Measurement of mucociliary transport velocity in ventilated patients. Short-term effect of general anesthesia on mucociliary transport.

OBJECTIVES: The objectives of this study were to evaluate a method for measuring BTV in ventilated patients and to study the short-term effect of general anesthesia with midazolam, Fentanyl, pancuronium and O2:N2O on BTV. DESIGN: The study included phantom measurements on a bronchoscopy model and the determination of BTV in patients in a convenience sample trial. SETTING: The study took place in a university hospital. PATIENTS: Fourteen patients undergoing major abdominal surgery with planned postoperative mechanical ventilation were included in the study. All patients gave their written informed consent to participate in the study. INTERVENTIONS: Bronchial mucus transport velocity was measured with a small volume (0.05 to 0.08 ml) of technetium 99m-labeled albumin microspheres with an activity of 3 MBq. The radiolabeled bolus was deposited on the dorsal mucosal surface at the distal end of the right and left main bronchus via flexible bronchoscopy. The movement of the microspheres toward the trachea was visualized and recorded using a scintillation camera; quantitative evaluation utilized the condensed image. MAIN MEASUREMENTS AND RESULTS: The technique was validated in a bronchoscopy model and in an intubated patient by moving a radioactive drop in a catheter through the main bronchi at velocities from 0 to 20 mm/min. The velocities determined by the image processing technique correlated well with the data by the model and patient determination (right bronchus, r = 1.0; left bronchus, r = 1.0). In seven ventilated patients, mechanical irritation by the fiberscope produced no significant effect on BTV. The BTV was measured preoperatively in seven conscious patients one day before surgery while they received local anesthesia with 10 ml of 1 percent lidocaine and postoperatively while they received intubation anesthesia. The preoperative and postoperative BTV values showed no significant differences (10.5; 5.7 to 13.7 mm/min; vs 9.7 (3.7 to 15.3) (median with range). CONCLUSION: By this method, bronchial transport velocity can be determined in a relatively short time in ventilated patients. General anesthesia with midazolam, Fentanyl, pancuronium and O2:N2O does not influence BTV.

Midazolam does not antagonize fentanyl-mediated analgesia in surgical patients.

STUDY OBJECTIVE: To determine whether midazolam possesses a clinically significant antianalgesic action in surgical patients. DESIGN: Randomized, controlled study. SETTING: Inpatient anesthesia at a university department of neurosurgery. PATIENTS: 2 groups of 10 patients each who were scheduled for supratentorial brain surgery, did not have elevated intracranial pressure, and were free from systemic disease. INTERVENTIONS: Patients underwent anesthesia induction with hexobarbital, succinylcholine, and pancuronium; anesthesia was maintained with injections of droperidol-fentanyl (Group 1) or with midazolam-fentanyl (Group 2) following a predetermined repetitive dosing schedule, such that fentanyl 0.1 mg was injected upon predominant increases in heart rate, whereas droperidol 2.5 mg or midazolam 2.5 mg was injected upon increases in blood pressure. MEASUREMENTS AND MAIN RESULTS: Duration of anesthesia and invasiveness of surgery were similar in both groups. The amount of fentanyl required was 0.55 +/- 0.18 mg/hr (mean +/- SD) in Group 1 and 0.53 +/- 0.17 mg/hr in Group 2. Injections of droperidol 7.5 +/- 3.4 mg/hr (Group 1) and midazolam 5.9 +/- 2.3 mg/hr (Group 2) were administered intraoperatively. This redosing regimen was associated with uninterrupted hemodynamic stability, indicating comparable and adequate anesthetic depth. Plasma concentrations of metabolites and hormones indicative of humoral stress activation did not differ between groups. CONCLUSION: Under these clinical conditions, the administration of midazolam, when compared with droperidol, was not associated with signs of any antagonistic or antianalgesic action toward fentanyl-mediated analgesia.

[Low-dose midazolam. Effect on the induction doses of fentanyl and on hemodynamics in the coronary patient]. / Midazolam à faible dose. Effet sur les doses d'induction de fentanyl et sur l'hémodynamique chez le malade coronarien.

A study was carried out to see whether the administration of a small dose of midazolam determined a reduction of the dose of fentanyl necessary for induction of anaesthesia. Sixteen patients undergoing coronary artery bypass surgery were randomly allocated to either of two groups. Patients in group M received 0.075 mg.kg-1 midazolam intravenously 3 to 5 min prior to induction with fentanyl (5 micrograms.kg-1.min-1), whereas patients in group P only received placebo. The mean dose of fentanyl administered to obtain complete loss of reaction to a painful stimulus was 20 +/- 3 micrograms.kg-1 in group M and 21.5 +/- 2.5 micrograms.kg-1 in group P (NS). However the small dose of midazolam associated with fentanyl caused a significant drop in blood pressure by 20%. After the administration of pancuronium (0.15 mg.kg-1), the patients in group P showed a significant increase in heart rate (+ 14 b.min-1), accompanied by an increase in cardiac index (+0.45 l.min-1.m-2). Pretreatment with midazolam seemed to protect the patient from this undesirable reaction. It was concluded that induction with a combination of a small dose of midazolam and fentanyl did not lead to a reduction in the dose of fentanyl necessary to obtain profound analgesia. However, it gave rise to a haemodynamic pattern quite distinct from that seen during induction with fentanyl alone.

[Comparison of the effects of midazolam and thiopental on the neuromuscular response of vecuronium, atracurium, and pancuronium]. / Comparación de los efectos del midazolam y del tiopental en la respuesta neuromuscular del vecuronio, atracurio y pancuronio.

To assess the possible interactions of midazolam and thiopental with the muscular relaxants vecuronium (0.08 mg/kg), atracurium (0.5 mg/kg), and pancuronium (0.1 mg/kg), a comparative analysis was undertaken in two groups of 18 and 32 patients treated respectively with midazolam (0.3 mg/kg) and thiopental (5 mg/kg). The beginning of the effect, maximal blockade, duration of the clinical response, and the spontaneous recovery index were measured on electromyographic recordings of action potentials evoked by train of four supramaximal stimuli delivered every 20 sec on the ulnar nerve. Conditions for intubation were assessed 2 minutes after administration of muscular relaxant. There were no significant differences in neuromuscular parameters in either of the two groups of patients treated with midazolam or with thiopental independently of the relaxant drug administered.

Effects of anesthetic induction in patients with diastolic dysfunction.

PURPOSE: To evaluate the effects of anesthetic induction on bi-ventricular function in patients with known preoperative left ventricular (LV) diastolic dysfunction undergoing coronary artery bypass grafting surgery (CABG). METHODS: Fifty patients with diastolic dysfunction undergoing CABG were studied. Preoperative transthoracic echocardiographic (TTE) examination was performed on the day before surgery and transesophageal echocardiography (TEE) assessment was undertaken after induction of anesthesia with sufentanil, midazolam, isoflurane, and pancuronium. Mean arterial pressure (MAP) and heart rate (HR) were recorded. The diameters of the left atrium (LA) and right atrium (RA) and right ventricular (RV) end-diastolic area (EDA), end-systolic area (ESA) and fractional area change (FAC) were obtained from the apical 4-chamber view. The LV EDA, LV ESA and LV FAC were measured from a transgastric midpapillary view. Pulsed wave Doppler of the transmitral flow (TMF) and transtricuspid flow (TTF), pulmonary venous flow (PVF) and hepatic venous flow (HVF) were measured. Mitral (Em, Am) and tricuspid (Et, At) annulus velocities were assessed by tissue Doppler imaging (TDI). Assessment of diastolic dysfunction was graded from normal to severe using a validated score. RESULTS: Following induction of anesthesia, HR decreased (66 +/- 12 vs 55 +/- 9 beats.min(-1), P < 0.0001) while MAP remained unchanged (86.1 +/- 9.0 vs 85.6 +/- 26.5 mmHg, P = 0.94). The diameters of the LA, RA and RV chambers increased, and these increases were associated with opposite changes in LV dimensions. The RV FAC decreased, but the LV FAC remained unchanged. While most Doppler velocities decreased (P < 0.05), a greater reduction in the atrial components of the TMF, TTF and TDI ratios was observed. The LV diastolic function score improved after induction of anesthesia (100% of patients with a score > or = = 3 pre-induction compared to 58% of patients with a score > or = 3 post-induction; P = 0.0004). CONCLUSION: In patients with left ventricular diastolic dysfunction, cardiac dimensions and bi-ventricular filling patterns are significantly altered after induction of general anesthesia. These changes can be explained to some extent by a reduction in venous return with general anesthesia, reduced atrial contractility, and the effect of positive pressure ventilation. Although the LV diastolic function score improved after induction of anesthesia, it is difficult to dissociate this effect from that of altered loading conditions.

[Changes in expression of lymphocyte surface markers following administration of etomidate, midazolam or methohexital]. / Veränderte Expression lymphozytärer Oberflächenmarker nach Gabe von Etomidat, Midazolam oder Methohexital.

Stress alters cellular immunity, affecting lymphocyte function, total lymphocyte count, and the frequency distribution of the lymphocyte subpopulations. Cortisol may mediate these stress-related changes, and drugs affecting cortisol levels might therefore alter lymphocyte patterns. Etomidate and midazolam both prevent the normal perioperative cortisol increase in minor surgery, but the mechanisms by which they do this are not identical: etomidate inhibits steroid synthesis in the adrenal cortex, leading to low cortisol and high ACTH levels, whereas midazolam primarily prevents ACTH increases. Methohexital has little or no influence on cortisol levels. By comparing the effects of these three drugs on the expression of lymphocyte surface markers and the interleukin-2 (Il-2) receptor, we hoped to gain further information on the effects of perioperative cortisol changes on cellular immunity. METHODS. Healthy, young male patients scheduled for routine body surface operations were premedicated with 2 mg flunitrazepam the evening before surgery and 50 mg promethazine and 15 mg piritramide i.m. 1 h before arrival in the operating room. Anaesthesia was induced with 0.2-0.3 mg fentanyl, 2 mg pancuronium, and either etomidate (0.3 mg/kg body wt.), midazolam (0.2 mg/kg body wt.), or methohexital (1.5 mg/kg body wt.). The induction bolus was followed by an infusion at the rate of 0.36 mg/kg/h for etomidate, 0.09 mg/kg/h for midazolam, and no infusion for methohexital. Intubation was facilitated with 100 mg succinylcholine. The patients were ventilated to normocapnia with 66% nitrous oxide in oxygen. Fentanyl was given as 0.1 mg bolus injections whenever necessary.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of two benzodiazepines and a benzodiazepine antagonist on neuromuscular blockade in the anaesthetized cat.

The interaction of diazepam and midazolam with non-depolarizing neuromuscular blocking drugs was studied in the sciatic nerve-tibialis anterior muscle preparation of the anaesthetized cat. Both diazepam and midazolam (0.3 mg/kg i.v.) caused a significant enhancement of a constant 50% neuromuscular block, produced by infusions of vecuronium or pancuronium. Increasing the dose of midazolam from 0.3 to 1.5 mg/kg, caused no significant further potentiation of vecuronium, but decreased the onset time of potentiation. Ro 15-1788, a selective benzodiazepine antagonist, did not antagonize the vecuronium potentiation caused by midazolam 0.3 mg/kg. However, when given before midazolam (1.5 mg/kg), Ro 15-1788 delayed the onset of potentiation. Ro 15-1788 antagonized and prevented the considerable blood pressure decrease produced by midazolam 0.3 and 1.5 mg/kg. There appears to exist a ceiling to the benzodiazepine-induced blood pressure decrease and potentiation of vecuronium in the cat.

Left-ventricular performance, volumes, and catecholamine responses during anaesthesia induction--monitoring by combined radionuclide cardiography and right heart catheterization.

Sequential radionuclide imaging and continuous recording of arterial and right heart pressures were carried out during anaesthesia with midazolam 0.2 mg kg-1, pancuronium 0.15 mg kg-1 and fentanyl 10 micrograms kg-1 in eight patients with normal cardiopulmonary status scheduled for craniotomy. The aim was to examine how a stress-free anaesthetic induction tailored to protect against the hypertension and tachycardia provoked by laryngoscopy and intubation influenced left-ventricular performance, left-ventricular loading conditions and plasma catecholamine concentrations. During the 20-min study period no significant changes were observed in heart rate, left-ventricular ejection fraction, ratio of peak systolic pressure to left-ventricular end-systolic volume, pulmonary capillary wedge pressure, left-ventricular end-systolic volume, cardiac output, dopamine and noradrenaline concentrations. Except for a minor increase in mean arterial pressure after laryngoscopy and intubation, mean arterial pressure decreased 24%, left-ventricular end-diastolic volume decreased 15%, and left-ventricular stroke volume decreased 21%. Central venous pressure increased by 75% but there was no parallel increase in pulmonary wedge pressure, which in turn did not reflect the alterations in ventricular end-diastolic volume. Plasma adrenaline concentrations decreased significantly (66%). The chosen induction regimen preserved global left-ventricular pump function during laryngoscopy and intubation without any activation of the sympathetic nervous system. Central venous and pulmonary wedge pressures were unreliable in the assessment of ventricular preload during induction of general anaesthesia.

The influence of propofol and midazolam/halothane anesthesia on hepatic SvO2 and gastric mucosal pH during cardiopulmonary bypass.

OBJECTIVE: Because propofol is known to reduce vascular resistance, the objective of this study was to compare the indices of hepatosplanchnic circulation and oxygenation during cardiopulmonary bypass (CPB) in patients anesthetized with either propofol or midazolam/halothane. DESIGN: A prospective, randomized, nonblinded study. SETTING: A university hospital. PARTICIPANTS: Twenty patients undergoing cardiac surgery with CPB. INTERVENTIONS: Nine patients were anesthetized with propofol/fentanyl/pancuronium and 11 patients were anesthetized with midazolam/halothane/fentanyl/pancuronium. All patients had a nasogastric tonometer tube and two fiberoptic thermodilution catheters inserted; one in the pulmonary artery and one in the upper right hepatic vein. During bypass, SvO2s were measured from the venous line of the heart-lung machine. MEASUREMENTS AND MAIN RESULTS: Gastric mucosal pH (pHi) was measured prebypass, 30 minutes after the start of CPB, and just before weaning off CPB. Hepatic SvO2 (HSvO2) values were recorded every 5 minutes. The pH gap was less at 30 minutes of hypothermic CPB in the propofol group. In the midazolam/halothane group, the HSvO2 decreased after the start of rewarming, whereas in the propofol group the values remained almost at the prebypass levels. At the end of rewarming, the HSvO2 was almost identical in the two groups. CONCLUSION: Propofol preserved the HSvO2 during CPB and produced a more optimal relationship between the hepatosplanchnic blood flow and oxygen consumption.