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Biomedical subjects

A M Lam

Publications and source records attributed to A M Lam.

At least 91 records · Page 5Linked to original sources
PubMed1993

The effect of alfentanil on cerebral blood flow velocity and intracranial pressure during isoflurane-nitrous oxide anesthesia in humans.

BACKGROUND: Intravenous opioids often are used as a component of anesthesia during neurosurgical procedures. However, the cerebrovascular effects of alfentanil administered to patients are controversial. In this study, the effect of alfentanil in patients with and without intracranial pathology was studied. METHODS: Sixteen neurosurgical patients and 16 patients scheduled for orthopedic procedures were studied. Anesthesia was maintained with isoflurane (0.4-0.6 vol% inspired) and nitrous oxide (50%) in oxygen. Within each group, the patients were assigned randomly to receive either 25 or 50 micrograms/kg intravenous alfentanil. During normocapnia and without surgical stimulation, the right middle cerebral artery flow velocity, and mean arterial pressure were measured every minute for 10 min after the administration of alfentanil. In the neurosurgical patients, intracranial pressure, cerebral perfusion pressure, and cerebral arteriovenous oxygen content difference were determined also. Neurosurgical patients received intravenous phenylephrine to maintain mean arterial pressure as needed. RESULTS: There was no significant change in middle cerebral artery flow velocity and arteriovenous oxygen content difference in the neurosurgical patients. In the high-dose group, intracranial pressure increased by 2 mmHg at 4 min but was otherwise unchanged. Despite phenylephrine administration, there was an immediate but transient decrease in mean arterial pressure in the high-dose group and a corresponding decrease in cerebral perfusion pressure. In the orthopedic patients, mean arterial pressure decreased significantly. Middle cerebral artery flow velocity decreased in the high-dose group but remained unchanged in the low-dose group. CONCLUSIONS: Based on the flow velocity and metabolic data, alfentanil is neither a cerebral vasodilator nor a vasoconstrictor in these doses. Furthermore, there was no clinically significant increase in intracranial pressure when alfentanil was administered in either dose.

Adult↗
PubMed1993

Acoustic impedance of the maternal abdomen.

Contact sensors to monitor fetal heart, breathing, and movement sounds with increased sensitivity and bandwidth are under development. To understand the inherent acoustical properties of the maternal abdomen and its interaction with these sensors, the driving-point impedance Z(j omega) was measured in nine women during their last trimester of pregnancy. An electromechanical shaker with a contact area of 2.85 cm2 produced abdominal vibrations between 10 and 500 Hz, and the resulting force and acceleration were measured. After digitally integrating the acceleration signal to obtain the velocity and removing the massive effects of the coupling between the shaker and the abdomen, Z(j omega) was estimated using spectral techniques. The imaginary part of Z(j omega) depicted a dominant compliance effect at low frequencies, a resonance at a frequency of 28 +/- 16 Hz (mean +/- s.d.), and a dominant mass effect at higher frequencies. The real part of Z(j omega) increased steadily with frequency. A series resistance-mass-compliance (R-M-C) circuit modeled these characteristics of Z(j omega) well when R was allowed to exactly mimic the frequency dependence of the real part of Z(j omega). Estimated element values of 6.6 +/- 2.2 x 10(-3) kg for M, 2.1 +/- 1.4 x 10(-3) m/N for C, and roughly 10 Ns/m for R (at resonance) were similar to those estimated for other body tissues such as the thigh but quite different from that of the often-studied chest wall.

Abdomen↗
PubMed1992

Change in cerebral blood flow velocity pattern during induced hypotension: a non-invasive indicator of increased intracranial pressure?

A neurologically intact patient underwent spinal instrumentation under hypotensive anaesthesia 10 days after a mild closed head injury. Transcranial Doppler monitoring of the right middle cerebral artery revealed an abnormal flow pattern, suggesting increased intracranial pressure, impaired autoregulation, or both. Patients with a mild head injury may have altered intracranial haemodynamics and the time course of recovery from these changes is unknown.

Adult↗
PubMed1992

Changes in the rate of formation and resistance to reabsorption of cerebrospinal fluid during deliberate hypotension induced with adenosine or hemorrhage.

Adenosine is recommended for induction of deliberate hypotension. Although its effects on brain vasculature and metabolism and intracranial pressure have been reported, its effects on cerebrospinal fluid dynamics have not. In this study the rate of cerebrospinal fluid formation (Vf), resistance to reabsorption of cerebrospinal fluid (Ra), and electroencephalogram (EEG) activity were determined in rabbits before and during decrease of cerebral perfusion pressure (CPP) with intravenous (iv) adenosine or hemorrhage. In the adenosine group (n = 6), Vf and Ra were determined at control CPP, at CPP of 50, 35, and 28 mmHg achieved with iv adenosine, and at CPP greater than 60 mmHg achieved with iv adenosine combined with iv phenylephrine. In the hemorrhage group (n = 6), Vf and Ra were determined at the first four experimental conditions only. Control values for Vf (9 +/- 3 and 9 +/- 4 microliter.min-1, mean +/- SD) and Ra (428 +/- 567 and 412 +/- 144 cmH2O.ml-1.min) did not differ between groups. In the adenosine group, Vf did not change significantly when CPP was decreased. However, in the hemorrhage group, Vf decreased significantly at CPP of 50 and 35 mmHg and became unmeasurable at CPP of 28 mmHg. Ra did not change significantly in either group. An increase of low-frequency (0.5-3.0 Hz) EEG activity and/or decrease of higher-frequency (3.5-30 Hz) EEG activity occurred at CPP of 28 mmHg in the adenosine group and at CPP of 35 mmHg in the hemorrhage group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1992

Effect of nitrous oxide on intracranial pressure after cranial-dural closure in patients undergoing craniotomy.

After cranial-dural closure, nitrous oxide (N2O) may diffuse into and expand an entrapped volume of intracranial air, thereby increasing intracranial pressure (ICP). We performed a prospective clinical study to determine the effect of continuation of N2O after dural closure on ICP in patients undergoing craniotomies. Patients were randomly assigned in a 1.5:1 ratio into a group in which N2O was continued after dural closure (N2O, n = 15) or a group in which N2O was discontinued and replaced with nitrogen (N2, n = 9) at the time of dural closure. PaCO2 was normal prior to closure, and end-tidal PCO2 was kept constant after dural closure. Ipsilateral ICP was recorded at 5-min intervals after dural closure until completion of skin closure and immediately postoperatively. Presence of intracranial air was determined by head computed tomography scan within the first postoperative hour. ICP at the time of dural closure did not differ between the groups (N2O: 3 +/- 2 mmHg vs. N2:5 +/- 1 mmHg). Intraoperatively, ICP did not change after dural closure, regardless of whether N2O was continued or discontinued. Postoperatively, ICP was reduced, with a significant decrease in ICP (P less than 0.01) observed only in the N2O group. Postoperative computed tomography scans demonstrated the presence of intracranial air in all patients, with most exhibiting a mild to moderate degree of pneumocephalus. We conclude that continuation of N2O after dural closure did not affect ICP during the craniotomy closure. These results suggest that it is not necessary to discontinue N2O prior to dural closure for reasons of avoiding expansion of intracranial air and increasing ICP.

Adult↗
PubMed1992

The influence of propofol with and without nitrous oxide on cerebral blood flow velocity and CO2 reactivity in humans.

The cerebrovascular response to CO2 has been reported to be preserved during propofol anesthesia, but no comparison with awake control values has been made, and the additional influence of N2O has not been investigated. Using the noninvasive technique of transcranial Doppler ultrasonography, this study investigated the cerebrovascular response to varying levels of PaCO2 while awake and during anesthesia with propofol and propofol/N2O. Seven adults without systemic diseases undergoing nonneurologic surgery were studied. A pulsed-wave Doppler monitor was used to measure the mean middle cerebral artery flow velocity (Vmca) during varying levels of PaCO2 (25-55 mmHg) under the following conditions: 1) awake; 2) propofol 2.5 mg.kg-1 bolus followed by continuous infusion of 150 micrograms.kg-1.min-1; and 3) propofol as in the condition above plus 70% N2O. During the awake study condition, hypocapnia was induced by voluntary hyperventilation, and hypercapnia was induced with rebreathing of 7% CO2 in a closed circuit. During the anesthetized study conditions, hypocapnia and hypercapnia were induced by adjustment of minute ventilation. A minimum of five to six simultaneous Vmca and PaCO2 measurements were obtained under each of the study conditions. Systemic blood pressure was monitored via a radial arterial catheter, and phenylephrine was administered if mean arterial blood pressure decreased below 60 mmHg (phenylephrine was used in three of five patients in the propofol-N2O group). Linear regression and analysis of covariance were used for statistical analysis of Vmca-PaCO2 relationships.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Autoregulation of cerebral blood flow in response to adenosine-induced hypotension in dogs.

During induced hypotension for surgical procedures, cerebral blood flow (CBF) autoregulation and cerebrovascular responsivity to CO2 may be impaired-changes that appear to be agent-specific. Adenosine is a potent endogenous systemic vasodilator and has been investigated as a hypotensive agent. In this study in dogs we investigated cerebral vascular responses to graded decreases of cerebral perfusion pressure (CPP) (100%, 60%, 45%, and 35% of control CPP) during normocapnia (PaCO2 = 37 mm Hg) and hypocapnia (PaCO2 = 21 mm Hg). CBF was measured using the venous outflow technique. Six mongrel dogs were anesthetized with halothane (0.6% inspired) and nitrous oxide (70%) in oxygen and studied during both normocapnic and hypocapnic hypotension. The entry sequence was randomized with >/= 1 h of recovery between normocapnia and hypocapnia. Hypocapnia reduced control CBF from 60.6 +/- 7.1 to 45.1 +/- 5.4 ml 100 g min (mean +/- SEM, p <0.05) during normotension. CBF was unchanged from control values during both graded normocapnic and hypocapnic hypotension until CPP reached 60% of control CPP (50 and 47 mm Hg for normocapnia and hypocapnia, respectively). Thereafter CBF decreased significantly from control values at 45% (37 mm Hg for both groups) and 35% (29 mm Hg for both groups) of control CPP. The lower limit of CBF autoregulation derived by applying linear regression analysis to the CBF-CPP relationship above and below the inflexion point was similar under both experimental conditions (60 +/- 1% of control CPP during normocapnia and 63 +/- 3% of control CPP during hypocapnia). CBF was significantly greater during normocapnia compared with hypocapnia at all levels of CPP, except at 35% of control when the values were similar. Cerebral metabolic rate was unchanged throughout the study. We conclude that neither CBF nor CO2 responsivity is appreciably altered during adenosine-induced hypotension when GPP remains above the lower limit of autoregulation of CBF.

Journal Article↗
PubMed1992

Ketamine decreases cerebral infarct volume and improves neurological outcome following experimental head trauma in rats.

In brain injury, concentrations of extracellular excitatory amino acids are increased and stimulate glutamate receptors in general and the N-methyl-D-aspartate (NMDA)-preferring subtype in particular. That stimulation causes substantial calcium influx, which appears to initiate a cascade of events leading to neuronal death. Blockage of NMDA receptors with specific antagonists or noncompetitive ion channel blockers provides protection against excitatory amino acid-induced neurotoxicity. We previously reported that the NMDA receptor antagonist dizocilpine maleate improved the neurological severity score (NSS) after head trauma in rats. The present study was designed to determine whether ketamine, a NMDA receptor antagonist like dizocilpine maleate, improves neurological outcome following head trauma in rats. Thirty-two male Sprague-Dawley rats (235-250 g) were divided into four groups. Groups A and B were surgically prepared only. Groups C and D were surgically prepared and then a nonpenetrating impact was delivered to the cranium over the left hemisphere. Groups A and C received no treatment. Groups B and D were treated with ketamine, 180 mg/kg i.p., 1 h after head trauma. The NSS was determined at 1, 2, 4, 10, 24, and 48 h following head trauma. After killing at 48 h, cortical slices were taken adjacent to the lesion on the traumatized hemisphere and from comparable sites on the nontraumatized hemisphere to measure the tissue specific gravity and water content. Brains were then placed in 4% formaldehyde and the volume of hemorrhagic necrosis measured 4 days later. Head trauma increased the NSS and, in the traumatized hemisphere, decreased the specific gravity, increased the water content, and caused cerebral infarction. With ketamine, the NSS at 24 and 48 h following head trauma was 7.4 +/- 2.6 and 6.7 +/- 2.6 (mean +/- SEM), respectively, significantly improved compared to the NSS in the untreated group of 12.6 +/- 2.6 and 11.3 +/- 2.6, respectively (p <0.02, Mann-Whitney U test). With ketamine, the volume of hemorrhagic necrosis was 88.0 +/- 23.1 mm, significantly less than that in the untreated group (147.4 +/- 22.4 mm; p <0.05, unpaired t test). The brain tissue specific gravity and water content at 48 h and the rectal temperature at 4 and 48 h after head trauma were not significantly different between treated and untreated groups. It is concluded that in this model of closed cranial impact, ketamine improves neurological outcome and decreases the volume of hemorrhagic necrosis without altering brain edema.

Journal Article↗
PubMed1991

Comparison of integrated evoked EMG between the hypothenar and facial muscle groups following atracurium and vecuronium administration.

In 17 healthy patients undergoing O2.N2O.isoflurane anaesthesia, following atracurium or vecuronium administration, we compared simultaneous integrated evoked electromyograms (IEEMGs) during spontaneous recovery of the adductor digiti minimi (ADM) and orbicularis oris (OOM) muscle groups in response to train-of-four (TOF) stimulation of the ulnar and facial nerves, respectively. In all patients, the onset of neuromuscular recovery occurred first in the OOM. The time required to recover to a T4/T1 = 0.70 +/- 0.01 (SD) was earlier in the OOM compared with the ADM muscles in both the atracurium (33.4 +/- 5 vs 46.5 +/- 8, P less than 0.005) and vecuronium (46.5 +/- 12 vs 60.3 +/- 20, P less than 0.005) groups. When the OOM attained a T4/T1 = 0.70 +/- 0.01, the simultaneous T4/T1 in the ADM was 0.29 +/- 0.15 (P less than 0.05) in the atracurium group and 0.41 +/- 0.16 (P less than 0.01) in the vecuronium group. We conclude that (1) the facial muscles (OOM) recover earlier than the hypothenar muscles (ADM) and (2) an EMG T4/T1 = 0.70 in the facial muscles may not indicate adequate recovery of neuromuscular function.

Adolescent↗
PubMed1991

Monitoring electrophysiologic function during carotid endarterectomy: a comparison of somatosensory evoked potentials and conventional electroencephalogram.

There is no consensus as to the most appropriate monitor for detecting ischemia during carotid endarterectomy. Accordingly, simultaneous 16-channel continuous electroencephalogram (EEG) and somatosensory evoked potential (SSEP) monitoring were performed in 64 normocapnic patients undergoing carotid endarterectomy and anesthetized with isoflurane or halothane-nitrous oxide (supplemented with fentanyl). Recordings were obtained before, during, and for 15 min after cross-clamping of the internal carotid artery. Internal shunt was not used in any patient, regardless of EEG and SSEP changes. Significant amplitude reduction in the cortical component of the primary negative peak (greater than 50%) in SSEP occurred in 6 patients, and an increase in central conduction time (CCT) (greater than 1 ms) occurred in 5 patients. Major EEG changes occurred in 6 patients, 4 of whom also had SSEP changes. Two patients had transient neurologic deficits postoperatively, with both having SSEP changes (amplitude reduction greater than 50%), whereas one had EEG changes. Based on these observations, the relative sensitivity and specificity for EEG and SSEP (amplitude reduction greater than 50%) in detecting postoperative neurologic deficits were 50% and 92% for EEG and 100% and 94% for SSEP, respectively, differences that were not statistically significant. Regarding SSEP, the use of latency change (CCT) as a criterion was associated with a sensitivity of 0% (P = 0.046 from sensitivity of amplitude) and a specificity of 87% (P = 0.17 from specificity of amplitude).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗