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Showing papers in "Anesthesiology in 1976"


Journal ArticleDOI
TL;DR: It is hoped that future studies will reveal the maximum dose of nitroprusside that can safely be metabolized in a 24-hour period, and may indicate that cofactors of rhodanase such as thiosulfate, or cobalamins such as hydroxocobalamin, can be administered with nitro Prussia to prevent cyanide poisoning.
Abstract: Sodium nitroprusside is a potent, effective, and readily reversible direct vasodilating agent. It is broken down by hemoglobin into cyanide, which is in part detoxified by liver and kidney to thiocyanate. Some cyanide, especially in nitroprusside- "resistant" individuals who need large amounts of the drug, appears to remain free to cause cyanide poisoning. Patients requiring inordinate amounts probably should not continue to receive the drug, although maximum dosage limits for long-term therapy are not established. Blood thiocyanate levels do not indicate the extent to which free cyanide is limiting oxygen utilization in essential tissue, nor do blood cyanide levels. Metabolic acidosis, elevated lactate levels, elevated lactate/pyruvate ratios, and elevated mixed venous blood oxygen content are at present the best indications of the presence of cyanide poisoning during nitroprusside administration. Nitroprusside appears useful for induction of hypotension during surgery, and for treatment of hypertensive emergencies from all causes, although continuance for more than a few days is probably unwise. The reductions of cardiac afterload and ventricular filling pressure by nitroprusside appear useful in treatment of severe myocardial failure or infarction, but studies of myocardial cyanide toxicity are needed before complete acceptance of this therapy is warranted. Initial dose rates between 0.5 and 1.5 mug/kg/min are recommended only as starting points for very careful titration. Total projected intra-operative dosage should be calculated as quickly as possible and should not exceed 3-3.5 mg/kg. It is hoped that future studies will reveal the maximum dose of nitroprusside that can safely be metabolized in a 24-hour period, and may indicate that cofactors of rhodanase such as thiosulfate, or cobalamins such as hydroxocobalamin, can be administered with nitroprusside to prevent cyanide poisoning.

313 citations


Journal ArticleDOI
TL;DR: The most reliable method of measuring neuromuscular function is to stimulate an accessible peripheral motor nerve and measurement of the evoked response of the skeletal muscle or muscles innervated by the stimulated motor nerve.
Abstract: Monitoring neuromuscular transmission provides valuable information to the anesthesiologist. The aquisition of relevant data contributes to a more predictable and rational approach to the use of muscle relaxants and assures improved patient care during and in the immediate postoperative period.

311 citations


Journal ArticleDOI
TL;DR: The results suggest that the rapid penetrance of naloxone into the brain and the high brain-serum concentration ratio contribute to its rapid onset of action and potency as a narcotic antagonist.
Abstract: Using a specific and sensitive radioimmunoassay, naloxone concentrations in the brains and sera of rats were measured at intervals for four hours following iv injection (5 mg/kg). Decrement curves of naloxone were compared with those after iv injection of morphine (5 mg/kg). Serum concentration of naloxone at 5 minutes was 1.45 +/- 0.1 mug/ml (mean +/- SE) and that of morphine was 1.0 +/- 0.08 mug/ml. Their serum half-lives from one to four hours were approximately the same, 30-40 minutes. With naloxone, the brain-serum concentration ratios ranged from 2.7 to 4.6. Concentration of naloxone in the brain declined parallel to that in the serum. However, with morphine the initial brain concentration was approximately one tenth that in the serum (0.096 +/- 0.04 mug/ml). The brain morphine concentration was sustained for one hour, while serum morphine concentrations declined from 1.0 to 0.19 mug/ml during this period. Two minutes after iv injection of naloxone HCl (0.4 mg) in nine healthy volunteers, the serum drug concentration was 0.01 +/- .001 mug/ml. At 5 minutes, 97 per cent of the administered dose was no longer found in the serum, the serum concentration being 0.004 +/- .0003 mug/ml. From 20 minutes to two hours after injection, the calculated mean serum half-life of naloxone was 64 minutes. These results suggest that the rapid penetrance of naloxone into the brain and the high brain-serum concentration ratio contribute to its rapid onset of action and potency as a narcotic antagonist. The rapid decline of naloxone concentration in the brain found in the animal model, in contrast to that of morphine, could be the basis for its relatively short duration of action.

287 citations


Journal ArticleDOI

276 citations


Journal ArticleDOI
TL;DR: Evidence from voltage-clamp studies of single nerve fibers indicates that anesthetic molecules interact with the sodium channels directly, from the inner side of the nerve membrane, providing a simple explanation for Wedenski inhibition.
Abstract: Local anesthetics block nerve conduction by preventing the increase in membrane permeability to sodium ions that normally leads to a nerve impulse. Among anesthetics containing tertiary amine groups, the cationic, protonated form appears to be more active than the neutral form. However, the neutral forms, as well as uncharged molecules like benzocaine and the aliphatic alcohols, also depress sodium permeability. Studies of single myelinated nerves and squid axons show no direct interaction between calcium ions and local anesthetics, thus disproving theories based on competition between these two agents. Likewise, hypotheses attributing local anesthesia to changes in electrical potentials at the membrane-water interface are disproven by the demonstrated potencies of electrically uncharged anesthetics. Hypotheses that propose that local anesthetics act by expanding the nerve membrane and causing a change in protein conformation that blocks sodium permeability are vague in conception and difficult to test experimentally. Evidence from voltage-clamp studies of single nerve fibers indicates that anesthetic molecules interact with the sodium channels directly, from the inner side of the nerve membrane. Anesthetics bind within sodium channels which have opened during membrane depolarization, preventing the normal sodium ion flux. Anesthetic molecules can dissociate from open channels, but not from channels that remain closed when the nerve is kept at rest. The "gating" properties that regulate the opening and closing of sodium channels are reversibly modified during anesthesia. Specifically, the inactivation function responds more slowly and requires more negative membrane potential changes to reach the same values as in unanesthetized nerves. A second, slow inactivation is observed following external application of tertiary amine anesthetics. The selective binding of anesthetics to open sodium channels provides a simple explanation for Wedenski inhibition, in which the block increases with the frequency of nerve impulses. When impulses occur at higher frequencies more sodium channels are open over a period of time comparable to the time necessary for the anesthetic binding reaction, thus more channels are blocked. In addition the changes of the inactivation function result in a longer refractory period and, thus, a decrease of impulse height at higher frequencies. Charged anesthetic molecules may bind in the pore of the sodium channel. Their binding can be modulated by the electrical field in the membrane. The channel has a higher affinity for larger anesthetic molecules, but this may result from their greater hydrophobicity as well as from their size. The binding site favors molecules that contain more polar linkages between the amine group and the aromatic residue. Binding of amine anesthetics is weakly stereospecific and, surprisingly, shows no absolute requirement for the terminal alkyl ammonium moiety present in most local anesthetics...

230 citations




Journal ArticleDOI
TL;DR: More than 70 per cent of the individuals tested were amnesia for the visual stimuli 15 minutes to 4 hours after 4 mg lorazepam, but was not related to the antirecall effect.
Abstract: The time of onset and duration of the anti-recall action of lorazepam were assessed under clinical conditions by measuring recall and recognition of visual stimuli 24 hours after intravenous administration of lorazepam. The visual stimuli were first presented 5-240 minutes after 2 mg and 5-360 minutes after 4 mg lorazepam. Retrograde amnesia was not produced. Lorazepam, 2 mg, produced a short anti-recall effect (anterograde amnesia) in 50 per cent of the cases, with a latency of 30 minutes and a duration of less than half an hour. Duration and frequency of the anti-recall effect were greater after 4 mg, while the latency was shorter. More than 70 per cent of the individuals tested were amnesic for the visual stimuli 15 minutes to 4 hours after 4 mg lorazepam. Sedation was satisfactory and long-lasting following both doses of lorazepam, but was not related to the anti-recall effect.

157 citations


Journal ArticleDOI
TL;DR: Halo thane decreased the severity of experimentally-induced myocardial ischemia in the non-failing canine heart, suggesting that, in the absence of ventricular failure, halothane influences the relationship betweenMyocardial oxygen supply and demand in a favorable direction when coronary blood flow is limited.
Abstract: The effect of halothane on net myocardial oxygen balance of ischemic myocardium was studied in the non-failing canine heart. Myocardial ischemia was produced by repeated reversible occlusions of a coronary artery; the severity of ischemia was estimated by summating ST-segment elevations (sigma ST) obtained by epicardial ECG mapping at 15 to 18 sites. Control measurements were obtained before and after administration of halothane (0.75 per cent) to six dogs with chloralose-urethane basal anesthesia. Halothane was associated with significant decreases of systemic arterial pressure (P less than .001), heart rate (P less than .01), and the product of systolic arterial pressure X heart rate (P less than .01), an indirect index of myocardial oxygen consumption, while left atrial pressure remained unchanged at normal levels. sigmaST during occlusion was less (P less .001) during halothane (26.5 +/- 7.4 (SD) mv) than before (36.6 +/- 5.4 mv) or after (34.4 +/- 8.2 mv) its administration. Thus, halothane decreased the severity of experimentally-induced myocardial ischemia in the non-failing canine heart. The data suggest that, in the absence of ventricular failure, halothane influences the relationship between myocardial oxygen supply and demand in a favorable direction when coronary blood flow is limited.

148 citations


Journal ArticleDOI
TL;DR: Either fentanyl or Innovar was administered to supplement nitrous oxide anesthesia for operations on 29 patients, and full recovery appeared to be more rapid with Innovar than with fentanyl alone.
Abstract: Either fentanyl or Innovar (fentanyl, 0.05 mg/ml, and droperidol 2.5 mg/ml) was administered to supplement nitrous oxide anesthesia for operations on 29 patients. Both fentanyl and Innovar depressed the slope of the rebreathing CO2 response curve during operation to 42 per cent +/- 6 (mean of all intraoperative values, +/- SE) of the awake control value. Following the last injection of drug but with continuation of operation, the slope increased such that it was 77 per cent +/- 8 of control on the patients' arrival in the recovery room. The slope continued to increase to a peak of 103 per cent +/- 9 of control. Soon therafter respiratory depression recurred, as indicated by a decline in the slope to 55 per cent +/- 5 of control, with a subsequent gradual return to 85 per cent +/- 8 of control 230 minutes after the last injection. This biphasic response occurred in 90 per cent (26 of 29) of the patients treated either with fentanyl alone or with Innovar. Full recovery appeared to be more rapid with Innovar than with fentanyl alone. Droperidol did not augment and may have attenuated fentanyl-induced respiratory-depression.

144 citations



Journal ArticleDOI
TL;DR: It is suggested that nitroglycerin decreases myocardial oxygen demand and relieves myocardian ischemia and reduces systolic diastolic blood pressures during coronary-artery surgery.
Abstract: The effects of an intravenous infusion of nitroglycerin were studied in 20 acutely hypertensive patients during coronary-artery surgery. Eight patients had histories of essential hypertension and six had been treated for it. They were anesthetized with morphine, diazepam, N2O, O2, pancuronium, and enflurane. Control measurements were obtained after sternotomy. Nitroglycerin was then administered until the blood pressure returned to normal, and the measurements then repeated. The mean dose of nitroglycerin was 80.0 +/- 4.7 mug/min, or 0.96 mug/kg/min. This produced significant decreases (P less than .05) in systolic, diastolic, and mean arterial blood pressures, central venous pressure, pulmonary capillary wedge pressure, systemic vascular resistance, and left ventricular stroke work index. Cardiac index, stroke index, and heart rate were unchanged. Two indices of myocardial oxygen demand (rate-pressure product and tension-time index) were significantly decreased by nitroglycerin (P less than .005). Fifty per cent of the patients had improvement in ST-segment depression on the electrocardiogram. These findings demonstrate that nitroglycerin can be safely administered intravenously during operation, and suggest that nitroglycerin decreases myocardial oxygen demand and relieves myocardial ischemia.

Journal ArticleDOI
TL;DR: Metabolism of enflurane to inorganic fluoride was insufficient to cause clinically significant renal dysfunction and postanesthetic renal function was normal in both groups of surgical patients without renal disease.
Abstract: The metabolism and renal effects of enflurane were studied during and after anesthesia in ten surgical patients without renal disease; ten control patients received halothane. Enflurane was metabolized to inorganic fluoride with a mean peak serum level of 22.2 ± 2.8 µM four hours after anesthesia. U


Journal ArticleDOI
TL;DR: This study was undertaken to see whether nitrous oxide-oxygen sedation caused any depression of the pharyngo-laryngeal reflexes.
Abstract: Nitrous oxide-oxygen sedation is in daily use in dental practice, following the pioneering work of practitioners such as Langa.1 With this technique, nitrous oxide is administered in analgesic concentrations, together with oxygen, using special apparatus with built-in oxygen fail-safe devices.2 Although no fatality or severe complication from this technique has been reported, it has been suggested by Pleasauts3 that the pharyngeal protective reflexes may be deminished. If this is so, then material from the oral cavity could be inhaled during dental treatment using nitrous oxide—oxygen sedation, which is an inherently dangerous situation. This study was undertaken to see whether nitrous oxide-oxygen sedation caused any depression of the pharyngo-laryngeal reflexes.

Journal ArticleDOI
TL;DR: The neurobehavioral status of 20 newborn infants was evaluated and demonstrated no measurable difference from control infants and did not have the decrease in muscle tone and strength observed in infants whose mothers had received continous lumbar epidural anesthesia with lidocaine or mepivacaine in a previous study.
Abstract: The neurobehavioral status of 20 newborn infants was evaluated after two to four hours of life following maternal epidural anesthesia with bupivacaine for labor and vaginal delivery. All infants were normal products of uncomplicated full-term gestations. The 20 infants, whose mothers had received continuous lumbar epidural anesthesia with bupivacaine, demonstrated no measurable difference from control infants and did not have the decrease in muscle tone and strength observed in infants whose mothers had received continuous lumbar epidural anesthesia with lidocaine or mepivacaine in a previous study.

Journal ArticleDOI
TL;DR: It is hypothesized that the products produced by this reductive metabolic pathway are also potentially more hepatotoxic than the oxidative metabolites, based upon the increased covalent binding of halothane metabolites under hypoxic conditions.
Abstract: Fluoride release and covalent binding of halothane metabolites were studied in rats pretreated with phenobarbital and anesthestized with halothane in the presence of high (40 per cent) and low (7 per cent) oxygen tensions. The purpose of producing hypoxia was to promote the reductive path ways invol


Journal ArticleDOI
TL;DR: It is concluded that stump pressure is an unreliable index of CBF during carotid occlusion and that its relationship to CBF is considerably influenced by the anesthetic.
Abstract: Carotid endarterectomy requires temporary surgical occlusion of the involved carotid artery. During occlusion, the minimally acceptable (critical) internal carotid artery stump pressure is reported to be 50 torr, whereas for regional cerebral blood flow (rCBF), a critical range is reported to be 18-24 ml/100 g/min. During 90 carotid endarterectomies, rCBF and stump pressure were measured and the EEG continuously monitored. A positive correlation between rCBF and stump pressure (i.e., when both were either above or below their respective critical values) was observed in only 58 per cent of the cases. In 28 per cent stump pressures of less than 50 torr were observed despite rCBF's above 24 ml/100 g/min and normal EEG's. In 8 per cent stump pressures were more than 50 torr but rCBF's were less than 18 ml/100 g/min and EEG changes of ischemia were commonly observed. In the remaining 6 per cent rCBF's were marginal (18-24 ml/100 g/min) while stump pressures were more than 50 torr and EEG changes were not observed. The relationship between stump pressure and rCBF was influenced by the anesthetic. In the absence of transient ischemia during occlusion (that is, rCBF greater than 18 ml/100 g/min), halothane and enflurane anesthesia were associated with significantly higher rCBF's and lower stump pressures than was neuroleptanesthesia. Pre-occlusion and post-occlusion rCBF measurements also demonstrated cerebral vasodilation by halothane and enflurane (halothane greater than enflurane) and vasoconstriction by neuroleptanesthesia. It is concluded that stump pressure is an unreliable index of CBF during carotid occlusion and that its relationship to CBF is considerably influenced by the anesthetic.

Journal ArticleDOI
TL;DR: A nitrogen-dilution technique for measurement of airway closing volumes (CV) and functional residual capacity (FRC) not requiring subject cooperation was tested in five healthy, awake, spontaneously breathing subjects and subsequently used in 20 patients during anesthesia with mechanical ventilation.
Abstract: A nitrogen-dilution technique for measurement of airway closing volumes (CV) and functional residual capacity (FRC) not requiring subject cooperation was tested in five healthy, awake, spontaneously breathing subjects and subsequently used in 20 patients during anesthesia with mechanical ventilation. Incomplete exhalation before inhalation of oxygen did not significantly alter CV. Inspiration of a volume of oxygen equal to 75 per cent of vital capacity (VC) did not affect CV, whereas inspiration to 50 percent VC resulted in a 20 per cent decrease in CV. Expiratory resistance tended to reduce CV. By means of this technique, the validity of which had been thus demonstrated, airway closure could be shown to occur at lung volumes larger than FRC (and thus within a normal tidal volume) in six patients prior to anesthesia, and in a further 11 (total 17 of 20) during anesthesia with mechanical ventilation. FRC decreased by an average of 0.5 liters during anesthesia with mechanical ventilation and was only 0.2 liters above residual volume. Significant hypoxemia was observed in association with airway closure.

Journal ArticleDOI
TL;DR: The authors conclude that pentobarbital and fentanyl-droperidol (Innovar) limit the extent of cerebral edema, but that inhaled anesthetics do not.
Abstract: Localized edema follows the freezing of a small area of cerebral cortex. Effects of five subsequent hours of anesthesia on this edema were studied in six groups of six dogs each. Six anesthetic techniques were studied. In six additional "awake" dogs, anesthesia (halothane) was discontinued immediately after the lesion was made. Eight control dogs received neither anesthesia nor cryogenic injury. Control white matter contained 67.4 +/- .4 (mean +/- SE) per cent water by weight. Twenty-four hous after the cryogenic injury, water accounted for the following percentages of total weight of white matter adjacent to the lesion: 60 mg/kg pentobarbital, 73.2 +/-.9; 70 per cent N2O/Innovar, 73.6 +/- .9; "awake", 77.9 +/- .9; 1.95 per cent enflurane, 78.2 +/- .9; 1.33 per cent isoflurane, 78.6 +/- .8; 0.86 per cent halothane, 78.2 +/- .6; 1.89 per cent halothane, 79.7 +/- .6. Peak intracranial pressures (ICP) were 15.4 +/- 1.3 torr with pentobarbital, 21.6 +/- 1.8 torr with N2O/Innovar, and 31.1 +/- 2.6 to 38.3 +/- 4.5 torr with the halogenated anesthetics. The water content of white matter and ICP were significantly lower (P less than 0.05) in animals receiving pentobarbital or N2O/Innovar anesthesia than in animals receiving inhalation anesthetics. The authors conclude that pentobarbital and fentanyl-droperidol (Innovar) limit the extent of cerebral edema, but that inhaled anesthetics do not.

Journal ArticleDOI
TL;DR: Compared to previous suggestions, enflurane appears to be at least as depressant to the dog heart as halogthane, suggesting that the cardiovascular dose-effect curve for en flurane is steeper than that for halothane.
Abstract: Trained dogs with chronically implanted catheters and left ventricular (LV) pressure transducers were anesthetized with 2.3 per cent (1 + MAC) and 3.6 per cent enflurane. Left ventricular function and metabolism were studied while the dogs were awake and during exposure to the two anesthetic concentrations. Enflurane depressed LV function in a dose-dependent fashion. Myoeardial blood flow and oxygenation mirrored the functional changes. Mayocardial oxygen extraction decreased and lactate extraction incrcased during enflurane anesthesia, suggesting adequate oxygen delivery to the myocardium. Low concentrations of halothane in the same dogs on different days had similar effects. However, 2 MAC halothane resembled 1.6 MAC enflurane, suggesting that the cardiovascular dose-effect curve for enflurane is steeper than that for halothane. Both anesthetics produce dose-dependent negative inotropic effects in the intact dog, accompanied demand. Contrary to previous suggestions, enflurane appears to be at least as depressant to the dog heart as halogthane.

Journal ArticleDOI
TL;DR: Metabolic, hemodynamic and neuroendocrine responses to halothane were measured in five normal and five malignant hyperthermia-susceptible swine and initial increases appeared to be non-hypoxic in origin.
Abstract: Metabolic, hemodynamic and neuroendocrine responses to halothane were measured in five normal and five malignant hyperthermia-susceptible (MHS) swine. Constant-volume ventilation was used. There was no therapeutic intervention. In NHS animals, blood lactate concentrations increased first, and the initial increases appeared to be non-hypoxic in origin. Lactate concentrations increased progressively to more than 20 mum/ml. Whole-body oxygen consumption increased almost twofold, and hind limb muscle oxygen consumption increased almost threefold. Extrapolated increases in muscle oxygen consumption accounted for about 55 per cent of the increase in whole-body oxygen consumption. Respiratory and metabolic acidosis, marked hyperkalemia, and increases in catecholamines and temperature occurred secondarily and were accompanied by progressive circulatory failure.

Journal ArticleDOI
TL;DR: This review is an attempt to summarize the known factors infuencing relaxant blocks and to identify the unknown factors.
Abstract: Although acetylcholinesterase inhibitors are accepted antagonists of nondepolarizing neuromuscular blockade, many basic questions are still unanswered. What is the relationship between receptor occupancy and adequate ventilation? What are the effects of changes in acid-base balance and temperature? What are the mechanisms of the various antibiotic-induced neuromuscular blockades, and what antagonizes them? This review is an attempt to summarize the known factors infuencing relaxant blocks and to identify the unknown factors. The need for further studies is obvious.


Journal ArticleDOI
TL;DR: Arterial and peripheral venous plasma levels of huptvacaine were determined in 30 patients following epidural anesthesia using 150 and 225 mg, as well as following intercostal nerve block with 400 mg, and the results suggest that bupivacaine may have a wider margin of safety in man than is now stated.
Abstract: Arterial and peripheral venous plasma levels of bupivacaine were determined in 30 patients following epidural anesthesia using 150 and 225 mg, as well as following intercostal nerve block with 400 mg. Arterial levels were consistently higher than levels in simultaneously sampled venous blood, and the highest levels occurred with bilateral intercostal nerve block. No evidence of systemic toxicity was observed. The results suggest that bupivacaine may have a wider margin of safety in man than is now stated.

Journal ArticleDOI
M R Salem1, A Y Wong, M Mani, E.J. Bennett, T. Toyama 
TL;DR: It is concluded that because of its selective inhibitory effect on gastric acid secretions, glycopyrrolate appears superior to other anticholinergic drugs and bile staining of gastric contents is not a reliable indicator of Gastric juice pH.
Abstract: The effects of premedication on gastric juice volume and pH were evaluated in five groups of 206 pediatric patients undergoing elective surgical procedures: Group 1 (Control) received no premedication; Group 2 was given morphine sulfate and pentobarbital as premedicants. The other groups received, in addition to morphine and pentobarbital, atropine (Group 3), scopolamine (Group 4), or glycopyrrolate (Group 5). After endotracheal intubation, gastric aspirates were examined for volume, pH and color. Neither premedication with morphine and pentobarbital nor addition of atropine or scopolamine to the premedication significantly altered volume. In patients treated with glycopyrrolate, volume was reduced to less than a third of that of patients in Group 1 (P less than 0.001), and the percentage of pH's higher than 2.5 was significantly greater than in other groups. The incidences of unobtainable samples and samples with pH's higher than 2.5 were greatest with atropine (32.0 per cent, P less than 0.05) and glycopyrrolate (58.1 per cent, P less than 0.01). In 60 per cent of the bile-stained specimens, pH's were below 2.5. It is concluded that because of its selective inhibitory effect on gastric acid secretions, glycopyrrolate appears superior to other anticholinergic drugs. The reduction of gastric juice volume and acidity produced by glycopyrrolate would have important clinical implications in case of accidental aspiration. It is also concluded that bile staining of gastric contents is not a reliable indicator of gastric juice pH.

Journal ArticleDOI
TL;DR: A potential for PEEP to evoke neurologic complications in patients who have intracranial disease and that the presence of pulmonary disease may attenuate these deleterious side effects is indicated.
Abstract: Elevated intrathoracic pressure due to positive end-expiratory pressure (PEEP) has the potential for increasing intracranial pressure (ICP) and reducing arterial blood pressure (BP). Such changes could critically reduce cerebral perfusion pressure (CPP = BP - ICP), This possibility was investigated in 15 cats with artificially-produced expanding intracranial masses (intracranial balloon). The interrelationships among ICP and central venous and arterial pressures were observed during application and removal of graded levels of PEEP (5, 10, 15 cm H2O). The electroencephalogram and pupillary diameters were monitored. At various levels of ICP, nine of the cats were given oleic acid intravenously to embolize the lung and cause pulmonary dysfunction. In cats not given oleic acid, PEEP caused a maximal reduction in cerebral perfusion pressure of 45 +/- 4 torr(SEM), accompanied by variable changes in ICP. PEEP application in the absence of oleic acid embolization of the lungs caused electroencephalographic abnormalities in 77% of these cats, while pupillary diameters increased in 56%. Animals embolized wwith oleic acid had significantly less (P less than .001) severe CPP reductions (mean 21 +/- 4 torr) than did the non-embolized animals, and developed no EEG change due to PEEP. However, increases in pupillary diameter still occurred in 33% of cats given oleic acid when PEEP was applied. In 82% of the PEEP applications (n = 44) in both experimental groups only insignificant increases in intracranial tension occurred (average peak ICP gain less than 1.5 torr). Abrupt increases in ICP exceeding 11 torr (15 cm H2O) occurred in four animals in each group. This happened most frequently (63 per cent) when the intracranial tension before PEEP was above 15 torr. Sudden removal of or reduction in PEEP was accompanied by increases in arterial and intracranial pressures in both groups, although this response was attenuated in the cats given oleic acid. The results indicate a potential for PEEP to evoke neurolgic complications in patients who have intracranial disease and that the presence of pulmonary disease may attenuate these deleterious side effects. Monitoring of neurologic function as well as blood-gas and cardiovascular effects of PEEP in patients who have intracranial disease is suggested.


Journal ArticleDOI
TL;DR: The dose-dependent negative inotropic effect of halothane resulted in a decrease in cardiac oxygen demand which was equal to or greater than the decrease in oxygen delivery.
Abstract: Chronically catheterized dogs were studied awake and during anesthesia with high and low concentrations of halothane to assess the relationship between cardiac function and metabolism. Low concentrations of halothane (0.79 per cent endtidal) increased heart rate and decreased left ventricular stroke volume, stroke work, and dP/dt without producing other hemodynamic changes. However, similar heart rate increases produced by atrial pacing in awake animals increased aortic pressure and cardiac output and decreased left atrial pressure. Consequently, the halothane-induced tachycardia partially compensated for the negative inotropic effect of the halothane. High concentrations of halothane (1.74 per cent endtidal) further increased heart rate and elevated left atrial pressures. Cardiac output, stroke volume, stroke work, aortic pressure, LV dP/dt, myocardial blood flow and oxygen consumption were markedly decreased. Myocardial glucose extraction was also decreased. Myocardial oxygen extraction was unchanged, and lactate extraction rose with both concentrations of halothane. Consequently, the dose-dependent negative inotropic effect of halothane resulted in a decrease in cardiac oxygen demand which was equal to or greater than the decrease in oxygen delivery. Whether the same relationship would be seen in the ischemic heart is yet to be demonstrated.