More on nitrous oxide and laser surgery.
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Humans↗
Biomedical subjects
D M Gaba
Publications and source records attributed to D M Gaba.
A comprehensive anesthesia simulation environment: re-creating the operating room for research and training.
Simulation is used extensively in industries that involve routine, but risky activities. The authors describe an anesthesia simulation environment that provides a re-creation of the anesthesiologist's task environment in a real operating room. The system provides appropriate inputs to standard monitoring equipment in common use during anesthesia, including ECG (with arrhythmias); invasive systemic arterial, pulmonary arterial, and central venous pressures (all coupled to ECG arrhythmias); automated cuff blood pressure; pulse oximetry; mass spectrometry; breathing circuit spirometry; and oxygen analysis. An intubation/thorax mannequin allows tracheal intubation and tube manipulation, and provides for simulation of occlusion, malposition, or disconnection of the tracheal tube, as well as regurgitation of gastric contents. The simulation is comprehensive in that it is "hands-on" and requires actual performance of most interventions using actual equipment. The simulation is conducted by a systems operator and a simulation director; the latter also acts in the roles of surgeon and circulating nurse. The simulator outputs are determined by a "script" that defines the consequences of routine anesthetic actions and pre-established critical incidents. Decisions about timing and override of the script are made by the simulation director. This control system offers maximum flexibility while maintaining clinical realism. The simulator experiences were judged as highly realistic by 21 subjects. Limitations in this version have centered on the mannequin (e.g., no patient movement, minimal or confusing physical signs) and will be addressed in future versions of the system. The authors suggest that anesthesia simulation can be accomplished at nominal expense and has major potential for training, continuing education, certification, and research.
Anesthesia↗
Internal countershock produces myocardial damage and lactate production without myocardial ischemia in anesthetized dogs.
The global myocardial extraction of lactate was measured in 13 halothane anesthetized dogs to assess the effect of electric countershock applied directly to the heart. Seven animals received two countershocks of 30 delivered joules each, while six animals were not shocked but were atrially paced to a rate of 190-200, both with and without occlusion of the vena cava to produce a mean arterial pressure of 40-50 mmHg. All animals had substantially positive lactate extraction in the baseline state (36 +/- 10% for countershock group vs. 41 +/- 3% for pacing group). Myocardial lactate extraction reached a markedly negative nadir 2.5 min after countershock (-19 +/- 15%), but returned toward normal by 6 min (10 +/- 6%). Lactate extraction was not significantly changed from baseline in the pacing group. The relationship between changes in regional myocardial blood flow (radiolabeled microspheres) and post-countershock myocardial damage (technetium pyrophosphate uptake) was assessed in six dogs shocked as above. Mean myocardial blood flow was increased minimally immediately after countershock (0.78 +/- 0.08 ml X min-1 X g-1 vs. 1.16 +/- 0.3), but there was no difference in blood flow between damaged and undamaged tissue at either time point. The epicardial-to-endocardial ratio of blood flow was unchanged after countershock (0.97 +/- 0.05 vs. 0.99 +/- 0.08). There was no relationship between myocardial damage and either the absolute amount of blood flow after countershock (r = -0.03) or the change in blood flow compared with the pre-shock period (r = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Anesthetic mishaps: breaking the chain of accident evolution.
Anesthesia and surgery are a risk for all, the healthy as well as the sick. While the prevention of adverse outcomes in healthy patients is paramount, enhancement of safety for critically ill patients is also essential, since they are more likely to suffer a SNO after a critical incident. Dangers originate from a variety of sources, not solely from errors by the anesthesiologist. Simple incidents of all description are inevitable, and we should focus on promoting recovery as well as avoiding error. Processes that lead to negative outcomes after critical incidents should be investigated to reduce the uncertainty complexity associated with managing the human body during anesthesia, and to establish the most effective detection and recovery techniques. Outcome studies are lacking, and clinical and animal research is highly dependent on the chosen model or population, making the results hard to apply to variable clinical conditions. Wherever possible, a consensus should be sought on therapeutic and adverse effects of drugs and techniques in common, specific patient populations. These can serve as a basis for developing therapeutic plans, recognizing that customizing to individuals is always necessary. A mainstay of anesthetic practice already involves attempts to loosen couplings, by keeping homeostatic mechanisms intact when possible (awake intubation, regional anesthesia); providing temporal buffers (titration of drugs, and use of drugs with short onset times and rapid termination of effect); and providing safety margins using appropriate pre-treatments (pre-oxygenation, atropine in children, etc.). Further means of loosening coupling should be identified and promoted. Specific attention to recovery from simple incidents should attack several facets of the problem.(ABSTRACT TRUNCATED AT 250 WORDS)
Accident Prevention↗
Epinephrine arrhythmogenicity is enhanced by acute, but not chronic, aminophylline administration during halothane anesthesia in dogs.
The authors determined the effect of acute and chronic aminophylline treatment on the arrhythmogenicity of epinephrine during halothane anesthesia. The dose of epinephrine required to achieve an arrhythmia threshold (ADE) was determined in nine unpremedicated dogs anesthetized with halothane (1.5% v/v) in oxygen (A0). Aminophylline was then infused to achieve and sustain a therapeutic theophylline level (mean +/- SD) of 17 +/- 2 micrograms X ml-1 (A1), at which time the ADE was reassessed. The aminophylline infusion regimen was then adjusted to provide a supratherapeutic level of theophylline of 34 micrograms X ml-1 (A2) and the ADE was reassessed. In an additional seven dogs the ADE was assessed before and after 6 weeks of oral aminophylline treatment that yielded a plasma theophylline level of 18 +/- 3 micrograms X ml-1. The ADE was significantly (P less than 0.01) reduced from a basal value (mean +/- SD) of 2.63 +/- 0.97 micrograms X kg X -1 X min-1 to 1.39 +/- 0.47 in the A1 state. There was no further decrement in the ADE at the A2 state (1.17 +/- 0.36). The plasma epinephrine level at the arrhythmia threshold decreased commensurately from 50.7 +/- 40.2 ng X ml-1 (A0) to 20.0 +/- 7.9 and 19.2 +/- 7.6 in the A1 and A2 states, respectively (P less than 0.01). In contrast to these acute treatment experiments, neither the ADE (2.65 +/- 0.95 vs. 2.97 +/- 1.49 micrograms X kg-1 X min-1) nor the plasma epinephrine levels at the arrhythmia threshold (47.2 +/- 13.7 vs. 51.1 +/- 22.0 ng X ml-1) were different after chronic aminophylline treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Aminophylline↗
Incendiary characteristics of a new laser-resistant endotracheal tube.
Endotracheal tube fires are the most frequent complication of laser surgery of the larynx. We investigated the incendiary characteristics of a new laser-resistant endotracheal tube, compared to polyvinyl chloride (PVC) and red rubber (RR) tubes, with different gas mixtures. A CO2 laser was focused on each tube and the probability of fire was assessed with oxygen fractions (FiO2) of 30%, 40%, 50%, 70%, and 100%, the balance being N2 or N2O. The laser-resistant tube could not be penetrated by a single laser pulse, regardless of laser energy or gas composition. PVC and RR tubes were readily ignited, the probability of ignition being related to oxygen concentration and laser energy. Nitrous oxide readily supported combustion. We suggest that laser surgery of the larynx can be most safely performed with a laser-resistant endotracheal tube and with gas mixtures containing the minimal safe O2 concentration (without nitrous oxide).
Anesthesia, Inhalation↗
Effects of hypoxia and hyperoxia on the human standing potential.
We report that the human standing potential, measured by the EOG, rises slowly when oxygen saturation is lowered to near 80% by breathing a controlled oxygen-nitrogen mixture. The standing potential falls abruptly by 20-30% of its amplitude when the oxygen saturation returns to 100%. These changes can be generated reproducibly, with minimal discomfort, under conditions that could be adopted for clinical use. Animal experimental studies by Linsenmeier and Steinberg suggest that this hypoxia-hyperoxia response may be a delayed response to potassium concentration changes in the subretinal space. Since there is no requirement for light and no involvement of the Müller cells, the hypoxia-hyperoxia response may be more specific for pigment epithelial pathology than the c-wave.
Adult↗
Postcountershock myocardial damage after pretreatment with adrenergic and calcium channel antagonists in halothane-anesthetized dogs.
Transthoracic electric countershock can cause necrotic myocardial lesions in humans as well as experimental animals. The authors investigated the effect on postcountershock myocardial damage of pretreatment with prazosin (0.1 mg/kg), an alpha-1 antagonist; L-metoprolol (0.5 mg/kg), a beta-1 antagonist, and verapamil (0.5 mg/kg), a calcium channel-blocking agent. Twenty dogs were anesthetized with halothane and given two transthoracic countershocks of 295 delivered joules each after drug or vehicle treatment. Myocardial injury was quantitated 24 h following countershock by measuring the uptake of technetium-99m pyrophosphate in the myocardium. Elevated technetium-99m pyrophosphate uptake occurred in visible lesions in most dogs regardless of drug treatment. For each of four parameters of myocardial damage there was no statistically significant difference between control animals and those treated with prazosin, metoprolol, or verapamil. These data suggest that adrenergic or calcium channel-mediated mechanisms are not involved in the pathogenesis of postcountershock myocardial damage.
Anesthesia, Inhalation↗
Anesthesia and the automatic implantable cardioverter/defibrillator.
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Anesthesia↗
Alpha 1-adrenergic blockade raises epinephrine-arrhythmia threshold in halothane-anesthetized dogs in a dose-dependent fashion.
The authors determined whether increasing alpha 1-adrenergic blockade resulted in progressively less arrhythmic activity in the canine halothane-epinephrine arrhythmia model. Dogs (n = 7) were anesthetized with halothane (1.5%) in oxygen. Stepwise increases in steady-state plasma levels of either of two alpha 1-adrenoceptor antagonists (droperidol, doxazosin) were produced by applying Wagnerian principles to the known pharmacokinetic parameters of these drugs. At each steady state plasma level of these antagonists, the extent of the alpha 1-adrenergic blockade produced was assessed by defining a phenylephrine (PE) dose pressor response curve. The degree of alpha 1-blockade produced was quantitated as the dose of PE that caused a 25-mmHg increase in mean arterial pressure (ED25) as derived by polynomial regression analysis. By analysis of variance (ANOVA) the ED25 increased significantly for each targeted steady state plasma level of either droperidol (P less than 0.001) or doxazosin (P less than 0.001). For an assessment of the antiarrhythmic activity of these alpha 1-antagonists, the arrhythmogenic dose of epinephrine (ADE) was determined at each of the states of alpha 1-adrenergic blockade previously defined. By ANOVA there was a significant increase in the ADE over the range of alpha blockade produced for either droperidol (P less than 0.001) or doxazosin (P less than 0.001). A close correlation (r2) existed between the ED25 and the ADE for the target steady state levels that were achieved for either droperidol (0.99) or doxazosin (0.74).(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic alpha-Antagonists↗
Myocardial damage following transthoracic direct current countershock in newborn piglets.
The effect of transthoracic direct current countershock on the myocardium of 21 newborn piglets was studied. Myocardial damage was quantified by measuring the myocardial uptake of technetium-99m pyrophosphate injected 24 hours after countershock. Substantial myocardial damage occurred in animals given greater than 150 joules/kg but not at lower energy doses. Damage occurred in both ventricular free walls, but more frequently in the right ventricle. The epicardial half of the myocardium was more severely affected than the endocardial half. The relationship between myocardial damage and total countershock energy dose was well modeled by an exponential function. Transthoracic direct current countershock appears unlikely to cause myocardial damage in newborn piglets unless greatly elevated energy doses are employed.
Animals↗