Enflurane Anesthesia Research Articles

Is Milrinone Equivalent to Amrinone during Enflurane Anesthesia in the Dog?

Dose-response curves for milrinone during 2.1-2.3% end-tidal enflurane anesthesia were studied in six dogs given three successive boluses and 30-minute infusions of milrinone: 1) 40 microgram/kg plus 3 microgram.kg-1.min-1 (plasma level at 5 and 30 minutes after beginning of infusion: 122 +/- 14 and 136 +/- 14 ng/ml); 2) 60 microgram/kg plus 6 microgram.kg-1.min-1 (285 +/- 31 and 304 +/- 19 ng/ml); 3) 80 microgram/kg plus 12 microgram.kg-1.min-1 (498 +/- 32 and 581 +/- 28 ng/ml), demonstrating a progressive improvement of cardiac performance. Differences between milrinone and amrinone were also studied during enflurane anesthesia in six other dogs given milrinone or amrinone at 3- to 4-week intervals using both a low dose that did not decrease mean arterial pressure significantly and a dose that decreased mean arterial pressure 20-25% below baseline values. There was a dose-related effect with both drugs on the measured hemodynamic variables. Plasma catecholamine levels did not change significantly in either group. The results of our studies show that during enflurane anesthesia 1) there is a correlation between milrinone plasma levels and improvement of cardiac performance and, 2) milrinone, at low and high doses studied without or with a significant decrease in mean arterial pressure, respectively, is similar to amrinone in its activity to improve cardiac performance by similar positive inotropic, chronotropic, and vasodilating effects.

Effects of the volatile anesthetic agents on sinus node function and atrioventricular conduction in dogs: A comparison with chloralose anesthesia

The effects of equipotent concentrations (1.5 times minimum alveolar concentration) of the inhalational agents halothane, enflurane, and isoflurane on sinus node function, and atrioventricular (A-V) conduction and refractoriness were compared with chloralose anesthesia in 49 mongrel dogs. Sinus node function was assessed using corrected sinus node recovery time. Atrial-His and His-ventricular conduction times were measured at paced heart rates of 150, 180, and 200 beats/min, and A-V refractoriness was assessed by Wenckebach periodicity. There was no evidence that sinus node function was impaired by any of the inhalational agents. Enflurane anesthesia was associated with a significant prolongation of atrial-His conduction at paced heart rates of 180 and 200 beats/min when compared to chloralose anesthesia and the other two inhalational agents ( P < .001). Atrioventricular refractoriness was impaired by enflurane ( P < .001) and halothane ( P < .05), but not isoflurane, when compared with chloralose anesthesia. Ventricular-His conduction was not altered by any of the agents. The authors conclude that enflurane is associated with a greater impairment of AN conduction and refractoriness than halothane or isoflurane, and that these changes are related to the anesthetic agent .and not the anesthetic state.

Interaction between diltiazem and halothane or enflurane in the canine blood-perfused papillary muscle and sinoatrial node preparations cross-circulated by chronically instrumented conscious donor dog.

Interaction of cardiovascular effects of diltiazem with those of halothane or enflurane was estimated in the canine isolated papillary muscle and sinoatrial node preparations perfused by arterial blood of the chronically instrumented conscious and halothane- or enflurane-anesthetized donor dog, into which diltiazem was infused i.v. at a rate of 20 micro g/kg/min for 60 min. One hour after diltiazem infusion, in the conscious donor dog, mean arterial pressure (MAP) and heart rate (DHR) were decreased to 84 +/- 3 and 84 +/- 2% and PQ interval (PQ) was prolonged to 148 +/- 5%, while in the isolated preparations, developed tension (DT) of the papillary muscle and sinoatrial rate (SAR) were decreased to 68 +/- 3 and 74 +/- 3% and blood flow (BF) was increased to 155 +/- 5% (n = 10). On the other hand, halothane (0.8%) anesthesia per se decreased MAP, DHR, DT and SAR to 89 +/- 8, 84 +/- 3, 79 +/- 3 and 89 +/- 5% (n = 7) of each basal value in conscious state 20 min after the inhalation. During halothane anesthesia, the same dose of diltiazem infused decreased MAP to 74 +/- 4 (n = 7), DHR to 66 +/- 4 (n = 6), DT to 62 +/- 7 (n = 7) and SAR to 69 +/- 1% (n = 3) of each value suppressed by halothane itself. Meanwhile, enflurane (1.7%) anesthesia itself decreased MAP, DHR, DT and SAR to 81 +/- 3, 85 +/- 2, 81 +/- 2 and 88 +/- 2% (n = 10) of each basal value in conscious state 30 min after enflurane inhalation. During enflurane anesthesia diltiazem decreased MAP to 74 +/- 3 (n = 10), DHR to 67 +/- 3 (n = 8), DT to 45 +/- 5 (n = 10) and SAR to 74 +/- 6% (n = 3) of each value under enflurane anesthesia alone. PQ interval of the donor dog heart was prolonged by halothane alone to 111 +/- 5% (n = 7) and by enflurane alone to 110 +/- 2% (n = 10) of the value before each anesthesia, and then diltiazem prolonged PQ interval to 160 +/- 8% (n = 6) and 174 +/- 10% (n = 8) of each value suppressed by the anesthetic itself during halothane- or enflurane-anesthesia, respectively. The second degree AV conduction block was induced in 1 of 7 halothane- and in 2 of 10 enflurane-anesthetized donor dogs, respectively. The sinus arrest was induced by diltiazem in 4 of 7 sinoatrial node preparations under halothane and in 7 of 10 ones during enflurane anesthesia. Moreover, plasma concentration of diltiazem 60 min after the start of infusion was 556 +/- 121 ng/ml in conscious dogs and tended to increase to 752 +/- 101 ng/ml in enflurane anesthetized donor dogs (n = 4), but there was no significant difference between two values (0.05 < P < 0.1). These results indicate that effects of diltiazem could be potentiated during halothane or enflurane anesthesia by elimination of compensatory reflex noted in conscious state, and that the negative inotropic effect of diltiazem was enhanced by enflurane anesthesia due to unknown mechanisms which probably include a slight but insignificant increase in plasma concentration.

Continuous infusion of vecuronium in children.

The average dose of vecuronium required in children continuous infusion to attain a steady state block of 90% was determined. The electromyographic (EMG) response and mechanical response to supramaximal stimulation of the ulnar never recorded simultaneously, were significantly correlated in four children. The steady-state infusion rate requirement of vecuronium was 1.4 +/- 0.03 micro g/kg/min during 2% enflurane anesthesia and 3.1 +/- 0.03 micro g/kg/min during 1% halothane anesthesia. The spontaneous recovery time to 25% of the control by EMG during halothane and enflurane anesthesia was 12.6 +/- 1.1 and 10.3 +/- 1.5 min, respectively, after termination of the infusion. There was no cumulative effect after prolonged vecuronium infusion.

MOUTH OPENING REDUCTION ASSOCIATED WITH SUCCINYLCHOLINE DURING ENFLURANE ANESTHESIA.

Vanderspek, A FL MD; Fang, W B MD; Ashton-Miller, J A PhD; Stohler, C S DDS; Reynolds, P I MD Author Information

Breathing pattern of anesthetized humans during pancuronium-induced partial paralysis.

We investigated the breathing patterns of 17 subjects anesthetized with enflurane before and after partial muscle paralysis produced by pancuronium bromide. In the face of significant muscle weakness produced by pancuronium, breathing patterns are characterized by decreases in both tidal volume and respiratory frequency. The decreased tidal volume corresponded to the decrease in occlusion pressure, indicating that the decreased tidal volume results solely from a decreased contractile force of the respiratory muscles. The decreased respiratory frequency was due to prolongation of both inspiratory and expiratory time without changing the ratio of the inspiratory time to the total breath time. Withdrawal of phasic vagal influence by airway occlusion before partial muscle paralysis revealed that an active Breuer-Hering inflation reflex was operative in only 8 of all 17 subjects. Since the contribution of the Breuer-Hering inflation reflex alone does not seem to account for the consistent decrease in respiratory frequency, some other mechanisms modulating respiratory frequency might be involved in the characteristic breathing patterns during partial muscle paralysis under enflurane anesthesia.

The Effects of Glycopyrrolate-Pyridostigmine Mixture on Heart Rate and Blood Pressure during Halothane and Enflurane Anesthesia

The Effects of Glycopyrrolate-Pyridostigmine Mixture on Heart Rate and Blood Pressure during Halothane and Enflurane Anesthesia

Response of the Heart to Acute Hypertension during Halothane, Enflurane, and Isoflurane Anesthesia

In the open chest dog model, the response of the left ventricle exposed to acute mechanical hypertension was evaluated while the animals were receiving various concentrations of halothane, enflurane, and isoflurane. Myocardial contractility was quantified by the end-systolic pressure-length relation (ESPL). When the mean aortic pressure was increased by 40% above the control value for a given concentration of inhalation agent, the end-diastolic volume increased and thereby maintained stroke work. However, as the end-tidal concentrations of the anesthetics increased, this compensatory mechanism became progressively more ineffective as a result of myocardial depression caused by the anesthetics. No evidence could be found of an improvement in myocardial contractility as the aortic pressure was increased. Mild depression of myocardial contractility could be demonstrated for 1.1 MAC halothane, 0.6 MAC enflurane, and 1.0 MAC isoflurane. Severe depression of contractility occurred at 2.3 MAC halothane, 1.2 MAC enflurane, and 1.5 MAC isoflurane.

Mechanisms of Succinylcholine-Induced Arrhythmias in Hypoxic or Hypoxic

To evaluate the effects of succinylcholine on cardiac arrhythmias and serum levels of potassium and catecholamines, dogs with hypoxia alone and with hypoxia and hypercarbia were studied during anesthesia with halothane or enflurane. After the injection of succinylcholine (0.3 mg/kg), cardiac arrhythmias occurred in all halothane:hypoxia dogs and in 70% of dogs given halothane during hypoxia:hypercarbia. No dogs given enflurane anesthesia developed arrhythmias. Serum potassium levels increased significantly 3 and 5 min after succinylcholine in all groups. Serum epinephrine levels increased in the halothane-hypoxia:hypercarbia and enflurane:hypoxia groups and, after the injection of succinylcholine, epinephrine levels increased further in dogs in the halothane:control, halothane:hypoxia, halothane-hypoxia:hypercarbia, enflurane:hypoxia, and enflurane-hypoxia:hypercarbia groups. Norepinephrine levels increased with enflurane-hypoxia:hypercarbia and after the succinylcholine in the halothane:hypoxia, halothane-hypoxia:hypercarbia, and enflurane-hypoxia:hypercarbia groups. The results suggest that succinylcholine induces arrhythmias by sympathetic stimulation and that halothane sensitizes the myocardium to arrhythmias at the same levels of serum catecholamines and potassium in the presence of hypoxia or hypoxia:hypercarbia more than does enflurane.

Plasma fluoride concentration and urinary fluoride excretion in obese and non-obese patients following enflurane anesthesia.

Plasma fluoride concentrations and urinary fluoride excretions were measured following enflurane anesthesia (1.5%, 2 hours) in obese (8 cases) and non-obese (9 cases) patients. At the end of anesthesia, there was no significant difference in plasma fluoride concentrations between the two groups. In the several days following anesthesia, however, plasma fluoride concentrations in obese patients were higher than those in non-obese patients. Urinary fluoride excretions after anesthesia were greater in obese patients than those in non-obese patients, and the period of increased fluoride excretion was prolonged in obese patients. These results suggested that obese patients metabolized more enflurane than non-obese patients during the postanesthetic period. In obese patients, their excess fatty tissue may cause a greater and more prolonged elevation of blood enflurane concentrations after anesthesia.

Cardiovascular effects of and interaction between calcium blocking drugs and anesthetics in chronically instrumented dogs. V. Role of pharmacokinetics and the autonomic nervous system in the interactions between verapamil and inhalational anesthetics.

To assess the role of both pharmacokinetics and the autonomic nervous system in the interaction between inhalational anesthetics and verapamil, dogs were chronically instrumented to measure heart rate, PR interval, dP/dt, cardiac output, and aortic blood pressure. In a first group of seven dogs, studied awake and during halothane (1.2%), enflurane (2.5%), and isoflurane anesthesia (1.6%), verapamil was infused for 30 min in doses calculated to obtain similar plasma concentrations (83 +/- 10, 82 +/- 6, 81 +/- 10, and 77 +/- 9 ng.ml-1, respectively). For the latter purpose, the infusion dose was 3 and 2 micrograms.kg-1.min-1 awake and during anesthesia, respectively, preceded by a loading dose of 200, 150, and 100 micrograms.kg-1, awake, during isoflurane, and halothane and enflurane, respectively. In awake dogs, verapamil induced an increase in heart rate (24 +/- 5 bpm) and PR interval (35 +/- 9 msec) and a decrease in mean arterial pressure (-5 +/- 2 mmHg) and dP/dt (-494 +/- 116 mmHg/s). Although plasma concentrations were similar in awake and in anesthetized dogs, the only statistically significant changes induced by verapamil were an increase in heart rate and a decrease in dP/dt during halothane and enflurane, while left atrial pressure increased only with enflurane. In a second group of six dogs, verapamil pharmacokinetics were determined in the presence and absence of a ganglionic blocking drug (chlorisondamine, 2 mg.kg-1 iv). Blockade of ganglionic transmission resulted in a decrease in both initial volume of distribution and total clearance of verapamil--changes similar to those previously reported with inhalational anesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed Convulsions Following Enflurane Anaesthesia

Summary A case of convulsions which occurred 3 days after recovery from enflurane anaesthesia is reported.

Neostigmine antagonism of vecuronium paralysis during fentanyl, halothane, isoflurane, and enflurane anesthesia.

Neostigmine antagonism of vecuronium paralysis during fentanyl, halothane, isoflurane, and enflurane anesthesia.

Clinical pharmacokinetics of the inhalational anaesthetics.

At present, the most widely used inhalational anaesthetics are the halogenated, inflammable vapours halothane, enflurane, isoflurane and the gas nitrous oxide. The anaesthetic effect of these agents is related to their tension or partial pressure in the brain, represented at equilibrium by the alveolar concentration. The minimum alveolar concentration for a specific agent is remarkably constant between individuals. The uptake and distribution of inhalational anaesthetics depends on inhaled concentration, pulmonary ventilation, solubility in blood, cardiac output and tissue uptake. Inhalational anaesthetics are mainly eliminated by pulmonary exhalation, but significant amounts of halothane are removed by hepatic metabolism. Inhalational agents currently in use have acceptable pharmacokinetic characteristics, and clinical acceptance depends on their potential for adverse effects. Induction of anaesthesia with halothane is rapid and relatively pleasant and it is the agent of choice for paediatric anaesthesia. Between 20 and 50% is metabolised, and the parent drug is a potent inhibitor of drug metabolism. Post-operatively enzyme induction may follow. The major disadvantages of halothane are myocardial depression, propensity to evoke cardiac arrhythmias and the rare but serious halothane hepatitis. Induction and recovery from enflurane anaesthesia is rapid. Metabolism accounts for 5 to 9% of the elimination. The metabolic product inorganic fluoride may in rare cases cause renal toxicity. Enflurane is a weak inhibitor of drug metabolism at anaesthetic concentrations. Enflurane depresses circulation more than halothane by reducing both myocardial contractility and systemic vascular resistance, but cardiac rhythm is stable. Enflurane anaesthesia may, unlike the other agents, induce epileptic activity. Enflurane is widely used as replacement for halothane in adults. Despite its low blood-gas solubility, the airway irritability of isoflurane precludes a faster induction of anaesthesia than with halothane. Isoflurane is almost resistant to biodegradation. Myocardial contractility is maintained during isoflurane anaesthesia and cardiac rhythm is stable except for the occurrence of tachycardia in some patients. Isoflurane is the inhalational agent of choice for neurosurgical operations. Sevoflurane is an experimental ether vapour: induction and recovery is fast and pleasant. It is metabolised to the same extent as enflurane and subnephrotoxic concentrations of inorganic fluoride may result. Sevoflurane has fewer respiratory and cardiovascular depressant effects than halothane and may be a future alternative for paediatric anaesthesia.(ABSTRACT TRUNCATED AT 400 WORDS)

Halothane Hepatotoxicity in Guinea Pigs

A recently reported animal model of halothane-associated hepatotoxicity in males of a colored strain of guinea pig was further characterized as to possible sex and strain specificity in outbred albino Amana, inbred albino Hartley, inbred colored strain 2, and inbred colored strain 13 guinea pigs. Exposure to 1% halothane for 4 hr in 21% O2 proved to be hepatotoxic in both sexes. Forty-eight hours after halothane exposure fatty vacuolization of hepatocytes was present in all animals. Histologically identifiable hepatic necrosis occurred in 60% of the guinea pigs exposed, along with concomitant increases in SGPT. Approximately one half of these responding animals had extensive centrilobular necrosis, which was still present 96 hr after halothane exposure. Females of the inbred strain 2 and males and females of strain 13 were the most susceptible to halothane-induced hepatic necrosis whereas the inbred Hartley strain was almost totally refractory to necrosis. Outbred Amana and male inbred strain 2 animals exhibited an intermediate hepatotoxic response. Comparison of the halothane-associated hepatic lesion with that induced by anoxic/ischemic mechanisms, (exposure to low (8%) oxygen during 1.7% enflurane anesthesia) showed obvious differences in the morphology of the hepatic necrosis and the apparent time course of lesion development. This guinea pig model of halothane-associated hepatotoxicity appears to be superior to previous animal models in that no pretreatment of the guinea pigs is required, both sexes are affected, and the resulting hepatic lesion is more persistent.

Amrinone Blunts Cardiac Depression Caused by Enflurane or Isoflurane Anesthesia in the Dog

The effects of two infusion rates of amrinone, a positive inotrope and vasodilator, were studied during high and low concentrations of either enflurane or isoflurane anesthesia in a canine model. The anesthetic concentrations used were: "low" = 2.1-2.2% enflurane or 1.7-1.8% isoflurane, and "high" = 3.4-3.5% enflurane or 3.0-3.1% isoflurane. The two infusion rates of amrinone were: "low" = 2 mg/kg plus 30 micrograms X kg-1 X min-1 and "high" = 4 mg/kg plus 100 micrograms X kg-1 X min-1. In the present study, amrinone, in sufficient doses, blunted the deleterious effects of enflurane or isoflurane on myocardial function, reduced systemic vascular resistance (SVR) and pulmonary capillary wedge pressure, restored left ventricular dP/dtmax (LVdP/dtmax), and maintained cardiac index, even at the high concentrations of enflurane or isoflurane that caused marked cardiac depression. However, with reduced SVR, mean arterial pressure remained low. With lower enflurane or isoflurane, high concentrations of amrinone elevated LVdP/dtmax and heart rate above baseline, which might be of concern if myocardial oxygen supply were limited. No arrhythmias were observed at any time in this study. Amrinone did not increase plasma catecholamine levels with either anesthetic. Elevated amrinone plasma concentrations persisted for at least 1 hr after cessation of the high amrinone infusion and continued stimulatory effects on the cardiovascular system were observed. These results suggest that in selected patients amrinone may be beneficial in the short-term treatment of perioperative depression of cardiac performance.

Respiratory Depression During Enflurane Anaesthesia in Children

The author studied the rate of induction and recovery, occurrence of airway problems and the degree of respiratory depression in 30 children breathing spontaneously during inhalational induction for intubation. Two equi-anaesthetic gas mixtures were compared, 5.0% enflurane in 50% N2O (group E50) and 3.2% enflurane in 70% N2O (group E70). Induction time and time for 'partial recovery' were significantly shorter in group E70 than in group E50 (P less than 0.05). Airway problems during the excitational stage and during intubation were less common in group E70 than in group E50 (P less than 0.05). Also respiratory depression, as measured by end-tidal CO2 tension and by the occurrence of apnoea, was significantly less pronounced in group E70 than in group E50. It was concluded that 3.2% enflurane-N2O/O2 (70/30) was quite acceptable for mask induction for intubation in spontaneously breathing children, while 5.0% enflurane-N2O/O2 (50/50) caused a marked respiratory depression with delayed induction and offered less suitable conditions for intubation.

Postoperative Hepatic Dysfunction After Halothane or Enflurane Anesthesia in Patients with Hyperthyroidism

SEINO, H.; DOHI, S.; AIYOSHI, Y.; MIZUTANI, T.; NAKAMURA, K.; NAITO, H. Author Information

Total Body Oxygen Supply-Demand Balance in Burned Patients Under Enflurane Anesthesia

The effects of enflurane anesthesia on the oxygen supply-demand balance have been studied in nine hypermetabolic-hyperdynamic burned patients undergoing debridement and skin-grafting procedures. Mean burn size was 55% of total body surface area. The patients were without cardiac, lung, hepatic, and kidney dysfunction and were not septic. Anesthesia was induced with sodium pentothal and maintained with enflurane and nitrous oxide in oxygen. Ventilation was controlled to maintain PaCO2 within normal limits. Crystalloid solutions and blood were administered to maintain adequate heart filling pressures. Serial measurements of cardiac output, arterial and mixed venous blood gases, and oxygen content were made before, during, and after anesthesia. Following induction of anesthesia and enflurane administration, cardiac output, oxygen delivery, and oxygen consumption decreased in a parallel fashion to approximately 60% of control. These variables did not change significantly throughout the procedure and returned to control values when enflurane was discontinued. Arteriovenous oxygen content difference did not increase and metabolic acidosis did not develop, suggesting that tissue perfusion remained adequate. Under anesthesia, oxygen consumption in burned patients was similar to that observed in normal subjects, indicating that enflurane blunts the hypermetabolic effects of thermal injury. It is concluded that in burned patients enflurane decreases metabolic rate and cardiac output, and maintains an adequate oxygen supply-demand balance.

Dramatic Control of Tachycardia during Enflurane Anesthesia in a Patient with Hyperthyroidism by Verapamil - A case report

Dramatic Control of Tachycardia during Enflurane Anesthesia in a Patient with Hyperthyroidism by Verapamil - A case report