Anesthesia and analgesia
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Anesthesia and analgesia · Feb 1998
Pneumoperitoneum as a risk factor for endobronchial intubation during laparoscopic gynecologic surgery.
Patients undergoing gynecological surgery under laparoscopic guidance usually receive general anesthesia with endotracheal intubation and mechanical ventilation. The creation of a pneumoperitoneum and the Trendelenburg position, both of which are used to improve visualization, are associated with cephalad movement of the diaphragm. This may increase the risk of endobronchial intubation. We studied the change in the distance from the tip of the endotracheal tube (ETT) to the carina with a fiberoptic bronchoscope in 30 patients aged 21-40 yr who were undergoing laparoscopic tubal ligation (n = 28) or hysterectomy (n = 2). Measurements were taken in the supine and Trendelenburg positions before and after pneumoperitoneum. The average distance from the ETT to the carina in the supine position was 2.1 +/- 0.8 cm and in the Trendelenburg position was 1.8 +/- 0.8 cm (P = not significant). After insufflation of the abdominal cavity, the mean distance decreased to 0.7 +/- 1.4 cm in the supine position (P < 0.05) and was associated with endobronchial intubation in eight patients. The addition of the Trendelenburg position to an established pneumoperitoneum resulted in minimal displacement (0.54 +/- 1.4 cm, P < 0.05) and one additional endobronchial intubation. We conclude that the insufflation of gas in the abdominal cavity, and not the change in patient position, is the main risk factor for endobronchial intubation in patients undergoing laparoscopic gynecologic surgery. ⋯ This study demonstrated that in anesthetized women, the insufflation of gas into the abdomen during laparoscopy for gynecologic surgery is the main risk factor for migration of the endotracheal tube into a bronchus.
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Anesthesia and analgesia · Feb 1998
The effect of halothane and sevoflurane on fatigue-induced changes in hamster diaphragmatic contractility.
The purpose of this study was to examine the effect of halothane and sevoflurane on fatigue-induced changes in diaphragmatic contractility. Forty-two hamster diaphragm strips were randomly allocated according to anesthetics (no anesthesia control, 1%-3% halothane, 2%-6% sevoflurane) and stimulated directly in an organ bath. Under the influence of the anesthetics, muscle fatigue was induced by repetitive tetanic contraction, and diaphragmatic contractilities (i.e., peak twitch and tetanic tension, twitch contraction time, and half-relaxation time) were measured before and after fatigue. Neither halothane nor sevoflurane changed tension generation before or after fatigue, but each anesthetic significantly enhanced fatigue-induced prolongations of the contraction time and half-relaxation time after fatigue. Specifically, the half-relaxation times after fatigue in the 3% halothane, 4% sevoflurane, and 6% sevoflurane groups (225.6 +/- 37.6, 236.0 +/- 76.5, and 287.3 +/- 55.5 ms, respectively) were more than twice as long as those of the control group (104.7 +/- 19.7 ms, P < 0.05). We conclude that halothane and sevoflurane augment fatigue-induced prolongations of the contraction and relaxation times. Diaphragmatic function may deteriorate when there is a fatiguing task during the clinical administration of halothane or sevoflurane anesthesia. ⋯ This study implicates diaphragmatic fatigue during anesthesia. An in vitro hamster diaphragm muscle preparation was used to study the effect of halothane and sevoflurane on fatigue-induced change in contractility. Our findings suggest that increased load on the diaphragm during volatile anesthesia may lead to impaired diaphragmatic contractility.
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Anesthesia and analgesia · Feb 1998
Catecholamine activation in the vasomotor center on emergence from anesthesia: the effects of alpha2 agonists.
The rostral ventrolateral medulla (RVLM) controls the vascular system and may contribute to postoperative hypertension. It comprises adrenergic cardiovascular neurons, a site for action of alpha2-adrenergic agonists. Because alpha2 agonists minimize perioperative circulatory activation, we asked the following question: do alpha2 agonists, such as clonidine and mivazerol, blunt the catecholamine activation observed in the RVLM on emergence from anesthesia? Halothane-anesthetized, paralyzed rats had their ventilatory, circulatory, and acid-base stability controlled. All pressure points and incisions were infiltrated with local anesthetics. With in vivo electrochemistry, a catechol signal was recorded in the RVLM during 150 min of stable halothane anesthesia (saline-halothane group); for 120 min after halothane discontinuation (saline-emergence group); after emergence and administration of the reference alpha2 agonist, clonidine 7 microg/kg or 21 microg/kg I.V. (50% or 90% effective dose [ED50 or ED90], respectively); and after emergence and administration of a new alpha2 agonist, mivazerol 20 microg/kg or 150 microg/kg I.V. (ED50 or ED90). Under halothane, dose-response curves for the RVLM catecholamine signal were constructed for mivazerol and an alpha2 antagonist, idazoxan (ED50 2.3 mg/kg I.V.). Stable halothane anesthesia (n = 5) led to no change in mean arterial pressure (MAP), heart rate (HR), or catechol signal (CAOC). During emergence from anesthesia, the MAP, HR, and CAOC increased (n = 5). Clonidine led to a near total suppression of the RVLM catecholamine activation noticed on emergence from anesthesia (n = 5). Hypertension was partially blunted with clonidine 7 microg/kg (n = 5). Tachycardia was partially blunted with mivazerol 20 microg/kg (n = 5). Pretreatment with idazoxan suppressed all the effects of mivazerol (n = 5). ⋯ On emergence from anesthesia, alpha2 agonists modify the activity of adrenergic cardiovascular neurons located within the vasomotor center, as assessed by in vivo electrochemistry. We provide a rationale for the use of alpha2 agonists on emergence from anesthesia in coronary/hypertensive patients.
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Anesthesia and analgesia · Feb 1998
Extension of sensory blockade after thoracic epidural administration of a test dose of lidocaine at three different levels.
To evaluate the relationship between the level of thoracic epidural injection and the extension of sensory blockade, we inserted radiopaque epidural catheters in 87 patients at the high (C7-T2, n = 28), mid (T3-5, n = 29) or low (T7-9, n = 30) thoracic levels. Fifteen minutes after the epidural administration of 60 mg of lidocaine, the mean (+/- SD) sensory block extension varied from 5.4 +/- 3.1 to 7.7 +/- 1.8 segments. The level of epidural puncture was a statistically significant factor in determining the cranial and caudal borders of sensory blockade (P = 0.0001, analysis of variance), but in determining for the total number of segments blocked. The number of blocked dermatomes located cranially of the puncture level increased significantly with descending injection site (P = 0.0001). We acquired chest radiographs in 61 patients to determine epidural catheter tip position. Direction of the epidural catheter tip was not a significant factor in determining the extension or borders of sensory blockade. We conclude that the extension of sensory blockade in thoracic epidural anesthesia is not influenced by the level of epidural puncture or catheter tip direction. There is, however, a more cranial spread of sensory blockade in the low thoracic region compared with the high thoracic region. ⋯ After evaluating the extension and pattern of sensory blockade in high, mid, and low thoracic epidural analgesia, the authors suggest that it is safe to use similar dosage regimens in all three regions, and that in high thoracic epidural analgesia, it is important to insert the epidural catheter at the level of the intended cranial border of blockade.
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Anesthesia and analgesia · Feb 1998
Propofol and thiopental in a 1:1 volume mixture is chemically stable.
Propofol and thiopental have been used clinically in combination for induction of anesthesia. Studies suggest that this mixture has synergistic activity, recovery characteristics similar to propofol alone, and bactericidal effects on multiple organisms. It may therefore be both clinically useful and cost-effective. In this study, we examined the chemical stability of this mixture. We used high-performance liquid chromatography to quantify the concentration of both propofol and thiopental in a given sample. This technique allows the detection of loss in total drug mass and of the appearance of breakdown products resulting from drug interaction. Ten samples of a 1:1 mixture by volume were prepared and assayed at Time 0 and Days 1, 3, and 7. Half the samples were incubated at 23 degrees C and the rest were stored at 4 degrees C. Other mixtures were assayed before and after filtration at Time 0 and Days 1 and 7 after storage at 23 degrees C. The assay was able to measure accurately the quantity of drug present in the samples. There was no significant decrease in the quantities of either propofol or thiopental in the mixture over the 7-day period. We conclude that the 1:1 volume mixture of propofol and thiopental is chemically stable for 1 wk at room temperature. ⋯ A mixture of propofol and thiopental has been used to induce anesthesia. We investigated the chemical stability of this mixture using high-performance liquid chromatography and found it to be stable for at least 24 h.