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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiocirculatory responses to equianaesthetic concentrations (MAC 0.5 and MAC 1.0 plus 67% N2O) of halothane, methoxyflurane, enflurane and isoflurane were studied in a total of 35 closed-chest dogs during ventilation controlled to produce normocapnia. Each anaesthetic produced a dose-related decrease in mean arterial pressure and in values reflecting cardiac function. These included cardiac output, stroke volume, left ventricular max dp/dt and ejection fraction. Isoflurane seemed slightly less depressant to the heart than the other 3 anaesthetics. Total peripheral resistance remained nearly unaffected during halothane and methoxyflurane anaesthesia but decreased significantly with MAC 1.0 enflurane and isoflurane. There was no change in heart rate at low anaesthetic concentrations. The deeper levels of anaesthesia were associated with moderate increases in heart rate. In spite of the obvious depression of myocardial contractility there was a fall in pulmonary artery and left ventricular end-diastolic pressures and in left ventricular end-diastolic volumes with each of the agents. We take this as an expression of decreased ventricular filling resulted from pooling of blood in peripheral capacitive vessels. With the exception of isoflurane, each of the other three anaesthetics reduced coronary blood flow. Coronary vascular resistance was not substantially influenced by halothane and methoxyflurane, but decreased with MAC 1.0 enflurane and isoflurane. Myocardial oxygen availability was always found to be adequate. Isoflurane even produced a significant rise in coronary venous oxygen saturation indicating coronary vasodilation. Parallel with the depression in cardiac performance and blood pressure as two of the main predictors of energy demand, myocardial oxygen consumption was found to be significantly reduced by each of the anaesthetics. The ratio of the external work of the left ventricle to its oxygen consumption indicated that myocardial efficiency deterioated. The clinical implications are discussed.
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PMID:[Influence of modern inhalation anaesthetics on haemodynamics, myocardial contractility, left ventricular volumes and myocardial oxygen supply (author's transl)]. 87 90

Isoflurane or halothane was administered at two different inspired concentrations to 21 surgical patients whose average age was 62 years. Most were in physical status (ASA) II or III. Patients were premedicated with diazepam and atropine, anesthesia was induced with thiopental, and tracheal intubation was facilitated with succinylcholine. Respiration was controlled manually or with a ventilator. Anesthesia was maintained with 60 percent N2O and halothane 1 percent, then 0.5 percent, or with N2O-isoflurane 1.2 percent, then 0.6 percent in O2. Variations in the cardiovascular responses among patients given the same anesthetic were as great as the variation in responses between anesthetics. Both produced similar decreases in arterial pressure, cardiac output, and stroke volume. Changes in pulse rate were minimal, and total peripheral resistance changes quite variable, for both drugs. Both halothane and isoflurane appear satisfactory for inhalation anesthesia in the elderly.
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PMID:Cardiovascular effects of isoflurane and halothane during controlled ventilation in older patients. 123 3

We have studied haemodynamic responses to 0, 0.25, 0.5, 0.75 and 1 MAC isoflurane administration in 10 patients during a zero-order propofol infusion and normocapnia. Isoflurane reduced mean arterial pressure (MAP), systemic vascular resistance and left ventricular stroke work in a dose-dependent manner (29%, 38% and 33%, respectively, at 1 MAC), while cardiac output (CO), stroke volume (SV) and heart rate were not affected significantly. Mean pulmonary artery pressure, pulmonary vascular resistance and right ventricular stroke work decreased by 13%, 10% and 17%, respectively (not significant). Pulmonary capillary wedge pressure and central venous pressure were affected minimally, while intrapulmonary shunting and PaO2 remained constant. It is concluded that administration of isoflurane during infusion of propofol caused a dose-dependent decrease in MAP as a result of afterload reduction without modification in CO or SV.
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PMID:Haemodynamic effects of isoflurane during propofol anaesthesia. 163

Haemodynamic changes and catecholamine responses were measured during anaesthesia with sufentanil (total dose 7 micrograms kg-1) supplemented with isoflurane in 14 patients undergoing coronary artery surgery. Isoflurane was used to control systolic arterial pressure, which was allowed to decrease to 100 mm Hg. Mean inspired isoflurane concentration was 0.22 (SD 0.19)% (induction), 0.34 (0.18)% (pre-bypass) and 0.22 (0.17)% (post-bypass). During cardiopulmonary bypass 0.22 (0.13)% isoflurane was administered to control mean perfusion pressure. During induction and the pre-bypass period, significant decreases in systolic and diastolic arterial pressure, systemic vascular resistance and left ventricular stroke work index (LVSWI) (P less than 0.01) were noted. The decrease in LVSWI with unchanged filling pressures indicated myocardial depression. Serum catecholamine concentrations remained at the pre-induction value until cardiopulmonary bypass, when a significant increase was noted. Tracheal intubation, sternotomy and sternal spread were not associated with hypertension or tachycardia. Clinical signs that could reflect myocardial ischaemia were not observed peroperatively. After operation, cardiac enzymes were within the normal clinical range and ECG was unchanged.
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PMID:Low-dose sufentanil-isoflurane anaesthesia for coronary artery surgery. 252 26

In rats with incomplete cerebral ischemia the effects of 70% N2O alone, isoflurane alone (0.5 and 1 MAC), and the combination of N2O + isoflurane on neurologic outcome, neurohistopathology, and EEG were compared. Moderate and severe ischemia were produced by right carotid artery occlusion combined with hemorrhagic hypotension (moderate ischemia, MAP = 30 mmHg, FIO2 = 0.30; severe ischemia, MAP = 25 mmHg, FIO2 = 0.20). Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke), and neurohistopathology was evaluated using a 40-point scale from 0 = normal to 40 = total hemisphere infarct at the level of the caudate nucleus in coronal section. Compared with N2O alone, isoflurane (0.5 and 1 MAC) improved neurologic outcome following moderate ischemia (P less than 0.05). Isoflurane also decreased histopathologic damage following moderate ischemia (N2O control = 33 +/- 1 vs. 0.5 MAC isoflurane = 11 +/- 4 and 1 MAC isoflurane = 12 +/- 3, P less than 0.05), whereas only 0.5 MAC isoflurane decreased histopathologic damage following severe ischemia (N2O control = 38 +/- 1 vs. 0.5 MAC isoflurane = 25 +/- 5; P less than 0.05) Adding N2O to 0.5 MAC isoflurane attenuated the neurologic protective effect of isoflurane alone and increased histopathologic damage following both moderate and severe ischemia (moderate = 23 +/- 5, severe = 37 +/- 2; both P greater than 0.05 compared with N2O controls). The effect of adding 70% N2O to isoflurane on cerebral blood flow (CBF) and cerebral oxygen consumption(CMRO2) was also evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The interaction of nitrous oxide and isoflurane with incomplete cerebral ischemia in the rat. 271 9

This study examined global hemodynamic responses to increasing concentrations of halothane and isoflurane in pigs with an acute critical coronary stenosis (CCS) on the left anterior descending coronary artery (LAD). The CCS was caused by graded inflation of an hydraulic occluder to the point where no hyperemic response was observed following a 10 sec. total LAD-occlusion. A minute, piezoelectric epicardial Doppler probe applied without dissection was used to monitor the stenosis. Previously reported minimum alveolar concentrations (MAC) were used as endtidal concentrations ([ Et]). The [Et] was increased stepwise until each animal died. Recordings obtained in this study were compared to recordings obtained during similar stepwise increments of these anesthetics in pig preparations without CCS. Isoflurane had a significantly less depressant effect on global hemodynamics compared to halothane and caused death at higher MAC than halothane in either case. A critical LAD-stenosis caused no major changes in the general dose-response pattern of isoflurane but further aggravated the depression of cardiac output and stroke volume induced by increasing concentrations of halothane.
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PMID:Hemodynamic dose-responses to halothane and isoflurane are different in swine with and without critical coronary artery stenosis. 273 40

Cardiac output and myocardial blood flow decrease dramatically in a dose-dependent pattern in the young lamb during isoflurane anesthesia. This raises important questions about the ability of the young lamb to increase myocardial performance if oxygen delivery were compromised by a decrease in oxygen content during anesthesia and surgery. To investigate the ability of the young lamb to increase oxygen delivery during isoflurane anesthesia, the response to hypoxemia, which is known to increase myocardial performance, was studied in awake 1-week-old lambs. Mean systemic arterial pressure, heart rate, cardiac output, and regional distribution of blood flow were measured during three states: awake, 1.0 minimum alveolar concentration (MAC) of isoflurane in an FIO2 of 1.0, and 1.0 MAC of isoflurane in an FIO2 of 0.09. Stroke volume, total body and myocardial oxygen consumption, and fractional extraction of oxygen were calculated for the total body and for the myocardium. Isoflurane anesthesia decreased mean systemic arterial pressure (70 +/- 8 mmHg), heart rate (222 +/- 29 beats/min), and cardiac output (277 +/- 72 ml.kg-1.min-1) significantly (43 +/- 11 mmHg, 163 +/- 20 beats/min, 191 +/- 34 ml.kg-1.min-1). Hypoxemia returned heart rate to control (191 +/- 23 beats/min), increased stroke volume (1.71 +/- 0.2 ml/kg) above both control (1.23 +/- 0.2 ml/kg) and 1.0 MAC isoflurane levels (1.19 +/- 0.3 ml/kg), and increased cardiac output (325 +/- 61 ml.kg-1.min-1) above the level during 1.0 MAC isoflurane.
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PMID:The young lamb can increase cardiovascular performance during isoflurane anesthesia. 281 70

The global and regional coronary hemodynamic and myocardial metabolic effects of isoflurane administered intraoperatively as an adjunct to sufentanil were studied in seven of nine patients who experienced increased systemic arterial pressure while undergoing elective coronary artery bypass grafting. All patients were premedicated and maintained on their preoperative medications (beta-blockers, nitrates, Ca++ entry blockers) up to and including the morning of surgery. Systemic and pulmonary hemodynamics and global (coronary sinus, CS) and regional (great cardiac vein, GCV) coronary blood flows were measured, and blood samples were obtained for systemic and myocardial metabolic parameters: after induction with 30 mcg/kg of sufentanil and 0.12 mg/kg vecuronium (FIO2 1.0), but prior to incision (control); 5 min after sternotomy; and during ventilation with isoflurane-oxygen. Heart rate, cardiac output, stroke volume, and GCV/CS flow ratio did not change throughout the study. Neither global nor regional myocardial lactate production was detected in any patient at any time, and the electrocardiogram (lead II, V5) remained unchanged. In response to sternotomy, seven of nine patients experienced an increase in mean systemic arterial pressure of 20% or more (27 +/- 3% from control values), due to an elevation in systemic vascular resistance (30 +/- 5%). Coronary sinus (CS) and great cardiac vein (GCV) flows, as well as CS and GCV lactate extractions, were unchanged 5 min after sternotomy. Both global and regional myocardial oxygen extraction increased, while coronary venous oxygen content decreased. Isoflurane was administered in a dose that restored systemic arterial pressure to baseline values (inspired concentration 0.75-1.0%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial circulatory and metabolic effects of isoflurane and sufentanil during coronary artery surgery. 295 72

The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsed Doppler and two-dimensional echocardiography: comparison of halothane and isoflurane on cardiac function in infants and small children. 360 47

Mean arterial pressure (MAP) decreased by 10, 20, 40, and 50% of its baseline value in six anesthetized baboons with the administration of increasing concentrations of isoflurane. Mean arterial pressure, right atrial pressure, pulmonary artery pressures, and cardiac output were measured at each decrement in arterial pressure, and after the withdrawal of the isoflurane. At the same times, cerebral blood flow, the cerebral metabolic rate for oxygen, and the cerebral metabolic rate for glucose were determined. Cerebrovascular reactivity was assessed before, during, and after the administration of isoflurane, and morphologic evidence of ischemic cell change was sought at the end of the investigation. Isoflurane produced dose-related decreases in systemic vascular resistance and MAP; heart rate, cardiac output, and stroke volume did not change significantly. Although cerebral metabolism was depressed in a dose-related manner, the response of the cerebral blood flow (CBF) was biphasic. At low isoflurane concentrations, CBF decreased significantly and then increased to reach baseline values at the highest concentration. Cerebrovascular reactivity was intact at baseline and at the 20% decrement in MAP; it was impaired at the 50% decrease in MAP and when studied 100 min after the withdrawal of isoflurane. There was no morphologic evidence of ischemic cell damage in any animal.
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PMID:Cardiovascular and cerebrovascular effects of isoflurane-induced hypotension in the baboon. 370 97


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