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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary complications after cardiac surgery under extracorporeal circulation remain frequent and sometimes grave, in spite of the great progress which has been made over the past 20 years in the methods of cardiorespiratory assistance. The authors analyse the clinical and radiological repercussions of perfusion on the lung, in 40 patients operated under ECC for coronary revascularisation. The simutaneous study of the arterial, and mixed venous blood gasses and of the alveolar gases, in 20 of these patients showed the constant occurrence of a shunt syndrome, without alveolar hypoventilation or disorders in peripheral circulatory flow. Ventilatory alcalosis, hypocapnia, hypoxemia and the rise in the alveolar arterial oxygen gradient is increased during the second post-operative day. Among the variables studied (duration of ECC, degree of hypothermia, duration of the intervention, duration of anesthesia, pleurotomy) only the latter intervened in a statistically significant manner in this study, in the increase in hypoxemia. 46 pulmonary biopsies carried out before and after ECC in 23 coronary patients were examined with the electron microscope. The initial alveolar involvement affects the septal microcirculation with signs of an increase in capillary permeability leading to an interstitial and epithelial destruction. The use of a membrane oxygenator prevents some of the alveolar lesions, as has been proved by the study of five pulmonary biopsies carried out in dogs submitted to ECC of long duration. Catherterization of the pulmonary artery carried out in 35 patients by means of a SWAN-GANZ catheter, before the intervention enabled supervision of the degree of importance and speed of the hemodynamic variations in the pulmonary circulation during the different phases of ECC (during the phase of ventricular fibrillation). The rise in the flow of left output can lead to the occurrence of negative pulmonary intravascular pressures which can be prejudicial for capillary trophicity. The syndrome of "ECC lung", a veritable "induced post-agressive lung" must be placed in the group of refractory hypoxemia of which it represents one of the most typical pictures.
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PMID:[Pulmonary complications after extracorporeal circulation. ECC lung syndrome]. 1 38

Six dogs, premedicated with pethidine 10 mg kg-1 b.w, were anaesthetized with mebumal natrium (NFN) 25 mg kg-1 b.w. and 80 mg gallamoni jodidum (NFN). Anaesthesia was continued with O2-N2O-halothane and artificial ventilation. Non-carbonic acidosis was induced by i.v. infusion of hydrochloric acid, during which the related values of pulse, blood pressure, cardiac output, total splanchnic prefusion and portal pressure were measured. The pulse remained unchanged down to pH 7.0. At this pH, arrhythmia suddenly occured and developed into ventricular fibrillation. Before this occured falling cardiac output was observed (cardiac output 1 min-1 = -21.49+3.21 x pH, N = 23, r = 0.75, P less than 0.001) and rising oxygen consumption (O2 ml min-1 kg-1 = 25.79--2.96 x pH, N =28, r = 0.52, P less than 0.01), rising oxygen extraction and rising peripheral resistance, while the mean pressure in the aorta was almost unaltered. During this course towards circulatory failure, an unchanged to slightly rising total splanchnic perfusion (Qsp1) was demonstrated, which with the lowest pH, represented up to 40% of the cardiac output (Qtot): Qsp1/Qtot = 3.11--0.39 x pH (N = 28, r = 0.52, P less than 0.01). Portal pressure rises slightly during acidosis, and oxygen saturation in the portal vein is high. It is probable that the retained splanchnic blood flow is caused by retention of the portal flow. This is quite different from observations during anaesthesia with barbiturates. It is concluded that halothane modifies considerably the circulatory response in the systemic circulation and the splanchnic region during non-carbonic acidosis.
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PMID:Effect of non-carbonic acidosis on total splanchnic perfusion and cardiac output during anaesthesia with O2-N2O-halothane. 3 17

Sinus tachycardia bigeminy, ventricular rhythm, ventricular tachycardia, and ventricular fibrillation are produced by relatively small intravenous doses of epinephrine in nonanesthetized dogs and in dogs anesthetized with thiamylal sodium. Origin of the abnormal beat in coupled bigeminal rhythms generated from the bundle o of His or above. Increases in arterial blood pressure may predispose to arrhythmia formation during thiamylal anesthesia.
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PMID:Arrhythmias in dogs associated with epinephrine and thiamylal anesthesia. 5

The effects of Forane anesthesia for deep surface hypothermia with 30 minutes of total circulatory occlusion were evaluated. With 100% O2 6 of 7 dogs developed motor disorders postoperatively, while 3 of 5 with 98% O2/2% CO2 and none with 95% O2/5% CO2 developed motor disorders. Cooling was uneventful except for 1 episode of ventricular fibrillation in the 5% CO2 group at 23 degrees C. Resuscitation was easy, but the early rewarming period was characterized by repeated episodes of ventricular fibrillation and delayed recovery of cardiac function, especially in the 100% O2 group. Blood lactate levels remained low during cooling and gradually increased during rewarming in all groups, with the highest levels in the 100% O2 group and the lowest in the 5% CO2 group. It is concluded that Forane can be used for surface hypothermia with 30 minutes' circulatory occlusion when administered in 95% O2/5% CO2. A Comparison of these results with previously reported series indicates that Forane is inferior to ether but may be superior to halothane for surface hypothermia.
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PMID:The use of Forane anesthesia for surface-induced deep hypothermia. 24 Mar 30

Lignocaine is widely used as a local anaesthetic and antiarrhythmic drug. It is commonly administered to patients with acute myocardial infarction as prophylaxis for ventricular fibrillation, although its efficacy in preventing primary ventricular fibrillation is still debated. Toxicity, sometimes with serious clinical consequence, is not uncommom and is usually related to overdosage. Blood lignocaine concentrations correlate roughly with antiarrhythmic and toxic effects and might be useful as an end point for monitoring prophylactic therapy. Administration of lignocaine as a local anaesthetic may result in blood lignocaine concentration in the antiarrhythmic or even toxic ranges. Expected peak levels for various routes of local anaesthesia are tabulated so that 'safe' total doses can be calculated. Intramuscular injection of high doses results in sustained therapeutic levels but is often associated with early minor toxicity. Lignocaine is eliminated primarily by hepatic metabolism, which appears to be limited by liver perfusion. Active metabolites may contribute to therapeutic and/or toxic effects. Disease states such as cardiac failure or drugs that alter hepatic blood flow may significantly affect lignocaine clearance. Pharmacokinetic studies in man show wide variability in drug disposition between patients, even when cardiac and hepatic status is considered, making specific dosing recommendations a problem. With intravenous injection, multicompartment kinetics is observed, with an initial rapid decline phase and initial decline in antiarrhythmic activity due to redistribution. With constant infusion, steady state concentrations of lignocaine are seen after 3 to 4 hours in normal subjects and after 8 to 10 hours in patients with myocardial infarction without circulatory insufficiency. In patients with cardiac failure, blood lignocaine concentration may continue to rise for 24 to 48 hours. In the presence of cardiac failure, decreased volumes of distribution and clearance require reduction in loading and maintenance doses. Lignocaine clearance is reduced in patients with liver disease and appears to be a sensitive index of liver dysfunction. A dosing algorithm for treatment of patients with myocardial infarction is presented.
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PMID:Clinical pharmacokinetics of lignocaine. 35 Apr 70

Mitral valve prolapse is a common cardiac abnormality associated with arrhythmias and sudden death. In most instances it can be diagnosed on the basis of physical findings. Those patients who are symptomatic or who display electrocardiographic abnormalities appear to be most susceptible to arrhythmias and, therefore, may be at increased risk for anaesthesia. Because the syndrome is relatively common and may present a very innocent clinical picture, anaesthetists should be aware of this condition and the problems it may present. A case of mitral valve prolapse syndrome associated with ventricular fibrillation on induction of anaesthesia is reported. The symptoms and pathophysiology of the disorder are reviewed and the potential problems and the anaesthetic management are discussed.
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PMID:Ventricular fibrillation in a patient with unsuspected mitral valve prolapse and a prolonged Q-T interval. 48 37

The authors studied the effect of sympathetic denervation of the heart (removal of the stellate ganglion together with the sympathetic trunk up to the level of the 5th thoracic ganglion) on the ventricular fibrillation threshold (VFT) in dog. The acute experiments were performed under general anaesthesia with pentobarbital. Unilateral left sympathetic denervation raised the VFT to 144% of the initial value (14 measurements) and unilateral right sympathectomy to 214% (9 measurements). Immediately after bilateral denervation the VFT increased to 242% (23 observations). Atropine blockade of the vagus nerve (0.1 mg/kg b.w.) displayed no effect on the VFT increase. The observed increase in VFT corresponded with the finding that bilateral sympathetic denervation of the heart protected the dogs from spontaneous ventricular fibrillation after ligating the intraventricular branch of the left coronary artery. The authors compared their own results with those reported in the literature and discuss the possible clinical use of sympathetic denervation of the heart in the treatment of tachyarrhythmia.
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PMID:Antiarrhythmic effect of cardiac sympathectomy. 54 95

A case is described of a 22 years old, high risk female patient who underwent an ophtalmological operation. She developed a ventricular fibrillation during halothane anesthesia by an excess of adrenaline (epinephrine) administered in eye drops.
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PMID:A case of ventricular fibrillation during halothane anesthesia caused by eye drops. 54 40

The role of cardiac nerves in the production of cardiac arrest during surgical anaesthesia on coronary ligated hypoxic heart has been studied. When atropinished coronary ligated dogs were exposed to hypoxia the terminal event was a cardiac asystole in 88% of the dogs. In propranolol treated dogs, or in dogs where sympathetic ganglia upto T6 were bilaterally removed earlier, coronary ligation and hypoxia produced ventricular extrasystoles, ventricular tachycardia and repeated sinus arrest followed by ventricular fibrillation. The possibility of the origin of arrythmia from the damaged myocardium, and the presence of an intact vagus in the production of ventricular fibrillation has been discussed.
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PMID:The role of nerves in the production of cardiac arrest during surgical anaesthesia. 77 18

Observations during 935 anesthesias for implantation or revision of permanent pacemakers are presented. Using different methods of anesthesia we found the light halothane anesthesia introduced by inhalation to be best, provided that only atropine was used for premedication. Applying this method we saw asystolies or ventricular fibrillation in 3% of all cases--3 patients (i.e. 0.4%) died in tabula. Tachycardia (2.4%) occuring mostly during the introduction period were successfully treated by verapamil or practolol. Hypotension (5.4%) mostly took place in the course of anesthesia after implantation of the pacemaker. This depression may be due to a normalisation of the enhanced stroke volume whedication with pethidine or induction with propanidid was followed by comparatively more complications such as exitus letalis (2% resp. 1.5%), cardiac arrest (6.5% resp. 9%) and hypotension (24% resp. 10.5%). Regional anesthesia did not bring specific advantages. The good experiences with soft halothane anesthesia for implantations or revisions of pacemakers include 125 high risk patients (ASA classification IV to VII).
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PMID:[Anesthesia in pacemaker implantation. Experiences in 935 cases of anesthesia for the implantation or revision of a cardiac pacemaker]. 86 62


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