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Biomedical subjects

A M Lam

Publications and source records attributed to A M Lam.

At least 127 records · Page 7Linked to original sources

Electrocardiographic changes during and after isoflurane-induced hypotension for neurovascular surgery.

We evaluated the effects of isoflurane anaesthesia and induced hypotension in 33 neurosurgical patients by electrocardiographic monitoring and serial cardiac enzyme measurements. An electrocardiogram (ECG) and serum enzymes were obtained preoperatively, intraoperatively and postoperatively in the recovery room and for three consecutive days. ECG leads II, V1 and V5 were monitored continuously during anaesthesia. Patients who had had a subarachnoid haemorrhage and a high incidence of abnormal preoperative ECG (42 per cent). Ten patients developed ECG changes intraoperatively, but these changes were unrelated to isoflurane-induced hypotension. Fifty-three per cent of patients developed an abnormal postoperative ECG. These abnormalities consisted mostly of nonspecific ST segment or T wave changes. At no time was there an elevation in cardiac enzyme activity. We found that nonspecific ECG changes are relatively common in patients undergoing vascular neurosurgical procedures. There was no enzymatic evidence of myocardial infarction and we can only speculate that these ECG changes are related to intracranial surgical manipulation.

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The effect of high-dose mannitol on serum and urine electrolytes and osmolality in neurosurgical patients.

The effect of mannitol on serum and urine electrolytes and osmolality was investigated intraoperatively in neurosurgical patients. Patients in Group A (n = 7) received 1 gm . kg-1 of 20 per cent mannitol ("low"-dose) and in Group B, (n = 7) 2 gm . kg-1 ("high"-dose). There was a significant decrease in serum sodium and bicarbonate, and a significant increase in serum osmolality in both groups after mannitol administration. The decrease in serum sodium and the increase in serum osmolality were significantly greater in patients receiving the larger dose of mannitol. The infusion of low-dose mannitol resulted in a slight decrease in serum potassium. In contrast, after high-dose mannitol there was a significant rise in serum potassium reaching a maximum mean increase of 1.5 mmol . l-1. Urine electrolyte concentration and osmolality showed a similar decrease in both groups. The significant changes that occurred with the administration of mannitol were of short duration in these patients with normal cardiac and renal function. The clinically most important change is the increase in serum potassium with high-dose mannitol. The exact mechanism of this increase remains unclear.

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The effects of cimetidine and ranitidine with and without metoclopramide on gastric volume and pH in morbidly obese patients.

The efficacy of preanaesthetic intravenous cimetidine versus ranitidine with and without metoclopramide for acid aspiration prophylaxis was assessed in 60 morbidly obese patients in a double-blind manner. Group 1 patients received cimetidine 300 mg + saline. Group 2 patients received cimetidine 300 mg + metoclopramide 10 mg. Group 3 patients received ranitidine 100 mg + saline. Group 4 patients received ranitidine 100 mg + metoclopramide 10 mg. Gastric fluid was aspirated for analysis of volume and pH following induction of anaesthesia. All four premedication regimens were equally effective in reducing the gastric volume and acidity and the inclusion of metoclopramide had no additive effect. Although statistically not significant, two patients in the cimetidine groups remained at risk (volume greater than 25 ml and pH less than 2.5) while no patients in the ranitidine groups remained so.

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The effect of isoflurane-induced hypotension on cerebral blood flow and cerebral metabolic rate for oxygen in humans.

Deliberate hypotension was induced with isoflurane (mean inspired concentration 2.3 +/- 1.0%) in 12 patients undergoing craniotomy for clipping of cerebral aneurysms. Global cerebral blood flow (CBF) was measured before, during, and after hypotension. Arterio-venous O2 content difference was measured concomitantly, and the cerebral metabolic rate for oxygen (CMRO2) was calculated from these data. Mean arterial pressure (MAP) was reduced from 78 +/- 5 mmHg to 51 +/- 7 mmHg and then returned to 82 +/- 8 mmHg. Mean CBF before hypotension was 49 +/- 14 ml X 100 g-1 X min-1 and was unchanged during (45 +/- 12 ml X 100 g-1 X min-1) and after (49 +/- 15 ml X 100 g-1 X min-1) hypotension. The CMRO2 before hypotension was 2.0 +/- 0.6 ml X 100 g-1 X min-1. This was statistically significantly (P less than 0.025) reduced to 1.5 +/- 0.5 ml X 100 g-1 X min-1 during hypotension and then returned to 2.2 +/- 0.6 ml X 100 g-1 X min-1 on return to normotension. This indicates that the global cerebral O2 supply-demand balance was favorably influenced by isoflurane. No complications could be attributed to the hypotensive technique. We conclude that, with regard to global cerebral oxygenation, isoflurane is a safe agent with which to induce hypotension during neurosurgery.

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Monitoring of brainstem auditory evoked potentials during basilar artery occlusion in man.

Brainstem auditory evoked potentials (BAEP) were recorded during surgery as a monitor of brainstem function in three patients undergoing posterior fossa surgery for clipping of basilar aneurysms. In two patients, ligation of the basilar artery, and of a vertebral artery, was associated with deterioration in BAEP and resulted in postoperative brainstem dysfunction. In the third patient, postoperative transient neurological dysfunction occurred following temporary occlusion of the basilar artery and this correlated with intra- and postoperative changes in BAEP. BAEP monitoring is recommended where temporary or permanent occlusion of the vertebrobasilar system is planned.

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The effects of isoflurane and isoflurane-nitrous oxide anesthesia on brainstem auditory evoked potentials in humans.

Monitoring of brainstem auditory evoked potentials (BAEP) during neurological surgery can provide useful information. However, in order to interpret intraoperative BAEP changes, it is necessary to delineate the influence of anesthesia, including inhalation agents. In this study, we examined the influence of isoflurane and isoflurane-nitrous oxide anesthesia on BAEP in ten healthy volunteers during normothermic, normocapnic, and normotensive conditions. Isoflurane significantly increased the latencies of peaks III, IV, and V at all end-tidal concentrations studied (1.0%, 1.5%, and 2.0%). Addition of 50% nitrous oxide did not influence these findings. The increase in latencies with isoflurane anesthesia, however, was nonlinear and appeared to plateau after 1.5%. We suggest that during isoflurane anesthesia, an intraoperative increase in peak V latency beyond 1.0 msec is best explained by factors other than direct effects of isoflurane.

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Effect of cimetidine premedication on morphine-induced ventilatory depression.

The potential respiratory interaction between morphine and cimetidine was studied by determining resting ventilation, PETCO2 and ventilatory response to added carbon dioxide in eight healthy volunteers on three separate occasions following administration of : (1) cimetidine 600 mg p.o., (2) morphine 10 mg IM, (3) morphine 10 mg IM preceded by cimetidine 600 mg p.o. Individual entry into the study was randomized and separated by at least one week. All measurements were determined at time 0, 30, 60, 120, 180, 240, 360, 480, 600, 720 minutes and at the end of 24 hours. In addition, serum morphine levels were measured in six subjects during the first six hours following morphine administration. Cimetidine alone had negligible respiratory effects. Morphine alone reduced resting ventilation, elevated PETCO2 and reduced the ventilatory response to added CO2, while the morphine-cimetidine combination caused a more profound depression of the CO2 response and delay in its recovery. No significant difference between resting ventilation and PETCO2 was observed. We conclude that cimetidine premedication interacts with morphine to prolong the respiratory depression but the magnitude of this interaction is small and clinically insignificant in healthy subjects. Caution, however, should be exercised in susceptible patients.

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Continuous in-vivo monitoring of arterial oxygen tension in a patient treated with bleomycin.

Patients receiving bleomycin therapy may develop pulmonary fibrosis. The risk of fibrosis is increased by the administration of general anaesthesia and fatal cases with pulmonary lesions resembling those of "oxygen toxicity" have been reported. The causes are not entirely clear but the enriched inspired oxygen given intraoperatively or postoperatively has been identified as an etiological factor. Optimal intraoperative management thus requires the administration of the lowest inspired oxygen fraction (FIO2) compatible with adequate oxygenation. To achieve this aim safely, continuous in vivo monitoring of arterial oxygen tension would be preferable to intermittent sampling of blood gases. We report the successful management of a patient undergoing thoracotomy following bleomycin therapy using an intravascular PO2 sensor to monitor arterial oxygen tension continuously. The uses and limitations of the PO2 sensor are discussed.

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Isoflurane-induced hypotension does not cause impairment in pulmonary gas exchange.

Induced hypotension during anaesthesia can result in deterioration in gas exchange with increases in intrapulmonary shunting and physiological deadspace. Cardiovascular stability has been previously demonstrated with isoflurane-induced hypotension but the effects on gas exchange have not been carefully studied. We have examined the shunt fraction (QS/QT) and physiological dead space to tidal volume ratio (VD/VT) before, during and following deliberate hypotension in twelve patients. Group I (n = 6) received an isoflurane-oxygen-air mixture with an FIO2 of 0.5 while Group II (n = 6) received an isoflurane-oxygen mixture with an FIO2 of 1.0. Mean blood pressure was reduced from 76 +/- 2 mmHg to 47 +/- 2 mmHg in the combined group. Neither QS/QT nor VD/VT changed significantly during the hypotensive state in either group. We conclude that isoflurane induced hypotension is associated with minimal pulmonary derangement.

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Blood solubility of isoflurane measured by a multiple gas phase equilibration technique.

Using a multiple gas phase equilibration technique, we determined the solubility of isoflurane in arterial blood at 37 degrees C obtained from patients anaesthetized with isoflurane. Goodness of fit of individual sets of data to a predicted decline of isoflurane concentration in successive equilibrated gas phases and reproducibility of results indicate that the analytical technique was acceptably accurate. In blood samples taken from twenty-three patients undergoing minor surgical procedures, the blood/gas partition coefficient of isoflurane was 1.20 +/- 0.08 (mean +/- S.D.). Individual values were not detectably related to absolute tension of isoflurane, preoperative haemoglobin concentration nor patient age. In samples taken from twenty neurosurgical patients, the blood/gas partition coefficient was slightly less, 1.14 +/- 0.09 (p less than 0.05), a difference we attribute to the effect of previously infused mannitol. In vitro, blood solubility of isoflurane was decreased by haemodilution with normal saline, mannitol 20 per cent or plasma, was increased by hypothermia (30 degrees C) and was decreased by hyperthermia (40 degrees C). We conclude that the solubility of isoflurane in human blood is approximately half that of halothane.

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Cardiovascular effects of isoflurane-induced hypotension for cerebral aneurysm surgery.

Deliberate hypotension was induced with isoflurane in 13 patients, undergoing craniotomy for clipping of aneurysms. Cardiovascular function and gas exchange were monitored before, during, and after hypotension. In all cases, the desired level of hypotension [40 +/- 1 (SEM) mm Hg] was achieved readily with prompt onset (5.7 +/- 1.0 min) and recovery (6.3 +/- 0.7 min). Cardiac output during hypotension (4.6 +/- 0.3 L/min) was not significantly different from the control normotensive value (4.80 +/- 0.3 L/min). Gas tensions during hypotension and during normotension were; PaO2 116 +/- 6 and 111 +/- 8 mm Hg; PaCO2 33 +/- 1 and 34 +/- 1 mm Hg; respectively. No complication could be attributed to the use of isoflurane. We conclude that isoflurane can be employed safely and effectively as a hypotensive agent in neurosurgery.

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Respiratory effects of nitrous during enflurane anesthesia in humans.

The authors measured resting ventilation, the ventilatory response to added CO2, the VD/VT ratio, the rate of carbon dioxide output, and arterial PCO2 in four healthy volunteers, awake and anesthetized with, in order (I) enflurane 0.4 MAC with nitrous oxide 70 per cent, (II) enflurane 1.1 MAC with nitrous oxide 70 per cent, and (III) enflurane 1.1 MAC alone. Enflurane 1.1 MAC reduced ventilation and the response to added CO2 markedly, increased the VD/VT radio, reduced rate of CO2 output, and elevated values of PaCO2 from 41 +/- 1 to 65 +/- 3 mmHg (mean +/- SEM). Enflurane 1.1 MAC with nitrous oxide 70 per cent had similar effects. Enflurane 1.1 MAC with nitrous oxide 70 per cent had similar effects. Enflurane 0.4 MAC with nitrous oxide 70 per cent caused much smaller changes in each measured respiratory variable, increasing PaCO2 values to only 49 +/- 1 mmHg. The results indicate that enflurane 1.1 MAC alone is too potent a depressant of alveolar ventilation to permit spontaneous breathing, but that the "equi-anesthetic" enflurane 0.4 MAC with nitrous oxide 70 per cent may not be. The magnitude of the beneficial respiratory effects of substituting nitrous oxide for an equivalent amount of vapor is substantially greater with enflurane than with either halothane or isoflurane.

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