Measurement of cerebral blood flow and volume with positron emission tomography during isoflurane administration in the hypocapnic baboon.

Using positron emission tomography, cerebral blood flow (CBF) and cerebral blood volume (CBV) were measured after the addition of isoflurane (1.3 vols %, end-tidal concentration) to neuroleptanesthesia (fentanyl/droperidol) in hypocapnic baboons. The study was designed to determine whether isoflurane, when administered during hypocapnia, acted as a cerebral vasodilator to increase either CBF or CBV. Mean arterial pressure was maintained within 10% of preisoflurane levels with an angiotensin infusion. In the first protocol (A), CBF and CBV were measured as close together in time as possible in order to detect divergent effects of isoflurane on these variables. When PaCO2 was reduced from 40 mmHg to 25 mmHg, CBF decreased from 44 +/- 4 to 31 +/- 4 ml.100 g-1.min-1 (P less than 0.05) and CBV decreased from 3.1 +/- 0.3 to 2.6 +/- 0.3 ml/100 g (P less than .05). Neither CBF nor CBV was significantly changed by the addition of isoflurane. In the second protocol (B), serial CBV scans were performed frequently during the addition of isoflurane in a fashion designed to detect transient changes in CBV at the time isoflurane was first added to the breathing circuit. Induction of hypocapnia again reduced CBV from 3.1 +/- .3 to 2.7 +/- .2 ml/100 g, (P less than .05) and addition of isoflurane did not change CBV. From these results the authors conclude that in the normal hypocapnic baboon the addition of 1.3% isoflurane does not significantly change cerebral blood flow or volume.

Pulling versus guiding: a modification of retrograde guided intubation.

We describe a modification of retrograde guided intubation. With the help of a gliding knot fixed around the side hole of the tracheal tube, we use the catheter to pull and guide the tracheal tube down the larynx and trachea. The technique offers several advantages: it is surprisingly fast, relatively atraumatic, easy to perform, and eliminates most causes of failure.

Changes in CSF pressure after mannitol in patients with and without elevated CSF pressure.

In view of the current concern that rapid infusion of mannitol might initially aggravate intracranial hypertension, the effects of a mannitol infusion on lumbar cerebrospinal fluid pressure (CSFP) were investigated in 49 patients. The studies were performed when the patients were under general anesthesia prior to elective craniotomy for tumor resection or intracerebral aneurysm clipping. The patients were divided into two groups: 24 patients with normal CSFP (Group I, mean CSFP 10.5 mm Hg) and 25 with raised CSFP (Group II, mean CSFP 20.8 mm Hg). Measurements of CSFP, mean arterial blood pressure (MABP), and central venous pressure (CVP) were made serially during and after the infusion of 20% mannitol (1 gm.kg-1 infused over a 10-minute interval). In both groups, mannitol infusion provoked a fall in MABP and an increase in CVP. An immediate decrease [corrected] in CSFP was observed in Group II, whereas CSFP increased transiently but significantly in Group I. Analysis of the arterial and venous driving pressures which contribute to CSFP suggests that the transient increase in CSFP after mannitol in Group I was partly due to the increase in CVP. The presence of intracranial hypertension may thus alter the CSFP response to arterial and venous pressure changes. Cerebral blood volume (CBV) was measured in dogs in a separate study analogous to the human protocol. The CBV increased approximately 25% over control values after mannitol infusion both in the normal animals and in those with CSFP raised by an epidural balloon. The response of the CSFP to mannitol infusion differed between both groups in a fashion similar to that observed in the human subjects. Thus, differences in CBV changes after mannitol do not account for the difference in CSFP response between normal subjects and those with raised CSFP.

Cerebral blood volume is increased in dogs during administration of nitrous oxide or isoflurane.

Positron emission tomography was used to study the effects of nitrous oxide (N2O) and isoflurane on regional cerebral blood volume (rCBV) in dogs during normocapnia and hypocapnia. Regional cerebral blood volume was measured serially during the addition of 50% N2O to a background anesthetic of fentanyl in normocapnic (group 1) and hypocapnic (PaCO2 25 mmHg, group 2) dogs. In each group, after 15 min of N2O administration accompanied by rCBV measurement, elimination of N2O with 100% O2 was continued for 15 min. This was followed by introduction of 2% isoflurane (no N2O), again accompanied by serial measurements of rCBV. In the normocapnic animals, the addition of 50% N2O caused an 11% increase in rCBV (6.1 +/- 1.4 to 6.8 +/- 1.0 ml/100 g, P less than 0.02) while 2% isoflurane caused a 36% increase (6.1 +/- 1.3 to 8.0 +/- 1.7 ml/100 g, P less than 0.02). The initial induction of hypocapnia during infusion of fentanyl in group 2 animals was associated with a 17% decrease in rCBV. In the hypocapnic dogs, there was no change in rCBV when N2O was introduced; however, an increase of 15% occurred following the addition of isoflurane (3.9 +/- 0.6 to 4.5 +/- 0.7 ml/100 g, P less than 0.02). Isoflurane, even during hypocapnia, may increase cerebral blood volume which in some circumstances may lead to an increase in ICP.

Does a bolus of mannitol initially aggravate intracranial hypertension? A study at various PaCO2 tensions in dogs.

In two groups of anaesthetized dogs, with (n = 28) or without (n = 28) induced intracranial hypertension, we compared the effects on intracranial pressure (ICP) of the rapid administration of mannitol 2 g kg-1 i.v. at PaCO2 2.7, 4.0, 5.3, and 6.7 kPa (n = 7). In dogs with no induced intracranial hypertension, ICP increased during the administration of mannitol, reached a peak at 2 min after infusion, and then gradually decreased (P less than 0.05). More marked changes in ICP were observed in response to higher values of PaCO2 (P less than 0.05). In dogs with induced intracranial hypertension, the rapid infusion of mannitol caused an exponential decrease in ICP, without initial increase, which was significantly steeper at higher values of PaCO2 (P less than 0.05). This was followed by a more gradual decrease which achieved pre-balloon inflation values 10 min after infusion. We postulate that the absence of the initial increase in ICP is the result of a concomitant decrease in arterial pressure, a reduction in the volume-pressure response of the brain, the failure of mannitol to dilate further the cerebral arterial vascular bed and a hitherto unnoticed early water-drawing effect. Our study confirmed the safety of rapidly expanding the circulating blood volume with mannitol in circumstances of increased ICP in dogs.

Selective neuromuscular blockade for intraoperative electrocorticography.

Local anesthesia is advocated for cortical mapping in certain neurological procedures. Occasionally, however, a modified general anesthetic is necessary. We describe a technique of balanced anesthesia in which the arm opposite to the craniotomy is selectively isolated from the effect of the neuromuscular blocking agent and hence preserves its motor response to cortical stimulation. The technique secures complete immobility of the patient during mapping of the brain, shortens the stimulation time, facilitates the localization of the motor cortex, precludes the development of full-blown seizures, increases safety and is well tolerated.

Effects of rapid mannitol infusion on cerebral blood volume. A positron emission tomographic study in dogs and man.

Positron emission tomography was used to study the effect of a rapid infusion of mannitol on cerebral blood volume (CBV) in five dogs and in three human subjects. The ability of mannitol to reduce intracranial pressure (ICP) has always been attributed to its osmotic dehydrating effect. The effects of mannitol infusion include increased osmolality, total blood volume, central venous pressure (CVP), and cerebral blood flow, and decreased hematocrit, hemoglobin concentration, serum sodium level, and viscosity. Mannitol's ability to dilate the cerebral vasculature, either directly or indirectly, and thus to transiently increase ICP, is a subject of controversy. By in vivo labeling of red cells with carbon-11, the authors were able to demonstrate an early increase in CBV in dogs of 20%, 27%, and 23% (mean increase, p less than 0.05) at 1, 2, and 3 minutes, respectively, after an infusion of 20% mannitol (2 gm/kg over a 3-minute period). The animals' muscle blood volume increased by 27% (mean increase, p less than 0.05) 2 minutes after infusion. In the human subjects, lower doses and a longer duration of infusion (1 gm/kg over 4 minutes) resulted in an increase in CBV of 8%, 14% (p less than 0.05), and 10% at 1, 2, and 3 minutes, respectively, after infusion. In dogs, ICP increased by 4 mm Hg (mean increase, p less than 0.05) 1 minute after the infusion, before decreasing sharply. The ICP was not measured in the human subjects. Hematocrit, hemoglobin, sodium, potassium, osmolality, heart rate, mean arterial pressure (MAP), and CVP were measured serially. Results of these measurements, as well as the significant decrease in MAP that occurred after mannitol infusion, are discussed. This study demonstrated that rapid mannitol infusion increases CBV and ICP. The increase in muscle blood volume, in the presence of a decreased MAP and an adequate CVP, suggests that mannitol may have caused vasodilation in these experiments.

The effects of rapid infusions of saline and mannitol on cerebral blood volume and intracranial pressure in dogs.

The role of osmotic brain dehydration in the early reduction of intracranial pressure (ICP) following mannitol administration has recently been questioned and a decrease in cerebral blood volume (CBV) proposed as the mechanism of action. To evaluate this hypothesis, relative CBV changes before and after mannitol infusion were determined by collimated gamma counting across the biparietal diameter of the exposed skull in six dogs. Red blood cells were labelled with chromium-51. Cerebral blood volume (CBV), total blood volume (TBV), ICP, mean arterial pressure (MAP), central venous pressure (CVP), haematocrit and osmolality were serially measured after infusions of 10 ml X kg-1 of normal saline (control study) and of 20 per cent mannitol (mannitol study). The solutions were administered over a two-minute period; a 30-minute equilibration period intervened between the saline and mannitol infusions. We demonstrated that the mannitol infusion was associated with significant increases in relative CBV (25 per cent), ICP (7 mmHg), CVP (11 cm H2O), and TBV (50 per cent). MAP declined significantly (14 per cent) after mannitol infusion. The administration of saline, although associated with an increase in TBV (18 per cent), was not associated with any significant change in CBV, ICP, MAP or CVP. The increase in relative CBV persisted for 15 minutes after mannitol infusion, while the ICP returned to control within five minutes and continued to decrease. This study supports the fact that after rapid mannitol infusion, ICP begins to decrease only once the dehydrating effect has counteracted the increase in brain bulk caused by the increase in cerebral blood volume.

Anaesthetic considerations in percutaneous radiofrequency coagulation of the Gasserian ganglion.

This study determined the cardiovascular effects of percutaneous radiofrequency coagulation of the Gasserian ganglion, performed under neuroleptanalgesia and intermittent ultrashort-acting barbiturate anaesthesia. Twelve ASA physical status class II patients were studied. Highly significant increases in mean heart rate and arterial blood pressure followed the insertion of the cannula electrode into the Gasserian ganglion (p less than 0.001). In six randomly assigned patients severe tachycardia and hypertension also accompanied the progress of the thermal lesion (p less than 0.0001). Three patients developed premature ventricular contractions, and two developed significant ST segment depression. Intravenous nitroglycerin, used during current generation, successfully controlled the hypertensive response in the other six patients. In percutaneous thermocoagulation of the Gasserian ganglion the patient's co-operation is essential. In addition to providing suitable operating conditions for both surgeons and patient, we should also be able to maintain normal and stable cardiovascular haemodynamics. Intravenous nitroglycerin used as an adjunct to light general anaesthesia safely maintained intraoperative normotension. It is also suggested that patients with coronary artery disease be adequately monitored and protected during the procedure.

Use of hypertension and electroencephalographic monitoring during carotid endarterectomy.

Intraoperative hypertension and continuous electroencephalographic (eeg) monitoring were used during 42 carotid endarterectomies performed on 37 patients from 1970 to 1978. Computer spectral analysis of a majority of the electroencephalograms was also performed. Under supplemented nitrous oxide general anesthesia, elevation of the mean arterial blood pressure to 20% above the individual's preoperative mean blood pressure resulted in reversal to normal of an ischemic EEG pattern in 19% of the patients. The authors discuss the benefit of this technique. they present guidelines for patient selection and analyse the data to help the surgeon decide whether to use shunt during carotid endarterectomy.

[Arterial hypotension induced by artificial cardiac pacing under general anaesthesia (author's transl)]. / Hypotension artérielle induite par l'entraînement électrosystolique ventriculaire sous anesthésie générale.

A case of haemodynamic decompensation is reported in a patient with a sick-sinus syndrome on a demand cardiac pacemaker, under-going surgery under general anaesthesia. While systemic arterial blood pressure showed adequate stability under the patient's own sinus drive, it consistently fell by 15 to 20 p. cent when artificial pacing was established. The possible mechanisms are discussed. The drop in arterial blood pressure with artificial pacing is probably due to the loss of the atrial contribution in maintaining adequate cardiac output. In the conscious patient, the resulting decrease in cardiac output is compensated by an increase in the peripheral resistance. Under general anaesthesia, this compensatory mechanism is lost, resulting in a drop in cardiac output and systemic arterial blood pressure. It needs to be emphasized therefore, that the patient who has a permanent pacemaker has significant under-lying cardiovascular disease and, that, continuous monitoring is indicated not only during surgery but also postoperatively until patient has stabilized.

Aetiology and control of cardiovascular reactions during trans-sphenoidal resection of pituitary microadenomas.

Two groups of 12 patients were studied to determine the causes of hypertension during trans-sphenoidal resection of pituitary microadenomas. Two concentrations of lidocaine, 0.5 and 1.0 per cent with epinephrine 1/200,000, were used to infiltrate the nose and upper gingiva. Heart rate, electrocardiogram lead II and systolic and diastolic arterial blood pressures were monitored. Three stages were observed for changes in above parameters: nasal infiltration, nasal dissection and sellar exploration. Highly significant reductions in arterial blood pressure and pulse rate responses to infiltration and nasal dissection were achieved by increasing the lidocaine concentration used for infiltration from 0.5 to 1.0 per cent (p < 0.05). Our findings implicate reflex from nasal stimulation as the main cause of the adverse cardiovascular effects. Only minimal changes accompanied the progress of the intrasellar dissection in both groups.