Anesthesia and analgesia
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Anesthesia and analgesia · Dec 1997
Carbon dioxide spirogram (but not capnogram) detects leaking inspiratory valve in a circle circuit.
Expiratory valve incompetence in the circle circuit is diagnosed by using capnography (PCO2 versus time) when significant CO2 is present throughout inspiration. However, inspiratory valve incompetence will allow CO2-containing expirate to reverse flow into the inspiratory limb. CO2 rebreathing occurs early during the next inspiration, generating a short extension of the alveolar plateau and decreased inspiratory downslope of the capnogram, which may be indistinguishable from normal. We hypothesized that CO2 spirography (PCO2 versus volume) would correctly measure inspired CO2 volume (VCO2) during inspiratory valve leak. Accordingly, a metabolic chamber (alcohol combustion) was connected to a lung simulator, which was mechanically ventilated through a standard anesthesia circle circuit. By multiplying and integrating airway flow and PCO2, overall, expired, and inspired VCO2 (VCO2,br = VCO2,E - VCO2,I) were measured. When the inspiratory valve was compromised (by placing a wire between the valve seat and diaphragm), VCO2,I increased from 2.7 +/- 1.7 to 5.7 +/- 0.2 mL (P < 0.05), as measured by using CO2 spirography. In contrast, the capnogram demonstrated only an imperceptible lengthening of the alveolar plateau and did not measure VCO2,I. To maintain effective alveolar ventilation and CO2 elimination, increased VCO2,I requires a larger tidal volume, which could result in pulmonary barotrauma, decreased cardiac output, and increased intracranial pressure. ⋯ Circle circuit inspiratory valve leak will allow CO2-containing expirate to reverse flow into the inspiratory limb, with subsequent rebreathing during the next inspiration. This CO2 rebreathing causes imperceptible lengthening of the alveolar plateau of the capnogram and is detected only by using the CO2 spirogram (PCO2 versus volume).
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Anesthesia and analgesia · Dec 1997
Comparative StudyArgon pneumoperitoneum is more dangerous than CO2 pneumoperitoneum during venous gas embolism.
We investigated the possibility of using argon, an inert gas, as a replacement for carbon dioxide (CO2). The tolerance of argon pneumoperitoneum was compared with that of CO2 pneumoperitoneum. Twenty pigs were anesthetized with enflurane 1.5%. Argon (n = 11) or CO2 (n = 9) pneumoperitoneum was created at 15 mm Hg over 20 min, and serial intravenous injections of each gas (ranging from 0.1 to 20 mL/kg) were made. Cardiorespiratory variables were measured. Transesophageal Doppler and capnographic monitoring were assessed in the detection of embolism. During argon pneumoperitoneum, there was no significant change from baseline in arterial pressure and pulmonary excretion of CO2, mean systemic arterial pressure (MAP), mean pulmonary artery pressure (PAP), or systemic and pulmonary vascular resistances, whereas CO2 pneumoperitoneum significantly increased these values (P < 0.05). During the embolic trial and from gas volumes of 2 and 0.2 mL/kg, the decrease in MAP and the increase in PAP were significantly higher with argon than with CO2 (P < 0.05). In contrast to CO2, argon pneumoperitoneum was not associated with significant changes in cardiorespiratory functions. However, argon embolism seems to be more deleterious than CO2 embolism. The possibility of using argon pneumoperitoneum during laparoscopy remains uncertain. ⋯ Laparoscopic surgery requires insufflation of gas into the peritoneal cavity. We compared the hemodynamic effects of argon, an inert gas, and carbon dioxide in a pig model of laparoscopic surgery. We conclude that argon carries a high risk factor in the case of an accidental gas embolism.
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Anesthesia and analgesia · Dec 1997
Time-dependent changes in heart rate and pupil size during desflurane or sevoflurane anesthesia.
To better characterize alterations in autonomic function associated with prolonged anesthesia, we tested the hypothesis that the time-dependent effects of sevoflurane and desflurane differ. We studied seven male volunteers, each anesthetized for 8 h with 1.25 minimum alveolar anesthetic concentration desflurane on one study day and with 8 h sevoflurane on another. These volunteers did not undergo surgery and were minimally stimulated during the study. Measurements included blood pressure, heart rate, pupillary size and light reactivity, concentrations of serum catecholamines, and carbon dioxide production. Over time, heart rate and pupil size increased significantly. During 6 of the 14 anesthetics (45%), heart rate at some point exceeded 95 bpm; similarly, pupil size at some time exceeded 5 mm during 8 anesthetics (57%). In contrast, plasma catecholamine concentrations and carbon dioxide production remained unchanged, and blood pressure remained nearly constant. There are thus substantial time-dependent changes in autonomic functions during prolonged anesthesia, even in unstimulated, nonsurgical volunteers, but we could not detect a difference in these changes during desflurane compared with sevoflurane anesthesia. ⋯ Pupil size and heart rate changes are used to guide the delivery of anesthesia. In volunteers, pupil size and heart rate increased with increasing duration of constant desflurane or sevoflurane anesthesia. Thus, anesthetic duration alters heart rate and pupil size independent of surgery and changes in anesthetic delivery.
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Anesthesia and analgesia · Dec 1997
Dehydration of Baralyme increases compound A resulting from sevoflurane degradation in a standard anesthetic circuit used to anesthetize swine.
In a model anesthetic circuit, dehydration of Baralyme brand carbon dioxide absorbent increases degradation of sevoflurane to CF2=C(CF3)OCH2F, a nephrotoxic vinyl ether called Compound A. In the present study, we quantified this increase using "conditioned" Baralyme in a circle absorbent system to deliver sevoflurane anesthesia to swine. Mimicking continuing oxygen delivery for 2 days after completion of an anesthetic, we directed a conditioning fresh gas flow of 5 L/min retrograde through fresh absorbent in situ in a standard absorbent system for 40 h. The conditioned absorbent was subsequently used (without mixing of the granules) in a standard anesthetic circuit to deliver sevoflurane to swine weighing 78 +/- 2 kg. The initial inflow rate of fresh gas flow was set at 10 L/min with the vaporizer at 8% to achieve the target end-tidal concentration of 3.0%-3.2% sevoflurane in approximately 20 min. The flow was later decreased to 2 L/min, and the vaporizer concentration was decreased to sustain the 3.0%-3.2% value for a total of 2 h (three pigs) or 4 h (eight pigs). Inspired Compound A increased over the first 30 +/- 60 min to a peak concentration of 357 +/- 49 ppm (mean +/- SD), slowly decreasing thereafter to 74 +/- 6 ppm at 4 h. The average concentration over 2 h was 208 +/- 25 ppm, and the average concentration over 4 h was 153 +/- 19 ppm. Pigs were killed 1 or 4 days after anesthesia. The kidneys from pigs anesthetized for both 2 h and 4 h showed mild inflammation but little or no tubular necrosis. These results suggest that dehydration of Baralyme may produce concentrations of Compound A that would have nephrotoxic effects in humans in a shorter time than would be the case with normally hydrated Baralyme. ⋯ The vapor known as Compound A can injure the kidney. Dehydration of Baralyme, a standard absorbent of carbon dioxide in inhaled anesthetic delivery systems, can cause a 5- to 10-fold increase in Compound A concentrations produced from the inhaled anesthetic, sevoflurane, given at anesthetizing concentrations in a conventional anesthetic system.
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Anesthesia and analgesia · Dec 1997
Neurotoxicological assessment after intracisternal injection of liposomal bupivacaine in rabbits.
Experiments were performed on rabbits randomly assigned to intracisternally receive 0.3 mL of plain bupivacaine 5 mg/mL, liposomal bupivacaine 5 mg/mL, bupivacaine-free liposomes, or isotonic phosphate-buffered saline. Mechanical ventilation was initiated or intravenous dopamine was infused when respiratory depression or hypotension occurred. Seven days after the injection, the whole spinal cord was removed and histopathologic characteristics were studied on transverse sections. All preparations were devoid of phosphatidylcholine hydrolysis or oxidation compounds. Solutions without bupivacaine produced transient irritative signs that required sedation in most rabbits. Despite the similar duration of respiratory depression in groups receiving liposomal or plain bupivacaine, liposomes produced significantly prolonged motor blockade (126 vs 70 min). Correction of hypotension after plain bupivacaine required a longer dopamine infusion and larger doses than after liposomal bupivacaine (28 vs 18 min and 74 vs 47 mg). Necrosis was observed in the cervical area of two rabbits (one in the liposomal bupivacaine group and another in the phosphate buffer group). No demyelinated areas were noted in spinal cord examinations. We conclude that liposomal bupivacaine leads to a less severe sympathetic block and to a prolonged motor block, whereas histologic changes are not significantly different among groups. ⋯ Multilamellar liposomes containing bupivacaine administered intracisternally to rabbits produce spinal cord histopathologic changes not significantly different from those observed with plain bupivacaine. Sustained release of bupivacaine from liposomes is suggested by the prolonged motor blockade and the reduced severity of arterial hypotension. Use of these liposomes could prolong the local anesthetic effects of bupivacaine.