Caution during double cannulation of the internal jugular vein.
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Biomedical subjects
Publications and source records attributed to C R Monk.
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We conducted a randomized, double-blind investigation to determine whether enoximone affects the actions of dobutamine in patients taking beta adrenoceptor antagonists. We studied sixteen patients with good ventricular function after coronary artery bypass operations. All patients were taking a beta adrenoceptor antagonist. The patients received a standardized intravenous anaesthetic, which was maintained throughout the investigation. They received a masked infusion, containing either normal saline or enoximone. Haemodynamic data were recorded before, during, and after an infusion of dobutamine, which was given at three different rates. Patients receiving enoximone had a greater cardiac output, a higher heart rate and a lower systemic vascular resistance than patients receiving saline. They also required an average of 1500 ml more intravenous colloid in the immediate postoperative period to achieve haemodynamic stability. Dobutamine produced a consistent, significant peripheral vasoconstriction, but no inotropic or chronotropic effect. There was no significant difference in this effect between the two groups, and it was not influenced by concurrent therapy with enoximone. The alpha adrenergic action of dobutamine prevented us from using high enough rates of infusion to explore any interaction between the inotropic actions of dobutamine and enoximone.
Adrenaline is the single most important therapeutic agent used in advanced cardiac life support (ACLS). Ideally it should be given into a large central vein but the European Resuscitation Council, the American Heart Association and the Resuscitation Council (U.K.) advise that adrenaline may be given into the trachea if i.v. access is not available. We have studied the effects of intra-tracheal and i.v. adrenaline in 16 patients undergoing mechanical ventilation. Log dose-response curves were constructed for systolic arterial pressure and heart rate responses. Intra-tracheal doses of adrenaline up to 10 micrograms kg-1, approximately one-third of that recommended for resuscitation, had no effect on arterial pressure or heart rate, whereas adrenaline 0.1 microgram kg-1 i.v. produced a mean increase in systolic pressure of 24 mm Hg. The intra-tracheal doses recommended for resuscitation (2-3 mg) are likely to be ineffective and consideration should be given to abandoning the tracheal route for adrenaline in ACLS.
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There is general concern that major blood loss during deliberate hypotension could produce severe organ ischemia, but documentation of the magnitude of this response remains obscure. To examine this response, we studied 43 male Sprague-Dawley rats that were divided into seven groups: the control animals received 1 MAC (1.4%) isoflurane only; the hypotensive animals received a 1.4% isoflurane baseline anesthetic and were then rendered hypotensive by either increasing the isoflurane concentration (dISO), or by adding sodium nitroprusside (SNP), or 2-chloroadenosine (2AD) to the baseline anesthetic, decreasing the MAP to 51 mmHg; hemorrhaged animals had hypotension produced in the same manner as for the hypotensive animals, but additionally were bled 20% of estimated blood volume during deliberate hypotension produced with either deep isoflurane (dISOH), sodium nitroprusside (SNPH), or 2-chloroadenosine (2ADH). After a 25-min period of hypotension, or hypotension plus hemorrhage, cardiac output and blood flow to brain, heart, gastrointestinal tract, kidney, and liver were measured with 141Ce-labelled 15-microns microspheres. Hypotension was associated with decreased blood flow to the kidneys in all groups and to the liver in the 2AD group and an increased blood flow to the heart in the SNP and 2AD groups. Hemorrhage decreased blood flow during deliberate hypotension to the brain and the gastrointestinal tract in the dISOH and 2ADH groups and to the liver in the dISOH group. Our results suggest that hemorrhage during deliberate hypotension with dISO or isoflurane plus 2AD may be associated with compromised organ blood flow, whereas blood flow to vital organs is maintained after 20% hemorrhage during isoflurane and superimposed SNP-induced hypotension.
We have studied the effect of i.v. metoclopramide on renal vascular resistance in nine healthy volunteers. Peak systolic and end-diastolic frequencies were measured using duplex Doppler ultrasound of a renal interlobar artery, before and after the administration of i.v. metoclopramide 10 mg, and the resistance index derived. There was no significant change in mean arterial pressure or resistance index following metoclopramide.
The haemodynamic effects of total i.v. anaesthesia with a combination of propofol and alfentanil infusions were studied in eight patients with good left ventricular function undergoing coronary artery bypass surgery. Haemodynamic indices were measured before anaesthesia and at specified intervals before cardiopulmonary bypass. The technique resulted in haemodynamic changes comparable to those reported with opioid-based anaesthesia for coronary artery surgery, and has potential advantages.
To compare the effectiveness of two routinely used methods of preoxygenation in protecting against hypoxia in the elderly, the arterial O2 saturation was measured using an oximeter. Twenty-four elderly patients (greater than or equal to 65 yr) presenting for elective orthopedic surgery were randomly allocated to receive either 3-min or four-maximal-breaths of 100% O2 via a Bain circuit. After preoxygenation, anesthesia was induced, tracheal intubation performed with patients kept apneic, and the endotracheal tube left open to air. The arterial O2 saturation was measured before preoxygenation and continually recorded during desaturation. Although attaining similar arterial O2 saturation values after preoxygenation, patients in the four-maximal-breath group had significantly shorter times (P less than 0.0001) to all levels of desaturation. We suggest that preoxygenation with 3-min breathing of 100% O2 offers more protection against hypoxia due to prolonged apnea after induction of anesthesia in the elderly than does four maximal breaths of 100% O2.
A self-tuning, closed-loop controller, based on the algorithm of Clarke and Gawthrop, was used to regulate the inspired concentration of isoflurane to reduce arterial pressure electively in 33 patients undergoing ENT surgery. The patients were allocated randomly to one of four groups and received differing doses of fentanyl and labetalol to vary the range of sensitivities to the hypotensive action of isoflurane. The performance of the controller was evaluated at two target arterial pressures (AP), by its response to simulated changes in AP and by a comparison with a further group of eight patients with manual control of AP. The controller's undershoot of AP (range 2.8 +/- 0.5-4.5 +/- 1.3 mm Hg) and % time spent within +/- 5 mm Hg of the target AP (range 83 +/- 3.4-89 +/- 2.2%) were acceptable and equalled the manual performance figures (range 3.3 +/- 0.8 mm Hg; 90 +/- 5%). The regulation of induced hypotension in all four groups was rapid, accurate, stable and reproducible.
A method is presented for the pre-column derivatization of agmatine, arginine, citrulline or ornithine with o-phthalaldehyde-2-mercaptoethanol, and subsequent separation of the derivatives by reversed-phase liquid chromatography. Fluorescent response is linear from 10 to 150 pmol of injected analyte and detection limits range from 28 to 100 fmol. Response factors relative to the internal standard, homocysteic acid, were 1.16 (agmatine and arginine), 1.03 (citrulline) and 0.34 (ornithine). The applicability of the method to the measurement of arginase, arginine deaminase, arginine decarboxylase and other enzyme activities in bacterial extracts was examined.
The infusion rate of propofol required to supplement 67% nitrous oxide in oxygen to maintain surgical anaesthesia was determined in 72 patients premedicated with lorazepam. Following an induction dose of propofol 2 mg kg-1, groups of eight patients received an infusion of propofol varying from 60 to 200 micrograms kg-1 min-1. Probit analysis was used to determine the ED50 (130 micrograms kg-1 min-1; 95% confidence limits: 106-167 micrograms kg-1 min-1) and ED95 (348 micrograms kg-1 min-1; 95% confidence limits: 233-1296 micrograms kg-1 min-1) for propofol infusion. Whole blood propofol concentrations at the time of surgical incision correlated strongly with the infusion rate, giving an EC50 value of 2.5 micrograms ml-1, and an EC95 value of 5.92 micrograms ml-1. There was no significant correlation between the rate of infusion of propofol, or the total propofol dose, and the times to response to command, or to recall of birthdate.
The haemodynamic effects of propofol at two infusion rates (54-65 and 108-130 micrograms kg-1 min-1) have been studied during peripheral arterial surgery in eight elderly patients premedicated with morphine sulphate 0.15 mg kg-1. The haemodynamic response to laryngoscopy and intubation was partially suppressed: neither arterial pressure nor heart rate exceeded awake values. During stable anaesthesia at the lower infusion rate before surgery, systolic (SAP) and diastolic (DAP) arterial pressures were significantly decreased from awake values (SAP: -47%; DAP: -46%) as a result of decreases in cardiac output (-32%) and systemic vascular resistance (SVR) (-9%). During surgery, with either spontaneous (SV) or intermittent positive pressure (IPPV) ventilation, both infusion rates were associated with decreases in arterial pressures when compared with the awake state. Cardiac output was decreased (SV: -35%, IPPV: -36%) and SVR increased (SV: +22%, IPPV: +45%) at the lower infusion rate; similar changes were observed during the faster infusion rate.
The hemodynamic response to anesthesia with the aqueous emulsion formulation of propofol was studied in healthy patients (ASA I or II), aged 39-57 yr, premedicated with morphine, 0.15 mg/kg. Anesthesia was induced in all patients with propofol, 2 mg/kg. Subsequently, patients were randomly assigned to two groups and maintained by a continuous intravenous infusion (group 1 received 54 micrograms X kg-1 X min-1, group 2 received 108 micrograms X kg-1 X min-1) to supplement 67% nitrous oxide. Three minutes after induction, systolic arterial pressure (SAP) decreased 28% (P less than 0.01) and was associated with decreased (-12%) cardiac output (Q70) and decreased (-15%) systemic vascular resistance (SVR). The hemodynamic response to tracheal intubation was not obtunded, but peak values of arterial pressures and heart rate did not exceed those recorded awake. Thirty minutes elapsed before repeating measurements prior to the first surgical incision. In group 1, SAP and Q70 decreased to 65% and 68% of awake values and in group 2 to 55% and 74% (P less than 0.05). Mild ventilatory depression persisted for the duration of spontaneous ventilation and was not reduced by the stimulus of surgery, which caused no significant hemodynamic responses in either group. Decreasing arterial PCO2 to the awake value by controlled ventilation increased SVR (P less than 0.05), but the associated increased SAP and decreased Q70 did not reach statistical significance. No patient reported awareness. The infusion of the emulsion formulation of propofol was associated with satisfactory anesthesia and recovery and with hemodynamic effects similar to those recorded with other intravenous anesthetics.
The study was performed to determine the ED50 and ED95 of a continuous infusion of the emulsion formulation of propofol during 67% nitrous oxide anaesthesia in 57 patients premedicated with morphine sulphate 0.15 mg kg-1. Anaesthesia was induced with propofol 2 mg kg-1, and maintained before incision with a fixed-rate infusion of propofol to supplement nitrous oxide. The response to the first surgical incision, made at least 30 min after induction of anaesthesia, was observed. The ED50 was 53.5 micrograms kg-1 min-1 and the ED95 was 112.2 micrograms kg-1 min-1. At the time of the first surgical incision, the venous whole blood concentrations of propofol at the ED50 and ED95 infusion rates (EC50 and EC95) were 1.66 micrograms ml-1 and 3.39 micrograms ml-1, respectively. The satisfactory maintenance of anaesthesia provided by nitrous oxide supplemented with propofol was associated with haemodynamic stability and rapid, uncomplicated recovery.
The new formulation of propofol appears to be approximately equipotent to the previous formulation when used as an infusion to supplement nitrous oxide anaesthesia in patients premedicated with morphine. Preliminary haemodynamic studies indicate that the emulsion formulation causes more arterial hypotension than the original Cremophor formulation, though larger numbers are required to confirm this finding.