid-collicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells, responding primarily to noxious peripheral stimuli, were sampled with a microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period, ventilation was changed to induce hypocapnia of PCO2 20-25 mmHg. After activities were well suppressed, phentolamine 0.5 mg with normal saline 1.0 ml was injected on the spinal cord. Changes of firings were investigated. When normocapnia was resumed, recovery followed. Hypocapnia of PCO2 20-25 mmHg significantly suppressed the activities of WDR cells. Phentolamine significantly antagonized the suppressive effects of hyperventilation upon the activities of WDR cells. Our results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell and the mechanisms of those suppressive effects are related to adrenergic pain modulating system.
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PMID:[Effects of hyperventilation upon the spinal pain modulating system (third report)]. 781 94


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