Coronary and left ventricular hemodynamic responses following reversal of flunitrazepam-induced sedation with flumazenil in patients with coronary artery disease

The effects of reversal of flunitrazepam-induced sedation with flumazenil on coronary hemodynamics, myocardial oxygen consumption (MVO2), and left ventricular (LV) performance were investigated, in a double-blind trial, in 12 patients with stable coronary artery disease undergoing cardiac catheterization. Coronary sinus blood flow was measured by continuous thermodilution. Arterial and coronary sinus blood were analyzed for oxygen and lactate contents. The determinants of LV performance were obtained from the cardiac output measured by thermodilution and from left heart catheterization data. To reverse flunitrazepam-induced sedation, patients were randomly allocated to receive placebo or flumazenil (by increment, up to 1 mg) at the end of procedure. In the placebo group, no significant hemodynamic changes were observed. In the flumazenil group, heart rate, cardiac index, maximum velocity of shortening, and relaxation time constant were not significantly altered. By contrast, mean aortic pressure and LV end-diastolic pressure (baselines: 90 +/- 5 and 7.3 +/- 4.1 mmHg, respectively) increased (9%, P less than 0.05 and 67%, P less than 0.05, respectively) after flumazenil administration, but these changes represented mainly a return toward presedation values. MVO2 and coronary resistance were not significantly altered, whereas CSBF increased slightly (baseline: 119 +/- 20 ml/min; increase 10%, P less than 0.05). No electrocardiographic evidence of myocardial ischemia was observed during the study. These data show that reversal of benzodiazepine effects with flumazenil is not associated with a major alteration of LV systolic function, relaxation, or coronary hemodynamics in patients with coronary artery disease. Nevertheless, it should be cautiously used when LV end-diastolic pressure is increased at the time of its administration.     

Effects of intubation on coronary blood flow and myocardial oxygenation

Effects on haemodynamics and myocardial oxygenation of endotracheal intubation were examined in 17 patients after halothane induction and 12 after 1 mg X kg-1 of IV morphine. Six patients having each anaesthetic were pretreated with IV propranolol (0.1 mg X kg-1) 45 minutes earlier. Arterial and intracardiac pressures, cardiac output and total coronary sinus blood flow (CSBF), both by thermodilution, were determined plus arterial-coronary differences of oxygen, haemoglobin and lactate. Blood pressure (BP), heart rate and CSBF were recorded continuously during intubation. The subjects were candidates for coronary bypass grafts, but had good ventricular function (mean ejection fraction 0.68 +/- 0.13 SD). From their reduced levels after induction, BP, cardiac index and systemic vascular resistance increased to awake levels following intubation. Mean CSBF in nonbetablocked patients increased to awake level along with BP. More myocardial oxygen was extracted and consumed after intubation, but lactate extraction continued: these data are evidence of adequate oxygen supply. Induction with either halothane or morphine effectively prevented the hypertensive response to intubation. Acute beta blockade led to less increase in heart rate from intubation.     

EFFECTS OF FLUNITRAZEPAM ON LEFT VENTRICULAR PERFORMANCE, CORONARY HAEMODYNAMICS AND MYOCARDIAL METABOLISM IN PATIENTS WITH CORONARY ARTERY DISEASE

The effects of flunitrazepam 15 µg kg^–1, on leftventricular (LV) performance, coronary sinus blood flow (CSBF),myocardial oxygen uptake and myocardial lactate balance werestudied in nine patients with coronary artery disease undergoingcardiac catheterization. Flunitrazepam produced a decrease inmean aortic pressure (MAP) and in systemic vascular resistance(SVR) with maximal changes from control value observed at 15min for MAP and at 5 min for SVR. No change in cardiac indexwas observed. The following changes in variables related toLV performance were observed: (1) a transient increase in heartrate and left ventricular contractility (V^max); (2) a sustaineddecrease of left ventricular end-diastolic pressure, maximumat 15 min. Myocardial oxygen consumption was decreased at 15min but CSBF did not change, whereas total coronary vascularresistance was decreased. Since myocardial lactate extractionwas increased and no change in ECG was observed, a coronarysteal induced by coronary vasodilatarion did not appear to takeplace.     

Effects of calcium on the coronary and systemic circulation in patients after coronary surgery

Nine patients were studied three hours after aorto-coronary bypass. Before anaesthesia a radial arterial cannula was inserted and a thermodilution catheter placed into the pulmonary artery by fluoroscopy. A special thermodilution catheter was manipulated into the coronary sinus. Haemodynamic measurements were made plus cardiac output and coronary sinus blood flow. Content of oxygen and lactate in arterial and coronary sinus blood was determined. Series of measurements were done before and after 1 gm of CaCl₂ given intravenously over 15 minutes. Calcium increased cardiac index and arterial pressure but not systemic vascular resistance. Total coronary sinus blood flow did not change, nor did myocardial oxygen consumption or coronary sinus oxygen content. Content of lactate in arterial and coronary sinus blood was unaltered and lactate extraction by the heart continued, in eight of nine patients. The improved haemodynamics were accomplished without inordinate risk to global ventricular energy metabolism.     

Effects of sevoflurane on cardiovascular dynamics,coronary circulation and myocardial metabolism in dogs

The effects of 2.5% and 5% of sevoflurane anesthesia on hemodynamics and myocardial metabolism were studied in pentobarbital-pancuronium anesthetized dogs. The interaction between nicardipine and 2.5% sevoflurane was also examined. Sevoflurane produced dose-dependent ( P < 0.05 to P < 0.01) decreases in systolic arterial pressure (SAP), heart rate (HR), cardiac index (CI), left ventricular minute work index (LVMWI), maximum rate of rise of left ventricular pressure (LV dP/dt), the time constant of fall in isovolumic left ventricular pressure (T) and systemic vascular resistance (SVR), whereas stroke volume index (SVI) and left ventricular end-diastolic pressure (LVEDP) remained unchanged. Central venous pressure (CVP) was significantly ( P < 0.05) increased at 5%. Myocardial oxygen consumption (MV(O)(2)), and myocardial lactate extraction ratio (ML ext) were decreased in a dose-dependent manner ( P < 0.05). Myocardial oxygen extraction ratio (M(O)(2) ext) was significantly ( P < 0.01) decreased at 5%. The ratio of the left ventricular minute work index to myocardial oxygen consumption (LVMWI/MV(O)(2)), i.e., left ventricular efficiency was significantly decreased only at 5% ( P < 0.05). Coronary sinus blood flow (CSBF) was significantly ( P < 0.05) decreased only at 2.5% sevoflurane and coronary vascular resistance (CVR) was significantly ( P < 0.01) decreased only at 5% sevoflurane. The ratio of CSBF to CO (CSBF/CO) showed a tendency to increase as sevoflurane concentrations were increased. Nicardipine (0.01 mg.kg(-1)) administered intravenously under 2.5% sevoflurane caused significant ( P < 0.05 to P < 0.01) decreases in SAP, HR, LV dP/dt, SVR, and CVR, and increases in CVP, SVI, CI, and CSBF ( P < 0.05 to P < 0.01). CSBF/CO remained unchanged. MV(O)(2), M(O)(2) ext, and ML ext were significantly ( P < 0.05 to P < 0.01) decreased. LVMWI/MV(O)(2) showed a tendency to increase. It is concluded that sevoflurane causes a rapidly and easily controlled cardiovascular depression and may not have unfavorable effects on coronary circulation and myocardial metabolism. Nicardipine exerts a synergistic myocardial depressant effect on sevoflurane, in terms of both cardiovascular dynamics and myocardial metabolism.     

Nitrous Oxide Augments the Systemic and Coronary Haemodynamic Effects of Isoflurane in Patients with Ischaemic Heart Disease

The effects of 70% nitrous oxide, added to 1% end-tidal isoflurane and administered by intermittent positive pressure ventilation (IPPV), on coronary haemodynamics and myocardial oxygenation were investigated in 10 patients with ischaemic heart disease. Standard methods were used for determination of their central haemodynamic effects. Coronary blood flow was measured by the retrograde thermodilution technique and coronary sinus blood sampled for measurement of myocardial oxygen consumption and lactate extraction. One per cent end-tidal isoflurane decreased systemic blood pressure (-39%) by a combination of systemic vasodilation and reduction in cardiac performance. Coronary blood flow remained unaltered despite the fall in coronary perfusion pressure and myocardial oxygen consumption (-30%) and extraction (-30%) fell significantly. Ischaemic ECG changes parallelled by decreased myocardial lactate extraction or lactate production were recorded in 6 of the 10 patients during steady state isoflurane anaesthesia. When nitrous oxide was added to isoflurane there was a fall in heart rate (-13%), a further reduction in systemic blood pressure (-18%) and myocardial oxygen consumption (-31%) and extraction (-17%) whereas all other variables including coronary blood flow remained unaltered. The myocardial ischaemia was worsened in three of the six patients with ECG and metabolic signs of impaired oxygenation during isoflurane alone. It is concluded that nitrous oxide potentiates the systemic and coronary haemodynamic effects of isoflurane in patients with coronary artery disease. The mechanisms for myocardial ischaemia seem to be decreased coronary perfusion pressure and/or redistribution of coronary blood flow by direct coronary vasodilation.     

Myocardial metabolism and haemodynamic responses during high-dose fentanyl anaesthesia for coronary patients

Fentanyl (mean dose 109 micrograms X kg-1) and oxygen were given to ten patients having coronary vein grafts. Serial studies were done before, during and after operation, of central and mean arterial pressures (MAP), cardiac index (CI) and coronary sinus flow (CBF) by thermodilution, myocardial oxygen consumption (MVO2) and lactate extraction (MLE). On induction CI and stroke work index decreased, but heart rate and MAP were unchanged as systemic resistance increased. Mean MAP and heart rate remained at the awake levels. Mean CBF remained unchanged along with stable MAP and coronary resistance. Oxygen content of CS blood increased on induction and remained elevated until the incision; it was above the awake level early postoperatively. MVO2 was low normal when the patients were awake and remained so. Normal MLE continued with a few exceptions. High-dose fentanyl did not uniformly abolish autonomic reflexes. Heavy premedication, complete beta adrenergic blockade and a high initial doses of fentanyl plus its continued infusion, aided in retaining a hypodynamic circulation and myocardial oxygenation.     

Myocardial Oxygen Consumption and Coronary Haemodynamics during Fentanyl-Droperidol-Nitrous Oxide Anaesthesia in Patients with Ischaemic Heart Disease

Eight patients with stable ischaemic heart disease were investigated to determine the effects of fentanyl (15 μg/kg) - droperidol (150 μg/kg) - nitrous oxide (75%) anaesthesia, without concomitant fluid challenge, on myocardial oxygen consumption and lactate uptake, and central and coronary haemodynamics. Anaesthesia induced reductions in mean arterial pressure (— 35%, P<0.01), systemic vascular resistance (— 30%, P<0.01), left ventricular stroke work index (—50%, P<0.01) and total body oxygen consumption (— 23%, P<0.01), with no changes in heart rate, cardiac output or mean pulmonary arteriolar occlusion pressure. Mixed venous oxygen content increased (P< 0.05). Systemic vasodilatation, circulatory adaptation to an overall lower metabolic rate, and clinically negligible cardiodepression are the likely mechanisms behind the central haemodynamic response to this form of anaesthesia. Coronary sinus blood flow (measured by the continuous thermodilution technique) decreased (P<0.01) in parallel with the decrease in coronary perfusion pressure. Thus coronary vascular resistance remained unchanged. As expected from the haemodynamic findings, myocardial oxygen consumption decreased (—37%, P<0.01). Coronary sinus oxygen content and myocardial oxygen extraction did not change, nor was myocardial lactate uptake affected. No ST-T-segment depressions or dysrhythmias were recorded. These observations indicate that myocardial oxygenation was adequate in spite of the reduction in coronary perfusion pressure. There was poor correlation between changes in myocardial oxygen consumption and rate pressure product (R=0.455) or triple product (R=0.375).     

Effects of magnesium sulphate on the cardiovascular system, coronary circulation and myocardial metabolism in anaesthetized dogs

We have studied the effects of i.v. bolus doses of magnesium sulphate (MgSO4) 60, 90 and 120 mg kg-1 on haemodynamic state, the coronary circulation and myocardial metabolism in nine dogs anaesthetized with pentobarbitone and fentanyl. MgSO4 produced dose-dependent decreases in arterial pressure, heart rate, left ventricular dP/dtmax and left ventricular minute work index (LVMWI) and an increase in the time constant of left ventricular isovolumic relaxation. Stroke volume increased, systemic vascular resistance decreased and cardiac output did not change significantly. MgSO4 produced decreases in coronary perfusion pressure, coronary vascular resistance and myocardial oxygen consumption (MVO2). Coronary sinus blood flow, lactate extraction ratio and the ratio of LVMWI to myocardial MVO2, that is an index of cardiac efficiency, did not change significantly. This study indicated that the depressant effect of MgSO4 on cardiac function was offset by lowering of peripheral vascular resistance, so that cardiac pump function remained effective, and the almost constant coronary sinus blood flow resulted from the decrease in coronary vascular resistance even at higher doses.      

Nitrous oxide added to halothane reduces coronary flow and myocardial oxygen consumption in patients with coronary disease

The haemodynamic and myocardial metabolic effects of adding 50 per cent nitrous oxide to 0.5 per cent halothane were studied in 13 patients, before the surgical incision for coronary artery vein grafts. Cardiac output and coronary sinus blood flow were determined by thermodilution, along with haemodynamic measurements. Measurements 15 minutes after addition of nitrous oxide revealed a significant decrease in heart rate, arterial pressure, cardiac index, coronary sinus blood flow and myocardial oxygen consumption. There was a significant increase in coronary sinus lactate content, and a significant decrease, from 27 to 11 per cent, in myocardial lactate extraction. We conclude that these circulatory changes were likely to be due to a depression of ventricular function by the nitrous oxide. The myocardia of these patients with severe coronary disease were becoming globally ischaemic while they were receiving 50 per cent oxygen, in the presence of hypotension. Nitrous oxide should be turned off when hypotension occurs in coronary patients.     

Rate-pressure product correlates poorly with myocardial oxygen consumption during anaesthesia in coronary patients

In 26 patients having coronary grafts, haemodynamics, coronary sinus blood flow and the arterio-coronary sinus difference of oxygen content were determined, awake and at four intervals during morphine-oxygen or halothane--oxygen anaesthesia. Rate-pressure product (RPP), triple product (TP) and myocardial oxygen consumption (MVO2) were calculated. The correlation of the two indirect indices to MVO2 were tested by repeated measures and regression analyses. No significant correlations were seen at four of five study times, when outlying data points were appropriately excluded. A pitfall of using more than one data point from each patient in the linear regression analysis is pointed out. In addition to the lack of correlation of RPP to MVO2, RPP was an imprecise predictor of myocardial lactate production and of postoperative infarction.     

Myocardial metabolism and haemodynamic responses with enflurane anaesthesia for coronary artery surgery

Ten patients were studied before, during and after enflurane anaesthesia for coronary vein grafting. All had good ventricular function and nine were receiving effective beta blockade. Cardiac output and vascular pressures were measured, plus coronary sinus blood flow (CBF), myocardial oxygen consumption (MVO2) and lactate extraction (MLE). Enflurane induction (10 minutes, mean 1.72 per cent end tidal) reduced blood pressure (MAP), due to decreased cardiac index (CI), with no change in heart rate or systemic resistance. Intubation returned MAP and CI to control level but the heart rate increased. Subsequently, enflurane kept MAP, CI and stroke work below the awake level. CBF decreased on induction, rose again on intubation and remained normal before bypass. MVO2 fell on induction from an increase in CS oxygen content, which remained elevated. Normal MLE continued in every patient. There was no evidence of myocardial ischaemia in patients on beta blockade, when haemodynamics were maintained at or below those of the sedated, awake state.     

Comparison of isradipine with nitroprusside for control of blood pressure following myocardial revascularization: effects on hemodynamics, cardiac metabolism, and coronary blood flow

The effects of isradipine (ISR) on cardiac performance, myocardial metabolism, and coronary blood flow were compared with those of sodium nitroprusside (SNP) when used to control blood pressure following myocardial revascularization. Twenty patients were randomized to receive either intravenous ISR or SNP if arterial blood pressure increased above 130 mm Hg systolic. Hemodynamic and metabolic parameters were studied using radial, pulmonary arterial, and coronary sinus catheters. Cardiac output and coronary blood flows were measured by thermodilution and blood was taken for calculation of myocardial oxygen consumption and lactate extraction. Electrocardiographic changes were recorded by Holter monitoring throughout the study. ISR and SNP both produced a satisfactory reduction in blood pressure accompanied by a decreased systemic vascular resistance (P less than 0.001). ISR infusion was associated with increases in cardiac output and stroke index (P less than 0.01), which were not apparent in the SNP group. Tachycardia occurred with SNP (P less than 0.01) but not with ISR therapy. Right and left ventricular stroke work indices and myocardial oxygen consumption were reduced with SNP. The ISR group showed unchanged myocardial oxygen consumption with increased right ventricular stroke work index. Coronary vascular resistance decreased (P less than 0.01) during ISR infusion but decreased only slightly in the SNP group. Great cardiac vein blood flow was significantly increased with ISR but not with SNP, resulting in a significant difference between the groups (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of thoracic epidural anesthesia on coronary arteries and arterioles in patients with coronary artery disease

The effect of cardiac sympathetic blockade by high thoracic epidural anesthesia (TEA) (T1-T6, bupivacaine) on the luminal diameter of normal and diseased portions of epicardial coronary arteries was determined by quantitative coronary angiography in patients (n = 27) with severe coronary artery disease (CAD). In a separate group of patients (n = 9) with severe CAD, the effects of TEA on coronary arterioles (resistance vessels) were studied, by measuring total and regional myocardial blood flow and metabolism with the retrograde coronary sinus thermodilution technique. At the stenotic segments, TEA induced an increase in luminal diameter from 1.34 +/- 0.11 to 1.56 +/- 0.13 mm (P less than 0.002), but did not change the diameter of the nonstenotic segments (3.07 +/- 0.13 to 2.99 +/- 0.13 mm). In the second group of patients, TEA induced no changes in coronary perfusion pressure, total or regional myocardial blood flow, coronary venous oxygen content, coronary blood flow distribution, regional myocardial oxygen consumption, or lactate extraction or uptake. Two patients had chest pain in the control situation and had regional myocardial lactate production that was attenuated by TEA. We conclude that TEA may increase the diameter of stenotic epicardial coronary artery segments in patients with CAD without causing a dilation of coronary arterioles. These effects may be beneficial when high TEA is used to treat severe ischemic chest pain in patients at rest.     

Myocardial circulatory and metabolic effects of isoflurane and sufentanil during coronary artery surgery

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)     

Effects of Halothane on Coronary Haemodynamics and Myocardial Metabolism in Patients with Ischaemic Heart Disease and Heart Failure

Halothane was administered at an end-tidal concentration of 1% to 10 patients with stable ischaemic heart disease and clinical and haemodynamic signs of moderate heart failure. Measurements of central haemodynamic variables, coronary sinus blood flow and oxygen, lactate and hypoxanthine balances over the myocardium were done before and at steady state during halothane anaesthesia. Halothane induced marked haemodynamic changes with decreases in mean arterial pressure; (-43%), mean pulmonary arteriolar occlusion pressure (-42%), systemic vascular resistance (-31%), cardiac index (-20%), stroke volume index (-31%) and left and right stroke work indices (-62% and -55%, respectively). Heart rate and pulmonary vascular resistance did not change. Coronary sinus blood flow decreased in parallel with perfusion pressure, and myocardial oxygen consumption decreased (-40%), as did myocardial oxygen extraction. Rate pressure product and triple product correlated better with changes in myocardial oxygen consumption in the present subset of patients than in healthy volunteers during halothane anaesthesia. The findings suggest that halothane, through its systemic vasodilatory effect, unloads the failing left ventricle and that this peripheral action predominates over the direct cardiodepressant action of the agent. The combined findings of unchanged coronary vascular resistance, decreased myocardial oxygen extraction and absence of increasing or pathological levels of lactate and hypoxanthine in coronary sinus blood imply a direct dilatory effect of halothane on the coronary vasculature.     

Global and regional myocardial blood flow and metabolism during equipotent halothane and isoflurane anesthesia in patients with coronary artery disease

Global and regional myocardial blood flow and metabolism were examined in 20 patients with coronary artery disease before surgical stimulation. Half were anesthetized with halothane (0.8%) and half with isoflurane (1.2%). Coronary perfusion pressure decreased similarly in both groups. During halothane anesthesia coronary sinus blood flow, an index of global perfusion, decreased from an awake value of 129 +/- 7 to 97 +/- 7 ml/min (P less than 0.05), and great cardiac vein blood flow, an index of regional perfusion, decreased from 60 +/- 8 to 44 +/- 5 ml/min (P less than 0.05). In contrast, during isoflurane anesthesia global coronary blood flow increased from 131 +/- 13 to 153 +/- 16 ml/min (P less than 0.05), while regional blood flow decreased from 68 +/- 7 to 56 +/- 6 ml/min (P less than 0.05). Thus, the ratio of great cardiac vein blood flow to coronary sinus blood flow was unchanged during halothane anesthesia but decreased significantly during isoflurane. Neither global nor regional coronary vascular resistance was altered by halothane, whereas isoflurane decreased global coronary vascular resistance without affecting regional coronary vascular resistance. All patients receiving halothane had net myocardial lactate extraction. In the isoflurane group, four patients showed global lactate production and three regional lactate production. All patients demonstrating lactate production also developed electrocardiographic evidence of myocardial ischemia, which was not present before induction. The authors conclude that halothane is a preferable anesthetic to isoflurane in patients with coronary artery disease because the latter has the propensity to induce maldistribution of the coronary circulation and myocardial ischemia.     

The effects of hypothermia on myocardial oxygen consumption and transmural coronary blood flow in the potassium-arrested heart.

Hypothermia remains the primary adjunct employed to lower cellular metabolism during various cardiac procedures. In these experiments, left ventricular myocardial oxygen consumption (MVO2) and transmural blood flow (TBF) were measured during cardiopulmonary bypass with the range of temperatures used clinically. Determinations were made in empty beating normothermic hearts and after potassium cardioplegia at 37, 32, 28, 22, 18, and 15 degrees (K+ = 15--37 meq/L: Hct 25 volumes %). Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer (vs Van Slyke, R = 0.98). Transmural blood flow was measured at each temperature using microspheres (8 microns), and perfusion was maintained at 80 mmHg. Asystole (37 degrees) alone decreased MVO2 from 5.18 +/- 0.55 to 1.85 +/- 0.20 ml O2/min/100 g of left ventricle or approximately 65% (p less than 0.001). With progressive cooling to 15 degrees an additional 82% decrement in oxygen uptake occurred during asystole (p less than 0.001). During asystole at 37 degrees the decrease in MVO2 was reflected mainly by a large decrement (p less than 0.01) in TBF (1.27 +/- 0.19 to 0.74 +/- 0.17 ml/min/g of mean left ventricular flow). However, with cooling below 32 degrees, the arteriovenous oxygen difference narrowed progressively (p less than 0.001) while TBF paradoxically returned to control levels. Endocardial/epicardial flow ratios were not altered by cooling. These data not only confirm earlier reports describing a sequential drop in MVO2 with incremental myocardial cooling, but also establish MVO2 levels for perfused hearts arrested by potassium at lower temperatures (18--15 degrees). Moreover, as transmural blood flow becomes independent of metabolic necessity during hypothermia, coronary autoregulation appears to be impaired, possibly affecting detrimental tissue over perfusion.     

Muscle relaxants change myocardial metabolism in patients with ischemic heart disease during high-dose fentanyl anesthesia

Although not unanimously accepted, high-dose fentanyl anesthesia has been associated with hemodynamic stability and little derangement of myocardial oxygen balance. This apparent inconsistency inspired us to investigate the effects on cardiac function and myocardial metabolism of stepwise increasing doses of fentanyl, accumulating to 15, 30, and 50 micrograms.kg-1, with the least possible interference from other drugs. Subjects were unpremedicated patients with ischemic cardiac disease scheduled for coronary artery bypass grafting or major vascular surgery. In an initial study employing succinylcholine for muscle relaxation, we found that heart rate (HR), coronary sinus blood flow (CSF) and coronary vascular resistance (CVR) remained unchanged, while systemic arterial pressure (SBP), rate-pressure product (RPP), coronary perfusion pressure (CPP) and left ventricular work (LVW) decreased. Myocardial uptake of oxygen (MVO2) and free fatty acids (FFA) both decreased in a dose-dependent manner. Arterial lactate concentration and myocardial lactate uptake both increased. These findings opposed the postinduction myocardial ischemia noted by some other investigators. In most of these studies pancuronium bromide had been used for muscle relaxation. Since the latter agent has been claimed to increase cardiac work, a second group of correspondingly diseased patients was studied in which succinylcholine was replaced by pancuronium bromide. In this group HR, RPP, CSF and MVO2 all increased at the lowest dose of fentanyl and HR additionally also at 30 micrograms.kg-1. The cardiac index was higher in the pancuronium group at the lowest and middle dose steps of fentanyl. Lactate uptake decreased with higher doses of fentanyl and relative myocardial lactate extraction declined.(ABSTRACT TRUNCATED AT 250 WORDS)     

Successful percutaneous coronary intervention significantly improves coronary sinus blood flow as assessed by transthoracic echocardiography

Background

Transthoracic echocardiography (TTE) has been used to assess coronary sinus blood flow (CSBF), which reflects total coronary arterial blood flow. Successful angioplasty is expected to improve coronary arterial blood flow. Changes in CSBF after percutaneous coronary intervention (PCI), as assessed by TTE, have not been systematically evaluated.

Hypothesis

TTE can be utilized to reflect increased CSBF after a successful, clinically indicated PCI.

Methods

The study cohort included 31 patients (18 females, 62 ± 11 years old) referred for diagnostic cardiac catheterization for suspected coronary artery disease and possible PCI, when clinically indicated. All performed PCIs were successful, with good angiographic outcome. CSBF per cardiac cycle (mL/beat) was measured using transthoracic two-dimensional and Doppler flow imaging as the product of coronary sinus (CS) area and CS flow time–velocity integral. CSBF per minute (mL/min) was calculated as the product of heart rate and CSBF per cardiac cycle. In each patient, CSBF was assessed prospectively, before and after cardiac catheterization with and without clinically indicated PCI. Within- and between-group differences in CSBF before and after PCI were assessed using repeated measures analysis of variance.

Results

Technically adequate CSBF measurements were obtained in 24 patients (77%). In patients who did not undergo PCI, there was no significant change in CSBF (278.1 ± 344.1 versus 342.7 ± 248.5, p = 0.36). By contrast, among patients who underwent PCI, CSBF increased significantly (254.3 ± 194.7 versus 618.3 ± 358.5 mL/min, p < 0.01, p-interaction = 0.03). Other hemodynamic and echocardiographic parameters did not change significantly before and after cardiac catheterization in either treatment group.

Conclusions

Transthoracic echocardiographic assessment can be employed to document CSBF changes after angioplasty. Future studies are needed to explore the clinical utility of this noninvasive metric.