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Biomedical subjects

E Lowenstein

Publications and source records attributed to E Lowenstein.

At least 109 records · Page 6Linked to original sources
PubMed1978

Ventricular performance and myocardial water content during hemodilution in dogs.

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.

Anemia↗
PubMed1976

Kinetics of high-dose intravenous morphine in cardiac surgery patients.

Ten patients received 1.0 mg/kg of morphine sulfate by constant-rate intravenous infusion at 5 mg/min over 9 to 27 min. Multiple arterial blood samples were drawn during the first 30 to 151 min after termination of the infusion, prior to institution of cardiopulmonary bypass. Postinfusion plasma concentrations were fitted by computer to biexponential functions consistent with a 2-compartment open pharmacokinetic model. Mean (+/- SE) pharmacokinetic parameters were: volume of central compartment, 0.09 +/- 0.03 L/kg; total apparent volume of distribution, 1.02 +/- 0.09 L/kg; distribution T 1/2, 0.90 +/- 0.09 min; apparent elimination T 1/2, 137 +/- 14 min; total clearance, 378 +/- 63 ml/min. Thus distribution of morphine is very rapid, but the apparent volume of distribution is only slightly larger than body weight, suggesting limited tissue uptake. Since apparent elimination T 1/2s are similar to those reported after smaller doses, evidence of saturable or capacity-linked elimination is lacking. Total clearances, representing mainly hepatic clearance, averaged about 25% of hepatic blood flow, suggesting clinically important first-pass metabolism of oral morphine.

Adult↗
PubMed1976

Lack of beta-adrenergic activity of isoflurane in the dog: a comparison of circulatory effects of halothane and isoflurane after propranolol administration.

The studies were undertaken to determine whether isoflurance inhalation is associated with a degree of beta-adrenergic action that is potentially important in clinical situations, and to compare the circulatory tolerance to isoflurane and halothane in dogs following beta blockade. We measured arterial and pulmonary artery pressure, left and right ventricular filling pressure, heart rate and cardiac output, and derived stroke volume and systemic and pulmonary vascular resistances in 13 mongrel dogs. The haemodynamic response to 1 MAC and 2 MAC isoflurane was studied in seven dogs and was similar before and after propranolol 0.1mg/kg i.v. In six dogs, propranolol 0.5mg/kg caused no significant changes in the circulatory response to 1 MAC and 2 MAC isoflurane or 1 MAC halothane. However, in three dogs, administration of 2 MAC halothane after propranolol 0.5mg/kg resulted in such profound circulatory depression as to preclude further study. These data suggest that (a) isoflurane possesses no clinically important beta-adrenergic stimulating activity; (b) there is no adverse drug interaction upon the circulation with the combination of isoflurane and propranolol; (c) in the presence of moderated profound beta-adrenergic blockade, 2 MAC isoflurane may be tolerated better than 2 MAC halothane.

Adrenergic beta-Agonists↗
PubMed1976

Halothane-induced decrease in experimental myocardial ischemia in the non-failing canine heart.

The effect of halothane on net myocardial oxygen balance of ischemic myocardium was studied in the non-failing canine heart. Myocardial ischemia was produced by repeated reversible occlusions of a coronary artery; the severity of ischemia was estimated by summating ST-segment elevations (sigma ST) obtained by epicardial ECG mapping at 15 to 18 sites. Control measurements were obtained before and after administration of halothane (0.75 per cent) to six dogs with chloralose-urethane basal anesthesia. Halothane was associated with significant decreases of systemic arterial pressure (P less than .001), heart rate (P less than .01), and the product of systolic arterial pressure X heart rate (P less than .01), an indirect index of myocardial oxygen consumption, while left atrial pressure remained unchanged at normal levels. sigmaST during occlusion was less (P less .001) during halothane (26.5 +/- 7.4 (SD) mv) than before (36.6 +/- 5.4 mv) or after (34.4 +/- 8.2 mv) its administration. Thus, halothane decreased the severity of experimentally-induced myocardial ischemia in the non-failing canine heart. The data suggest that, in the absence of ventricular failure, halothane influences the relationship between myocardial oxygen supply and demand in a favorable direction when coronary blood flow is limited.

Anesthesia, General↗
PubMed1976

Myocardial ischemia due to infrarenal aortic cross-clamping during aortic surgery in patients with severe coronary artery disease.

Hemodynamic measurements were performed and ECG recorded before and shortly after infrarenal aortic cross-clamping during operation for abdominal aortic aneurysm in five patients without evidence of heart disease (group I) and in ten patients with severe coronary artery disease (group II). All patients sustained an increase in systemic arterial pressure. Group I demonstrated a decrease in pulmonary artery, pulmonary capillary wedge (PCW), and central venous pressures when the aorta was clamped, whereas group II demonstrated an increase. The difference in response of the groups is significant (P less than 0.05). All three patients who responded to cross-clamping with increases of 7 mm Hg or greater in PCW demonstrated myocardial ischemia during cross-clamping. None of the values measured prior to cross-clamping predicted with certainty the response to cross-clamping. Sodium nitroprusside reversed the elevation of left ventricular filling pressure in all three patients, and in two patients, relieved evidence of myocardial ischemia concurrently. In the third patient, ventricular irritability was abolished by lidocaine and did not recur. We conclude that infrarenal aortic cross-clamping may cause myocardial ischemia in patients with severe coronary artery disease. This ischemia may be predicted by a rise in PCW at the time of cross-clamping, and vasodilator therapy is indicated in such patients.

Aged↗
PubMed1976

[Anesthetic considerations in patients with CAD (author's transl)].

The primary aim during anesthetic management of the patient with coronary artery disease is prevention of imbalance between myocardial oxygen supply and demand. Since oxygen supply is limited by restriction of coronary blood flow, prevention of increases in demand plus maintenance of supply, rather than increases in supply, will achieve this aim. The major determinants of myocardial oxygen demand are mechanical, i.e. (a) left ventricular wall tension, dependent in turn upon systolic pressure and ventricular volumn, (b) velocity of contraction, and (c) heart rate. Systolic pressure, pulmonary capillary wedge pressure, and heart rate monitoring will alert the anesthetist to increases associated with an enhanced oxygen demand. Decreased arterial diastolic and increased pulmonary capillary wedge pressure are associated with decreased supply. By appropriate manipulation of these variables and avoidance of episodes of myocardial ischemia, the perioperative morbidity and mortality rates associated with coronary artery disease may be decreased.

Adrenergic beta-Antagonists↗
PubMed1976

Hemodynamic effects of nitroprusside infusion during coronary artery operation in man.

The hemodynamic response to vasodilator therapy with sodium nitroprusside has been assessed in 33 patients with severe coronary artery disease (CAD) during coronary artery operation. The patients were divided into three groups; Group 1 included seven patients with CAD and normal left ventricular filling pressure (LVFP less than 12 mm Hg); Group 2 included 18 patients with CAD and chronic left ventricular (LV) dysfunction (LVFP greater than 12 mm Hg) and Group 3 included eight patients with CAD and acute LV dysfunction (LVFP greater than 12 mm Hg) associated with an intraoperative hypertensive episode. Nitroprusside was administered intraoperatively at an initial infusion rate of 10-15 mcg/min and the rate was gradually increased thereafter until the criteria for effective therapy were satisfied. The effective dose ranged from 10-120 mcg/min with an average of 52 +/- 4 (SEM) mcg/min. In all three groups, pulmonary and systemic arterial pressure, right and left ventricular filling pressure, and pulmonary and systemic vascular resistance decreased significantly with nitroprusside infusion. Heart rate increased significantly in Group 1 and remained unchanged in Group 2 and 3. Heart rate X systolic arterial pressure decreased significantly in Group 1 and 3 and did not change in Group 2. Stroke index increased significantly in both groups of patients with elevated control LVFP (Group 2 and 3) and remained unchanged in patients with normal left ventricular function (Group 1). Left ventricular stroke work index decreased in Group 1, increased in Group 2, and remained unchanged in Group 3. Right ventricular stroke work index decreased significantly in all groups. These findings suggest that judicious intraoperative administration of sodium nitroprusside improves left ventricular function in patients with acute or chronic elevation of LVFP and LV dysfunction associated with severe CAD. Furthermore, nitroprusside is an effective drug for control of intraoperative hypertensive episodes in such patients.

Adult↗
PubMed1975

Hemodynamic responses to mechanical ventilation with PEEP: the effect of hypervolemia.

The hemodynamic effects of prolonged mechanical ventilation with positive end-expiratory pressure (PEEP), with and without blood volume augmentation, were studied in 18 beagles anesthetized with halothane (0.7 per cent end-tidal). Addition of 12 cm H2O PEEP during mechanical ventilation in normavolemic dogs was associated with reductions of transmural cardiac filling pressures, cardiac index and stroke index to 50 per cent of control values. Circulatory adaptation did not occur. Filling pressures and flow remained unchanged during the ensuing 8 hours when PEEP was maintained. They returned to control levels when PEEP was discontinued, except for the transmural right ventricular end-diastolic pressure, which remained elevated above control levels. Systemic vascular resistance was unchanged, but pulmonary vascular resistance doubled upon addition of PEEP. Following autologous whole blood transfusion (25 ml/kg) during mechanical ventilation with PEEP, cardiac index returned to, and remained at, control levels. After PEEP was discontinued, cardiac index increased acutely and remained elevated for the remainder of the study period (as long as 7 hours). Comparable transfusion during mechanical ventilation without PEEP elevated cardiac index only transiently. Right atrial, pulmonary capillary wedge, and right and left ventricular end-diastolic pressures showed marked increases relative to atmospheric with PEEP and after transfusion. Calculated transmural pressures demonstrated clear reductions with application of PEEP, followed by increases to control levels with transfusion and further increases to above control when PEEP was discontinued. Study of ventricular function curves revealed that changes in filling pressures and not to changes in ventricular contractility. Transmural pulmonary arterial diastolic pressure rose throughout the 12 hours of study, despite return of pulmonary vascular resistance to control level with removal of PEEP. Thus, acute decreases in cardiac filling pressure, cardiac index, and stroke index persist consequent to application of PEEP, and circulatory adaptation does not occur. The apparent hemodynamic deterioration may be reversed by blood volume augmentation, but when PEEP is discontinued, hypervolemia with consequent increases in filling pressures and a move along a ventricular function curve will occur. Changes in cardiac index will depend upon the overall state of right and left ventricular contractility.

Animals↗
PubMed1975

Filling pressures of the heart and pulmonary circulation of the patient with coronary-artery disease after large intravenous doses of morphine.

Filling pressures of the heart and hemodynamic responses were studied before, during, and after administration of morphine, 2 mg/kg, intravenously (5 mg per minute) in eight patients with coronary-artery disease and normal ventricular contractility requiring myocardial revascularization. Left-heart filling pressure (LHFP) was estimated by measuring balloon-occluded pulmonary arterial pressure via a Swan-Ganz catheter, and right-heart filling pressure (RHFP) by right atrial pressure measurements. LHFP and RHFP were unchanged until 1.5 mg/kg morphine had been administered; after 2 mg/kg, LHFP had risen from a control level of 6.9 plus or minus 0.8 to 10.6 plus or minus 1.1 mm Hg (P less than .01) and RHFP from 2.9 plus or minus 0.4 to 4.9 plus or minus 0.8 mm Hg (P less than .05). Heart rate (P less than .02) and rate-pressure product (P less than .05), an indirect index of myocardial oxygen consumption, decreased throughout the study period. Systemic arterial pressure, cardiac index, and left ventricular stroke work decreased significantly only at the 0.5 mg/kg dose level, while systemic vascular resistance and stroke index remained unchanged. Mean pulmonary arterial pressure increased (P less than .05) after 1.5 mg/kg morphine, but pulmonary vascular resistance was unchanged. PaC02, pH, base excess, and hematocrit were constant throughout the study period. These data indicate that doses of morphine to 2 mg/kg, iv, are well tolerated by, and, presumably, decrease the myocardial oxygen consumption of, patients with coronary-artery disease. The hemodynamic response resembles that seen in man without hear or lung disease.

Blood Pressure↗
PubMed1975

Effects of fentanyl and droperidol on canine left ventricular performance.

The effects of fentanyl and droperidol on left ventricular performance were evaluated in the neurally intact dog right-heart-bypass preparation under conditions of constant cardiac output, arterial pressure, and heart rate. Fentanyl, .01 and .02 mg/kg body weight, and droperidol, 0.5 mg/kg, did not affect left ventricular performance. However 1.0 mg/kg droperidol caused a significant (P less than .05) increase in left ventricular end-diastolic pressure and a small decrease in maximum left ventricular dP/dt (.05 less than P less than .10). No significant change in myocardial oxygen consumption was observed. This study indicates that large doses of droperidol may depress left ventricular performance and may account for a portion of the hypotension observed after its administration in man. (Key words: Anesthetics, intravenous, fentanyl; Anesthetics; intravenous, droperidol; Heart, function, fentanyl; Heart, function, droperidol.).

Acid-Base Equilibrium↗
PubMed1975

Hemodynamic consequences of the combination of isoflurane anesthesia (1 MAC) and beta-adrenergic blockade in the dog.

The hemodynamic response to the combination of isoflurane (1 MAC) and propranolol (0.5 mg/kg) was studied in 12 intact ventilated dogs following basal anesthesia with chloralose-urethane. When propranolol was administered during isoflurane anesthesia, stroke volume was maintained with a higher pulmonary capillary wedge pressure (3.2 plus or minus 0.7 mm Hg to 6.3 plus or minus 1.4 mm Hg), while systemic vascular resistance remained unchanged. When isoflurane was administered to the previously beta-adrenergically blocked dog, there were declines in systemic pressure and cardiac output (P smaller than 0.01) and in pulmonary arterial pressure and stroke volume (P smaller then 0.05), without change in systemic vascular resistance. When isoflurane was subsequently discontinued, these changes were reversed, and in addition, systemic vascular resistance increased (P smaller than 0.05). These data indicate that isoflurane has pharmacologic properties compatible with a peripheral beta-adrenergic stimulating action.

Anesthesia↗
PubMed1975

Left ventricular performance and pulmonary circulation following addition of nitrous oxide to morphine during coronary-artery surgery.

The effects of nitrous oxide on ventricular performance and pulmonary circulation were studied in 12 patients with angiographically demonstrated coronary-artery disease and normal ventricular contractility who had received 2 mg/kg morphine intravenously. Seventeen studies were performed intraoperatively, five before and 12 after cardiopulmonary bypass and myocardial revascularization. Recordings were obtained during oxygen breathing and during nitrous oxide administration. Fifty per cent nitrous oxide significantly decreased mean arterial pressure (P less than 0.05), cardiac index (P less than 0.01), stroke index (P less than 0.01), left ventricular stroke work index (P less than 0.01), peak left ventricular dP/dt (P less than 0.05) and dP/dt/P (P less than 0.01), and heart rate-systolic arterial pressure product (P less than 0.01). Mean pulmonary arterial pressure (P less than 0.05), pulmonary artery occluded pressure (P less than 0.01), left ventricular end-diastolic pressure (P less than 0.01) and pulmonary vascular resistance (P less than 0.05) increased. Heart rate, right atrial pressure and systemic vascular resistance remained unchanged. When nitrous oxide was discontinued, all variables returned to control except mean pulmonary arterial pressure and pulmonary vascular resistance. Responses were similar before and after cardiopulmonary bypass and myocardial revascularization. These findings suggest that nitrous oxide depresses left ventricular performance when administered intraoperatively to patients who have received large doses of morphine for coronary-artery surgery. Nitrous oxide also increases pulmonary vascular resistance, possibly via alpha-adrenergic stimulation.

Anesthesia, Inhalation↗
PubMed1975

Lung water accumulation with acute hemodilution in dogs.

Extravascular lung water content was determined in vivo, gravimetrically, and histologically in severely hemodiluted (Ringer's lactate), supine, spontaneously breathing, halothane-anesthetized dogs. One group of dogs was studied immediately after undergoing hemodilution to a hematocrit value of less than 10 per cent; a second group was studied after hemodilution and 1 hour of circulatory maintenance with Ringer's lactate; and a third group was evaluated after hemodilution, maintenance for one hour with Ringer's lactate, and reconstitution of oncotic pressure with 75 Gm human salt-poor albumin. Lung water content was increased significantly from a normal of 3.88 Gm water per gram of dry weight to 4.70 Gm per gram of dry weight by hemodilution; it was increased further to 5.71 tgm per gram of dry weight during 1 hour of maintenance with Ringer's lactate. Reconstitution of oncotic pressure decreased the water content significantly to 4.96 and decreased the units demonstrating perivascular-peribronchial cuffing from 81 to 23 per cent. Double indication-dilution measurement of PEVW failed to reliably reflect changes in lung water. Arterial PO2 with the animals breathing 100 per cent oxygen was unchanged in all of the groups. We made the following conclusions: (1) lung water accumulation occurs during severe hemodilution and serum protein depletion; (2) this may be partially reversed by restoration of oncotic pressure; (3) double indicator-dilution PEVW measurements do not reliably reflect changes in extravascular lung water of less than 47 per cent; and (4) interstitial edema of this magnitude does not interfere with blood-gas exchange.

Animals↗