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

The cardiovascular effects of halothane-nitrous oxide anesthesia, and beta-receptor blockade with either propranolol or practolol, were studied in 15 dogs in which severe myocardial infarction had been induced ten days earlier. The hemodynamic responses to blood loss amounting to 25 per cent of estimated blood volume, and its subsequent replacement, were studied before and after induction of beta-receptor blockade. In terms of cardiac output and aortic blood flow acceleration, cardiac performance in the absence of beta-blockade was markedly impaired during steady-state anesthesia, compared with corresponding values in normal dogs. Practolol (2.0 mg/kg) administered during anesthesia induced no significant circulatory change other than a 14 per cent decrease in heart rate and a 25 per cent increase in strode volum. Propranolol (0.3 mg/kg) caused a comparable reduction of heart rate, but significantly reduced cardiac output (-27 per cent), aortic blood flow acceleration (-26 per cent), and peak LV power (-19 per cent), and increased systemic vascular resistance (+49 per cent). The two drugs caused comparable shifts of the isoproterenol dose-response curve during anesthesia. Graduated blood loss during anesthesia, to a total of 25 per cent of blood volume, caused consistent circulatory changes (decreased mean arterial pressure cardiac output, peak LV power, LV minute work) that were essentially similar before and after beta-receptor blockade with either propranolol or practolol. The positive inotropic effect of calcium gluconate during halothane anesthesia was significantly reduced following either propranolol or practolol, but the hemodynamic responses to changes of systemic vascular resistance induced with acetylcholine or phenylephrine were not modified by beta-receptor blockade.
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PMID:Interaction of anesthesia, beta-receptor blockade, and blood loss in dogs with induced myocardial infarction. 0 20

A 10-year experience of cardiac arrests in a district general hospital is reviewed. 1063 arrests in the general areas of the hospital were studied, excluding the coronary and intensive care units. In 718 (67-5%) initial resuscitation was unsuccessful; in 252 (23-7%) the patient died later in hospital, 93 patients (8-7%) were discharged alive. After discharge from hospital there was a progressive annual mortality of about 7% for the first five years, but thereafter no patient died. Significant incapacity after discharge was also unusual. The probability of successful resuscitation was greater in patients with primary cardiac disease (11-8% survival), drug overdose (22-2% survival), or undergoing anaesthesia (20-0% survival). The success-rate was significantly greater in the accident and emergency department (7-9%) than on the wards (2-1%), but this difference was due entirely to the more successful resuscitation of patients with myocardial infarction in the accident and emergency department. Within each diagnostic category the survival-rate was independent of the age of the patient. Prolonged survival after resuscitation but ending in death before discharge was unusual.
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PMID:Survival after cardiac arrest in hospital. 6 27

Twelve cardiorespiratory arrests in eight neuropathy are reported. Only one patient died at the time, but two others subsequently died suddenly at home. There was no evidence of myocardial infarction, cardiac arrhythmia, or hypoglycaemia at the time of arrest. In most of the episodes there was some interference with respiration, either by anaesthesia, drugs, or bronchopneumonia. Five of the episodes occured during or immediately after anaesthesia. It is suggested that the arrests were caused by defective respiratory rather than cardiovascular reflexes. Cardiorespiratory arrest appears to be a specific feature of diabetic autonomic neuropathy and may contribute to the mortality of this condition.
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PMID:Cardiorespiratory arrest and diabetic autonomic neuropathy. 7 96

5 patients developed pulmonary oedema after retrograde femoral arteriography under general anesthesia. Because of the haemodynamic changes associated with radiographic contrast media, a good preoperative cardiological assessment is essential. The volume and nature of the contrast media injected and any other fluid administered should be carefully monitored. There is no apparent safe maximum dose of radiographic contrast media, but this work suggests that for 'Conray 420' (sodium iothalamate 70% w/v) a total dose should be less than 200 ml in a fit patient. The dose should be substantially smaller in patients with a history of evidence of myocardial infarction, myocardial insufficiency, myocardial ischaemia, or hypertension.
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PMID:Pulmonary oedema after radiological investigation of peripheral occlusive vascular disease. Adverse reaction to contrast media. 7 42

Nitroglycerin is a vasodilating agent by virtue of its actions on vascular smooth muscle fibers. It may be administered intravenously (using either 5 p. cent dextrose, or propylene-glycol solvant), sublingually, orally or by topical administration. It is rapidly metabolized, principally by liver. Its is not toxic. The vasodilatation that is produced is both arterial and venous and is dose-related in dog (1 microgram to 100 micrograms/kg/min). However, resistance and tachphylaxis may occur. Its principal use is for angor treatment, but it has been used for the treatment of arteriopathy of the lower limbs, biliar hypertony and arterial hypertension. It has been recently administered for the treatment of acute phase of myocardial infarction and during pre, per- and post-operative periods in cardiac surgery, neurosurgery and hip surgery, as myocardial protector or anti-hypertensive agent or hypotensive agent. The absence of toxicity and the rapid reversibility of its cardio-vascular effects which are similar to the effects of sodium nitroprusside are important reasons for its use in anesthesia and cardiac intensive care.
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PMID:[Pharmacology of nitroglycerin (author's transl)]. 11 40

The incidence of operative myocardial infarction was assessed by electrocardiogram (ECG) and technetium-99m pyrophosphate (99mTc-PyP) myocardial scintigrams in 89 consecutive patients undergoing coronary artery bypass grafting (CABG). Myocardial scintigrams were performed on the day before operation and repeated 2 to 3 days postoperatively. All patients survived operation, with three in-hospital deaths not related to myocardial infarction (mortality rate 3 percent). Operative infarction was assessed to have occurred in four of 89 patients (4 percent). Two had new Q waves and positive scintigrams; one, major ST-T wave changes and a positive scintigram; and the fourth, new Q waves without a positive scintigram. Three further patients (3 percent) had Q waves and positive scintigrams postoperatively, but myocardial infarction was evolving before anesthesia and operation. Twenty-seven of 89 patients (30 percent) were found to have abnormal scintigrams preoperatively. In two patients, both operated upon with evolving myocardial infarction, the scintigram was worse postoperatively. In 13 patients the scintigram was improved after operation. In 12 patients (13 percent) the abnormal preoperative scintigram was unchanged after operation. Preoperative and postoperative myocardial scintigrams and ECG's must be compared to assess the incidence of operative myocardial infarction in patients undergoing CABG.
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PMID:Preoperative and postoperative technetium-99m pyrophosphate myocardial scintigraphy in the assessment of operative infarction in coronary artery surgery. 22 52

Fifteen patients were studied to detect unrecognized intraoperative ischemia or necrosis in perioperative myocardial infarction (MI) associated with coronary bypass. Simultaneous arterial and coronary sinus blood samples were analyzed for lactate and both total and MB-CPK. Coronary sinus flow measurements were done coincident with sampling in seven patients. Five had perioperative MI diagnosed by positive pyrophosphate scan and electrocardiogram. Although normal initially (mean 19 +/- 5.0%), lactate extraction after thoracotomy, before aortic cross-clamping, became abnormal in 12 patients with more pronounced abnormality in those with perioperative MI (-19 +/- 9.0%). Net efflux of lactate was higher in perioperative MI (mean 0.6 +/- 0.2 vs 0.016 +/- 0.04 mM/L) than in non-MI patients. All patients had detectable total and MB-CPK (mean 295 and 31 IU/L, respectively) and all those with coronary disease had a positive arterial-coronary sinus gradient for MB-CPK (mean 9 IU/L). Perioperative MI patients had a higher gradient than non-MI patients (mean 25 vs 2 IU/L) and with one exception that gradient exceeded 5-7 IU/L. It is concluded that severe ischemia before aortic cross-clamping precedes perioperative MI and may contribute to release of CPK into coronary sinus blood. Improvement in the techniques of anesthesia and intraoperative myocardial preservation are suggested.
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PMID:Coronary sinus blood flow and sampling for detection of unrecognized myocardial ischemia and injury. 30 99

Intra-aortic balloon pump assistance (IABPA) for cardiogenic shock is well established. The response to balloon pumping and patient survival are better after low output from cardiotomy than after myocardial infarction. Elective use of IABPA preoperatively allows an extra margin of safety for patients with acute coronary insufficiency, significant left main coronary artery stenosis, or depressed left ventricular function. However, advances in monitoring techniques during the induction of anesthesia and weaning from cardiopulmonary bypass support, as well as improved methods for myocardial preservation, have reduced the requirements for elective IABPA. Current indications for preoperative IABPA include: patients with acute coronary insufficiency who are totally unresponsive to full medical management and who continue to have pain and electrocardiographic changes at rest, and patients with serious left main coronary artery stenosis who also have acute coronary insufficiency or depressed left ventricular function. The survival of patients with valvular heart disease and left ventricular dysfunction is not improved with preoperative IABPA, while most patients with depressed left ventricular function from coronary artery disease may now undergo revascularization uneventfully, although inevitably some will still require postoperative IABPA.
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PMID:Changing patterns of intra-aortic balloon pump assistance. 30 76

The incidence of perioperative myocardial infarction (MI) was examined in 148 patients with known coronary artery disease (CAD) who underwent 226 noncardiac surgical procedures. In 168 operations in 99 patients who had prior coronary artery bypass grafting (CABG) there were no perioperative MI's whereas in the 49 patients who had not undergone prior CABG who underwent 58 noncardiac operations, there were three MI's (5 percent). The lower (p less than 0.02) incidence of perioperative MI in patients with CAD who had had prior CABG suggests a protective effect for subsequent noncardiac operation, which could not be explained by other differences in cardiac status between the groups. All three MI's occurred in patients with three-vessel CAD, evidence that this should be added to prior MI as a significant risk factor. The study indicates also that patients with prior CABG have less risk of MI during and following anesthesia and noncardiac operation than do patients without CABG who have had a previous MI.
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PMID:Perioperative myocardial infarction in patients with coronary artery disease with and without aorta--coronary artery bypass grafts. 30 29

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


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