Myocardial function and metabolism in the conscious dog and during halothane anesthesia.

Chronically catheterized dogs were studied awake and during anesthesia with high and low concentrations of halothane to assess the relationship between cardiac function and metabolism. Low concentrations of halothane (0.79 per cent endtidal) increased heart rate and decreased left ventricular stroke volume, stroke work, and dP/dt without producing other hemodynamic changes. However, similar heart rate increases produced by atrial pacing in awake animals increased aortic pressure and cardiac output and decreased left atrial pressure. Consequently, the halothane-induced tachycardia partially compensated for the negative inotropic effect of the halothane. High concentrations of halothane (1.74 per cent endtidal) further increased heart rate and elevated left atrial pressures. Cardiac output, stroke volume, stroke work, aortic pressure, LV dP/dt, myocardial blood flow and oxygen consumption were markedly decreased. Myocardial glucose extraction was also decreased. Myocardial oxygen extraction was unchanged, and lactate extraction rose with both concentrations of halothane. Consequently, the dose-dependent negative inotropic effect of halothane resulted in a decrease in cardiac oxygen demand which was equal to or greater than the decrease in oxygen delivery. Whether the same relationship would be seen in the ischemic heart is yet to be demonstrated.     

Reversal by acupuncture of cardiovascular depression induced with morphine during halothane anaesthesia in dogs

The cardiovascular effects of morphine sulphate and/or acupuncture by means of electrocautery at Jen Chung (Go-26) were studied in 35 dogs. All animals were maintained under anaesthesia with halothane 0.75 per cent supplemented by the intravenous administration of succinylcholine to allow controlled ventilation during a two hour period of monitoring. Cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, [H⁺] (pH) PaC0₂, Pa0₂ and base deficit were measured in each dog. Morphine 0.5 mg ·kg^-1, administered alone as a single bolus, significantly (P < 0.05) decreased cardiac output, heart rate, mean arterial pressure, and significantly increased stroke volume and pulse pressure in dogs under halothane anaesthesia. Acupuncture by electrocautery alone induced a significant increase in cardiac output, stroke volume, heart rate, mean arterial pressure and pulse pressure with a significant decrease in total peripheral resistance following halothane. Acupuncture at Jen Chung (Go-26) for 10 minutes following the intravenous administration of morphine caused a significant increase in cardiac output, heart rate and mean arterial pressure with a significant decrease in central venous pressure and total peripheral resistance during halothane anaesthesia. The depressant effect of morphine on cardiac output, heart rate and mean arterial pressure in dogs under halothane anaesthesia appears to be reversed by acupuncture by electrocautery at Jen Chung (Go-26). Stimulation of this acupuncture locus could be helpful in resuscitating patients whose cardiovascular system is depressed by morphine and/or halothane anaes-thesia.     

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.     

MYOCARDIAL BLOOD FLOW AND OXYGEN CONSUMPTION DURING HALOTHANE-NITROUS OXIDE ANAESTHESIA FOR CORONARY REVASCULARIZATION

The effects of halothane on myocardial blood flow and myocardialoxygen balance were studied in seven male patients with stableangina and normal left ventricular function. Patients were receivingmaintenance doses of ß-receptor antagonists and underwentcoronary artery bypass surgery. Anaesthesia consisted of halothaneand 50% nitrous oxide in oxygen. Halothane decreased myocardialblood flow and myocardial oxygen consumption by 29% and 32%,respectively, after induction of anaesthesia, and during sternotomy.Myocardial lnctatc production was not observed at any time.Cardiac index, stroke volume index, mean arterial pressure andmean diastolic arterial pressure were decreased significantlyafter induction of anaesthesia and during sternotomy. Heartrate remained unchanged. The global myocardial oxygen supplyand demand relationship was maintained. The results suggestthat halothane is a safe anaesthetic for coronary revascularizationin patients with unimpaired left ventricular function.     

Haemodynamic and plasma vasopressin responses with high-dose fentanyl anaesthesia during aorto- coronary bypass operations

Twelve male patients were given high dose fentanyl (75-100 u,g-kg-1) anaesthesia with oxygen during elective aorto-coronary bypass operations, and their haemodynamic and vasopressin responses were determined during induction, sternotomy, cardiopulmonary bypass, post-bypass and recovery periods. For comparison, a group of 12 male patients were anaesthetized with morphine, halothane 0.5 per cent, nitrous oxide and oxygen, and were similarly studied. Significant alterations in haemodynamics included increased mean arterial pressure after sternotomy in the fentanyl group, increased heart rate in both groups, increased systemic vascular resistance after sternotomy only in the halothane group, and decreased left ventricular stroke work index in both groups following induction, bypass, and during the recovery periods. Plasma vasopressin levels increased significantly in both groups during the bypass period, but returned to baseline levels following bypass. Serum sodium and osmolality did not change significantly, and urinary sodium and potassium excretion rose with the progress of the operation in both groups. A positive correlation was found between mean arterial pressure and vasopressin only in the halothane group. Systemic vascular resistance was correlated to vasopressin levels in both groups. Vasopressin response in both groups was similar, with significant but relatively low increases in levels during cardiopulmonary bypass. Fentanyl-oxygen anaesthesia did not provide haemodynamic stability in eight of 12 patients.     

Haemodynamic and plasma vasopressin responses with high-dose fentanyl anaesthesia during aorto-coronary bypass operations

Twelve male patients were given high dose fentanyl (75-100 microgram.kg-1) anaesthesia with oxygen during elective aorto-coronary bypass operations, and their haemodynamic and vasopressin responses were determined during induction, sternotomy, cardiopulmonary bypass, post-bypass and recovery periods. For comparison, a group of 12 male patients were anaesthetized with morphine, halothane 0.5 per cent, nitrous oxide and oxygen, and were similarly studied. Significant alterations in haemodynamics included increased mean arterial pressure after sternotomy in the fentanyl group, increased heart rate in both groups, increased systemic vascular resistance after sternotomy only in the halothane group, and decreased left ventricular stroke work index in both groups following induction, bypass, and during the recovery periods. Plasma vasopressin levels increased significantly in both groups during the bypass period, but returned to baseline levels following bypass. Serum sodium and osmolality did not change significantly, and urinary sodium and potassium excretion rose with the progress of the operation in both groups. A positive correlation was found between mean arterial pressure and vasopressin only in the halothane group. Systemic vascular resistance was correlated to vasopressin levels in both groups. Vasopressin response in both groups was similar, with significant but relatively low increases in levels during cardiopulmonary bypass. Fentanyl-oxygen anaesthesia did not provide haemodynamic stability in eight of 12 patients.     

Hemodynamic effects of desflurane/nitrous oxide anesthesia in volunteers.

We determined the cardiovascular effects of 0.91, 1.34, and 1.74 MAC of desflurane/nitrous oxide anesthesia (60% inspired nitrous oxide contributed 0.5 MAC at each level) in 12 healthy, normocapnic male volunteers. Desflurane/nitrous oxide anesthesia decreased systemic blood pressures, cardiac index, stroke volume index, systemic vascular resistance, and left ventricular stroke work index, and increased pulmonary arterial pressures and central venous pressure in a dose-dependent fashion, while heart rate was 10%-12% and mixed venous oxygen tension was 2-4 mm Hg higher at all MAC levels than at baseline (awake). Desflurane/nitrous oxide anesthesia modestly increased left ventricular end-diastolic cross-sectional area (preload) and decreased velocity of left ventricular circumferential fiber shortening, systolic wall stress (afterload), and area ejection fraction; this combination of changes indicates myocardial depression. At approximately comparable MAC levels, heart rate was lower and systemic blood pressures, central venous pressure, left ventricular stroke work index, and systemic vascular resistance usually were significantly higher during anesthesia with desflurane and nitrous oxide than during desflurane anesthesia alone (same volunteers, data collected in crossover design). After 7 h of anesthesia, regardless of the background gas, somewhat less cardiovascular depression and/or modest stimulation was apparent: cardiac index, area ejection fraction, and velocity of left ventricular circumferential fiber shortening recovered to or toward awake values, whereas heart rate was further increased. Evidence of circulatory insufficiency did not develop in any volunteers during the study. Segmental left ventricular function was normal at baseline, and no segmental wall-motion abnormalities, ST-segment change, or dysrhythmias developed.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Cardiovascular changes during deep halothane anaesthesia in infants and children

Cardiac output, blood pressure and heart rate were measured with noninvasive techniques before, during and after induction of anaesthesia with halothane and after intubation in unpremedicated infants and in diazepam-atropine premedicated children presenting for elective surgery. Cardiac output was measured with pulsed doppler echocardiography. Left ventricular shortening fraction was estimated with M-mode echocardiography during induction. Induction with halothane in infants caused significant decrements in blood pressure, cardiac index, stroke volume index and significant depression of left ventricular shortening fraction. Induction with halothane in diazepam-atropine premedicated children caused a significant increase in heart rate but significant decreases in blood pressure, stroke volume index and left ventricular shortening fraction while cardiac index decreased slightly. Intubation in infants caused a mild increase in heart rate compared with pre-induction values but blood pressure, cardiac index and stroke volume index remained below pre-induction values. Intubation in diazepam-atropine premedicated children caused significant increases in heart rate and cardiac index, and a non-significant increase in blood pressure but stroke volume index remained significantly below pre-induction values. Healthy infants and children tolerate induction of anaesthesia with halothane to a depth to permit intubation but large reductions in cardiac output and myocardial contractility are expected with subsequent reductions in blood pressure.     

Indices of myocardial oxygenation during coronary-artery revascularization in man with morphine versus halothane anesthesia.

A prospective study in 12 adult male patients undergoing coronary-artery revascularization was conducted to compare the effects of a morphine versus a halothane anesthetic technique on several indices of myocardial oxygen supply and demand. Indices reflecting myocardial contractility, preload, afterload, and heart rate were measured. Undesirable increases in systemic and pulmonary capillary wedge pressure were minimized using sodium nitroprusside as needed. In the period after sternotomy but before revascularization, patients anesthetized with morphine (mean 2.1 mg/kg) had significant (P less than .05) increases in rate-pressure product, tension-time index, blood pressure, and heart rate, as well as relative myocardial ischemia, evidenced by significant ST-segment depression in the V5 lead of the EKG and a decreased diastolic pressure-time index/tension-time index compared with patients anesthetized with halothane (mean .75 per cent inspired). Few difficulties associated with myocardial depression were seen in patients anesthetized with halothane. Halothane, at least in a well-monitored environment, is safe for use in patients without severe ventricular dysfunction undergoing coronary-artery revascularization.     

Correlation between the linearized Frank-Starling relationship and myocardial energetics in the ejecting heart. Afterload independence and sensitivity to inotropic state

Previous studies suggest that the relationship between end-diastolic volume and stroke work calculated as the area of the pressure-volume work loop is linear, afterload independent, and sensitive to the inotropic state. The correlation of myocardial oxygen consumption with this stroke work could provide an integrated measure of cardiac performance and metabolism to assess perturbations induced by ischemia or pathologic loading conditions. Fourteen canine hearts instrumented for computerized acquisition of instantaneous pressure-volume data and quantitation of myocardial oxygen consumption were studied during progressive volume infusion on right heart bypass (1.5 to 3.5 L/min in 250 ml/min increments). Data acquisition both in the control state and during continuous infusion of calcium chloride (0.03 mEq/kg/min, n = 7) to increase contractility or phenylephrine (2 micrograms/kg/min, n = 7) to alter afterload facilitated the construction of stroke work versus end-diastolic volume and myocardial oxygen consumption versus stroke work relationships by least-squares regression analysis. The cardiac mechanics assessment for this group of dogs confirmed a highly linear (mean r = 0.984) work versus preload relationship that was unaffected by changes in afterload but sensitive to increased contractility (71% increase in slope). The myocardial energetics correlation was also linear (mean r = 0.939) and demonstrated an increased oxygen utilization characteristic of the higher inotropic state produced by calcium chloride infusion (0.047 +/- 0.003 versus 0.070 +/- 0.008 ml oxygen/beat/100 gm left ventricular weight, p = 0.008). Although phenylephrine administration produced variable perturbations of myocardial oxygen consumption, the energetics relationship for this subgroup was not statistically altered by changes in afterload. The features of this cardiac energetics assessment suggest its value as a biological marker to evaluate the postischemic, hypertrophied, or failing heart.     

Haemodynamic evidence for per-operative cardiac stress during transurethral prostatectomy. Preliminary communication.

Haemodynamic changes were measured during routine transurethral prostatectomy (TURP). The heart rate and stroke volume fell progressively over the first 30 min of surgery, resulting in a steady reduction in cardiac output. There was a significant increase in left ventricular afterload from commencement of the procedure. These findings demonstrate that haemodynamic responses, which are not detectable using conventional methods of monitoring, occur during TURP. Increased left ventricular afterload indicates increased myocardial work and oxygen demand which could result in myocardial ischaemia. This may contribute to the increased cardiovascular morbidity and mortality which have been reported to occur after TURP. The possible underlying mechanisms are discussed.     

Comparison of tidal ventilation and high-frequency jet ventilation before and after cardiopulmonary bypass in dogs using two-dimensional transesophageal echocardiography

This study compared the use of high-frequency jet ventilation (HFJV) and tidal ventilation (TV) in a group of dogs with induced global myocardial ischemia before and after cardiopulmonary bypass. Transesophageal echocardiography was used to determine whether HFJV with its lower airway pressures could improve cardiac performance. The surgical procedure was separated into four study periods: closed chest before bypass, open chest before bypass, open chest after bypass, and closed chest after bypass. During each of these study periods, the dogs were randomly ventilated with alternate periods of TV and HFJV to maintain the PaCO2 at 34.3 +/- 3.3 mm Hg (mean +/- SEM). Cardiac output, stroke volume, systemic mean blood pressure, left ventricular ejection fraction, left ventricular end-diastolic volume, left ventricular dP/dt, left ventricular stroke work, and expiratory volumetric flows were higher during HFJV, whereas airway pressures and pulmonary vascular resistance were lower. Increases in cardiac output and stroke volume during HFJV were due to a combination of improved left ventricular contractility indicated by increased LV dP/dt and increased left ventricular end-diastolic volume accompanying decreased airway pressures. These data indicate that HFJV with its lower airway pressure is associated with significantly less impairment of cardiovascular function than TV in dogs with induced global myocardial ischemia.     

Haemodynamic Response to Nitrous Oxide during High-Dose Fentanyl Pancuronium Anaesthesia

Ten patients subjected to coronary by-pass surgery were studied to determine the haemodynamic effects of replacing Fio2 1.0 normoventilation with nitrous oxide in oxygen (Fio2 0.3) after induction of anaesthesia with fentanyl (50 micrograms/kg), flunitrazepam and pancuronium. In all patients the application of N2O decreased systemic arterial pressures by an average of 10% (P less than 0.001), but left pulmonary arterial pressures and systemic vascular resistance unchanged. The slight bradycardia induced was associated with moderate depression of the cardiac index and the left ventricular stroke work index (P less than 0.001) at the time when the rate-pressure product was decreased by 20% (P less than 0.001). The cardiac depression produced by N2O was most prominent in patients with left ventricular wall hypokinesia and an ejection fraction below 55%, in whom the cardiac work index was diminished by 29%. The replacement of oxygen with nitrous oxide in oxygen during high-dose fentanyl-pancuronium anaesthesia seems not to be associated with sympathetic stimulation, and the myocardial depressant effect of N2O should be weighed against the possible reduction in myocardial oxygen consumption with special care in patients with compromised myocardial function.     

Intravenous nitroglycerin administration during infrarenal aortic clamping

Twenty-five patients requiring infrarenal abdominal aortic clamping were studied during halothane, nitrous oxide anaesthesia. Aortic clamping caused reductions in cardiac index (CI), stroke volume index (SVI) and left ventricular stroke work index (LVSWI). Systemic vascular resistance (SVR) increased. In seven patients CI was less than 1.81 X min-1 X m-2. Intravenous administration of nitroglycerin, 1 microgram X kg-1 X min-1, for 20 minutes, accompanied by volume loading to maintain pulmonary capillary wedge pressure, resulted in a significant improvement in haemodynamic parameters. CI increased 24 per cent as a result of a 14 per cent increase in SVI and an eight per cent increase in heart rate. LVSWI increased 13 per cent and SVR decreased 21 per cent. The plasma nitroglycerin concentration at the time of these measurements was 2.9 +/- 1.0 ng X ml-1. Aortic unclamping resulted in a mean maximum decrease of 14 +/- 2 torr mean arterial pressure. Epinephrine, norepinephrine and plasma renin activity gradually increased during the period of the anaesthetic.     

Myocardial metabolism and oxygenation in man awake and during halothane anesthesia.

Cardiac catheters were placed in seven healthy conscious patients so that aortic and left ventricular pressures (and the derivative), cardiac output (thermodilution) and myocardial blood flow (argon washin) could be measured. Blood was drawn for measurement of arterial blood-gas and arterial and coronary venous oxygen, glucose, lactate, pyruvate and fatty acid values. After induction of anesthesia by inhalation of halothane, the measurements were made during administration of low (0.70%) and high (1.54%) end-tidal halothane concentrations. Myocardial function decreased in a dose-related fashion without a change in heart rate. Myocardial blood flow and oxygen consumption were depressed in a similar manner. Myocardial oxygen extraction decreased and lactate did not change, suggesting that myocardial oxygenation was adequate. The heart rate-systolic blood pressure product correlated poorly with myocardial oxygen consumption. Systolic blood and the contractile performance index dP/dt/IP were better correlated with myocardial oxygen consumption, but the value of the coefficient was still low. Without significant changes in heart rate, systolic blood pressure is the best correlate of myocardial oxygen consumption in healthy man during the myocardial depression produced by halothane.     

Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two0dimensional echocardiographic dimensions of the left ventricle and pulmonary artery bloodflow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg·kg⁻¹ IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in bothgroups, but decreases in EF (32 ± 5 percentvs18 ± 5 per cent) and increases in LVEDV (18 ± 7 per cent vs7 ± 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 ± 6 per cent), than during isoflurane anaesthesia (18 ± 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 ± 4 per cent) following atropine in both groups, and CO returned to control levels. Halothane decreased EF and increased LVEDV more than isoflurane at 1.5 MAC end— expired anaesthetic levels. Atropine did not diminish the myocardial depression produced by halothane or isoflurane. The increase in CO following atropine during halothane and isoflurane anaesthesia in infants and small children is the result of increases in HR alone. Nous avons utilisé un appareil à échocardiographie bi-dimensionnelle couplé à un Doppler pulsé chez des bébés et de jeunes enfants pour évaluer l’impact hémodynamique de l’halothane (n = 15) et de l’isoflurane (n = 16) et la modification possible de ces effets par l’atropine. Nous avons mesure la frequence cardiaque (FC), la pression artérielle moyenne (PAM), la dimension de la cavité ventriculaire gauche (par écho bi-dimensionnelle) et la vélocité du flot sanguin pulmonaire (par Doppler) et ce, en trois occasions soit avant l’induction, après l’instauration de 1.5 MAC d’halothane ou d’isoflurane et finalement, deux minutes après l’injection IV de 0.02 mg·kg⁻¹ d’atropine. On ne nota une baisse de la frequence cardiaque qu’avec l’halothane tandis que la PAM, le débit cardiaque (DC) et le volume d’éjection (VE) diminuaient autant avec l’un ou l’autre anesthésique. La diminution de la fraction d’éjection (FE) et l’augmentation du volume télédiastolique du ventricule gauche (VTDVG) significatives pour les deux groupes, étaienl plus marqué avec l’halothane qu’avec l’isoflurane: FE 32 ± 5 pour cent vs18 ±5 pour cent; VTDVG 18 ± 7 pour cent vs 7 ± 5 pour cent. Avec l’atropine, la FC monta plus dans le groupe halothane (31 ± 6 pour cent) que dans le groupe isoflurane (18 ± 5 pour cent), le DC augmentant dans les deux groupes, alors que le VE et la FE demeuraient inchangés. Comparée aux mesures pré-induction, l’atropine amenait une hausse significative de la FC, semblable dans les deux groupes (18 ± 4 pour cent) et restaurait le DC. Donc, chez les bebes et les jeunes enfants, a 1.5 MAC, l’halothane diminue la FE et augmente le VTDVG plus que ne le fait l’isoflurane. L’atropine ne modifie pas la depression myocardique et elle ne restaure le DC que par une hausse de la FC.

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Supported by PHS Grant No. 8507300 from the College of Medicine, University of Iowa Hospital, Iowa City, IA.     

The effect of halothane, enflurane and isoflurane on the circulation

This study, in open-chested dogs, sought to explore the relationship between whole-body oxygen delivery and oxygen consumption during anaesthesia, using increasing concentrations of halothane, enflurane and isoflurane. Results indicate that the cardiac index and oxygen delivery became critical at less than 1 MAC (minimal alveolar concentration of anaesthetic) for the three commonly used vapours. Halothane caused the least depression of contractility, but the stroke volume was reduced by the well-maintained afterload at 1 MAC. Enflurane and isoflurane were associated with more depression of contractility, but the cardiac output was maintained by an increase in heart rate in the case of isoflurane and reduced mean arterial pressure during the use of enflurane.     

Inotropic stimulation and oxygen consumption in a canine model of dilated cardiomyopathy

Inotropic support for the dilated, failing ventricle results in complex hemodynamic changes affecting preload, afterload, contractility, and heart rate, each of which affects myocardial oxygen consumption. Appreciation of a hierarchy of hemodynamic determinants of myocardial oxygen consumption may be helpful to the clinician trying to balance oxygen demands and hemodynamic performance. We tested the hypothesis that epinephrine alters the hierarchy of hemodynamic determinants of myocardial oxygen consumption in a canine model of dilated cardiomyopathy created by rapid ventricular pacing. Dogs (n = 10) were instrumented to record left ventricular pressure and dimension, and a modified right heart bypass preparation was used to control left ventricular workload. Coronary sinus effluent was quantitatively collected and analyzed for oxygen content and used to calculate myocardial oxygen consumption. Epinephrine administration significantly increased myocardial oxygen consumption in the empty, beating heart; however, when the relationships of multiple determinants of left ventricular work and load were compared before and after epinephrine administration, no oxygen wasting effect was observed. Using multivariate linear regression analysis, a hierarchy of hemodynamic determinants of myocardial oxygen consumption was created. In the untreated heart, stroke work and cardiac output were the primary hemodynamic determinants of oxygen consumption; epinephrine significantly altered the determinants such that wall stress became the dominant hemodynamic determinant of myocardial oxygen consumption. Focused manipulation of wall stress in the treated, failing heart may limit the potentially deleterious effects of inotropic stimulation in this setting.     

Circulatory effects of isoflurane during acute hypercapnia

Acute respiratory acidosis results in increases in cardiac output and in systemic and pulmonary arterial blood pressures. The aim of this investigation was to determine if isoflurane modifies these effects. Nine patients (ASA II or III) scheduled for major surgery took part in the investigation. After the induction of general anesthesia, CO2 was added to the inspiratory gas mixture. After 15 min, ventilation with addition of CO2 (PaCO2 8-9 kPa) isoflurane (3%) was added. Hemodynamic measurements were made to study the effects of acute hypercapnia and the effects of isoflurane during hypercapnia. The addition of carbon dioxide resulted in increases in cardiac output, systemic and pulmonary arterial blood pressures, and right and left ventricular stroke work. The addition of isoflurane during hypercapnia decreased systemic arterial blood pressure, but pulmonary arterial blood pressure was unaffected, cardiac output and stroke volume did not change, and left but not right ventricular stroke work decreased. In conclusion, acute pulmonary hypertension induced by hypercapnia was not affected by isoflurane but, despite increased right ventricular stroke work, there were no signs of right ventricular failure.