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Biomedical subjects

B Bissonnette

Publications and source records attributed to B Bissonnette.

At least 37 records · Page 2Linked to original sources
PubMed1998

Closure of persistently patent arterial duct and its impact on cerebral circulatory haemodynamics in children.

PURPOSE: Closure of a patent arterial duct (PDA) is suggested as a risk factor associated with intraventricular haemorrhage and/or cerebral ischemia in neonates. This study evaluate the effects of transcatheter closure of a patent arterial duct in children on cerebral blood flow velocity. METHODS: Twelve children, aged from one to eight years were enrolled. Anaesthesia induction consisted of thiopentone, fentanyl and diazepam. Tracheal intubation was facilitated with vecuronium. Anaesthesia was maintained with N2O 70% in O2 and a PaCO2 between 35 to 40 mmHg. No cerebral vasoactive agents were used. Mean arterial pressure (MAP), central venous pressure (CVP), heart rate were continuously recorded. Systolic (Vs) and diastolic (Vd) cerebral blood flow velocity (CBFV) were recorded. Cerebral perfusion pressure (CPP) was calculated. The mean CBFV, the systolic-mean ratio and the cerebral blood volume were estimated from the area under the velocity-time curve (AUC) before PDA closure, immediately after and for 10 min following occlusion. RESULTS: The mean (+/- SD) age and weight were 30 +/- 22 mo and 13 +/- 5 kg, respectively. Continuous recording during duct closure showed an abrupt increase in Vd (P < 0.05) whereas Vs remained constant. The AUC increased after closure and persisted for 10 min (P < 0.05). CONCLUSION: This study confirms that closure of a PDA leads to acute changes in intracerebral diastolic flow and volume. This observation gives weight to mechanisms involved in IVH in smaller infants after arterial surgical duct closure. The anaesthetic technique used for arterial duct closure in these procedure could influence these observations.

Area Under Curve↗
PubMed1998

-The effect of ondansetron on intracranial pressure and cerebral perfusion pressure in neurosurgical patients-.

OBJECTIVE: To determine the effect of ondansetron on intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP). STUDY DESIGN: Prospective, comparative, randomized double-blind study. PATIENTS: Twenty-six patients undergoing intracranial surgery. METHOD: Induction was obtained with propofol (1-2.5 mg.kg-1), fentanyl (1.5 micrograms.kg-1) and pancuronium (0.1 mg.kg-1), and maintenance was achieved with propofol and fentanyl. Intermittent positive pressure ventilation was used to ensure mild hypocapnia at 35 +/- 2 mmHg. Positioning of the patient was followed by 15 minutes steady-state. Patient received thereafter either 8 mg ondansetron or a placebo intravenously. The ICP was measured using a lumbar malleable spinal needle. CPP was calculated using the formula CCP = MAP-ICP. All variables were measured every minute for 15 minutes. RESULTS: The ICP, MAP and CPP did not differ between the two groups. There were no differences in the highest ICP values in patients receiving either ondansetron or placebo (11 +/- 5 versus 9 +/- 5, mean +/- SD), respectively. CONCLUSION: Intravenous administration of 8 mg ondansetron affects neither cerebral hemodynamics nor ICP.

Adolescent↗
PubMed1998

Recovery characteristics of propofol anaesthesia, with and without nitrous oxide: a comparison with halothane/nitrous oxide anaesthesia in children.

Few studies have examined whether nitrous oxide influences the recovery characteristics of propofol anaesthesia. The present study examined the effect of nitrous oxide on the recovery characteristics of propofol anaesthesia, and compared these data with those for halothane/nitrous oxide anaesthesia. Sixty children aged 3-12 years were assigned at random to receive one of three maintenance regimens: propofol with or without nitrous oxide (70%) or halothane/nitrous oxide (70%). During propofol/N2O anaesthesia, the infusion rate of propofol (180 +/- 39 micrograms.kg-1.min-1) required to maintain the mean arterial pressure and heart rate within 20% of the baseline values was significantly less than that during propofol/O2 (220 +/- 37 micrograms.kg-1.min-1; P < 0.005). The time from discontinuation of anaesthesia to eye-opening (11 +/- 6 min), to response to commands (12 +/- 6 min), and to return of full wakefulness (21 +/- 10 min) after propofol/N2O were similar to those after propofol/O2, but significantly less (by approximately 30%) than those after halothane (P < 0.05). The overall incidence of emesis after propofol/N2O (53%) was greater than that after propofol/O2 (17%, P < 0.05) and comparable to that after halothane/N2O (58%). These data suggest that N2O has little effect on the rate of recovery after propofol, but significantly increases the incidence of postoperative emesis, thereby attenuating one of the main attributes of propofol anaesthesia.

Anesthesia Recovery Period↗
PubMed1998

The impact of systemic vasoconstrictors on the cerebral circulation of anesthetized patients.

UNLABELLED: BACKGROUND. The effect of vasoconstrictors on intracerebral hemodynamics in anesthetized patients is controversial. The influence of phenylephrine and norepinephrine on the cerebral circulation was investigated in isoflurane- or propofol-anesthetized patients using transcranial Doppler ultrasonography. METHODS: Forty patients were randomly assigned to have vasoconstrictor tests with norepinephrine or phenylephrine during either isoflurane or propofol anesthesia. Blood flow velocities were simultaneously measured in the middle cerebral artery and ipsilateral extracranial internal carotid artery. Baseline recordings were done during stable anesthesia in a supine position (test 0). A second series of measurements were performed after norepinephrine or phenylephrine had increased mean arterial blood pressure by about 20% (test 1). With maintained norepinephrine or phenylephrine infusion, a final series of results were obtained after the increased mean arterial blood pressure was counteracted by a slightly head-up patient position (test 2). RESULTS: Both vasoconstrictors significantly increased mean flow velocities in the middle cerebral artery (norepinephrine: 43 +/- 11 cm/s to 49 +/- 11 cm/s; phenylephrine: 43 +/- 8 cm/s to 48 +/- 9 cm/s; +/- SD) and internal carotid artery (norepinephrine: 27 +/- 7 cm/s to 31 +/- 8 cm/s; phenylephrine: 27 +/- 9 cm/s to 31 +/- 10 cm/s) in the isoflurane-but not in the propofol-anesthetized patients. In the head-up position, only small and insignificant flow velocity changes were observed in both cerebral arteries independent of the vasoconstrictor or background anesthetic. CONCLUSIONS: The results of the present study indicate that norepinephrine and phenylephrine do not directly affect intracranial hemodynamics in anesthetized patients, but rather that hemodynamic changes observed with vasoconstrictors reflect the effect of the background anesthetic agents on cerebral pressure autoregulation.

Adult↗
PubMed1998

Interaction of vecuronium and atracurium during halothane anaesthesia in children.

The combination of vecuronium and atracurium was studied in 60 children of ASA physical status 1 or 2. In part I, the dose-response relationships were determined in 30 children who were randomly assigned to receive a single bolus of 0.02, 0.025 or 0.03 mg kg-1 of vecuronium or 0.075, 0.01 or 0.0125 mg.kg-1 of atracurium. The evoked electromyogram of the adductor pollicis brevis muscle to train-of-four stimulation was monitored. The speed of onset of the neuromuscular blockade was determined by a 95% depression of the train-of-four whereas the recovery index was established at 75% recovery of T1. In part II, 30 children were randomly assigned to receive 2 x ED95 of vecuronium, 2 x ED95 of atracurium, or a combination of 1 x ED95 of vecuronium + 1 x ED95 of atracurium. This study showed that the ED50 and ED95 for vecuronium were 0.021 mg.kg-1 and 0.037 mg.kg-1 and for atracurium 0.11 mg.kg-1 and 0.30 mg.kg-1, respectively. The slopes of the dose-response relationships were significantly different (p < 0.001). With vecuronium alone, the speed of onset of neuromuscular blockade was significantly slower (p < 0.001) and the duration of action less (p < 0.001) than that with atracurium alone or with the combination. There were no differences between atracurium and the combination of both medications. The recovery index was similar for all groups. We conclude that the dose-response relationships of vecuronium and atracurium in children undergoing halothane anaesthesia are not parallel and the neuromuscular effects of vecuronium and atracurium are neither additive nor synergistic. While vecuronium has a shorter duration of action than atracurium, this feature is not apparent when it is combined with atracurium in equipotent doses. Recovery is rapid and not prolonged when these two drugs are combined.

Anesthesia, Inhalation↗
PubMed1997

Heart rate and cardiac output after atropine in anaesthetised infants and children.

PURPOSE: Heart rate is considered to be a major determinant of cardiac output in infants and small children but the relationships between age, heart rate and cardiac output in humans have never been clearly established. This study was designed to determine the change in cardiac output following atropine iv to anaesthetised infants and small children. METHODS: Following Institutional Ethics Committee approval and written-informed consent, 20 ASA I or II unpremedicated patients aged from 1 to 36 mo were studied. Anaesthesia was induced with 5 mg.kg-1 thiopentone, 2 micrograms.kg-1 fentanyl and maintained with halothane 0.5% in nitrous oxide 66% in oxygen. Vecuronium 0.1 mg.kg-1 was used to provide muscular relaxation. Cardiac output was measured by non-invasive transthoracic blind continuous-wave Doppler echocardiography before and after the administration of 0.02 mg.kg-1 atropine iv. RESULTS: Atropine increased both heart rate and cardiac index by 31.1 +/- 12.8% and 29.4 +/- 17.3% respectively (P < 0.05). The cardiac index before atropine was 5.1 +/- 1.2 L.min-1.m-2 and the increase after atropine varied widely from 1.4 to 52.1%. Although atropine did not alter the overall stroke index the recorded changes ranged from -20.8 to +18.0%. There was no association between age and either cardiac index or % change in cardiac index after atropine. However, there was a positive but weak correlation between percentage change in heart rate and cardiac output (r2 = 0.46). CONCLUSION: Atropine causes a variable increase in cardiac output in infants and children aged between 1 and 36 mo. The change in cardiac output, considering the limits of the transthoracic echocardiography methodology, suggests that this is related to the increase in heart rate but is not dependent of age.

Anesthesia↗
PubMed1997

[Biomechanics and intracranial hypertension].

Biomechanics can be defined as the physical concepts exploring the effects of mechanical forces in biology. Biomechanics explores the consequences of an alteration in the steady-state normally existing between living tissues and their immediate environment. The application of this science in the field of brain physiopathology and intracranial hypertension is essential to understanding the sequence of events triggered during an alteration of the intracranial volume such as observed with intracranial pathologies. Furthermore, biomechanics allows the development of a logical and rational therapeutic approach, better adapted to the various intracerebral problems anaesthesiologists might be confronted with.

Adult↗
PubMed1997

[Cerebral hemodynamics and intracranial hypertension].

Various cerebral aggressions, either primary or secondary, can lead to the development of raised intracranial pressure. The presence of an elevated intracranial pressure often results in cerebral ischaemia/hypoxia and, eventually, neuronal death. In face of this cascade of events, several therapeutic approaches have been suggested. Two management concepts for patients with raised intracranial pressure have retained the most attention in recent years: the first suggests a therapeutic increase in cerebral perfusion pressure with the objectives to improve perilesional collateral perfusion and decreased cerebral blood volume, and consequently intracranial pressure in areas where autoregulation is preserved. The second concept supports the diminution in perilesional capillary pressure with the aim of decreasing vasogenic oedema. Although these two concepts are antagonistic and cannot be used simultaneously, they are probably complementary in the sequence of therapeutic events of patients experiencing severe head injury. This article reviews these therapeutic concepts and their clinical applications.

Anesthetics, Intravenous↗
PubMed1997

[Efficacy of ketanserin on postanesthetic shivering].

OBJECTIVE: To evaluate the clinical and electromyographic (EMG) effects of ketanserin (K), a serotoninergic receptor antagonist (5-HT2), on postoperative shivering (POS). STUDY DESIGN: Prospective, randomised, double-blind study. PATIENTS: Fifty ASA class 1 and 2 patients with major clinical postoperative tremor were studied. METHODS: POS was assessed clinically (0 = nil, 1 = moderate, 2 = severe). Inclusion criterion was a POS of 2 at admission in the recovery room. The mean arterial blood pressure, rectal temperature, SpO2 were recorded at admission (T0) and subsequently at T5, T10, T15, T30 and T60 minutes. Either 10 mg of K (n = 25) or a corresponding volume of a placebo (P) (n = 25) were intravenously injected. The EMG activity of the deltoid and quadriceps muscles was recorded continuously. Blood lactic acid concentration was measured at the end of POS. Results are expressed as mean +/- SEM. Parametric values were analysed with unpaired Student's t-test, and nonparametric values with chi 2 analysis. P < 0.05 was accepted. RESULTS: Demographic data, duration of anaesthesia, postoperative temperature, oxygen saturation, blood pressure and blood lactate concentration were similar between groups. The POS duration in the K group was significantly shorter than in the P group: 8.8 +/- 1.5 min and 15.5 +/- 1.5 min respectively (P < 0.01). The number of patients in the K group experiencing POS at T5 and T10 was significantly lower, when compared with those who had received the P (P < 0.05). CONCLUSION: At a dose of 10 mg, K administered in patients with POS during recovery, reduced significantly the duration and intensity of the shivering without noticeable side effects. This study suggests that this 5-HT2 antagonist is an efficient therapeutic tool for POS in adults.

Adult↗
PubMed1996

[Hypertonic solutions and intracranial pressure].

The properties of the endothelium differ between the brain and the remainder of the body. In most non-CNS tissues the size of the junctions between endothelial cells averages 65 A. Proteins do not cross these gaps, while sodium does. In the brain, the junction size is only 7 A, which is too small to allow crossing by sodium. Investigations with changes in osmotic and oncotic pressure have demonstrated that: (1) reducing osmolality results in edema formation in all tissues including normal brain; (2) a decrease in oncotic pressure is only associated with peripheral edema but not in the brain; (3) in case of brain injury, a decrease in osmolality elicits edema in the part of brain which remained normal; (4) similarly, a decrease in oncotic pressure does not cause an increase in brain edema in the injured part of the brain. The determinant factor of water exchange in the brain is mediated through the osmolality and not the oncotic pressure. The use of hypertonic solutions (Ringer lactate or NaCl) for intravascular fluid resuscitation of patients suffering from hypovolemic head trauma has gained popularity. A research survey in regard with this observation can be summarized as follows: NaCl 7.5% (2400 mOsm/l) is becoming the most popular hypertonic solution because of its favorable systemic and cerebral effects. It improves myocardial contractility, precapillary dilatation, and reactive venoconstriction, and it has a plasmatic expansion factor of 3.8. In regard to the brain tissue, it improves the PO2 and the cerebral blood flow (CBF) as a result of decreasing cerebrovascular resistance. Finally, it reduces the cortical water content of intact blood-brain barrier area. The overall consequence is reduction of intracranial pressure (ICP). Although the homeostasis of the cerebral intracellular compartment remains unknown, it is possible that brain cells are able to resist important osmolar overload. NaCl 7.5%/dextran 70.6% is clinically at this moment the most studied hypertonic/hyperoncotic agent in prehospital emergencies. Its effects on cerebral homeostasis are identical to NaCl 7.5%. However, the addition of a colloid agent has the advantage of prolonging the systemic effects without affecting the brain. The plasmatic expansion factor is 4.5, which is slightly superior to NaCl 7.5%. Mannitol improves CBF by maintaining autoregulation as a result of changes in viscosity and reactive cerebrovascular constriction. It generates an osmotic gradient which reduces the cerebral volume and subsequently the ICP. In the presence of a cryogenic cerebral lesion, its reductive effects on brain water are superior to the hypertonic/hyperoncotic solution. Because mannitol has less spectacular systemic responses than the other solutions, it is not indicated for resuscitation following hemorrhagic shock. In conclusion, it is important to note that hypotension and hypoxemia represent the determinant factors of secondary cerebral insults. Therefore, in the presence of patients with head injury and especially hemorrhagic shock, it is essential to ensure a cerebral perfusion pressure (CPP) of > 80 mm Hg. Hypertonic solutions have gained popularity in these clinical situations because of their combined effects on ICP, mean arterial pressure (MAP) and CPP. However, the therapeutic approach to polytraumatized patients with small intravascular volume (4-6 ml/kg) of hypertonic solutions should not be a substitute for the usual volemic resuscitation technique. The clinical indication for these solutions should be limited to the initial resuscitation maneuvers in traumatized patients. Prolonged use of hypertonic solutions for the purpose of intravascular resuscitation would only contribute to increasing the side effects and eventually counteract the initial beneficial advantages.

Blood Pressure↗
PubMed1996

[Peroperative risks in cerebral aneurysm surgery].

The perioperative complications associated with cerebral aneurysm surgery require a specific anaesthetic management. Four major perioperative accidents are discussed in this review. The anaesthetic and surgical management in case of rebleeding subsequent to the re-rupture of the aneurysm is mainly prophylactic. It includes haemodynamic stability assurance, maintenance of mean arterial pressure (MAP) between 80-90 mmHg during stimulation of the patient such as endotracheal intubation, application of the skull-pin head-holder, incision, and craniotomy. The aneurysmal transmural pressure should be adequately maintained by avoiding an aggressive decrease of intracranial pressure. Once the skull is open, the brain must be kept slack in order to decrease pressure under the retractors and avoid the risks of stretching and tearing of the adjacent vessels. If, despite these precautions, the aneurysm ruptures again. MAP should be decreased to 60 mmHg and the brain rendered more slack, in order to allow direct clipping of the aneurysm, or temporary clipping of the adjacent vessels. The optimal agents in this situation are isoflurane (which decreases CMRO2), intravenous anaesthetic agents (inspite their negative inotropic effect, they may potentially protect the brain) and sodium nitroprusside. Vasospasm occurs usually between the 3rd and the 7th day after subarachnoid haemorrhage. It may be seen peroperatively. The optimal treatment, as well as prophylaxis, is moderate controlled hypertension (MAP > 100 mmHg), associated with hypervolaemia and haemodilution, the so-called triple H therapy, with strict control of the filling pressures. Other beneficial therapies are calcium antagonists (nimodipine and nicardipine), the removal of the blood accumulated around the brain and in the cisternae, and possibly local administration of papaverine. Abrupt MAP increases are controlled in order to maintain adequate aneurysmal transmural pressure. Beta-blockers, local anaesthetics administered locally or intravenously, a carefully titrated level of anaesthesia, a maintained volaemia play a protective role. Cerebral oedema is sometimes already present at the opening of the skull or may arise later, due to a high pressure under the retractors, to the surgical manipulations of the brain or to brain ischaemia subsequent to temporary clipping. Its treatment is aggressive, with intravenous agents, mannitol, deep hypocapnia and/or lumbar drainage. Prophylaxis, according to the "brain homeostasis concept", is the preferred method to avoid these four peroperative accidents. It includes normal blood volume, normoglycaemia, moderate hypocapnia, normotension, soft manipulation of the brain and optimal brain relaxation.

Anesthesia, General↗
PubMed1996

[Enhancement of cardiac performance for prevention and treatment of delayed cerebral ischemia caused by vasospasm].

Following subarachnoid haemorrhage, delayed cerebral ischaemia from cerebral vasospasm remains the most important cause of mortality and morbidity in patients with surgically secured aneurysms. Therapy with haemodilution, hypertension and volume expansion has been recommended to prevent and treat delayed cerebral ischaemia in these patients on the basis of uncontrolled clinical series (level of evidence III to V, grade C recommendation). Despite the lack of controlled studies, the maintenance of a cardiac index > 3.5 L.min-1.m-2 and a systolic arterial pressure between 120 and 150 mmHg before clipping and 160 to 200 mmHg thereafter is recommended as a prophylactic or therapeutic measure for vasospasm. Close monitoring of neurological and cardiorespiratory status is important to avoid neurologic and systemic complications.

Cerebrovascular Circulation↗
PubMed1996

[Intubation conditions: importance of the rate of repetition of the train-of-four].

OBJECTIVES: To assess that neuromuscular relaxation onset of the adductor pollicis (AP) is related to neuromuscular stimulation rate. To assess that train-of-four (TOF) at 0.05 Hz is a more accurate indicator of optimal tracheal intubation time and conditions, than TOF at 0.08 Hz. STUDY DESIGN: Prospective, comparative, randomized double-blind study. PATIENTS: Forty adults, physical class ASA 1 or 2, undergoing general anaesthesia with tracheal intubation were allocated to two groups (n = 20) according to the sequence of stimulation of the AP: either TOF at 0.05 Hz (test group) or TOF at 0.08 Hz (control group). METHODS: Induction of anaesthesia was achieved with thiopentone, fentanyl and vecuronium (0.1 mg.kg-1). Neuromuscular monitoring was obtained with force displacement transducers attached to each AP. Tracheal intubation was performed once AP muscular response obtained with TOF at 0.05 Hz for test group and TOF at 0.08 Hz for control group was abolished. Results are expressed as mean +/- SEM. Fisher exact test was used for intubation conditions comparison. Curarization time between groups was compared with unpaired Student's t test (P < 0.05 accepted). RESULTS: TOF with 0.05 Hz stimulation significantly increased curarization time: 217 +/- 7 versus 162 +/- 6 s (P < 0.001). Intubation conditions were excellent in 95% and good in 5% of patients in the study group, compared to 15 and 40% in the control group, respectively (P < 0.01) in 45% of the control group patients coughing at intubation occurred. CONCLUSION: Low stimulation rate (TOF at 0.05 Hz) of AP is a reliable technique to determine the appropriate intubation time for patients paralyzed with vecuronium.

Humans↗
PubMed1996

Dimenhydrinate decreases vomiting after strabismus surgery in children.

Dimenhydrinate, an H1-receptor antagonist, has been used to both prevent and treat postoperative vomiting (POV) in children for several decades. However, its effectiveness for POV after strabismus surgery remains anecdotal. This study was designed to determine the effectiveness and side effects of dimenhydrinate for the prevention of POV in children after strabismus surgery. Eighty ASA physical status I or II children, ages 1-12 yr inclusive, who were undergoing strabismus surgery, were prospectively and randomly allocated to receive either dimenhydrinate 0.5 mg/kg intravenously (n = 40) or placebo (n = 40) at induction of anesthesia. The incidence of POV and the times to arousal (and discharge from the recovery room and hospital) were recorded postoperatively in a double blinded manner. For 24 h after discharge from the hospital, all emetic episodes and medications given were recorded by the parents. Demographic data did not differ between the groups. Children who received dimenhydrinate had significantly less POV both inhospital (10%) and overall (30%) than those who received placebo (in-hospital 38%, P < 0.008; overall 65%, P < 0.003). The times to arousal and discharge from the hospital did not differ between the two groups. Dimenhydrinate (0.5 mg/kg) is an effective, safe, and inexpensive antiemetic in children undergoing strabismus surgery. It significantly reduces the incidence of vomiting for 24 h postoperatively and is not associated with prolonged sedation or other adverse effects.

Antiemetics↗
PubMed1996

Enflurane decreases the threshold for vasoconstriction more than isoflurane or halothane.

Intraoperative hypothermia results largely from anesthetic-induced inhibition of tonic thermoregulatory vasoconstriction. Sufficient hypothermia, however, triggers peripheral vasoconstriction, which usually prevents further decrease in core temperature. The thermoregulatory effects of all volatile anesthetics have been tested in adults and/or children, but different anesthetics have not been directly compared. We therefore evaluated thermoregulatory responses during enflurane, isoflurane, and halothane administration. Anesthesia was maintained with 1 minimum alveolar anesthetic concentration (MAC) of halothane, isoflurane, or enflurane in 27 patients undergoing intraabdominal surgery. Patients were maintained normovolemic and normocapnic but were allowed to cool passively. A forearm minus fingertip, skin-temperature gradient of 4 degrees C identified significant vasoconstriction; the core temperature triggering vasoconstriction identified the threshold. Morphometric characteristics, initial core temperatures, ambient operating room temperatures, blood pressures, and anesthetic potencies were similar in each group. All eight patients given halothane vasoconstricted at a core temperature of 35.5 +/- 0.6 degrees C. Eight of the patients given isoflurane vasoconstricted at a core temperature of 35.2 +/- 0.5 degrees C. However, two others did not at minimum core temperatures of 34.0 and 33.8 degrees C. Only one patient given enflurane vasoconstricted at a core temperature of 34.6 degrees C. The other six patients never vasoconstricted, at minimum core temperatures of 33.6 +/- 0.4 degrees C. Our data indicate that enflurane profoundly inhibits thermoregulatory responses in children. The mechanism for this extraordinary inhibition remains unknown but does not result from any obvious anesthetic pharmacology or thermoregulatory physiology. We conclude that unwarmed pediatric patients will become colder when anesthetized with enflurane than with halothane or isoflurane.

Anesthetics, Inhalation↗