End-systolic pressure-volume relationship and arterial elastance: the optimal method to evaluate myocardial contractile effects of anesthetic agents?
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Heart↗
Biomedical subjects
T Deloof
Publications and source records attributed to T Deloof.
Propofol infusion with or without fentanyl supplementation for microlaryngoscopy.
20 patients (ASA I to III) scheduled for microlaryngoscopy were randomly allocated to receive by infusion either 12-15 mg/kg/h propofol alone (group A) or 6-9 mg/kg/h with fentanyl supplementation (group B). All patients were premedicated with oral diazepam one hour before the procedure; they received an induction dose of 2 mg/kg propofol, preceded in group B by a bolus dose of fentanyl 1 microgram/kg. Significant hypotension was observed at induction in both groups to a similar degree (A:--26%; B:--30.2% compared to baseline). Placement of the laryngoscope induced sustained hypertension throughout the procedure in both groups (A: +28%; B: +20%) subsiding only at the removal of the instrument. Heart rate was never significantly altered. Arterial blood concentrations of propofol at induction reached high peak values (A: 16.82 +/- 8.52 micrograms/ml--B: 19.52 +/- 8.87 micrograms/ml--mean +/- SD) then remained stable throughout the procedure (A: 5.44 +/- 1.40 micrograms/ml--B: 2.91 +/- 1.06 micrograms/ml). At awakening, they were lower in group B (0.62 +/- 0.2 micrograms/ml) than in group A (1.17 +/- 0.55 micrograms/ml--p less than 0.05). Recovery was a little faster in group A (at the limit of significance). Though patients may present some excitation at awakening, recovery was usually very pleasant and characterized by swift return to consciousness, alertness and of all reflexes. We conclude that a propofol infusion is particularly suitable for microlaryngeal surgery. The addition of a narcotic agent allows reduction of the propofol dose range and does not alter recovery significantly. The proper dose of narcotic agent necessary to abolish cardiovascular reactivity to laryngoscopy must still be ascertained.
Adult↗
Effects of propofol on pulmonary and systemic arterial pressure-flow relationships in hyperoxic and hypoxic dogs.
We have investigated the effects of a continuous infusion (18 mg kg-1 h-1) of the aqueous emulsion formulation of propofol on mean pulmonary arterial (PAP)/cardiac output (O) and mean systemic arterial pressure (SAP)/Q relationships in 15 intact pentobarbitone-anaesthetized dogs subjected to hyperoxia (F/O2 0.4) and hypoxia (F/O2 0.1). Five-point PAP/Q and SAP/Q plots were obtained by opening an arterio-venous femoral fistula or by stepwise inflations of an inferior vena cava balloon. Over the range of Q studied (2-5 litre min-1), hypoxia increased PAP in eight dogs ("responders") and did not affect PAP in seven others ("non-responders"). Hypoxic pulmonary vasoconstriction (HPV) was restored in non-responders by the administration of acetylsalicylic acid (ASA) 1 g i.v. Hypoxia did not affect SAP over the range of Q studied in the responders or in the non-responders treated with ASA. Propofol had no effect on hyperoxic or on hypoxic PAP at all values of Q either in responders or in non-responders with HPV restored by ASA. Propofol did not change Q at uncontrolled flow, but decreased SAP at the lowest Q (2 and 3 litre min-1) during hyperoxia and at all values of Q during hypoxia. The systemic vascular effects were the same in animals of both groups, treated with ASA or not. We conclude that propofol does not influence pulmonary vascular tone and does not inhibit HPV, but reduces systemic vascular tone when venous return or oxygenation is decreased. The haemodynamic response to propofol was not affected by cyclo-oxygenase inhibition.
Anesthetics↗
Multipoint pulmonary vascular pressure/flow relationships in hypoxic and in normoxic dogs: effects of nitrous oxide with and without cyclooxygenase inhibition.
The authors investigated the effects of 70% nitrous oxide on overall mean pulmonary artery pressure (MPAP)/cardiac index (CI) relationships in 13 intact pentobarbital anesthetized dogs ventilated alternatively in normoxic (fraction of inspired O2, FIO2 0.3) and in hypoxic (FIO2 0.1) conditions. Five-point MPAP/CI plots were constructed by opening an arterio-venous femoral fistula or by stepwise inflations of a balloon in the inferior vena cava. These MPAP/CI plots were rectilinear in all experimental conditions. Over the entire range of CI studied, 1-5 l.min-1.m-2, hypoxia increased MPAP in seven dogs ("responders"), and did not affect MPAP in six other dogs ("nonresponders"). Hypoxic pulmonary vasoconstriction (HPV) was restored in "nonresponders" by administration of 1 g acetylsalicylic acid (ASA) intravenously. In "responders," nitrous oxide partially inhibited HPV. In "nonresponders" with a hypoxic pressor response restored by ASA, nitrous oxide enhanced both normoxic and hypoxic pulmonary vascular tone, and did not affect HPV. These results suggest that pulmonary vascular effects of nitrous oxide depend on preexisting pulmonary vascular tone, and may be modulated by cyclooxygenase products of arachidonic acid metabolism.
Animals↗
Effect of propofol on cerebral blood flow and metabolism in man.
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.
Adult↗
Pulmonary artery pressure: flow relationships in hyperoxic and in hypoxic dogs. Effects of methylprednisolone.
Methylprednisolone has been reported to impair hypoxic pulmonary vasoconstriction in isolated lungs, possibly by inhibiting the generation of vasoconstricting products of arachidonic acid metabolism. We investigated the effects of methylprednisolone on mean pulmonary artery pressure (PAP):cardiac index (Q) relationships in intact pentobarbital anaesthetized dogs ventilated alternatively in hyperoxia (fraction of inspired O2, FiO2 0.4) and in hypoxia (FiO2 0.1). Cardiac output was increased by opening an arterio-venous femoral fistula or reduced by stepwise inflations of a balloon in the inferior vena cava. Five point PAP:Q relationships were found to be rectilinear in all experimental conditions. Over the entire range of Q studied (2 to 5 l/min.m2), hypoxia increased PAP in seven dogs ("responders") and did not affect PAP in three other dogs ("non-responders"). A hypoxic pulmonary pressor response was restored in these three "non-responders" by administration of 1 g acetylsalicylic acid iv. Methylprednisolone 30 mg/kg iv had no effect on hyperoxic and on hypoxic pulmonary vascular tone in the "responders" and in the "non-responders" treated with acetylsalicylic acid. An additional dog pretreated with methylprednisolone 30 mg/kg iv 24 h before the experiment still had a marked hypoxia-induced increase in PAP over the entire range of Q studied. Thus a large dose of methylprednisolone does not affect hypoxic or hyperoxic pulmonary vascular tone in intact dogs. These data do not support the hypothesis that products of arachidonic acid metabolism mediate hypoxic pulmonary vasoconstriction.
Animals↗
Pulmonary hemodynamic response to dopamine and dobutamine in hyperoxic and in hypoxic dogs.
The pulmonary hemodynamic response to dopamine and to dobutamine was investigated in dogs ventilated with hyperoxia (fraction of inspired O2 concentration [FIO2], 0.4 balance nitrogen) and challenged with short periods of inspiratory hypoxia (FIO2 0.125 or 0.1 for 10 min). Dopamine at doses of 5, 10, and 20 micrograms X kg-1 X min-1 (n = 7 dogs) increased cardiac index (CI) and pulmonary artery pressure (PAP) without change in indexed pulmonary vascular resistance (PVRI) at both FIO2 0.4 and 0.125. Hypoxia-induced increases in PVRI were unaffected by dopamine. Dobutamine at doses of 5, 10, and 20 micrograms X kg-1 X min-1 (n = 7 dogs) increased CI, with an increase in PAP without change in PVRI at FIO2 0.4, and at FIO2 0.125 there was no change in PAP and a decrease in PVRI. Hypoxia-induced increases in PVRI were inhibited by dobutamine, partially at 5 and 10 micrograms X kg-1 X min-1, and completely at 20 micrograms X kg-1 X min-1. In two additional groups of seven dogs the effects of reducing FIO2 from 0.4 to 0.1 without and with dopamine or dobutamine either at 10 micrograms X kg-1 X min-1 (n = 7) or at 20 micrograms X kg-1 X min-1 (n = 7) were studied at an unchanged CI obtained by stepwise inflations of a balloon placed in the inferior vena cava. At constant flow both amines increased PVRI at FIO2 0.4 and did not significantly affect hypoxia-induced increases in PVRI.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Pulmonary arterial pressure-flow plots in dogs: effects of isoflurane and nitroprusside.
We investigated the effects of nitroprusside and isoflurane on multipoint pulmonary arterial pressure (PAP)/cardiac index (Q) plots in pentobarbital sodium-anesthetized dogs ventilated alternatively in hyperoxia (fraction of inspired O2, FIO2, 0.4) and hypoxia (FIO2 0.1). Over the entire range of Q studied, 2-5 l.min-1.m-2, hypoxia increased PAP in 16 dogs ("responders") and did not affect PAP in 16 other dogs ("nonresponders"). A hypoxic pulmonary vasoconstriction (HPV) was restored in the nonresponders by intravenous administration of 1 g of acetylsalicylic acid (ASA). Nitroprusside (5 micrograms.kg-1.min-1) inhibited HPV in responders (n = 8) and nonresponders treated with ASA (n = 8). End-tidal 1.41% isoflurane (a minimal alveolar concentration equal to one for dogs) did not affect HPV in responders (n = 8) and nonresponders treated with ASA (n = 8). In the latter group isoflurane increased PAP at the highest Q studied (3-5 l.min-1.m-2) in hyperoxia and hypoxia. In a final group of eight dogs with Q kept constant, PAP remained unchanged during two consecutive sequences of alternated 30-min periods (maximum time to generate a PAP/Q plot) successively at FIO2 0.4 and 0.1, and the hypoxia-induced increase in PAP was reproducible. Thus the present experimental model appeared suitable for the study of the effects of hypoxia and drugs on pulmonary vascular tone of intact dogs. At the given doses HPV was inhibited by nitroprusside and not affected by isoflurane. Products of arachidonic acid metabolism possibly could be implicated in the pulmonary vascular effects of isoflurane.
Animals↗
Effects of dopamine and dobutamine on hyperoxic and hypoxic pulmonary vascular tone in dogs.
The pulmonary vascular effects of dopamine and of dobutamine have been reported variably in the literature. We investigated the effects of dopamine and of dobutamine, at doses of 10 and 20 micrograms/kg/min, on the relationships of overall mean pulmonary arterial pressure (Ppa) to cardiac index (Cl) in 14 dogs ventilated alternatively in hyperoxic (FIO2, 0.4) and in hypoxic (FIO2, 0.1) conditions. Five-point Ppa/Cl plots were constructed by opening an arteriovenous femoral fistula or by stepwise inflations of a balloon in the inferior vena cava. These Ppa/Cl plots were rectilinear in all experimental conditions. Hypoxia was associated with an increase in Ppa over the entire range of Cl studied (2 to 5 L/min/m2). A deterioration in arterial oxygenation and an increase in O2 consumption constantly occurred after dopamine as well as after dobutamine administration. At 10 micrograms/kg/min (n = 6 dogs) neither drug affected Ppa over the entire range of Cl at both 0.4 and 0.1 FIO2. At 20 micrograms/kg/min (n = 8 dogs), dopamine and dobutamine increased Ppa at the lowest Cl (2 to 4 and 2 to 3 L/min/m2, respectively) at 0.4 FIO2, and attenuated hypoxia-induced increases in Ppa over the entire range of Cl. Two repetitions of alternated 0.4 and 0.1 FIO2 exposures had no effect on Ppa/Cl plots in 6 additional dogs given no drug. We concluded that at dosages as great as 20 micrograms/kg/min, as generally given in clinical practice, dopamine and dobutamine exerted similar effects upon the pulmonary circulation of intact dogs; either no change or an increase in hyperoxic pulmonary vascular tone and either no change or an attenuation of hypoxic pulmonary vasoconstriction.
Animals↗
Turning the mass-spectrometer into an easy to handle clinical instrument for routine multipatient surveillance of respiratory and anesthetic gases during anesthesia.
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.
Anesthetics↗
Composition of fresh frozen plasma.
We analyzed 35 samples of fresh frozen plasma (FFP), finding mean concentrations of 535 mg/dl glucose, 172 mEq/L sodium, 73 mEq/L chloride, 3.5 mEq/L potassium, 15 mEq/L bicarbonate, and 5.5 g/dl protein with 60% albumin. Thus, FFP is a hyperosmolal, hyperglycemic, hypernatremic, and hypochloremic solution which may be a less effective volume expander than other albumin-containing solutions, due to its lower albumin content.
Plasma↗
Cardiovascular and blood gas responses to inhaled anaesthetics in normoxic and hypoxic dogs.
Changes in haemodynamics and blood gases were investigated before and after administration of 0.5, 1 and 1.5 MAC of halothane, enflurane and isoflurane in respectively 7, 7 and 9 dogs ventilated alternatively with a fraction of inspired O2 in N2 (FiO2) of 0.4 and with brief periods (10 min) of FiO2 of 0.1. Anaesthesia was induced with pentobarbital and the animals were paralysed with pancuronium. Acute hypoxic challenges with FiO2 of 0.1 consistently decreased arterial PO2 to 3.5-4.5 kPa and increased pulmonary vascular resistances by 60-100%. At identical inspired concentrations, as expressed in MAC units, all three inhaled anaesthetics induced a broadly comparable dose-related decrease in systemic blood pressures, due to a depression in cardiac performance as well as a reduction in systemic vascular resistances. Enflurane was the most potent myocardial depressor and isoflurane the most potent vasodilator, halothane being intermediate. Oxygen deprivation was associated with some enhancement of the cardiovascular depressant effects of the inhaled anaesthetics but, in spite of this, matching of O2 transport to tissue O2 demand appeared to be improved, probably in relation to a concomitant reduction in metabolic rate. Only isoflurane inhibited the hypoxic pulmonary pressor response, and this was associated with a slight deterioration in arterial oxygenation in both normoxic and hypoxic conditions.
Adaptation, Physiological↗
Immunological mechanisms of reactions to macromolecular solutions.
Hypersensitivity reactions to intravenous macromolecular solutions are an exacerbation of the organism defence mechanisms with production of exaggerated and deleterious effects. The immediate adverse reactions to drugs (anaphylaxis) have clinical manifestations-due to histamine release principally: cutaneous (rash, urticaria, edema); pulmonary (bronchospasm), and cardiovascular (hypotension, collapse, cardiac arrest); their intensity may be graded in degrees I to V. These reactions may be either truly anaphylactic (immunological): hypersensitivity type I with reaginic antibodies (IgE), requiring previous exposure to the drug (true allergy); other immune responses with antigen-antibody (IgG or IgM) complexes activating classical complement pathway; or anaphylactoid; indirect histamine release by direct activation of C3 (alternate complement pathway) direct histamine release by pharmacological effect; dose related effects. The incidence of reactions to plasma substitutes vary greatly according to authors. In most cases, gelatin derivatives act by direct action on mast cells (histamine release) and indeed prevention of reaction with antihistamines is effective; antibody related reactions occasionally occur (immune complexes). With dextrans, soluble immune complexes aggregates have been described; dextrans may react to specific antibodies (possibly previously produced by bacterial polysaccharides); complement activation occur only in severe reactions. HES is comparable to dextran, antibodies have been described. Other factors may predispose to anaphylactoid reactions such as genetic factors (atopy, primary complement anomalies) underlying immune processes and stress. All macromolecular solutions carry the risk of anaphylactoid side-reactions, the mechanisms of which are not completely clarified.
Anaphylaxis↗
Objective regression of unexcised melanoma in-transit metastases after hyperthermic isolation perfusion of the limbs with melphalan.
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Adult↗
Open trial of cimetidine in the prevention of upper gastro-intestinal haemorrhage in patients with severe intracranial injury.
The present study evaluates the efficacy of Cimetidine in the prevention of clinically important gastro-intestinal haemorrhage in patients suffering from severe head injury. Fifty patients (39 males and 11 females) were included in the study. We excluded from the trial patients on anticoagulant therapy or concomitant non-steroid anti-inflammatory agents, pregnant and lactating women, and patients with previous histories of peptic ulcer disease.
Adolescent↗
Is lumbar epidural analgesia an alternative in patients who have incomplete colonoscopy with standard premedication?
Total colonoscopy is unsuccessful in about 10% of attempts. In three fourths of the cases, failure is due to the patient's inability to tolerate the procedure and difficulty in negotiating the sigmoid colon. Lumbar epidural analgesia has been used in a series of 29 patients referred for total colonoscopy which had been unsuccessful using intravenous analgesia. The cecum was reached in 27 of 29 examinations. Mean time required to perform total colonoscopy was 10 min and took less than 5 min in one third of the cases. Complete visceral analgesia was responsible for one case of perforation.
Adolescent↗
[Medical management of intracranial hypertension in severe head injuries (author's transl)].
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Barbiturates↗
Etomidate infusion for laryngoscopy.
Reporting our experience with etomidate infusion in 37 cases of endoscopic examinations of the larynx, we recommend a method of general anesthesia ensuring easy examination conditions and rapid recovery. After premedication with atropine, IV Thalamonal is administered till obtention of somnolence. A dose of 0.25 mg/kg of etomidate is used for induction and an infusion at a rate of 25 mcg/kg/min for maintenance of anesthesia. Succinylcholine is used for intubation and whenever complementary muscular relaxation is required. Ventilation is ensured by the jet mixing technique with a manual injector. Fentanyl is given when reactions of tachycardia or arterial hypertension due to nociceptive stimuli are observed. The method described is safe, provides good conditions of anesthesia with complete amnesia and rapid recovery.
Adjuvants, Anesthesia↗