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Biomedical subjects

B Vigué

Publications and source records attributed to B Vigué.

12 recordsLinked to original sources
PubMed2001

Comparison of the cerebral effects of dopamine and norepinephrine in severely head-injured patients.

OBJECTIVE: To compare the cerebral effects of dopamine and norepinephrine after severe head injury. DESIGN: Prospective, clinical study. SETTING: Surgical intensive care unit in a university hospital. PATIENTS: Nineteen patients with severe head-injuries already requiring vasopressor therapy. Group 1: patients receiving dopamine (n = 9); group 2: patients receiving norepinephrine (n = 10). INTERVENTION: Vasopressor therapy was switched from dopamine to norepinephrine in group 1 and from norepinephrine to dopamine in group 2, maintaining the same mean arterial pressure (MAP). MEASUREMENTS AND RESULTS: MAP, intracranial pressure (ICP), jugular venous oxygen saturation (SjvO2), transcranial Doppler mean velocity in the middle cerebral artery (Vm), and transoesophagal Doppler aortic output (AO) were evaluated under dopamine and norepinephrine. Means for each group were compared with the paired Student's t-test. For the same MAP, ICP was significantly higher with dopamine than norepinephrine in both groups (respectively, group 1: 26 +/- 11 vs 23 +/- 11 mmHg, P < 0.005; group 2: 39 +/- 13 vs 31 +/- 9 mmHg, P < 0.005). SjvO2, Vm, and AO did not change significantly between treatments. The ICP variation between treatments was not correlated with the variation of any other measured parameter. The ICP variation between treatments was significantly higher in group 2 than group 1, which could be explained by autoregulation mechanisms. CONCLUSIONS: For the same MAP, ICP was significantly higher with dopamine than norepinephrine with no argument supporting an increase of cerebral blood flow.

Adolescent↗
PubMed2001

Hypoxia-hypotension decreases pressor responsiveness to exogenous catecholamines after severe traumatic brain injury in rats.

OBJECTIVE: To quantify the phenylephrine pressor responsiveness after severe brain injury combined with hypoxia-hypotension, and to study the respective roles of brain injury and hypoxia-hypotension in the observed alteration. DESIGN: Randomized study. SETTING: Accredited animal laboratory. SUBJECTS: Adult Sprague Dawley rats. INTERVENTIONS: Anesthetized animals were assigned to control, brain injury, hypoxia-hypotension, and brain injury combined with hypoxia-hypotension groups. Brain injury was induced with an impact-acceleration device. During the 15-min hypoxia-hypotension, arterial oxygen pressure was decreased to 40 torr (5.3 kPa) and mean arterial pressure to 30 mm Hg. Thirty-six of the 53 included rats were alive at the end of hypoxia-hypotension (nine animals per group). In an additional group (Hypo, n = 8), mean arterial pressure was lowered to the level observed in brain injury combined with hypoxia-hypotension with pentobarbital infusion. Sixty minutes after injuries (T60), animals received 0.1, 1, and 10 microg/kg phenylephrine in a random order. Pressor responsiveness to phenylephrine was defined as maximal postinjection minus preinjection mean arterial pressure. MEASUREMENTS AND MAIN RESULTS: During hypoxia-hypotension, mortality was higher and residual restored blood volume was lower (p <.01) in the animals with brain injury and hypoxia-hypotension compared with hypoxia-hypotension alone. At T60, mean arterial pressure (mm Hg) was lower (p <.01) in the brain injury group (83 +/- 22) compared with controls (110 +/- 10) and in brain injury combined with hypoxia-hypotension (76 +/- 18) compared with controls and hypoxia-hypotension (107 +/- 14). Pressor responsiveness (mm Hg) to 1 and 10 microg/kg phenylephrine was less (p <.05) in brain injury combined with hypoxia-hypotension (15 +/- 6 and 44 +/- 8) and hypoxia-hypotension (15 +/- 3 and 44 +/- 8) compared with controls (26 +/- 2 and 57 +/- 11). No significant difference was observed for phenylephrine pressor responsiveness between controls and the Hypo group (25 +/- 5 and 66 +/- 7). CONCLUSIONS: Combination of brain injury and hypoxia-hypotension induces a severe hemodynamic alteration associated with a decreased pressor responsiveness to phenylephrine. Transient hypoxia-hypotension is responsible for the depressed alpha-1 adrenergic reactivity.

Adrenergic alpha-Agonists↗
PubMed2000

Relationship between intracranial pressure, mild hypothermia and temperature-corrected PaCO2 in patients with traumatic brain injury.

OBJECTIVE: To study the effects of mild hypothermia and associated changes in temperature-corrected PaCO2 (cPaCO2) on intracranial pressure (ICP), mean velocity of the middle cerebral artery (Vm), and venous jugular saturation in O2 (SjvO2) in patients with severe traumatic brain injury (TBI). DESIGN: Prospective, observational study. SETTING: Intensive care unit. PATIENTS: Severe TBI patients mechanically ventilated, sedated and paralyzed. INTERVENTIONS: Twenty patients were subjected to four consecutive periods: (a) normocapnia-normothermia; (b) hypocapnia-normothermia, where hypocapnia was induced by an increase in minute volume; (c) hypocapnia-hypothermia, where hypocapnia was induced by hypothermia maintaining the ventilatory settings constant; (d) normocapnia-hypothermia, where normocapnia was achieved by a decrease in minute volume. MEASUREMENTS AND RESULTS: cPaCO2 was 41 +/- 8 mmHg in periods 1 and 4, and 31 +/- 7 mmHg in periods 2 and 3. Core temperature was 37.1 +/- 0.8 degrees C in periods 1 and 2, and 34.1 +/- 1.1 degrees C in periods 3 and 4. End-tidal CO2 and cPaCO2 values showed no difference between periods 1 and 4 and periods 2 and 3. ICP and Vm were dependent on cPaCO2 but independent of core temperature values. SjvO2 was related to cPaCO2 and was significantly higher during period 3 than during period 2 (P < 0.05). CONCLUSION: The decrease in ICP was similar when hypocapnia was induced by hyperventilation or as a result of hypothermia alone. The relationship between cPaCO2 and ICP might predict variations in ICP during changes in core temperature. Further studies are needed to confirm the cerebral metabolic effects of moderate hypothermia in TBI patients.

Adult↗
PubMed1999

Early SjvO2 monitoring in patients with severe brain trauma.

OBJECTIVE: To investigate early cerebral variables after minimal resuscitation and to compare the adequacy of a cerebral perfusion pressure (CPP) guideline above 70 mmHg, with jugular bulb venous oxygen saturation (SjvO2) monitoring in a patient with traumatic brain injury (TBI). DESIGN: Prospective, observational study. SETTING: Anesthesiological intensive care unit. PATIENTS: 27 TBI patients with a postresuscitation Glasgow Coma Scale score less than 8. INTERVENTION: After initial resuscitation, cerebral monitoring was performed and CPP increased to 70 mmHg by an increase in mean arterial pressure (MAP) with volume expansion and vasopressors as needed. MEASUREMENTS AND RESULTS: MAP, intracranial pressure (ICP), CPP, and simultaneous arterial and venous blood gases were measured at baseline and after treatment. Before treatment, 37% of patients had an SjvO2 below 55%, and SjvO2 was significantly correlated with CPP (r = 0.73, p < 0.0001). After treatment, we observed a significant increase (p < 0.0001) in CPP (78+/-10 vs 53+/-15 mmHg), MAP (103+/-10 vs 79+/-9 mmHg) and SvjO2 (72+/-7 vs 56+/-12), without a significant change in ICP (25+/-14 vs 25+/-11 mmHg). CONCLUSION: The present study shows that early cerebral monitoring with SjvO2 is critical to assess cerebral ischemic risk and that MAP monitoring alone is not sensitive enough to determine the state of oxygenation of the brain. SjvO2 monitoring permits the early identification of patients with low CPP and high risk of cerebral ischemia. In emergency situations it can be used alone when ICP monitoring is contraindicated or not readily available. However, ICP monitoring gives complementary information necessary to adapt treatment.

Adolescent↗
PubMed1996

Left ventricular function after severe trauma.

OBJECTIVE: To evaluate cardiac function at the early phase of severe trauma. DESIGN: Prospective, clinical study. SETTING: Anesthesiological Intensive Care Unit. PATIENTS: 7 consecutive patients admitted after severe trauma (ISS: 38 +/- 9, mean +/- SD), without preexisting cardiac disease. INTERVENTIONS: Each patient received midazolam and sufentanyl for sedation. Right heart catheterization (Swan-Ganz) and transesophageal echocardiography (TEE) were performed. The fractional area change (FAC) of the left ventricle was calculated within 6 h following trauma and at day 1 and day 2 in order to evaluate left ventricular function. MEASUREMENTS AND RESULTS: All of the patients had a low FAC value < 50% at day 0 (43.2 +/- 2.4%, range 39-46%), which increased significantly at day 2 (52.5 +/- 4%, range 47-59%, p = 0.001), whereas heart rate and preload (assessed by left ventricular end diastolic area and pulmonary arterial occlusion pressure) were constant and afterload, assessed by systolic blood pressure, increased significantly between day 0 and day 2 (112 +/- 21 to 145 +/- 24 mmHg, p = 0.02). CONCLUSION: The initial phase of severe trauma is associated with an abnormal cardiac function, suggested by a low FAC value. This myocardial dysfunction must be taken into account for early resuscitation after severe injury.

Adult↗
PubMed1995

Role of systemic inflammatory response syndrome and infection in the occurrence of early multiple organ dysfunction syndrome following severe trauma.

OBJECTIVE: To evaluate the role of infection and systemic inflammatory response syndrome (SIRS) on the occurrence of early posttraumatic MODS. DESIGN: Retrospective study. SETTING: University Teaching Hospital ICU. PATIENTS: 163 consecutive patients hospitalized for more than 48 hours following severe trauma. MEASUREMENTS AND MAIN RESULTS: The patients were classified into two groups in respect to the existence of MODS at day 2. There was 27 patients in the MODS group and 136 patients in the no MODS group. The two groups were similar with respect to age, sex ratio and Simplified Acute Physiology Score. The MODS group had a higher mortality (52 versus 7%), Injury Severity Score (45 +/- 14 versus 31 +/- 13), hypovolemic shock rate (74 versus 30%), massive volume replacement rate (59 versus 6%) and SIRS rate (81 versus 54%) than the no MODS group (P < 0.05). The rate of infection was similarly low in the MODS and no MODS group (4 versus 6% respectively). CONCLUSION: Early MODS is often associated with hypotension and massive volume administration but very rarely with infection, despite the high rate of SIRS.

Adult↗
PubMed1994

Role of vascular endothelium in exercise-induced dilation of large epicardial coronary arteries in conscious dogs.

BACKGROUND: The role of vascular endothelium in the control of epicardial coronary artery vasomotion during treadmill exercise remains unclear. Therefore, we examined the consequences of in vivo balloon endothelial denudation on external coronary diameter of the left circumflex artery during exercise in conscious dogs. METHODS AND RESULTS: Seven dogs instrumented for the measurement of arterial blood pressure, external coronary artery diameter, and coronary blood flow were studied during exercise before and up to 21 days after balloon endothelial denudation of the proximal left circumflex artery. Endothelial denudation was confirmed by abolition of the epicardial coronary artery dilation induced by acetylcholine (0.3 microgram/kg IV) and reactive hyperemia. Epicardial coronary vasodilation was observed in the control state during treadmill exercise (+5.2 +/- 1.0%). In contrast, a marked vasoconstriction was observed 3 (-4.6 +/- 0.6%) and up to 6 days after endothelial denudation. Complete epicardial coronary artery dilation in response to acetylcholine and exercise was restored 9 days after endothelial denudation. In addition, epicardial coronary artery vasomotor responses to acetylcholine and treadmill exercise were closely correlated (r = .82, P < .001). Reactive dilation was not completely restored 21 days after endothelial denudation, but reactive hyperemia and exercise vasomotor responses during the 21 days follow-up were correlated (r = .70, P < .001). Vasodilation induced by nitroglycerin (1 microgram/kg IV) was reduced by 25% (P < .01) 3 days after endothelial denudation and returned to its corresponding control level 3 days later. Prazosin (50 micrograms/kg IV) significantly attenuated the exercise-induced coronary artery constriction after endothelial denudation (+1.5 +/- 1.4% versus -4.6 +/- 1.0%). CONCLUSIONS: These data demonstrate that endothelium is essential for the mediation of epicardial coronary dilation during exercise and may protect these vessels against the vasoconstrictor effect of endogenous catecholamines.

Acetylcholine↗
PubMed1991

[Hemodynamic effects of the induction of general anesthesia after low thoracic epidural anesthesia].

Sixteen ASA 1 or 2 patients scheduled for abdominal surgery were included in the study after they had given their informed consent. Thirty minutes after starting a low-thoracic epidural anaesthesia (median level of sensitivity loss: T5), the patients were randomly given an intravenous bolus injection of either thiopentone (4 mg.kg-1, n = 8) or etomidate (0.5 mg.-1, n = 8), associated with succinylcholine 1 mg.kg-1. One minute after induction of general anaesthesia, the patients were intubated and mechanically ventilated (V(T) 8 ml.kg-1, rate 12 c.min-1). Mean arterial blood pressure (MAP) (oscillometric method), cardiac output (CO) (transthoracic bioimpedance) and heart rate were recorded semi-continuously. Total peripheral resistances (TPR) were calculated using the formula TPR = (MA/CO)*80. There were no differences between the groups in patient age, height, weight, and cardiovascular consequences of epidural anaesthesia. After anaesthetic induction and before endotracheal intubation, there was a slight decrease in CO in both groups, without any change in MAP. After intubation, MAP increased in both groups through peripheral vasoconstriction, whereas CO did not increase further. A significant tachycardia was occurred only seen in the thiopentone group, before and after tracheal intubation. This study showed that thiopentone and etomidate were suitable drugs for anaesthetic induction in a patient under epidural blockade. However, the absence of tachycardia following etomidate may be beneficial in cardiac patients. The monitoring of cardiac output determinants during thiopentone and etomidate anaesthesia require further invasive investigations.

Adult↗
PubMed1988

[Are combinations of local anesthetics dangerous?].

Although local anaesthetic mixtures are often used, there is often no scientific basis for this. Interactions between the local anaesthetics in the mixture can even increase their toxicity. Such interactions may be due to the physical chemical properties of each constituent (this is not a real problem for amide local anaesthetics), to a mutual displacement from the binding sites on the plasma proteins or to an additional effect on membrane receptors. This displacement would seem to benefit the least toxic drug: the toxicity of local anaesthetic mixtures may therefore be reduced; for example, lidocaine and mepivacaine are displaced by bupivacaine. Moreover, the fraction of drug which leaves the blood vessel is greater than the serum free fraction. During chronic administration, neurological toxicity and free fraction are narrowly linked. When using local anaesthetic mixtures, it must be remembered that potency and toxicity of a local anaesthetic are closely correlated and that the toxic effects are, at least, additive.

Anesthetics, Local↗