[Woman and medicine].
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Biomedical subjects
Publications and source records attributed to M de Rood.
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The effects of norepinephrine and dobutamine were compared during endotoxin shock in dogs anesthetized either with enflurane (E: 1.5%, N = 12) or with i.v. ketamine (K: 5 mg.kg-1 + 0.2 mg.kg-1.min-1, N = 12). An i.v. bolus of 1.5 mg.kg-1 E. coli endotoxin was followed by saline infusion to restore left-sided filling pressures at baseline. With E, heart rate, mean arterial pressure and stroke index decreased (P less than 0.01). The decrease in oxygen delivery (DO2) and in oxygen consumption (VO2) was associated with an increase in blood lactate. In contrast, K anesthesia was associated with remarkable hemodynamic stability. DO2 was well maintained, VO2 decreased (P less than 0.01) and blood lactate did not change. Under E anesthesia, mean arterial pressure increased more with norepinephrine and heart rate increased more with dobutamine. Under K anesthesia, cardiac index, stroke index and left ventricular stroke work index increased similarly with both agents. In both groups DO2 and VO2 increased markedly. The amount of fluid infused was higher with dobutamine than with norepinephrine. Thus, enflurane but not ketamine had depressant cardiovascular effects at the doses used in this model. With both anesthetics, norepinephrine and dobutamine could effectively improve cardiac function. Dobutamine could therefore represent a valuable alternative to norepinephrine for cardiovascular support during anesthesia in septic shock.
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The effects of four commonly used anesthetic agents, halothane, isoflurane, alfentanil, and ketamine, on cardiovascular function and oxygen balance were studied in a dog model of septic shock. After initial pentobarbital administration, the dogs were given Escherichia coli endotoxin (3 mg/kg) and, after 30 min, fluids to restore cardiac filling pressures to baseline levels. This resulted in a low resistance shock in all animals. Dogs were then given for 2 h either halothane (n = 9, 0.5 MAC), isoflurane (n = 9, 0.5 MAC), or alfentanil (n = 9, 150 micrograms/kg IV plus 2 micrograms.kg-1.min-1) or ketamine (n = 9, 2 mg/kg IV plus 0.2 mg.kg-1.min-1) or no anesthetic (control: n = 9). Mean arterial pressure increased in the control group (+11 +/- 18 mm Hg) and with ketamine (+10 +/- 20 mm Hg), remained unchanged with isoflurane (-2 +/- 11 mm Hg), and decreased with halothane (-22 +/- 23 mm Hg) and alfentanil (-9 +/- 23 mm Hg). Heart rate tended to increase in the control group but decreased with the four anesthetic agents, especially with alfentanil and halothane. Cardiac index and left ventricular stroke work index increased in the control group and in each anesthetic group except the halothane group. Systemic vascular resistance decreased in all groups except in the ketamine group. In the control group, the increase in cardiac index was associated with significant increases in oxygen delivery and consumption, and with a significant decrease in blood lactate levels. There was a dramatic decrease in oxygen consumption in all anesthetic groups, whereas oxygen delivery failed to increase only with halothane. Blood lactate increased significantly with halothane (5.0 +/- 1.5 to 6.3 +/- 1.4 mM/L) and isoflurane (4.8 +/- 1.1 to 5.3 +/- 1.2 mM/L), remained unchanged with alfentanil (4.5 +/- 1.5 and 4.6 +/- 0.8 mM/L), and tended to decrease with ketamine (4.9 +/- 1.4 to 4.5 +/- 1.4 mM/L). In conclusion, among the four anesthetic agents tested, halothane had the least desirable effects. Ketamine best preserved cardiovascular function and appeared to have the least deleterious effects on the hypoxic tissues. Thus, ketamine could be the anesthetic agent of choice in septic shock.
The aim of the present study was to evaluate right ventricular (RV) preload by measurements of right ventricular volumes during aortic clamping and unclamping. Nine patients (aged 67 +/- 9 years) undergoing infrarenal aortic aneurysmectomy were monitored with a pulmonary artery catheter equipped with a fast-response thermistor, allowing determination of RV volumes by the thermodilution technique. Anesthesia consisted of a continuous infusion of alfentanil and 50% N2O. Aortic clamping resulted in a significant decrease in cardiac index (CI) and a significant increase in systemic vascular resistance (SVR). There was no significant change in right ventricular ejection fraction (RVEF) (from 35% +/- 6% to 33% +/- 8%) in the presence of a significant decrease in stroke index (from 37.2 +/- 9.8 to 31.1 +/- 10.0 mL/beat/m2, P less than 0.05), indicating a significant decrease in RV end-diastolic volume (from 106 +/- 17 to 92 +/- 19 mL, P less than 0.01). There were no significant changes in cardiac filling pressures. Aortic unclamping was associated with a significant increase in CI and a significant decrease in SVR. There were no significant changes in cardiac filling pressures, RVEF, or RV volumes. Measurements of RV volumes indicated that aortic clamping resulted in a decrease in RV preload, which is usually not demonstrated by measurements of right atrial pressure alone.
The authors studied in a double-blind placebo-controlled study the effects of oral preoperative administration of 5 micrograms/kg clonidine upon the alfentanil and droperidol requirements, hemodynamic lability, distribution of the values of heart rate and blood pressure, and plasma noradrenaline levels, in two groups of ten normotensive patients undergoing infrarenal aortic surgery. The amounts of alfentanil supplementing a standardized continuous infusion, injected to maintain hemodynamic stability, were statistically identical between the groups (P = 0.23). The amount of droperidol, however, was significantly less (P = 0.004) in the group of patients that received clonidine. The norepinephrine plasma concentrations, during the entire procedure, were lower (P = 0.001) in the clonidine group. The variability of the heart rate, systolic (SBP) and diastolic (DBP) blood pressure recorded every 5 s, and assessed by the calculation of the coefficients of variation for each patient, showed no difference between the clonidine and the placebo group. However, when the values recorded were compared to the preoperative baseline values, and divided into three categories (baseline +/- 20%--greater than 20% decrease vs. baseline--greater than 20% increase vs. baseline), the clonidine group showed a higher frequency of low heart rate and fewer episodes of tachycardia. The frequency of SBP hypertension was lower and of SBP hypotension higher in the clonidine group. After induction of anesthesia, but before surgery, there were more episodes of DBP hypotension in the clonidine group, but during dissection and vascular sutures the placebo group experienced more episodes of DBP hypotension, owing probably to the greater amount of droperidol injected. The authors conclude that the preoperative administration of clonidine decreased the need to supplement anesthetic, and modifies the profile of distribution of heart rate and blood pressure.
Cerebral blood flow, cerebral oxygen consumption, lactate and glucose metabolism were measured in 13 patients during anaesthesia with nitrous oxide, oxygen and enflurane 0.5% and after 30 minutes infusion of propofol. The mean blood concentration of propofol was 4.06 micrograms/ml. Cerebral blood flow decreased by 27.6% and cerebral vascular resistance by 51%. There were no changes in lactate and glucose metabolism. Cerebral oxygen consumption decreased by 18.25%. Changes in the electro-encephalograph were related to the blood levels of propofol.
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Although most authors use it as the reference instrument for respiratory gases measurement, the use of mass-spectrometer in clinical routine in ICU and in anesthesia remains quite limited. We developed a fully automatically controlled system, carrying on a twinned goal: The ACS-2000 (Automatic Calibration System) turns the Airspec MGA-2000 mass-spectrometer into a true clinical instrument, as easy to use as any routine monitoring instrument, and lets the clinician and the anesthetist benefit from its uncomparable metrological performances. PAMS-M, multibed monitoring system, shares the mass-spectrometer time among 4 to 8 rooms, providing each anesthetist with full composition of inspired and end tidal gases composition, trend evolution of those data, as with the display of capnogram. Each room is equipped with an IBM PC compatible intelligent terminal, abling the user to select the nature of the displayed information and enter into an easy menu driven dialog with the system. As a subproduct, the informatic infrastructure on which the system is based allowed, beyond the standard monitoring function, to set the bases of a computerized patient's anesthesia or respiratory monitoring report.
Labetalol, an alpha and beta adrenergic blocking drug, was used during anesthesia for removal of a very large pheochromocytoma which was predominantly epinephrine secreting. The 70-year-old female patient suffered from angina pectoris and chronic bronchitis. A preoperative treatment including an alpha-adrenolytic drug was administered but beta-adrenergic blockers were avoided because of the risk of cardiac decompensation and bronchoconstriction. During the operation, hypertensive peaks were easily controlled by bolus injections of labetalol 20 mg. The removal of the tumor was followed by a transient moderate hypotension. Heart rate remained stable throughout the operation. No hemodynamic problems occurred during the postoperative period. With regard to this case, a summary of the literature concerning the properties of labetalol is presented.
This study is based on the same group of neurosurgical patients as our previous publication. All, except one, had suffered from head injury. We made a first measurement of rCBF under N2O anesthesia, a second under N2O + 1% enflurane anesthesia, both at a PaCO2 of 40 Torr. A third measurement was performed under N2O + 1% enflurane but at a PaCO2 of 30 Torr. The method we used consists of the intracarotid injection of 133Xe and recording of the radioactivity by a gammacamera. Mean arterial pressure was maintained constant by an intravenous phenylephrine drip. For each measurement of each patient, a map was drawn, representing the distribution of the regional cerebral blood flows (rCBF), compared to the mean value of the hemisphere. We have studied rCBF in one case of normal hemisphere, and in cases of traumtic lesions in acute and chronic states, taking into account that the normal brain exhibits areas with higher flow in the frontoparietal and insular regions. In the normal brain, introduction of 1% enflurane decreases uniformally mean CBF, rCBF repartition not being changed. Hyperventilation to 30 Torr shows that regions with previously higher flow react more to hypocapnia by a slightly more decreased flow. In severe brain trauma, mean CBF is generally low, and it is difficult to visualize the lesions under N2O and N2O + 1% enflurane anesthesia. Neither mean CBF, nor rCBF repartition are significantly modified. On the other hand, in the acute phase, hypocapnia causes a more decreased flow in the previously well irrigated areas, and shows a lack of vascular reactivity in the damaged region. Passing to the chronic state, the patient clinically recovering, the rCBF repartition is normalized and the contused area becomes agains vasoactive. Severe losses of neuronal tissue are characterized by definitive low flows without reactivity by hyperventilation.
We have measured the CBF in ten neurosurgical patients. A first measurment was made during anesthesia with nitrous oxide 70% and a second with nitrous oxide 70% + 1% enflurane, both at a PaCO2 of 40 Torr. A third measurement was performed also with nitrous oxide + 1% enflurane, but at a PaCO2 of 30 Torr. We used the method of intracarotid 133Xe injection, with a gammacamera recording. In order to avoid any decrease of cerebral perfusion pressure, which might influence the CBF, an infusion of phenylephrine was used, if needed. At a constant PaCO2 of 40 Torr, there was no statistically significant difference in CBF with nitrous oxide + 1% enflurane compared to nitrous oxide alone. No change in cerebral vascular resistance was observed. When PaCO2 was lowered to 30 Torr, under 70% nitrous oxide + 1% enflurane, there was a 43% decrease in CBF (from a mean of 42 ml/100 G/min. to a mean of 24 ml/100 g/min.). Cerebral vascular resistance had an increase of 79%. In some instances, the decrease in CBF reached values around 20 ml/100 g/min. and in one case, even less. That level is generally considered to be the lowest acceptable limit in the conscious man, though not necessarily in the anesthetised one. Under hypocapnia, the cerebral arterio-venous oxygen difference increased, but the CMRO2 did not change. There were little differences in lactate and pyruvate cerebral metabolic rates, all values remaining within normal ranges. In conclusion, we believe that enflurane is a favorable anesthetic agent for neurosurgical operations at the concentration of 1%, CMRO2 is reduced, there is no significant effect on cerebral blood vessels, CBF and CVR do not change. However, a complementary use of hypocapnia may reduce CBF to dangerously low levels, if at the start, it shows already a pathological decrease and if hyperventilation is applied at a marked degree.
We have studied the effects of enflurane on intracranial pressure (ICP) in 9 neurosurgical patients, whose ICP was continuously monitored for therapeutic or diagnostic purposes. The control ICP was under 15 Torr in 5 cases, under 20 Torr in 3 cases and of 25 Torr in one case. In order to achieve stable ventilatory conditions, the patients were kept under controlled ventilation, breathing a mixture of 60 to 70% nitrous oxide and oxygen. The PaCO2 was kept constant, at the pre-study level. Mean arterial pressure (MAP) was maintained stable with the administration of fluids and/or a phenylephrine drip. Cerebral perfusion pressure (CPP) was calculated as the difference between MAP and mean ICP. After a control stabilization period of about one hour, enflurane was introduced in the circuit at successive concentrations of 1 and 2% during 20 to 30 minutes. In seven patients, enflurane did not produce any change of ICP. ICP rose only in 2 patients, whose control values were of 16 and 25 Torr. The overall changes, however, are not significant. There is a small significant decrease of MAP and CPP under 2% enflurane when compared to control, of probably no clinical importance (under 10% change). Our results do not show that enflurane is entirely without effect on ICP, but we think that 1 to 2% enflurane may be used in neuroanesthesia with a reasonable margin of safety, in association with slight hyperventilation and other means or reducing ICP, in accordance to clinical requirements.
Cerebral blood flow was measured, under controlled conditions of stable ventilation and PaCO2, in 11 patients suffering from cerebro-vascular lesions. Comparing the results under N2O-enflurane 1% anesthesia with those under N2O-fentanyl anesthesia shows an average 8.4% decrease of blood flow. In 5 cases, a third measurement was performed under N2O-enflurane 2% anesthesia. This caused an average 8.5% complementary decrease. Whereas most inhalational anesthetic agents produce an increase of cerebral blood flow, this is not observed with enflurane, the tendency rather being towards a decrease.
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The adrenal cortex and the adrenal medulla, functionally quite distinct, re discussed separately. Knowledge of the steroid biosynthesis with its three productive pathways (glycocorticoids, mineralocorticoids and sex hormones) is essential not only to understand the physiopathology of the adrenal cortex, but also to delineate the necessary diagnostic hormonal screening tests and the applied treatment modalities. When surgery is indicated a precise preoperative evaluation of the patient is essential with correction of all possible anomalies. With this all in mind the Cushing syndrome, the adrenogenital syndrome and the primary aldosteronism (Conn) are discussed with regard to etiology and treatment. Patients who underwent a bilateral adrenalectomy are likely to live a normal life as long as the hormonal substitution therapy (glycocorticoids and mineralocorticoids) is adequate. When stress situations, such as surgery, do occur adjustments of this therapy are essential. The pathology of the adrenal medulla confronts us with the problems of pheochromocytoma. An adequate preoperative preparation of the patients with adrenergic blocking agents and fluid support allows for a surgical intervention with a low morbidity and mortality. In conclusion, surgery of the adrenals requires a perfect knowledge of the associated physiopathology and a close cooperation between the endocrinologist, the surgeon and the anesthesiologist.