Moderate Hypocapnia Research Articles

Parallel changes of blood flow and heterogeneity of capillary plasma perfusion in rat brains during hypocapnia.

Plasma perfusion patterns were investigated in brain capillaries during decreased cerebral blood flow induced by hyperventilation. Anesthetized rats were decapitated 3-4 s after being given an intravenous bolus injection of Evans blue dye. the measured steep increase of the arterial dye concentration at this moment ensures that different capillary plasma transit times are reflected in different intracapillary dye concentrations. The observed heterogeneity of capillary plasma transit time was expressed as the coefficient of variation (means +/- SD) of the intracapillary dye concentrations. For comparison, cerebral blood flow was determined at comparable PCO2 values in a second experimental group. At arterial PCO2 values between 40 and 25 mmHg, the cerebral blood flow and the coefficient of variation of the intracapillary dye concentration decreased with decreasing PCO2, whereas at PCO2 values <25 mmHg cerebral blood flow and coefficient of variation did not correlate with the arterial PCO2. However, it cannot be excluded that the coefficient of variation of the intracapillary dye concentration increases between 25 and 14 mmHg and decreases between 14 and 10 mmHg. It is concluded that the reduction of cerebral blood flow measured during moderate hypocapnia is paralleled by a decreased heterogeneity of the brain capillary perfusion. During severe hypocapnia this relationship is lost, indicating a potential disturbance of the cerebral microcirculation.

Risques peropératoires lors de chirurgie cérébrale anévrismale

The perioperative complications associated with cerebral aneurysm surgery require a specific anaesthetic management. Four major perioperative accidents are discussed in this review. The anaesthetic and surgical management in case of rebleeding subsequent to the re-rupture of the aneurysm is mainly prophylactic. It includes haemodynamic stability assur-ance, maintenance of mean arterial pressure (MAP) between 80–90 mmHg during stimulation of the patient such as endo-tracheal intubation, application of the skull-pin head-holder, incision, and craniotomy. The aneurysmal transmural pressure should be adequately maintained by avoiding an aggressive decrease of intracranial pressure. Once the skull is open, the brain must be kept slack in order to decrease pressure under the retractors and avoid the risks of stretching and tearing of the adjacent vessels. If, despite these precautions, the aneurysm ruptures again. MAP should be decreased to 60 mmHg and the brain rendered more slack, in order to allow direct clipping of the aneurysm, or temporary clipping of the adjacent vessels. The optimal agents in this situation are isoflurane (which decreases CMRO 2), intravenous anaesthetic agents (inspite their negative inotropic effect, they may potentially protect the brain) and sodium nitroprusside. Vasospasm occurs usually between the 3rd and the 7th day after subarachnoid haemorrhage. It may be seen peroperatively. The optimal treatment, as well as prophylaxis, is moderate controlled hypertension (MAP > 100 mmHg), associated with hypervolaemia and haemodilution, the so-called triple H therapy, with strict control of the filling pressures. Other beneficial therapies are calcium antagonists (nimodipine and nicardipine), the removal of the blood accumulated around the brain and in the cisternae, and possibly local administration of papaverine. Abrupt MAP increases are controlled in order to maintain adequate aneurysmal transmural pressure. Beta-blockers, local anaesthetics administered locally or intravenously, a carefully titrated level of anaesthesia, a maintained volaemia play a protective role. Cerebral oedema is sometimes already present at the opening of the skull or may arise later, due to a high pressure under the retractors, to the surgical manipulations of the brain or to brain ischaemia subsequent to temporary clipping. Its treatment is aggressive, with intravenous agents, mannitol, deep hypocapnia and/or lumbar drainage. Prophylaxis, according to the “brain homeostasis concept”, is the preferred method to avoid these four peroperative accidents. It includes normal blood volume, normoglycaemia, moderate hypocapnia, normotension, soft manipulation of the brain and optimal brain relaxation.

Effect of Ketanserin on Global Cerebral Blood Flow and Middle Cerebral Artery Flow Velocity

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.

Carbachol, norepinephrine, and hypocapnia stimulate phosphatidylinositol turnover in rat tracheal slices.

The intracellular mechanisms involved in the alpha-adrenoceptor- or hyperventilation-induced bronchoconstriction remain unknown. Because there is a direct relationship between phosphatidylinositol (PI) metabolism and airway smooth muscle contraction induced by muscarinic agonists, the authors examined the effects of carbachol (CCh), norepinephrine (NE), and hypocapnia on PI turnover in the airway smooth muscle. Rat tracheal slices were incubated in Krebs-Henseleit solution containing LiCl and [3H]myo-inositol in the presence of NE, CCh, or neither. The PCO2 in the solution was 36 +/- 3 mmHg (normocapnia), 19 +/- 2 mmHg (moderate hypocapnia), or 5 +/- 2 mmHg (severe hypocapnia), respectively. [3H]inositol monophosphate (IP1) formed was counted with a liquid scintillation counter. Basal IP1 formed was greater at severe hypocapnia than at normocapnia. Norepinephrine- and CCh-induced IP1 formation were also greater at hypocapnia than at normocapnia. These results indicate that CCh, NE, and hypocapnia stimulate PI turnover in the airway smooth muscle, which would cause bronchoconstriction, and hypocapnia also augments NE- and CCh-induced PI turnover, which could cause worsening of exercise-induced asthma and vagotonic asthma, respectively.

Transcranial doppler for detection of cerebral ischaemia during carotid endarterectomy

We evaluated transcranial Doppler sonography (TCD) for the detection of cerebral ischaemia during carotid endarterectomy in 30 male and 14 female patients with ipsilateral focal cerebro-vascular symptoms. Surgery was performed during halothane-nitrous oxide anaesthesia with moderate hypocapnia. Eight patients had a temporary shunt owing to contralateral occlusion or a stump pressure below 40 mmHg, and/or EEG flattening. Transcranial Doppler sonography was followed intra-operatively together with electro-encephalography (EEG), internal carotid artery (ICA) pressures and cerebral blood flow (CBF). Middle cerebral artery mean flow velocity (Vmean) was 38 (22-96) cm s-1 (median and range) and decreased during cross-clamping to 28 (10-60) cm s-1 (p less than 0.0001). After removal of the clamp it increased to 42 (20-102) cm s-1 (p less than 0.0001). AVmean clamp of less than 30 cm s-1 together with a Vmean clamp: Vmean pre-clamp ratio of less than 0.6 showed an accuracy with respect to CBF below 20 ml 100 g-1 min-1 of 89%. AVmeanclamp:Vmean pre-clamp ratio below 0.4 detected all all patients with EEG flattening (n = 3) (accuracy 97%). The corresponding level of accuracy obtained with stump pressure was 80%. The results indicate that middle cerebral flow velocity enables an increase in the accuracy of detecting cerebral ischaemia during carotid endarterectomy.

Per- and postoperative changes in the arterio-venous oxygen content difference (AVDO2) in patients subjected to craniotomy for cerebral tumours.

Sixteen patients with supratentorial cerebral tumours were subjected to craniotomy under thiopentone, fentanyl, nitrous oxide, halothane anaesthesia during moderate hypocapnia (PaCO2 level 4.0 kPa). The arterio-venous oxygen content difference (AVDO2) was measured peroperatively, and repeatedly during the first three hours after extubation. Peroperatively the level of AVDO2 averaged 8.0 vol% during opening of the dura, and decreased to 7.0 vol% during closure of the dura (P less than 0.05). Immediately after extubation the AVDO2 decreased to 4.3 vol% (P less than 0.05), and during the next 3 hours a gradual increase to 5.8 vol% (P less than 0.05) was disclosed. In individual cases the postoperative changes in AVDO2 correlated fairly well with changes in mean arterial blood pressure (MABP), but other factors including duration of the operation, age of the patients, size of the tumour, level of PaCO2 and adaptation to prolonged hyperventilation during operation are supposed to be responsible for the low levels of AVDO2 observed in the postoperative period.

Acidosis, hypoxia and stress hormone release in response to one-minute inhalation of 80% CO2 in swine.

The study pertains to a series of investigations on the effects of CO2 inhalation as used for pre-slaughter anaesthesia in swine. Acid/base parameters, blood oxygen tension, plasma Na, K, Ca and stress hormone concentrations were monitored in Yorkshire swine before, during, and for 10 min after the animals were descended for 1 min into 80% CO2 in air. Severe respiratory acidosis (PaCO2 approximately 50 kPa, arterial pH approximately 6.6) and hypoxia (PaO2 approximately 4kPa) had developed after 45 s of the CO2 inhalation. The corresponding changes in venous blood were less drastic (PvCO2 approximately 17 kPa, pH 7.1, PvO2 approximately 4 kPa). Readjustment to PaCO2 approximately II kPa, arterial pH 7.2, and PaO2 approximately 13 kPa had occurred at 1 min post CO2. Four minutes later the respiratory acidosis had become converted into metabolic acidosis subjected to partial respiratory compensation (arterial pH 7.3 in the presence of moderate hypocapnia and hyperoxaemia). The cause of this metabolic acidosis (present also at 10 min post CO2) was apparently hypoxia-induced anaerobic metabolism (= lactic acid production). Apparently due to hydrogen ion transport into the cells in exchange for other cations, hyperkalaemia (K approximately 6.6 mmol l-1), and a 7 mmol l-1 increase in plasma Na had developed at 1.5 min later. The CO2 inhalation did not change the total plasma Ca significantly. The transport of the swine from the stable to the immediate pre-experimental situation induced a 3-fold increase in plasma cortisol concentration (PC, to approximately 130 mmol l-1). No further increase in PC occurred in response to the CO2 inhalation. It indicates that no additional emotional strain was imposed upon the animals during the CO2 exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Room air ventilation for total intravenous general anaesthesia

The use of room air alone to ventilate patients who were anaesthetized with total intravenous anaesthesia, including morphine 2 mg · kg −1, was studied in ten patients. The were scheduled for gastrectomy for peptic ulcer or stomach carcinoma. The patient's minute-ventilation was measured the day previous to surgery ; this, together with a frequency of 14 c · min −1, was used to preset the ventilator. Alveolar ventilation, end-expiratory CO 2, arterial blood gases and acid-base balance were monitored throughout the procedure. The blood oxygen level was found to remain similar to the reference value ; there was a moderate hypocapnia, a low end-expiratory CO 2 and minimal changes in acid-base balance. No pulmonary complication was cncountered in the postoperative course. These results showed that room air could be used in unusual circumstances for healthy patients for whom a total intravenous anaesthetic technique has been chosen.

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.

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.

GAS EXCHANGE AND HAEMODYNAMICS DURING THORACOTOMY

Cardiac index, systemic and pulmonary arterial pressures, carbon dioxide elimination and ventilation of each lung were studied during thoracotomy. Seventeen patients, placed in the full lateral position, were ventilated mechanically through a Carlens' tube to moderate hypocapnia. Mean cardiac index increased by 12% as the pleura was opened (P less than 0.05), with no further change during surgery on the still ventilated upper lung. Mean arterial pressure was unchanged after opening the pleura, but decreased from 114 +/- 15 mm Hg (mean +/- 1 SD) to 104 +/- 18 mm Hg during surgery on the lung (P less than 0.01). Mean pulmonary artery pressure was unchanged. There was a significant (P less than 0.01) increase in carbon dioxide elimination from the upper lung when the pleura was opened. In addition, the ventilation of this lung increased significantly (P less than 0.05). Mean end-tidal PCO2 of the lower lung increased from 4.1 to 4.2 kPa after opening the pleura, while that of the upper lung increased from 3.0 to 3.6 kPa (P less than 0.01). VD/VT decreased from 43 to 38% as the pleura was opened (P less than 0.01). During surgical handling of the lung, marked decreases in ventilation, compliance, carbon dioxide elimination and end-tidal PCO2 were observed in the upper lung. We conclude that ventilation-perfusion mismatch decreased on opening the pleura, and that neither opening the pleura nor the subsequent lung surgery (both lungs being ventilated) caused any clinically important derangements in haemodynamics or oxygenation.

Thiopental loading during controlled hypotension for intracranial aneurysm surgery.

In this study we report our clinical experience with supplementary thiopental loading, based on 30 patients undergoing surgery for intracranial aneurysm after a recent episode of subarachnoid haemorrhage. As standard procedure we used pentobarbitone induction, pancuronium relaxation, endotracheal intubation, maintenance with halothane 0.5%, N2O 66% in oxygen, fentanyl, and moderate hypocapnia. A thiopental load of up to 20 mg X kg-1 was supplied while the aneurysm was approached. Satisfactory and well-controlled hypotension was obtained in five cases after thiopental alone, and after thiopental and sodium nitroprusside (SNP) (means +/- s.d.) 1.3 +/- 0.9 microgram X kg-1 X min-1 in the remaining 25 patients. No ECG sign of myocardial ischaemia was observed. One disadvantage was a prolonged recovery period, which in some cases necessitated controlled ventilation for some hours. We conclude that thiopental loading can be used safely as a supplement to neuroanaesthesia for aneurysm surgery.

CARBON DIOXIDE ELIMINATION FROM EACH LUNG DURING ENDOBRONCHIAL ANAESTHESIA: Effects of posture and pulmonary arterial pressure

The ventilation and carbon dioxide elimination of each lung, and pulmonary arterial pressure, were studied in 17 patients during the early phases of anaesthesia for pulmonary surgery. The patients were ventilated mechanically to moderate hypocapnia. Expired tidal volume and carbon dioxide elimination rate of the lung to be operated on, and of the other lung, were similar in the supine position. There was a significant (P less than 0.01) increase in ventilation and a decrease in end-tidal PCO2 of the upper lung after turning the patient on to the side. Simultaneously, the physiological deadspace fraction of tidal volume (VD/VT) increased from 42 to 45% (P less than 0.05). Mean pulmonary arterial pressure (MPAP) increased slightly as surgery on the chest wall commenced. A concomitant increase of carbon dioxide elimination from the upper lung occurred also, although the distribution of ventilation, between the lungs, was unchanged in comparison with the conditions during undisturbed anaesthesia. Individual changes in MPAP (delta MPAP) and corresponding changes in VD/VT (delta (VD/VT)) were negatively correlated (r = -0.68, P less than 0.01). The regression equation was delta (VD/VT) (%) = 0.7 - 0.83 X delta MPAP (mmHg). It was concluded that variations in pulmonary arterial pressure during surgical stimulation may significantly affect the pattern of carbon dioxide elimination in the lungs. However, there was no evidence that these effects were important clinically.

Effects of CO2 to modulate the norepinephrine constrictor response in isolated perfused rabbit carotid artery.

It has been suggested that large cerebral arteries contribute to cerebral vascular resistance and thus participate actively in the regulation of cerebral blood flow (CBF) during changes in arterial carbon dioxide tension (PCO2). In order to test this hypothesis, 3-cm segments of carotid artery from adult male rabbits were studied. The segments were mounted in a chamber with constant surrounding pressure and temperature and perfused at constant pressure. Inflow pressure, outflow pressure, and outflow rate were measured and values of resistance (R) were calculated before (C) and after stimulation with two sequential norepinephrine concentrations: 4 X 10(-6) M (NE1), 1 X 10(-5) M (NE2). During each sequence, the PCO2 of the surrounding and perfusion media were held equal and constant at one of four levels. The following mean R values were obtained: (table; see text) Symbols (*) represent significance (p less than 0.05) between the indicated R and the corresponding normocapnic (PCO2 = 35 mm Hg) R. Hypercapnia (PCO2 = 61 mm Hg) enhanced the response to both NE1 and NE2. Moderate hypocapnia (PCO2 = 27 mm Hg) had no effect. These studies support the claim that large cerebral arteries contribute to CBF regulation during PCO2 changes. However, the effect of large cerebral arteries may not be significant during PCO2 variations of less than 20 mm Hg.

Lactic acidosis in the brain: occurrence, triggering mechanisms and pathophysiological importance.

Brain cells are better protected against systemic acidosis (and alkalosis) than most other cells since they are surrounded by an extracellular fluid which is, in itself, subjected to pH regulation. For all practical purposes, therefore, cerebral intracellular acidosis is endogenous and arises when lactic acid accumulates. This occurs in three main conditions: hypocapnia, epileptic seizures, and hypoxia plus ischaemia. In the first of these, metabolic acidosis is compensatory but in the other two, a moderate or pronounced decrease in pH occurs. In all three, increased glycolytic rate involves activation of phosphofructokinase secondarily to a raised intracellular pH (moderate hypocapnia) or to a perturbation of cerebral energy state (seizures and hypoxia plus ischaemia). In seizure states, accumulation of lactic acid is usually moderate (about 10 mumol g-1). In complete ischaemia, the acidosis is only slightly more pronounced. However, in severe incomplete ischaemia, and in severe hypoxia, the continued substrate supply can lead to excessive accumulation of lactic acid (30-50 mumol g-1). When this occurs, the acidosis contributes to irreversible cell damage.

Effect of two levels of induced hypocapnia on cerebral autoregulation in the acute phase of head injury coma.

In eight unconscious and artificially ventilated patients with severe head injury, cerebral autoregulation (CA) was tested during angiotensin infusion, before and after a reduction of Paco2. Intracranial pressure (ICP) and systemic arterial pressure (SAP) were continuously recorded. Regional cerebral blood flow (rCBF) was measured by the intracarotid Xe133 washout technique as initial slope index, stochastic and compartmental analysis. In contradistinction to previous human studies, we found a preserved CA during moderate hypocapnia (mean Paco2 34.2 mmHg) while the CA after a further decrease in Paco2 (mean value 23.1 mmHg) was lost. The apparently preserved CA may be a "false phenomenon" due to a regional increase in ICP. After a decrease in Paco2, an association between high CO2 reactivity and rCBF increase during angiotensin was disclosed, while a decreased or unchanged rCBF was observed in regions with inverse steal or abolished CO2 reactivity. The study indicates that the interpretation of CA is facilitated by performing the test during two levels of Paco2, but the presence of impaired autoregulation in the acute phase of head injury indicates that deliberate increase in SAP may be dangerous, as it may provoke an increase of regional ICP and brain oedema.

Normocapnic Ventilation Using the Circle System

A formula is derived for maintaining normocapnia during controlled ventilation using a circle system without carbon dioxide absorption. In a series of 70 patients, unselected in terms of age, sex, obesity, ASA status, body position during operation, type of anaesthetic administered or type of circle system used, it was found that a total fresh gas flow of 50 ml/kg body weight/min and a minute ventilation of 120 to 150 ml/kg body weight at a rate of 10 to 12/min achieved normocapnia. For moderate hypocapnia a total fresh gas flow of 60 ml /kg body weight/min and a minute ventilation of 120 ml/kg at a rate of 10–12/min is suggested.

Normocapnic ventilation using the circle system.

A formula is derived for maintaining normocapnia during controlled ventilation using a circle system without carbon dioxide absorption. In a series of 70 patients, unselected in terms of age, sex, obesity, ASA status, body position during operation, type of anaesthetic administered or type of circle system used, it was found that a total fresh gas flow of 50 ml/kg body weight/min and a minute ventilation of 120 to 150 ml/kg body weight at a rate of 10 to 12/min achieved normocapnia. For moderate hypocapnia a total fresh gas flow of 60 ml/kg body weight/min and a minute ventilation of 120 ml/kg at a rate of 10-12/min is suggested.

Electroencephalographic activity in children under enflurane anesthesia.

EEG, end-tidal CO2, neck muscle EMG, eye movements, and ECG were recorded in 17 children undergoing enflurane anesthesia combined with N2O and O2. All subjects were classified in the lowest risk group and had normal pre-anesthetic EEG recordings. Eleven subjects were breathing spontaneously and six were under controlled ventilation. Thirteen subjects were hyperventilated for short periods. As previously reported for adults, various signs of increased central nervous excitability appeared. At the enflurane concentration of 4% all three cases with PaCO2 below 32 mmHg showed generalized high voltage epileptic activity of grand mal type followed by several minutes of postictal slowing. One of these subjects also showed motor manifestations of the electrographic seizure activity. At 3% enflurane, three out of eight subjects showed electrographic seizure activity of poly-spike-suppression type. One of these children also had motor manifestations during this type of seizure activity at a PaCO2 of 31 mmHg. The results indicate that electrographic seizure activity is common among children with moderate hypocapnia at enflurane concentrations of 3% or more.

Regional cerebral blood flow and intraventricular pressure in acute head injuries.

Twelve patients who were comatose after head injuries were studied with serial determinations of regional cerebral blood flow, jugular PO(2) tension, and intraventricular pressure. These determinations began a few hours after the injury, and were followed throughout the clinical course. Diffuse derangement of cerebral vasomotor regulation is confirmed after severe head trauma, which may contribute to deterioration and poor prognosis, and which indicates a need for therapeutic maintenance of rich oxygenation, hyperventilation with moderate hypocapnia, and steady blood pressure. Continuous recording of IVP (eventually sensitized by fluid infusion or CO(2) inhalation tests) may give an early indication of the subsequent clinical state and may suggest the need to submit the patients to further investigative and therapeutic procedures.