[Atrial fibrillation: from cardiology to perioperative management]. / Fibrillation atriale en anesthésie-réanimation : de la cardiologie médicale à la période périopératoire.

Atrial fibrillation (AF) is the most frequent arythmia. During the perioperative period and in intensive care units, management of patients with AF is frequent and difficult. As in cardiology, two main issues are present: the risk of acute hemodynamically instability and the risk of thromboembolic complication. Cardiological guidelines recently published must guide the management of patients in this context. Two main factors must be kept in mind: acute AF in these situations are often of short duration; the risk of anticoagulation can be superior to the risk of thrombotic complication in this situation. An individualized benefit-risk analysis must be done in each patient. New treatments, antiarrhythmic or mainly antithrombotic drugs, are under evaluation and will be soon available.

Role of nitric oxide and cyclooxygenase pathways in the coronary vascular effects of halothane, isoflurane and desflurane in red blood cell-perfused isolated rabbit hearts.

BACKGROUND: The coronary vascular endothelium could mediate some of the coronary effects of halogenated anaesthetic agents. The role of the endothelial vasodilator substances nitric oxide (NO) and prostaglandins (PGs) in the coronary effects of halothane and isoflurane remains to be determined and has not been investigated for desflurane. In this study, the roles of NO and cyclooxygenase pathways in the coronary effects of halothane, isoflurane and desflurane were studied in isolated red blood cell-perfused rabbit hearts. METHODS: Rabbit hearts were perfused by a Langendorf technique with red blood cells mixed with modified Krebs-Henseleit buffer. Coronary blood flow (CBF), oxygen consumption and myocardial performance were evaluated during exposure to 0.5, 1 and 2 rabbit minimum alveolar concentrations of halothane, desflurane and isoflurane. Thereafter, the same protocol was applied with the addition of N(G)-nitro-L-arginine (L-NNA), indomethacin or a combination of both inhibitors. RESULTS: Similar and significant increases in CBF were observed with increasing concentrations of isoflurane and desflurane. In contrast, CBF did not change with halothane. The combination of the two antagonists abolished desflurane-induced vasodilation, whereas it did not change the isoflurane-mediated increase in CBF. Halothane-induced vasoconstriction was observed in the presence of a combination of indomethacin with L-NNA. CONCLUSIONS: Halothane and desflurane induce the release of vasodilating prostaglandins and NO in rabbit coronary arteries. In contrast, these mediators are not involved in the coronary vasodilating properties of isoflurane.

The continuous recording of blood pressure in patients undergoing carotid surgery under remifentanil versus sufentanil analgesia.

UNLABELLED: We compared the hemodynamic stability during carotid endarterectomy of remifentanil with that of sufentanil anesthesia. Fifty-six patients were randomly assigned into Remifentanil (n = 27) or Sufentanil (n = 29) groups. In the Remifentanil group, IV propacetamol (2 g) and morphine (0.1 mg/kg) were infused 30 min before skin closure. In the Sufentanil group, patients received 2 g propacetamol. Beat-to-beat recordings of systolic arterial blood pressure (SBP) and heart rate (HR) were stored on a computer. The maximum and minimum values of BP and HR after induction, at intubation, during the surgical procedure, and after the operation and the coefficients of variation of SBP and HR were used as indices of hemodynamic stability. The coefficients of variation of SBP and HR were similar in both groups during and after surgery. However, at intubation, maximal SBP was higher in the Sufentanil group (P < 0.05). Decreased propofol doses and isoflurane end-tidal concentrations were used in the Remifentanil group. At recovery, a similar profile of SBP and HR was found in both groups. We conclude that intra- and posthemodynamic stability was similar with remifentanil or sufentanil in patients undergoing carotid endarterectomy. However, remifentanil was more effective for blunting the increase in SBP at intubation without increasing the blood pressure-decreasing effect of induction. Intraoperative remifentanil use was associated with a decreased amount of hypnotic drug administered. IMPLICATIONS: Beat-to-beat recordings of heart rate and blood pressure in patients undergoing carotid surgery revealed that hemodynamic stability was similar with remifentanil or sufentanil anesthesia both during and after surgery. Remifentanil was more effective in limiting the increase in blood pressure associated with intubation without increasing the blood pressure-lowering effect of induction or the blood pressure response to recovery.

Myocardial and coronary effects of propofol in rabbits with compensated cardiac hypertrophy.

BACKGROUND: Myocardial effects of propofol have been previously investigated but most studies have been performed in healthy hearts. This study compared the cardiac effects of propofol on isolated normal and hypertrophic rabbits hearts. METHODS: The effects of propofol (10-1,000 microM) on myocardial contractility, relaxation, coronary flow and oxygen consumption were investigated in hearts from rabbits with pressure overload-induced left ventricular hypertrophy (LVH group, n = 20) after aortic abdominal banding and from sham-operated control rabbits (SHAM group, n = 10), using an isolated and erythrocyte-perfused heart model. In addition, to assess the myocardial and coronary effects of propofol in more severe LVH, hearts with a degree of hypertrophy greater than 140% were selected (severe LVH group, n = 7). RESULTS: The cardiac hypertrophy model induced significant left ventricular hypertrophy (136+/-21%, P < 0.05). The pressure-volume relation showed normal systolic function but an altered diastolic compliance in hypertrophic hearts. Propofol only decreased myocardial contractility and relaxation at supratherapeutic concentrations (> or = 300 microM) in SHAM and LVH groups. The decrease in myocardial performances was not significantly different in SHAM and LVH groups. Propofol induced a significant increase in coronary blood flow which was not significantly different between groups. In severe LVH group, the degree of hypertrophy reached to 157+/-23%. Similarly, the effects of concentrations of propofol were not significantly different from the SHAM group. CONCLUSIONS: Propofol only decreased myocardial function at supratherapeutic concentrations. The myocardial and coronary effects of propofol were not significantly modified in cardiac hypertrophy.

Does desflurane alter left ventricular function when used to control surgical stimulation during aortic surgery?

BACKGROUND: Although desflurane is commonly used to control surgically induced hypertension, its effects on left ventricular (LV) function have not been investigated in this clinical situation. The purpose of the present study was to evaluate the LV function response to desflurane, when used to control intraoperative hypertension. METHODS: In 50 patients, scheduled for vascular surgery, anesthesia was induced with sufentanil 0.5 microg/kg, midazolam 0.3 mg/kg and atracurium 0.5 mg/kg. After tracheal intubation, anesthesia was maintained with increments of drugs with controlled ventilation (N2O/O2=60/40%) until the start of surgery. A 5 Mhz transesophageal echocardiography (TEE) probe was inserted after intubation. Pulmonary artery catheter and TEE measurements were obtained after induction (to)(control value), at surgical incision (t1) if it was associated with an increase in systolic arterial pressure (SAP) greater than 140 mmHg (hypertension) and after control of hemodynamic parameters by administration of desflurane (return of systolic arterial pressure to within 20% of the control value) (t2) in a fresh gas flow of 31/ min. RESULTS: Sixteen patients developed hypertension at surgical incision. SAP was controlled by desflurane in all 16 patients. Afterload assessed by systemic vascular resistance index (SVRI), end-systolic wall-stress (ESWS) and left-ventricular stroke work index (LVSWI) increased with incision until the hypertension returned to post-induction values with mean end-tidal concentration of 5.1+/-0.7% desflurane. No change in heart rate, cardiac index, mean pulmonary arterial pressure, stroke volume, end-diastolic and end-systolic cross-sectional areas, fractional area change and left ventricular circumferential fiber shortening was noted when desflurane was added to restore blood pressure. CONCLUSION: This study demonstrates that in patients at risk for cardiac morbidity undergoing vascular surgery, desflurane is effective to control intraoperative hypertension without fear of major cardiac depressant effect.

Treating anesthesia-induced hypotension by angiotensin II in patients chronically treated with angiotensin-converting enzyme inhibitors.

UNLABELLED: Although angiotensin II bolus administration may be used to increase blood pressure in patients chronically treated with angiotensin-converting enzyme inhibitors (ACEI) who have severe hypotension on anesthetic induction, no data are available describing its time course and its effects on the left ventricular function. Fourteen patients chronically treated with ACEI for hypertension and scheduled for vascular surgery were prospectively studied. Patients with cardiac insufficiency were excluded. A transesophageal echocardiography probe was inserted to assess systolic left ventricular function. When hypotension was observed (systolic arterial pressure [SAP] <85 mm Hg), an I.V. bolus of 2.5 microg of angiotensin II (AII) was given, and hemodynamic variables were recorded each 30 s over 5.5 min. Results are expressed as mean +/- SEM. Sixty seconds after the AII bolus injection, the SAP increased from 78 +/- 3 to 152 +/- 6 mm Hg. SAP remained higher than control until the 5th min. This was associated with significant increases in end-diastolic area (from 15.1 +/- 0.6 to 19.3 +/- 1.0 cm2, P < or = 0.001), end-systolic area (from 6.6 +/- 0.4 to 10.7 +/- 0.7 cm2, P < or = 0.001), end-systolic wall stress (from 32 +/- 0.05 to 82 +/- 7 kdynes/cm2, P < or = 0.001). In addition, a decrease in fiber-shortening velocity (from 1.1 +/- 0.05 to 0.76 +/- 0.04 circ/s, P < or = 0.05) and in fractional area change (from 0.57 +/- 0.02 to 0.44 +/- 0.02, P < or = 0.05) was observed. Heart rate did not significantly change during the study. Increases in preload and afterload were observed. However, the administration of AII causes a transient impairment in left ventricular function. We conclude that AII, given as an I.V. bolus of 2.5 microg, is effective in restoring arterial blood pressure within 60 s in patients chronically treated with ACEI. IMPLICATIONS: Severe hypotension on anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors for hypertension could be treated with an I.V. bolus of 2.5 microg of angiotensin II.

Mechanisms of coronary vasoconstriction induced by high arterial oxygen tension.

In isolated rabbit hearts perfused with suspension of red blood cells, we investigated the role of the endothelium and of several substances in the coronary vasoconstriction induced by a high arterial blood oxygen tension (PaO2). Red blood cells in Krebs-Henseleit buffer were oxygenated to obtain control and high-PaO2 perfusates. Arterial oxygen content was kept constant in both perfusates by reducing hemoglobin concentration in the high-PaO2 perfusate. Coronary blood flow was kept constant so that oxygen supply would not vary with the rise in PaO2. Increases in perfusion pressure therefore reflected increased coronary resistance. The high PaO2-induced coronary vasoconstriction was not affected by administration of indomethacin, nordihydroguaiaretic acid, NG-nitro-L-arginine, or superoxide dismutase and catalase but was abolished after endothelium damage or by cromakalim. These results demonstrate that 1) the endothelium contributes to the high PaO2-induced coronary vasoconstriction; 2) this effect is independent of cyclooxygenase or lipoxygenase products, nitric oxide, or free radicals; and 3) the closure of ATP-sensitive K+ channels mediates this vasoconstriction.

Effects of eltanolone on myocardial performance and coronary flow in intact and catecholamine-depleted isolated rabbit hearts.

BACKGROUND: Experimental studies suggest that the new short-acting intravenous anesthetic agent eltanolone does not markedly alter hemodynamics or cardiac function. However, because its intrinsic effects on myocardial performance and coronary blood flow are not yet known, they were examined in isolated blood-perfused rabbit hearts. METHODS: Coronary blood flow, myocardial contractility, relaxation, and oxygen consumption were measured during perfusion of hearts with 0.1 to 10 micrograms/ml eltanolone (n = 7) or its vehicle (n = 7). To determine whether the cardiac effects of eltanolone are mediated by indirect sympathetic activation, the same dose-response curve was studied in another group of five hearts depleted of catecholamine with reserpine treatment. RESULTS: Coronary blood flow significantly increased with 10 micrograms/ml eltanolone and significantly decreased with 10 micrograms/ ml eltanolone vehicle. At eltanolone concentrations less than 10 micrograms/ml, myocardial contractility and relaxation remained unchanged but decreased at 10 micrograms/ml. Myocardial contractility and relaxation were not affected by perfusion of eltanolone vehicle alone. In eltanolone-perfused hearts, unchanged myocardial oxygen consumption was associated with significant increases in coronary venous oxygen content and tension, but in vehicle-perfused hearts, it was associated with reduced coronary venous oxygen content and tension. In catecholamine-depleted hearts, the variations in myocardial performance and coronary blood flow induced by eltanolone were similar to those observed in intact hearts. CONCLUSIONS: Eltanolone (0.1 to 3 micrograms/ml) did not alter myocardial performance or coronary blood flow in isolated blood-perfused rabbit hearts. These effects were not due to an eltanolone-induced indirect sympathetic activation. Cardiac depression and coronary vasodilatation were only observed at concentrations of eltanolone far greater than those in clinical range.

Mechanisms of increased myocardial contractility with hypertonic saline solutions in isolated blood-perfused rabbit hearts.

Hypertonic saline improves organ perfusion and animal survival during hemorrhagic shock because it expands plasma volume and increases tissue oxygenation. Because both decreased and increased myocardial performance have been reported with hypertonic saline, the effects of hyperosmolarity and the mechanism accounting for it were investigated in isolated blood-perfused rabbit hearts. Coronary blood flow (CBF), myocardial contractility, relaxation, and oxygen consumption were measured during administration of blood perfusates containing 140-180 mmol sodium concentrations ([Na+]). In two other series of experiments, the role of Na(+)-Ca2+ exchange in the inotropic effect of hyperosmolarity (160 mmol sodium concentration) and hypertonicity (sucrose) were also investigated. Hypertonic [Na+] induced a significant increase in contractility and relaxation, combined with a coronary vasodilation. Myocardial oxygen consumption (MVO2) increased at all hypertonic [Na+] without significant change in coronary venous oxygen tension (PVO2) and content (CVO2). Amiloride (0.3 mmol) inhibited the improved contractility observed with 160 mmol sodium. Similar Na(+)-Ca2+ exchanger blockade did not inhibit the inotropic effect of sucrose. These results confirm the positive inotropic effect of hypertonic [Na+]. The inhibition of this improvement by amiloride suggests that calcium influx through the sarcolemna could be the major mechanism of this effect.

Amplification by phenylephrine and serotonin of coronary vasoconstriction induced by a high arterial blood oxygen tension.

OBJECTIVE: The aim was to investigate the effect on the coronary network of the interaction between high arterial blood oxygen tension (PaO2) and stimulation by the alpha adrenergic agonist phenylephrine or by serotonin in an isolated, blood perfused rabbit heart preparation. METHODS: Fresh pig erythrocytes in Krebs-Henseleit buffer were oxygenated to reach normal PaO2 [19.4(SEM 0.7) kPa] or high PaO2 [53.2(5.5) kPa]. Blood oxygen content was kept constant despite the higher PaO2, by slightly reducing the haemoglobin concentration from 9.3(0.2) to 8.8(0.2) g.100 ml-1 (p < 0.01). Coronary blood flow was kept constant throughout the study, so that the oxygen supply would not vary with the rise in PaO2. Increases in coronary resistance were therefore reflected by increased perfusion pressure. RESULTS: Switching from normal to high PaO2 induced coronary vasoconstriction, reflected by enhanced perfusion pressure of +21(5)%. After pretreatment with the alpha adrenergic agonist phenylephrine, perfusion of a high PaO2 solution increased coronary resistance by +35(7)% (p < 0.05), a value significantly higher than that found without phenylephrine. Oxygen consumption and myocardial performance did not vary throughout the study. To determine whether this amplification of the response was specifically due to alpha agonist stimulation or could be observed with other vasoactive agents, we applied the same protocol using serotonin instead of phenylephrine. Here again, coronary vasoconstriction rose in response to high PaO2 after serotonin infusion [+25(5)% versus +59(10)%]. CONCLUSIONS: The response of the coronary network to high PaO2 is amplified by pretreatment with the alpha adrenergic agonist phenylephrine or with serotonin, regardless of any changes in metabolic status.

Effects of propofol and thiopental on coronary blood flow and myocardial performance in an isolated rabbit heart.

BACKGROUND: Some clinical and experimental studies suggest that propofol decreases myocardial contractility and relaxation, whereas others report preserved cardiac function. To investigate the effects of propofol on intrinsic contractility and relaxation, increasing concentrations of propofol were infused in isolated blood-perfused rabbit hearts. Equimolar concentrations of thiopental were infused as a reference group. METHODS: Coronary blood flow, left ventricular contractility and relaxation (as maximal positive and negative left ventricular pressure derivatives [dP/dtmax and dP/dtmin], respectively), and myocardial oxygen consumption (MvO2) were measured during infusion of 10-1,000 microM propofol in blood-perfused hearts. To determine whether the effects of propofol depend on the heart's perfusate, propofol also was infused in isolated buffer-perfused rabbit hearts. In addition, the effects of propofol solvent were investigated in blood- and buffer-perfused preparations. RESULTS: In blood-perfused preparations, coronary blood flow increased with propofol concentrations greater than 30 microM and with 300 and 1,000 microM thiopental. Left ventricular dP/dtmax and dP/dtmin remained unchanged with propofol and decreased with concentrations of thiopental equal to or greater than 30 microM. MvO2 increased with 1,000 microM propofol, whereas coronary venous oxygen tension and content remained unchanged. MvO2 decreased with thiopental associated with a significant increase in coronary venous oxygen tension and content. In six buffer-perfused hearts, basal coronary blood flow was much greater and MvO2 less than in blood-perfused hearts. Left ventricular dP/dtmax and dP/dtmin decreased with 30, 100, and 300 microM propofol. Propofol vehicle did not change coronary blood flow, myocardial performance, or MvO2 of blood- or buffer-perfused hearts. CONCLUSIONS: When compared to a reference drug such as thiopental, propofol did not depress the myocardial performance of blood-perfused rabbit hearts. The type of the perfusate (blood vs. buffer), however, had a major influence on the myocardial effects of propofol.

Red blood cell aggregation and blood viscosity in an isolated heart preparation.

We studied the effects of moderate changes in red blood cell RBC aggregation on blood flow in the vasodilated vascular bed of an isolated rat heart. We compared a non-aggregating RBC suspension (in Krebs-albumin medium) with RBC suspensions in 1% and 2% Dextran 70 (MW 70000), exhibiting two different degrees of moderate aggregation. Degrees of aggregation were precisely estimated by in vitro laser aggregometry. Each heart was perfused by the non-aggregating RBC suspension and by one aggregating RBC suspensions. Blood flow was measured in a range of perfusion pressure from 40 to 80 mm Hg. For the three RBC suspensions, linear pressure/flow relationships were found. From the comparison between the pressure/flow relationships obtained with Krebs albumin medium and either 1% or 2% Dextran, it was possible to compare in vivo the contribution of RBC to the viscosity (i.e., the relative apparent viscosity) in the 2 aggregating RBC suspensions with that of the non-aggregating RBC suspension. The contribution of RBC to the viscosity was found to be 20% to 25% lower in the 1% RBC suspension than in the non-aggregating RBC suspension. With 2% Dextran which induced a higher degree of aggregation no differences were found between the relative apparent viscosities of the aggregating and the non-aggregating suspension. From the comparison between RBC in 1% Dextran and Krebs-albumin, we concluded that in vivo a moderate RBC aggregation reduces viscous resistance due to the presence of blood in a vascular network. Since no more effect of RBC aggregation per se was found when the degree of aggregation was higher (with RBC in 2% Dextran), this suggests that, in this case, aggregation induces opposite effects along the myocardial vascular network which cancel each other out, thus inducing a nil net balance.

Comparison of isoflurane with sodium nitroprusside for controlling hypertension during thoracic aortic cross-clamping.

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)

[Peri- and postoperative use of low molecular weight heparin in peripheral vascular surgery]. / Utilisation per et postopératoire d'une héparine de bas poids moléculaire en chirurgie vasculaire périphérique.

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.

Normovolemic hemodilution and lumbar epidural anesthesia.

This randomized study was designed to determine the cardiovascular effects of normovolemic hemodilution and lumbar epidural anesthesia in patients scheduled for vascular surgery. The patients were randomly assigned to three different groups: group 1 (N = 10) included patients undergoing lumbar epidural anesthesia without hemodilution; group 2 (N = 10) consisted of patients with normovolemic hemodilution without epidural anesthesia; and in group 3 (N = 10) normovolemic hemodilution was produced during lumbar epidural anesthesia. The three groups included several patients with a history of either myocardial infarction or stable mild angina or treated and controlled hypertension. In group 1, the level of epidural anesthesia reached T-9 +/- 1. After lumbar epidural anesthesia and 7 mL/kg colloid infusion, pulmonary capillary wedge pressure increased slightly but significantly above baseline, without significant changes either in mean arterial pressure or in cardiac index. In group 2, the same colloid infusion as in group 1 when infused before normovolemic hemodilution increased pulmonary capillary wedge pressure and cardiac index without significant effects on arterial blood pressure. Normovolemic hemodilution using a colloid solution decreased hemoglobin concentration (18%) and increased cardiac index significantly (9%). No significant change in systemic oxygen transport or in total body oxygen consumption was observed. In group 3, with anesthesia to T-9 +/- 1, hemodynamic changes were as observed in group 1. After normovolemic hemodilution, hemoglobin concentration decreased significantly (15%), whereas cardiac index increased significantly (15%) without significant changes either in mean arterial pressure or in heart rate. Systemic oxygen transport and total body oxygen consumption did not change significantly. No patient experienced chest pain or electrocardiographic evidence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

[Baroreflex activity in carotid endarterectomy during general anesthesia]. / Etude de l'activité baroréflexe lors de l'endartériectomie carotidienne sous anesthésie générale.

The baroreceptor reflex was studied in eleven patients, aged 69 +/- 6 years, scheduled for carotid endarterectomy under general anaesthesia. Nine were hypertensive. The anaesthetic protocol was the same for all the patients: premedication with morphine and scopolamine, induction with 5 mg.kg-1 thiopentone, 6 micrograms.kg-1 fentanyl and 0.01 mg.kg-1 pancuronium bromide. All the patients were intubated and ventilated with a mixture of nitrous oxide and oxygen. Fentanyl, 100 micrograms, was routinely given at the time of incision. Baroreflex sensitivity was tested using Smyth's method, with a bolus of 75 micrograms trinitrin and plotting changes in heart rate against those in systolic blood pressure. Electrocardiogram, invasive arterial blood pressure and airway pressure were simultaneously recorded. PaCO2 and PaO2 were measured during arterial clamping. The tests were carried out before clamping, 2 min later and 10 to 20 min after the last injection of fentanyl. In the seven patients for whom clamping lasted more than 15 min, a further test was carried out after administration of 0.4 +/- 0.05 vol% halothane (Datex analyser) for 5 min. During anaesthesia, baroreflex sensitivity was low (1.8 +/- 0.3 ms.mmHg-1). After clamping, there was only a significant change in Pasys, with no changes in heart rate or blood gas values (129 +/- 8 mmHg before clamping; 167 +/- 12 mmHg after clamping; n = 8; p less than 0.01). After halothane administration, the sensitivity slope decreased, but not significantly. Moreover, halothane decreased the R-R intervals (1140 +/- 84 after clamping; 963 +/- 76 under halothane; n = 6; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Ischemia, myocardial infarction and epidural anesthesia in patients with coronary disease]. / Ischémie, infarctus myocardique et anesthésie péridurale chez le coronarien.

In patients with coronary artery disease, the beneficial effects of epidural anesthesia are well known and often emphasized. Thus, several studies have shown a decrease in the determinants of myocardial oxygen consumption, and an improvement in regional and global left ventricular performance. The disadvantages of epidural anesthesia in patients with coronary artery disease are also well known, however, rarely reported. These detrimental effects are dominated by a decrease in arterial pressure which in turn may compromise the coronary perfusion pressure and induce myocardial ischemia. These 2 case reports illustrate the occurrence of myocardial complications in relation to epidural anesthesia. These case reports contrast with data from the literature showing a beneficial influence of epidural anesthesia on the myocardium. However, the severity of the coronary artery disease in these 2 reported patients may explain this discrepancy. These case reports pointed out that the decrease in arterial pressure is not the exclusive mechanism by which myocardial ischemia may be observed during epidural anesthesia since an hemodynamically-unrelated ischemic episode is described. The treatment of myocardial ischemia during epidural anesthesia is illustrated by these 2 case reports. A relationship between myocardial ischemia and myocardial infarction is discussed from these observations.