Absence of side effects of hydroxyethylstarch 200 in a porcine model of experimental arterial thrombosis.
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Biomedical subjects
Publications and source records attributed to P Viars.
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Experience with a new type of laryngoscope (Bullard) is reported. It weighs 1,200 kg, and has fiberoptic fibers both for lighting and viewing. Angle of vision is about 55 degrees. Endotracheal intubation with this device requires a semi-rigid stylet to bend the tracheal tube at 90 degrees just above its cuff, so as to reproduce the curvature of the laryngoscope blade. Intubation is carried out in five steps: 1) introducing the laryngoscope blade, and visualising the vocal cords through its lens; 2) introducing the tube with its stylet, just above the laryngoscope blade; 3) placing the tube between the vocal cords under fiberoptic vision; 4) adjusting tube position in the trachea, the stylet still in place; 5) removing both stylet and laryngoscope. The use of this apparatus in an obese patient with reduced mobility of the cervical spine, who was ranked 4 on the Mallampati scale, is reported. The Bullard laryngoscope enabled easy tracheal intubation (duration 1 min 30 s), whereas direct laryngoscopy and the use of a Huffman prism were unsuccessful. The fiberoptic laryngoscope may be of help in case of difficult intubation.
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The peripheral vascular effects of thiopental 5 mg/kg and propofol 2.5 mg/kg were compared in five patients whose lungs were being ventilated and in whom a Jarvik-7 artificial heart had been implanted. The patients were monitored, using catheters that had been surgically inserted into the radial artery, the right and left atria, and the pulmonary artery. The Jarvik-7 settings were modified to render the artificial heart "preload independent" and to maintain cardiac output constant. Each patient received both drugs, with the interval between each drug ranging from 16 to 28 h. Hemodynamic parameters and catecholamine and atrial natriuretic peptide plasma concentrations were measured before drug administration and 5, 10, 15, 30, and 45 min later. Both drugs significantly decreased arterial pressure, systemic vascular resistance index, pulmonary arterial pressure (PAP), and right and left atrial pressures (RAP and LAP, respectively). However, propofol 2.5 mg/kg induced a significantly greater and more prolonged decrease in arterial pressure, systemic vascular resistance index, and RAP than that after administration of thiopental 5 mg/kg (P less than 0.05). Five minutes after drug injection, mean arterial pressure decreased by 21% after thiopental and by 39% after propofol (P less than 0.01); systemic vascular resistance index decreased by 21% after thiopental and by 44% after propofol (P less than 0.05); RAP decreased by 20% after thiopental and by 50% after propofol (P less than 0.05); mean PAP decreased by 18% after thiopental and by 32% after propofol (P less than 0.09); and LAP decreased by 40% after thiopental and by 46% after propofol (P less than 0.2). With both drugs, atrial natriuretic peptide, norepinephrine, and epinephrine plasma concentrations remained stable throughout the study period. Because cardiac output was maintained constant throughout the study, these results suggest that propofol 2.5 mg/kg is a more potent vasodilator of venous and arterial beds than is thiopental 5 mg/kg.
The goal of this randomized study of high-risk surgical patients was to determine whether intraoperative thoracic epidural anesthesia in combination with light general anesthesia alters postoperative morbidity when compared to a standard technique of "balanced" general anesthesia. A total of 173 patients scheduled for abdominal aortic reconstruction were admitted to the study; 86 were to receive "balanced" general anesthesia (group 1) and 87 thoracic epidural anesthesia in combination with light general anesthesia (group 2). Preoperative evaluation included standard clinical tools, dipyridamole thallium gammatomography, and radionuclide angiography. In these patients, all of whom had peripheral artery disease, there were no significant differences in associated coronary artery disease, hypertension, and cardiovascular treatment. The distribution of left ventricular ejection fraction and the number of patients with thallium redistribution were not statistically different between the two groups. During the postoperative period, group 1 received analgesia of subcutaneous morphine (n = 35), epidural fentanyl (n = 30), or epidural bupivacaine (n = 21). In group 2, 6 patients with a nonfunctioning epidural catheter due to technical failure received a balanced general anesthesia and were eliminated from the study. During the postoperative period, group 2 received analgesia of subcutaneous morphine (n = 26), epidural fentanyl (n = 25), or epidural bupivacaine (n = 30). Cardiovascular morbidity did not differ between the two groups: 22 patients in group 1 and 19 patients in group 2 had a major postoperative cardiac event.(ABSTRACT TRUNCATED AT 250 WORDS)
The ventilatory effects of medical antishock trousers (MAST) were investigated using 10 healthy volunteers. Use of the MAST (60-80 mm Hg) decreased forced expiratory volume (-8% +/- 4%, p less than 0.01), vital capacity (-8% +/- 5%, p less than 0.01), and functional residual capacity (-12% +/- 6%, p less than 0.01) and induced a significant decrease in tidal volume (-30% +/- 17%, p less than 0.05), but minute ventilation was unmodified because of a concomitant increase in respiratory rate (+17% +/- 8%, p less than 0.001). The MAST modified the breathing pattern: the abdominal contribution to ventilation was markedly decreased (-57% +/- 22%, p less than 0.001), suggesting a decrease in the diaphragmatic contribution to ventilation. The MAST increased both the end-expiratory (+131% +/- 115%, p less than 0.01) and inspiratory variation (delta Pgas: +42% +/- 40%, p less than 0.05) of gastric pressure, whereas the end-expiratory and inspiratory variation of esophageal pressure remained unchanged. Because of a higher delta Pgas, the dynamic compliance of the abdominal compartment markedly fell (-77% +/- 10%, p less than 0.001). Transdiaphragmatic pressure (Pdi: +28% +/- 30%, p less than 0.05) significantly increased and the pressure-time index of the diaphragm significantly increased (+32% +/- 32%, p less than 0.05) after inflation of the MAST, suggesting an increase in the diaphragmatic cost of breathing. Inspiratory activity of the parasternal intercostal muscles significantly increased after the MAST was inflated. Computerized tomography showed that the MAST induced a cephalad shift of the diaphragm, which reduced pulmonary height.(ABSTRACT TRUNCATED AT 250 WORDS)
The aims of this randomized study were (1) to determine if isoflurane is effective in controlling blood pressure during thoracic aortic cross-clamping, and (2) to compare its effects on hemodynamics and oxygen transport to those of sodium nitroprusside. Sodium nitroprusside (SNP group, n = 10) or isoflurane (ISO group, n = 10) was started 2 minutes before cross-clamping and was adjusted to maintain systolic arterial pressure as near as possible to preinduction values. The duration of thoracic aortic cross-clamping was 26 +/- 4 minutes in the SNP group and 30 +/- 4 minutes in the ISO group. Administration of isoflurance and sodium nitroprusside was stopped 2 minutes before unclamping. The same anesthetic technique using fentanyl, 6 micrograms/kg, flunitrazepam, 0.02 mg/kg, pancuronium, 0.1 mg/kg, and 50% N2O was used for all patients. At the time of clamping, either isoflurance (maximal expired concentration, 2.5% +/- 0.3%) or sodium nitroprusside (cumulative dose, 11.1 +/- 1.0 mg) was effective in maintaining the systolic blood pressure below 160 mm Hg, whereas the pulmonary capillary wedge pressure did not change. However, only SNP was able to bring the arterial pressure above the cross-clamp back to postinduction levels. During clamping, stroke index values were similar in both groups, but cardiac index increased only in patients receiving SNP. In both groups, at clamping and unclamping, PvO2 was higher than postinduction values, indicating that throughout the study the oxygen needs of the perfused area were adequately met. There was no evidence of acute left ventricular decompensation because pulmonary capillary wedge pressures did not abruptly increase, nor did pulmonary edema occur.(ABSTRACT TRUNCATED AT 250 WORDS)
A pilot study has been conducted in ten consecutive patients undergoing femoro-popliteal reconstruction or distal vascular surgery under epidural anaesthesia. Immediately before arterial cross-clamping, enoxaparin (E) (75 anti-Xa IU.kg-1) was injected intravenously (i.v.). During surgery, washing of the saphenous or polytetrafluoroethylene (PTFE) graft has been performed using enoxaparin. Enoxaparin (75 anti-Xa IU.kg-1) was administered subcutaneously (S.C.) 8 hours after the i.v. injection, and then every 12 hours during 10 days. The patency of the vascular reconstruction and the side-effects of E administration were evaluated clinically before and during surgery, then by a daily clinical examination. Echo-Doppler and/or arteriography were also performed preoperatively and on the 10th postoperative day. Haematocrit, platelet count, activated partial thromboplastin time, prothrombin time, thrombin time, fibrinogen and anti-Xa activity were assessed. None of the patients developed venous or arterial thrombosis and all the by-pass grafts remained patient. Only one minor surgical bleeding occurred on the first post operative day, despite anti-Xa levels in the expected range. One patient developed minor haematomas at the injection site. No bleeding was observed. Further randomized studies comparing LMWH and UH are required in order to substantiate these preliminary clinical and biological findings.
This study, including 33 consecutive patients was designed to assess the haemostatic alterations occurring during repair of thoracoabdominal aneurysms. The surgical procedure consisted in Dacron graft replacement of the diseased aorta, using neither cardiopulmonary bypass, nor any shunting technique, nor any heparin. Blood samples were drawn before anaesthesia, before and 30 min after unclamping, and on the first postoperative day. The measured parameters were: haematocrit, platelet count, bleeding, activated cephalin, thrombin and prothrombin times, and concentrations of fibrinogen, factors V, VII, X and II, anti-thrombin III, proteins C and S, fibrin degradation products, D-dimers, alpha 2-antiplasmin, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor, and serum protein. Eight patients developed severe multiple haemorrhages; 3 of them died during the procedure because of uncontrollable bleeding. Although the measured parameters were similar in the "bleeding" and control (n = 25) groups before surgery, there was, before unclamping in the first group, an important increase in activated cephalin and thrombin times, with a fall in concentrations of factor II and V, protein C, fibrinogen, and alpha 2-antiplasmin, and in platelet numbers. After unclamping, these changes worsened further, with an increase in prothrombin time and in fibrinogen levels (0,8 g.l-1), without any increase in fibrin degradation products. Abnormal bleeding started about 30 min after this in all the patients of the "bleeding" group. These changes, involving the fibrinolytic system as well as a fall in concentration of all the coagulation factors, can probably be partly explained by the clamping and unclamping of mesenteric vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
Indirect and experimental evidence suggests that polymorphonuclear leukocytes, responding to an activating signal presumably related to the complement cascade activation, are involved in the pathogenesis of the adult respiratory distress syndrome (ARDS). The pathologic changes seem to be result of the polymorphonuclear leukocyte margination within the pulmonary capillary vessels and their activation with subsequent release of vasoactive peptides (thromboxane A2, prostaglandin E2) and toxic intracellular compounds. This study confirms that adherence, chemotaxis, and chemiluminescence are increased in polymorphonuclear leukocytes from patients with ARDS. Enhanced chemotactic and chemiluminescence capacities are likely specific to ARDS, whereas increased polymorphonuclear leukocyte adherence seems to be nonspecific. If increased polymorphonuclear leukocyte activation is important in the pathogenesis of ARDS, the inhibition of this phenomenon could play a therapeutic role. This double-blind prospective study was undertaken to assess if polymorphonuclear leukocyte activity is inhibited in vivo by the iv administration of prostaglandin E1 (PGE1) in patients with ARDS. A continuous infusion of PGE1 at a dose of 30 ng.kg-1.min-1 for 7 days did not modify the functional activity of polymorphonuclear leukocytes in patients with ARDS. Because hemodynamic instability was seen during infusion of this dose of PGE1, an increased dose was not tested. At the dose of PGE1 tested, no significant effect upon the function activity of polymorphonuclear leukocytes in patients with ARDS could be demonstrated.
Etomidate is available in two different solvents: propylene glycol for induction of anesthesia and ethanol for maintenance of anesthesia. The direct effect of etomidate (1 and 5 micrograms/ml) and of its solvents on cardiac muscle was studied using rat left ventricular papillary muscle. Etomidate induced a slight positive inotropic effect in both solvents, as shown by an increase in maximum unloaded shortening velocity (Vmax) but not in force. At 0.5 mM Ca++ 5 micrograms/ml etomidate increased Vmax (128 +/- 18%, P less than 0.05) but not force (103 +/- 16%, NS). Using various afterloaded twitches, the peak power output (Emax) was calculated: 1 and 5 micrograms/ml etomidate increased Emax (107 +/- 8%, P less than 0.05, and 108 +/- 10%, P less than 0.05, respectively). This increase was related to the increase in Vmax and not in isometric force. Etomidate did not modify the elastic components of papillary muscle, isometric relaxation, and contraction-relaxation coupling under high load. Several findings suggest that etomidate in propylene glycol impaired the sarcoplasmic reticulum (SR) function: 1) it impaired the isotonic relaxation, the contraction-relaxation coupling under low load, and the load sensitivity of relaxation; and 2) it decreased postrest potentiated contraction, which is highly dependent on the SR. Nevertheless, alteration of SR function was only significant at high [Ca++]o and the beat-to-beat postrest recovery was not modified, indicating that the deleterious effects on SR function were moderate. The isotonic relaxation (max Vr) was more impaired by etomidate in propylene glycol (78 +/- 9%, P less than 0.001) and by propylene glycol alone (69 +/- 9%, P less than 0.001) than by etomidate in ethanol (97 +/- 12%, NS) and by ethanol alone (92 +/- 8%, P less than 0.05). This suggests that propylene glycol was responsible for the decrease in SR function. Etomidate in propylene glycol thus has a dual action on rat myocardium: 1) a slight positive inotropic effect due to etomidate per se, and 2) a slight decrease in SR function probably related to propylene glycol. However, because etomidate in propylene glycol induced a slight decrease in isometric force under certain experimental conditions (i.e., after isometric stabilization), etomidate in propylene glycol may induce a slight negative inotropic effect in some clinical conditions as a result of its dual action on the myocardium.
The peripheral vascular effects of isoflurane and halothane were compared in five critically ill patients in whom a Jarvik-7 artificial heart had been implanted. The lungs of all patients were mechanically ventilated in the postoperative period and the patients were monitored with an arterial catheter and with catheters that had been surgically inserted into the right and left atria and into the pulmonary artery. Norepinephrine and epinephrine plasma concentrations were measured using a radioenzymatic assay. The Jarvik-7 settings were modified to render the artificial heart "preload independent" and to maintain cardiac output constant. Each patient was anesthetized twice using halothane and isoflurane at two different MAC levels, 1 and 1.5 (Datex vapour analyzer), with the interval between each anesthetic ranging from 12 to 26 h. Both anesthetics significantly decreased mean arterial pressure (from 100 +/- 11 mmHg to 66 +/- 13 mmHg for halothane and from 102 +/- 17 mmHg to 48 +/- 11 mmHg for isoflurane; mean +/- SD) and systemic vascular resistance index (from 27 +/- 11 Wood units/m2 to 18 +/- 6 Wood units/m2 for halothane and from 30 +/- 6 Wood units/m2 to 13 +/- 3 Wood units/m2 for isoflurane; mean +/- SD), but with isoflurane to a significantly greater extent than with halothane (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of ketamine (10(-5) and 10(-4) M) on the intrinsic contractility of left ventricular papillary muscle from normal hamsters and those with cardiomyopathy (BIO 82.62, 6-month old) was investigated. At these concentrations, ketamine induced a positive inotropic effect on normal papillary muscle, as shown by an increase in maximum unloaded shortening velocity (+19 +/- 4 and +34 +/- 5%, P less than 0.05), active isometric force (+32 +/- 8 and +57 +/- 11%, P less than 0.05), and peak power output (+40 +/- 8 and +80 +/- 16%, P less than 0.05), and induced a slight decrease in sarcoplasmic reticulum function. Ketamine had no effect on the curvature of the total force-velocity curve, suggesting that it does not modify myothermal economy. Contractility of papillary muscle from hamsters with cardiomyopathy was less than that of controls, as shown by the decrease in isometric active force (-41%, P less than 0.02), peak power output (-33%, P less than 0.05), and sarcoplasmic reticulum function. The positive inotropic effect of ketamine on papillary muscle from hamsters with cardiomyopathy was less marked than in controls and almost suppressed in some cases: only the maximum unloaded shortening velocity was significantly increased with 10(-5) M ketamine (+7 +/- 6%, P less than 0.05), whereas no significant changes were observed in active isometric force (+14 +/- 8 and +13 +/- 11%; nonsignificant [NS]) and peak power output (+9 +/- 5 and +13 +/- 8%; NS) with ketamine (10(-5) and 10(-4) M, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
This study evaluates the respiratory effects of laparoscopy under epidural anesthesia in seven female patients (ASA physical status I) scheduled for a gamete intrafallopian transfer procedure. Epidural anesthesia was performed with 15-18 mL of 1.5% plain lidocaine using a catheter inserted at the L3-4 level. The upper level of analgesia to pinprick was measured 20 min after lidocaine injection. Ventilatory measurements and arterial blood gas analyses were performed (a) preoperatively, in the horizontal supine position with a T7-9 level of analgesia; (b) in the 20 degrees Trendelenburg position with a T2-5 level of analgesia; (c) during intraabdominal insufflation of CO2 through the laparoscope; and (d) after CO2 exsufflation by manual compression of the abdomen before removal of the laparoscope while in the horizontal position. On-line measurements of VO2, VCO2, VE, VT, F, and PETCO2 were made using a Beckman metabolic cart, while the patients breathed room air through an anesthetic face mask. No significant changes in the ventilatory variables were observed in the Trendelenburg position. In contrast, CO2 insufflation significantly increased VE (from 9.1 +/- 1.0 L/min to 11.8 +/- 2.6 L/min, mean +/- SD), and F (from 16.9 +/- 1.9 breaths/min to 23.1 +/- 3.3 breaths/min, mean +/- SD), whereas VCO2 remained unchanged. PaCO2 remained constant throughout the study. These results suggest that epidural anesthesia may be a safe alternative to general anesthesia for outpatient laparoscopy, as it is not associated with ventilatory depression.
Thirty-one critically ill patients with acute respiratory failure and circulatory shock were divided into three groups. Group 1 included 11 patients with an inserted mixed venous saturation (SvO2) catheter using three-reference wavelengths and characterized by one transmitting and one detecting fiberoptic filament (Oximetrix opticath catheter); group 2 included eight patients with an inserted SvO2 catheter using two-reference wavelengths and characterized by one transmitting and one detecting fiberoptic filament; (Edwards sat-one catheter); group 3 included 12 patients with an inserted SvO2 catheter using two-reference wavelengths and characterized by one transmitting and two detecting fiberoptic filaments. Once calibration procedures were performed, SvO2 measured by the catheter and by an hemoximeter OSM 3 (reference value) were compared following each therapeutic intervention. Over a period of 1.5 to 6 hours during which the hematocrit value remained unchanged, 119 measurements were obtained in group 1, 91 in group 2 and 181 in group 3. The dispersion of SvO2 values was much more pronounced with the two-reference wavelength systems using either one or two detecting fiber optic filaments, and the correlation coefficient was significantly higher with the three-reference wavelength system (r = 0.970 for the Oximetrix catheter vs r = 0.855 for the Edwards catheter and r = 0.826 for the Spectramed catheter, p less than 0.001). After 24 hours, the spontaneous drifts in the two-reference wavelength systems, using either one or two detecting fiber optic filaments (expressed as the SvO2 value measured by the catheter minus the reference SvO2 value) were significantly higher than the spontaneous drift in the three-reference wavelength system (9.3 +/- 7 percent for the Edwards catheter and +/- 6 +/- 4.1 percent for the Spectramed catheter vs 3.3 +/- 3.1 percent for the Oximetrix catheter, p less than 0.05). This study shows that a three-wavelength system is more accurate than a two-wavelength system for measuring acute changes in SvO2. The addition of a second detecting fiber optic filament does not seem to improve the accuracy of the system when SvO2 changes occur in conditions of stable hematocrit.
The authors discuss the physiopathological mechanisms of intra and postoperative cardiac failure and the different means of treatment. A distinction is made between the intra and postoperative periods: the factors which predispose to cardiac failure are different and the immediate postoperative period would seem to be the most dangerous in patients with reduced coronary or contractile reserves. Enoximone is a valuable and effective inotropic agent in this situation.
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