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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxygen uptake, cardiac output, stroke volume and arterial and central blood pressures were measured before and after induction of neuroleptanaesthesia in 27 subjects. Nine were elderly patients operated on for obliterative arteriosclerotic disease, and the other 18--nine elderly and nine younger patients--underwent operation for varicose veins. Cardiac output, stroke volume and systolic arterial blood pressure decreased significantly with a corresponding decrease in oxygen uptake. The changes were most pronounced in the patients with arteriosclerotic disease. The arterio-venous oxygen difference was unchanged in the arteriosclerotics and decreased in the other two groups. The central pressures remained unchanged in all groups. It is concluded that the cardiovascular changes induced by neuroleptanaesthesia are due to a decrease in oxygen uptake and not to myocardial depression.
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PMID:The cardiovascular effects of neuroleptanaesthesia. 84 53

The cardiac response to volume loading was evaluated in fifty severely septic patients. After a rapid infusion of albumin or whole blood the cardiac index (CI) and left ventricular stroke work index (LVSWI) were recorded as the pulmonary arterial wedge pressure (PAWP) increased. Initial values of PAWP, CI, and LVSWI were similar in both the nineteen surviving and thirty-one nonsurviving patients. Surviving patients, however, demonstrated greater increases in CI and LVSWI as PAWP rose. Nearly half of both patient groups developed decreases in CI and LVSWI as the PAWP continued to increase. These downslopes occurred at relatively low PAWP and are taken as evidence of an abnormality of myocardial function in both survivors and nonsurvivors. The lower upslope of the performance curves in nonsurvivors indicates myocardial depression or a negative inotropic effect. Cardiac ischemia, acute respiratory failure, and high affinity red cells were found to diminish the cardiac response to volume loading, whereas hepatic and renal failure were associated with a good CI and LVSWI response.
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PMID:Myocardial depression during sepsis. 84 86

To study the effects of contraction mode on ventricular end-systolic pressure-volume relationship, we compared the end-systolic pressure of isovolumic contraction with that of ejecting contraction at an identical end-systolic volume. The left ventricle of excised cross-circulated canine hearts was fitted with a water-filled balloon. The balloon was connected to a hydraulic pump that allowed the ventricle to contract to a preset constant end-systolic volume (19-37 ml) from a variable end-diastolic volume. At each of control, enhanced, and depressed levels of contractility, differences of end-systolic pressures of steady state isovolumic and ejecting contractions were evaluated while stroke volume and velocity of ejection were widely varied. The end-systolic pressure in the ejecting contraction tended to decrease by 5-15% from that of the isovolumic beat with increases in either stroke volume to 20-25 ml or peak velocity of ejection to about 800 ml/sec. There was no obvious difference in the results at different levels of contractility. The magnitude of the end-systolic pressure depression due to ejection was, however, relatively small as compared to 4-fold changes in end-systolic pressure due to the changes in contracility. We, therefore, conclude that the ventricular end-systolic pressure-volume relationship is affected slightly by ejection, and that this effect is much smaller than the maximal effect of changing contractility on the end-systolic pressure-volume relationship.
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PMID:Effects of stroke volume and velocity of ejection on end-systolic pressure of canine left ventricle. End-systolic volume clamping. 85 81

1 Twelve men with untreated essential hypertension in WHO stage I were studied on an outpatient basis to evaluate the haemodynamic long-term effect of a new beta-adrenoceptor blocker, metoprolol. 2 Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intraarterial brachial pressure were recorded at rest in a supine and sitting position and during steady state work at 300, 600 and 900 kpm/min. 3 The subjects were treated with metoprolol (dose 50-250 mg/day) as the sole drug for 1 year and the haemodynamic study was repeated. 4 Mean arterial blood pressure was reduced about 12% at rest and 9% during exercise. The heart rate was decreased about 22% at rest and 20% during exercise. There was no significant compensatory increase in the stroke volume and consequently the cardiac index was reduced about 22% at rest sitting and about 17% during exercise. There was no decrease in total peripheral resistance. 5 No side-effects were seen. 6 The major haemodynamic long-term effects of metoprolol in mild and moderate essential hypertension resemble those seen by other beta-adrenoceptor blockers like alprenolol, atenolol and timolol. The study has not given support to the assumption that metoprolol should cause less depression in cardiac output than other beta-adrenoceptor blockers.
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PMID:Haemodynamic long-term effects of metoprolol at rest and during exercise in essential hypertension. 86 Nov 29

Observations during 935 anesthesias for implantation or revision of permanent pacemakers are presented. Using different methods of anesthesia we found the light halothane anesthesia introduced by inhalation to be best, provided that only atropine was used for premedication. Applying this method we saw asystolies or ventricular fibrillation in 3% of all cases--3 patients (i.e. 0.4%) died in tabula. Tachycardia (2.4%) occuring mostly during the introduction period were successfully treated by verapamil or practolol. Hypotension (5.4%) mostly took place in the course of anesthesia after implantation of the pacemaker. This depression may be due to a normalisation of the enhanced stroke volume whedication with pethidine or induction with propanidid was followed by comparatively more complications such as exitus letalis (2% resp. 1.5%), cardiac arrest (6.5% resp. 9%) and hypotension (24% resp. 10.5%). Regional anesthesia did not bring specific advantages. The good experiences with soft halothane anesthesia for implantations or revisions of pacemakers include 125 high risk patients (ASA classification IV to VII).
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PMID:[Anesthesia in pacemaker implantation. Experiences in 935 cases of anesthesia for the implantation or revision of a cardiac pacemaker]. 86 62

To access left ventricular function and compare pulmonary capillary wedge pressure and left ventricular end-diastolic pressure in the supine and sitting positions, 20 men with angina pectoris secondary to coronary artery disease underwent hemodynamic studies at rest and during exercise in the two positions. At rest the values for cardiac index, stroke index, systolic ejection rate index and left ventricular stroke work index were lower in the sitting position; heart rate, left ventricular end-diastolic pressure and pulmonary capillary wedge pressure were similar in the two positions. All patients experienced angina during both exercise periods. At angina during supine exercise, stroke index, systolic ejection rate index and left ventricular stroke work index did not increase significantly from the resting values. In contrast, during sitting exercise, significant increases in these variables were observed. Comparison of data during exercise revealed higher values for heart rate, mean systemic pressure, cardiac index, systolic ejection rate index, left ventricular stroke work index and rate-pressure product and lower values for mean pulmonary capillary wedge pressure (20 +/- 3 versus 27 +/- 3 [mean +/- standard error of the mean] mm Hg, P is less than 0.001), and left ventricular end-diastolic pressure (24+/- 3 versus 31 +/- 3 mm Hg, P is less than 0.02) in the sitting position; stroke index and S-T segment depression were similar during the two exercise periods. Four patients had insignificant increases in left ventricular filling pressure during both exercise periods. Of the 16 patients with abnormal left ventricular filling pressure during supine exercise, only 10 had a similar response during exercise in the sitting position. There was a good correlation between left ventricular end-diastolic pressure and mean pulmonary capillary wedge pressure at rest and during exercise in the two postures.
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PMID:Hemodynamics at rest and during supine and sitting bicycle exercise in patients with coronary artery disease. 87 Nov 6

The hemodynamic, coronary sinus blood flow and myocardial metabolic effects of 0.15 mg/kg body weight of intravenously administered propranolol were studied in 19 patients with coronary artery disease and 6 normal patients. Atrial pacing was performed in all patients and produced angina in 15 of the 19 patients with coronary artery disease. In these patients propranolol reduced heart rate from 78 to 69 beats/min, cardiac index from 3.0 to 2.6 liters/min per m2 and left ventricular stroke work index from 47 to 43 g-m/m2; it increased total peripheral resistance from 24 to 28 units and lactate extraction from 16.3 to 22.5%. There was no significant change in mean arterial pressure, left ventricular end-diastolic pressure, coronary sinus blood flow or myocardial oxygen consumption. During a second pacing stress propranolol produced clinical improvement in 9 of the 15 patients who experienced angina initially. The improvement was associated with less severe abnormalities in S-T depression and left ventricular end-diastolic pressure, increased lactate extraction and no significant change in coronary sinus blood flow or myocardial oxygen consumption. Thus, propranolol appears to be capable of modifying the anginal threshold as determined with atrial pacing, and the clinical response appears to be independent of global changes in coronary sinus blood flow and myocardial oxygen consumption.
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PMID:Effects of propranolol on the hemodynamic, coronary sinus blood flow and myocardial metabolic response to atrial pacing. 87 19

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

Although morphine is one of the oldest drugs known to man, it has only recently been used in large doses as an anesthetic agent. The main advantage is the cardiovascular stability. The purpose of this investigation was to study the circulatory response to high equianalgesic doses of morphine and meperidine. In 10 closed chest dogs during normoventilation and light background-anaesthesia (0.5 Vol. % halthane; N2O:O2 = 2:1) 2.0 mg/kg morphine and 15.0 mg/kg meperidine were given at random. Morphine produced a decrease in mean arterial blood pressure by 28%, which was paralleled by an identical fall in total peripheral resistance. No negative inotropic effects were found. In contrast to this, the severe hypotension developing with meperidine (decrease in blood pressure by 54%) was the result of peripheral vasodilatation (46%) and of myocardial depression indicated by a sharp drop in dp/dtmax (59%), dp/dtmax/IP (14%) and in left ventricular ejection fraction (33%). Utilizing the thermodilution technique, the cardiac output remained largely unaffected with both narcotic analgesics, as the increase in heart rate (morphine 27%; meperidine 101%) compensated for the fall in stroke volume (morphine 19%; meperidine 55%). In spite of the altered haemodynamics there was no change in the myocardial energy demand, which was adequately met by the coronary blood flow measured with the pressure-difference technique. Both, morphine and meperidine, produced initially an increase in coronary blood flow and coronary venous oxygen saturation indicating coronary vasodilation. While the mechanism for the change in cardiovascular status with high doses of morphine is vasodilatation probably due to histamine release, the results of this study suggest a peripheral as well as a central (myocardial depression) site of action with meperidine. The results obtained from this study were compared with the data from a previous investigation on equianalgesic doses of fentanyl and piritramide and their clinical implications were discussed.
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PMID:[Effect of high dosages of morphine and meperidine on haemodynamics, coronary blood flow and myocardial oxygen consumption in comparison to fentanyl and piritramide (author's transl)]. 87 92

The effect of the vasodilator nitroprusside (NP) on haemodynamics and myocardial oxygen consumption during drug induced myocardial oepression was examined in dogs (n = 7). The investigations were performed on closed chest dogs lightly anaesthetized with piritramide and N2O/O2 (ratio 2:1) under controlled ventilation and after beta-adrenergic blockade (1.5 mg/kg propranolol). After a loading dose and a continuous infusion of 0.3 mg/kg X min of pentobarbitone left ventricular maximum dp/dt was reduced to 50% of the control level, which was taken for granted as a standardized myocardial depression. Using an infusion of NP at a mean rate of 7 microgram/kg X min mean arterial pressure was then lowered to 80 mmHg for 20 min. The vasodilator therapy led to an increase in cardiac output and in stroke volume by 16%. Since the calculated endsystolic volume of the left ventricle decreased simultaneously (19%), the ejection fraction increased from 38% to 46%. There was also a significant reduction in left ventricular enddiastolic pressure (46%), which is supposed to result from the combined effects of an improved myocardial performance, a pooling of blood in peripheral vessels (indicated by decreases in enddiastolic volume by 6%, in mean pulmonary arterial pressure by 25% and in central venous pressure by 45%) and an increased ventricular compliance. Since the myocardial wall tension, a major determinant of myocardial energy demand, was lowered by increased ventricular compliance and reduced pre- and afterload, the oxygen consumption of the heart decreased by 22%. The smaller demand was supplied by an unchanged coronary blood flow. The narrowing of the a-v oxygen difference of the heart indicated a coronary dilatation (10%). The results obtained from this study support the clinical observations that NNP may improve an imbalanced ratio between myocardial oxygen supply and demand, in patients with impaired cardiac performance.
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PMID:[The effects of the vasodilator nitroprusside on haemodynamics and myocardial oxygen consumption during drug induced myocardial depression (author's transl)]. 87 94


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