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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

General anaesthesia is the reversible depression of central nervous system function. There is still no agreement over what constitutes depth of anaesthesia, and the clinical anaesthetist must thus titrate drug input according to clinical signs (heart rate, blood pressure, somatic movement, autonomic responses). The potency of inhalational agents may be expressed in terms of the MAC (minimum alveolar concentration); comparable end-points (including blood concentrations) have been proposed for the intravenous agents. Kinetic infusion regimens can be constructed for the intravenous agents to achieve the ED95 concentrations required to provide clinically adequate anaesthesia. However, because of individual differences in drug kinetics and dynamics, as well as the influences of disease states and intercurrent therapy, the clinician will titrate the dose according to response. Administration of volatile or intravenous anaesthetics by fixed regimens may result in either overdosage or the risk of patient awareness. The choice of anaesthetic drug is usually based on the nonhypnotic side effects of the different agents--including their central and regional cardiovascular effects, the speed and completeness of recovery, and the need to provide intraoperative analgesia. In addition, special techniques and drugs are often needed for neurosurgical, cardiothoracic and obstetric anaesthesia. All anaesthetic agents (inhalation and intravenous) have other side effects (such as cardiorespiratory depression and organ toxicity related to the liver or kidney). Both halothane and enflurane may be responsible for postoperative hepatic dysfunction, while the metabolism of enflurane can also result in nephrotoxicity in patients with pre-existing renal dysfunction. Isoflurane has been reported to cause 'coronary steal' in patients with ischaemic heart disease through its coronary vasodilator properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Practical treatment recommendations for the safe use of anaesthetics. 137 60

The effects of increasing inspired sevoflurane (Sev) concentrations (0.5, 1.0, 1.5, 2.0 MAC) on regional myocardial oxygen balance and metabolism were studied in 10 open-chest dogs with coronary artery stenosis. Regional myocardial oxygen balance was assessed by continuous recording of subendocardial and subepicardial oxygen tensions. After the basal measurement, the left circumflex coronary artery blood flow (CBFLCX) was reduced by 20% with a screw flow regulator. The institution of stenosis caused a slight but significant decline in subendocardial oxygen tension. Otherwise, there were no significant differences between basal values and those after the stenosis. During the subsequent inhalation of Sev at 0.5, 1.0 and 1.5 MAC, endocardial oxygen tension was maintained at the level of control value. Sev 2.0 MAC caused a severe reduction in systemic arterial pressure and resulted in a marked and significant decline of endocardial oxygen tension compared with control value. On the other hand, subepicardial oxygen tension remained unchanged during each Sev inhalation. The ratio of epicardial/endocardial oxygen tension did not show a significant decline with increasing Sev concentration. It seems that Sev may not possess sufficient potency to cause myocardial ischemia by redistribution of coronary blood flow.
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PMID:[Effects of sevoflurane on regional myocardial oxygen balance in the canine heart with coronary artery stenosis]. 143 75

The present study examined the postulate that the quotient of mean systemic arterial pressure and heart rate predicts the severity of myocardial ischemia during occlusion of the left anterior descending coronary artery. Studies were performed in open-chest fentanyl-anesthetized dogs before and during halothane (n = 8) or isoflurane (n = 8) anesthesia. The pressure-rate quotient (PRQ) decreased significantly in both groups during incremental increases in halothane or isoflurane to 68% and 57% of control values at 0.5 MAC and to 41% and 38% at 1.5 MAC for halothane and isoflurane, respectively. Myocardial lactate production was unchanged from the ischemic region, and no correlation between the PRQ and myocardial lactate production was observed. In contrast, heart rate correlated significantly (r = 0.376; P less than 0.05) with lactate production. The product of systolic systemic arterial pressure and heart rate (rate-pressure product) correlated with blood flow (r = 0.493; P less than 0.001) and with oxygen consumption (r = 0.571; P less than 0.001) in the normal myocardium. A weak correlation (r = 0.330; P less than 0.05) of rate-pressure product with myocardial lactate production from the ischemic region was observed. There were no correlations between the PRQ and myocardial lactate production from the ischemic region or indices of blood flow distribution (i.e., inner/outer ratio in the ischemic region or ischemic/normal ratio). The relationship of hemodynamic variables to measurements of regional myocardial metabolism was independent of background anesthetic agent of depth of anesthesia. The current data suggest that heart rate changes are weakly predictive of severity of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of systemic arterial pressure, heart rate, and derived variables in prediction of severity of myocardial ischemia during acute coronary occlusion in anesthetized dogs. 819 88

In anesthesiology and intensive care medicine it is often necessary to treat disorders involving cardiac failure or low-output syndrome. However, in patients who are endangered by ischemic heart disease, any pharmacologic therapy with positive inotropic agents should improve cardiac output without increasing myocardial oxygen demand significantly: the heart should perform its task as efficiently as possible. In the present study a mathematical model of myocardial efficiency was developed. The implications of this theoretical concept of myocardial efficiency were evaluated in animal experiments. THEORETICAL MODEL. Cardiac efficiency is predominantly dependent on preload, afterload, and inotropic state. Quantitatively, it can be calculated from end-diastolic volume, left ventricular systolic pressure (Psyst), stroke volume (SV), and ejection time. The implications of the theoretical analysis are: (1) the inotropic state, which leads to optimal myocardial efficiency, is specifically determined by preload and afterload: for each preload and afterload one matched inotropic state is necessary to achieve optimal efficiency; (2) an increase in blood pressure leads to a decrease in myocardial efficiency even if the inotropic state is optimally matched to preload and afterload; and (3) an increase in end-diastolic volume improves the efficiency of myocardial pump work. ANIMAL EXPERIMENTS. The validity of the theoretical model was studied in animal experiments with emphasis on the following items: (1) is theoretically optimal efficiency of myocardial pump work achieved by physiologic regulation of myocardial performance? (2) how does sympathetic stimulation influence myocardial efficiency? and (3) how do cardiodepressive agents such as beta-blockers or volatile anesthetics influence myocardial efficiency? METHODS. Experiments were performed on nine mongrel dogs after induction of piritramide--nitrous oxide anesthesia. Standard hemodynamics: heart rate, Psyst, maximum left ventricular pressure rise (dP/dtmax), and SV (thermodilution) as well as coronary blood flow (pressure difference catheter) and myocardial oxygen consumption (Fick principle) were measured. In order to create a broad range of different hemodynamic settings, blood withdrawal and retransfusion of blood and/or colloid osmotic solutions were used to modify intravascular volume. Additionally, the inotropic state was varied by infusion of catecholamines (isoproterenol 0.4-0.8 microgram.kg-1.min-1 or norepinephrine 1-2 micrograms.kg-1.min-1). Experimental myocardial failure was induced by adding halothane (0.8-1.5 MAC) to the basic anesthesia, beta-blockade with propranolol (125-250 micrograms.kg-1), and combination of beta-blockade with a pressure load imposed on the myocardium (propranolol 125-250 micrograms.kg-1 + norepinephrine 1-2 micrograms.kg-1.min-1). RESULTS. During variation of the intravascular blood volume by normo-, hypo-, and hypervolemia, the myocardial efficiency very closely matched the theoretically predicted values of optimal efficiency: the average observed efficiency was 98.8% of predicted optimal efficiency. Increasing afterload with norepinephrine did not alter this close relationship, although absolute values of efficiency decreased as predicted by the theoretical model. Application of isoproterenol resulted in SVs that exceeded optimal values by 41.5%. In contrast, during experimental myocardial failure SVs were too small to achieve the necessary values for optimal pump work; observed myocardial efficiency was therefore significantly lower than optimal efficiency. CONCLUSIONS. For pharmacological interventions, it can be concluded that maximal efficiency of cardiac pump work requires maximal end-diastolic filling in combination with minimal afterload. (ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The energetics and economics of the cardiac pump function]. 195 41

The use of isoflurane in patients with coronary artery disease remains controversial because of the possibility of "coronary steal". In this study, the effects of isoflurane and halothane on global and regional myocardial blood flow and metabolism were compared, and the relationship between steal-induced myocardial ischemia and the administered volatile anesthetic was investigated in 40 patients with steal-prone coronary anatomy undergoing elective coronary artery bypass operations. The patients were randomly assigned to receive either isoflurane or halothane (0.5 MAC inspired concentration) immediately after induction with fentanyl (50 micrograms/kg). Hemodynamic measurements and blood samples were obtained at preinduction, postintubation, preincision, poststernotomy, at 60 min after beginning isoflurane or halothane, and precannulation (a total of 238 study events). Throughout the study, heart rate was kept constant by atrial pacing at approximately postintubation values while arterial pressure was maintained within 10% of postintubation values with fluid administration or phenylephrine infusion. Overall, systemic hemodynamic changes observed during the study were similar in the two groups. Myocardial ischemic episodes were defined as a new electrocardiographic ST-segment shift of greater than or equal to 0.1 mV, new echocardiographic regional wall motion abnormalities (RWMA) and/or myocardial lactate production (MLP). A total of 18 new ischemic episodes were detected in 15 patients (7 episodes during isoflurane in 7 patients and 11 during halothane in 8 patients). Ten (56%) episodes were related to acute hemodynamic abnormalities, whereas 8 (44%) were random and unrelated to changes. Seven episodes were detected by echocardiography (38%), 6 by MLP (33%) and 1 by ECG (6%) only, whereas concomitant echocardiographic abnormalities and MLP were observed during 2 episodes (11%), echocardiographic and ECG during 1 (6%), and ECG and MLP during 1 other (6%). Ratios of regional to global coronary venous flow, coronary vascular resistance, myocardial oxygen content, and lactate extraction, along with hemodynamic data obtained during these episodes, do not support coronary steal for the development of myocardial ischemia. We conclude that in patients with steal-prone coronary anatomy anesthetized with fentanyl, neither isoflurane nor halothane administered at concentrations used in the current study is likely to cause myocardial ischemia by the coronary steal mechanism.
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PMID:Regional and global myocardial circulatory and metabolic effects of isoflurane and halothane in patients with steal-prone coronary anatomy. 195

Animal studies indicate that desflurane and isoflurane have similar hemodynamic effects when administered in equipotent anesthetic concentrations. The authors compared desflurane and isoflurane, used as primary anesthetics for patients undergoing elective coronary artery bypass surgery whose left ventricular ejection fractions were greater than 0.34. After induction of anesthesia with thiopental (dose 180 +/- 45 mg [mean +/- standard deviation]) and fentanyl, 10 micrograms.kg-1, either desflurane or isoflurane was administered to maintain systolic blood pressure within 70-120% of, and heart rates less than 120% of, the patients' average preoperative values. If adjusting the end-tidal anesthetic concentration within the range of 0-2.0 MAC could not maintain these predefined hemodynamic limits, additional fentanyl or vasoactive drugs were used. Induction and maintenance of anesthesia was accompanied by a significant decrease in mean arterial pressure in both groups (desflurane 97 +/- 12 mmHg at control, decreasing to 71 +/- 5 mmHg during skin preparation; isoflurane 95 +/- 9 mmHg at control, 74 +/- 9 mmHg during skin preparation). One minute after sternotomy, mean arterial pressure in the isoflurane group had returned to control, 97 +/- 9 mmHg, which was significantly greater than in the desflurane group, 87 +/- 12 mmHg. Systolic arterial pressure was also significantly greater in the isoflurane group 1 min after intubation, during skin preparation, and 1 min after sternotomy. Otherwise, the hemodynamic effects of these volatile agents were similar. There were no differences between groups in the incidence of ECG changes indicative of myocardial ischemia prior to cardiopulmonary bypass, perioperative myocardial infarction, or perioperative mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of desflurane and isoflurane in patients undergoing coronary artery surgery. 195 2

Active vasoconstriction of epicardial coronary arteries can cause myocardial ischemia in patients with coronary artery disease. Relief of vasoconstriction can improve blood flow to the heart. The purpose of this study was to determine if 1.5 MAC halothane and 1.5 MAC isoflurane would each attenuate contractions evoked by three putative mediators of coronary constriction in coronary arteries removed from the hearts of human beings. Hearts were obtained in the operating room from five patients undergoing cardiac transplantation and from six brain-dead patients undergoing organ donation procedures. Coronary arteries were dissected free, cut into rings, and studied in organ chambers. Endothelium-dependent relaxations to 10(-6) M bradykinin were examined; they indicated a variable degree of endothelial dysfunction in vessels used in the experiments. Contractile responses to 40 mM KCl were tested and were used as control contractions. Contractions evoked by serotonin, histamine, and prostaglandin F2 alpha were measured and were expressed as a percent of contractile responses evoked by 40 mM KCl. Halothane depressed the agonist-induced contractions. Maximal contractile responses to serotonin were 130% +/- 28% in untreated rings and 63% +/- 10% in rings exposed to halothane (P less than 0.03). Responses to histamine were 183% +/- 46% untreated and 121% +/- 26% during halothane administration (P less than 0.05), and responses to prostaglandin F2 alpha were 227% +/- 42% untreated and 148% +/- 18% with halothane (P less than 0.05). Isoflurane had no effect on contractions. The results demonstrate that 1.5 MAC halothane, but not 1.5 MAC isoflurane, attenuates contractile responses evoked by putative mediators of coronary vasoconstriction in coronary arteries removed from the hearts of human beings.
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PMID:Halothane 1.5 MAC, isoflurane 1.5 MAC, and the contractile responses of coronary arteries obtained from human hearts. 200 36

To determine the extent to which different electrocardiographic systems account for differences in reported incidence of perioperative myocardial ischemia, the authors simultaneously recorded in 109 patients undergoing coronary artery bypass grafting (CABG) the V5 or modified CM5 lead on five ECG systems by means of a specially constructed common V5 lead. The systems included a Spacelabs Alpha 14 Model Series 3200 ECG Cardule at bandwidths of 0.05-125 Hz and 0.5-30 Hz (a typical operating room monitor), a Marquette Electronics MAC II ECG at 0.05-40 Hz and 0.05-100 Hz (a standard ECG), and a Del Mar Holter recorder at 0.1-100 Hz. Relative ST-segment position and incidence of new ischemia compared to the preoperative ECG were determined in 109 sets of preinduction traces and 877 sets of intraoperative traces. ST-segment position on the three recording systems conforming with the American Heart Association (AHA) low-frequency response recommendations (0.05 Hz) were similar. Compared to the standard ECG, ST-segment position on the Spacelabs at 0.5-30 Hz was consistently more negative. Displacement on the Holter was consistently less negative and less positive. By the 0.1-mV displacement criterion for diagnosis of myocardial ischemia on any one ECG system, 16.5% of patients on arrival and 32.1% of patients intraoperatively suffered new myocardial ischemia. Based on the operating room monitor, arrival and intraoperative ischemia were present in 15.6 and 27.5% of patients, respectively. Ischemia at the same periods was less frequent by the standard ECG system (5.5 and 12.8%, respectively) and least frequent by the Holter recorder (4.6 and 8.3%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incidence of perioperative myocardial ischemia detected by different electrocardiographic systems. 204 84

Some coronary vasodilators, paradoxically, may endanger patients with coronary artery disease by causing "coronary steal." To determine the capacity of isoflurane and halothane to cause coronary steal, the authors studied their effects on coronary vascular resistance (CVR), diastolic coronary artery pressure, and collateral myocardial blood flow. Using ameroid constrictors, chronic occlusions of the left anterior descending (LAD) coronary artery were created in ten dogs. Six to eight weeks after implantation, the dogs were anesthetized with fentanyl and pentobarbital, and a stenosis was created on the circumflex (Cx) coronary artery. Isoflurane and halothane were each administered in doses of 0.5 and 1.5 MAC. Diastolic aortic pressure was held constant. Using small catheters in the circumflex and LAD coronary arteries, the authors measured diastolic coronary artery pressures. Collateral myocardial blood flow was measured by the microsphere method. In this model, halothane and isoflurane minimally affect CVR. The maximum change in CVR, which was found during 1.5 MAC isoflurane, was -8% (not significant). Diastolic coronary pressures distal to the Cx stenosis (54.5 +/- 11.5 mmHg) and distal to the LAD occlusion (44.5 +/- 5.2 mmHg) did not change significantly with either isoflurane or halothane. Transmural collateral blood flow distal to the LAD occlusion (0.51 +/- 0.11 cc.g-1.min-1) was unaltered by either drug. There was no evidence of coronary steal. Epicardial ECG S-T segments showed no evidence of ischemia. The finding of minimal direct effects of halothane and isoflurane on CVR, diastolic coronary pressure, and collateral myocardial blood flow suggest that, under the conditions of this study, neither agent, when used as an adjuvant to high-dose narcotic anesthesia, is likely to cause myocardial ischemia by a coronary "steal" mechanism.
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PMID:Effects of isoflurane and halothane on coronary vascular resistance and collateral myocardial blood flow: their capacity to induce coronary steal. 367 66

The systemic and coronary haemodynamic effects of 1.5 MAC enflurane-nitrous oxide anaesthesia and abdominal surgery were investigated in nine patients with ischaemic heart disease. Anaesthesia decreased systemic blood pressure (-56%) by a combination of cardiodepression and peripheral vasodilation. A marked fall in myocardial oxygen extraction suggested a moderate coronary vasodilation. Surgery markedly increased the circulating levels of adrenaline and noradrenaline, manifested by increases in blood pressure (+76%) and systemic vascular resistance (+83%). Pulmonary capillary wedge pressure increased by 70% without any change in cardiac or stroke volume index, suggesting that the patients were performing at the horizontal part of their left ventricular function curve. Despite the marked rise in coronary perfusion pressure and a 62% increase in myocardial oxygen demand, coronary blood flow remained unaltered. This could be due either to coronary vasoconstriction overriding the normal coronary autoregulation or to an increase in coronary back pressure opposing the diastolic aortic pressure. When coronary blood flow could not increase to meet the demand for oxygen, the myocardium had to extract more oxygen to ensure appropriate oxygenation, demonstrating interference with coronary autoregulation. Surgery markedly increased myocardial extraction of adrenaline and noradrenaline. We could not find any relationship between myocardial adrenaline extraction and heart rate response to surgery or between myocardial noradrenaline extraction and changes in coronary blood flow, calculated coronary vascular resistance, incidence of myocardial ischaemia or cardiac dysrhythmias.
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PMID:Coronary haemodynamic effects of surgery during enflurane-nitrous oxide anaesthesia in patients with ischaemic heart disease. 397 16


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