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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Septic shock associated with depressed myocardial function generally requires the use of catecholamine. Currently dopamine is often selected. Dobutamine is a newly developed catecholamine which has been shown to be of value in severe cardiomyopathic disease. The aim of this work was to determine the most appropriate drug by comparing haemodynamic responses to dopamine and dobutamine in 19 studies carried out in 11 patients with septic shock and heart failure. Cardiac index increased siliarly with dopamine and dobutamine (33%), as did stroke volume (respectively 26.4 and 25%). Arterial pressure increased by 17% with dopamine whereas it did not significantly change with dobutamine due to reduction in vascular resistance of 19%. Dobutamine decreased filling pressure, either right (14%) of left (28%) whilst they slightly but unsignificantly increased with dopamine. Pulmonary shunting increased more with dopamine (47%) than with dobutamine (16%), but PaO2 remained constant with both. Since septic shock is characterized by lowered arterial pressure and vasodilatation it is concluded that effects of dopamine on capacitance and resistance vessels make this drug more suitable. In addition it selectively increases renal blood flow. Nevertheless dobutamine could be appropriate, in case of very high filling pressures, severe peripheral vasoconstriction, marked pulmonary shunting and in some cases where dopamine becomes ineffective.
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PMID:Comparative haemodynamic effects of dopamine and dobutamine in septic shock. 50 Sep 39

Detailed hemodynamic and metabolic studies were performed during the course of phenformin related lactic acidosis in two patients. Arterial blood lactate was increased to 11.5 and 26.1 mM/L and arterial blood pH was reduced to 7.05 and 6.80 units, respectively. A marked reduction in cardiac indices (0.94 and 1.15 L/min/m2), stroke volume, and stroke work were observed, with either normal or increased arterial resistance. Mild increases in pulmonary artery systolic pressure (50/11), 45/25 mmHg) were observed, but necropsy in both cases disclosed no evidence of pulmonary vascular obstruction. In the absence of increases in central venous and pulmonary artery wedge pressure, a cardiac failure was excluded as primary cause of the low output state. Hypovolemia was excluded on the basis of radioisotope dilution measurements of plasma volume and red cell mass and no increase in cardiac output followed volume expansion. Oxygen extraction from blood was not grossly impaired. These observations indicate that phenformin-related lactic acidosis may evolve as a circulatory defect characteristic of shock in which oxygen delivery rather than oxygen utilization is impaired. The hemodynamic defect is best explained by a defect in the intravascular distribution of blood volume.
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PMID:Circulatory defects during phenformin lactic acidosis. 50 Sep 42

This report examines prospectively, in the Framingham cohort, the relation of diabetes and impaired glucose tolerance to each of the cardiovascular sequelae, taking into account age, sex, and associated cardiovascular risk factors. The incidence of cardiovascular disease, as well as the levels of cardiovascular risk factors, were found to be higher in diabetic than in nondiabetic men and women. The relative impact of diabetes on coronary heart disease, peripheral vascular disease, or stroke incidence was the same in men and women, but for cardiovascular mortality and cardiac failure the impact is greater for women. Present evidence suggests that alleviation of associated cardiovascular risk factors is the most promising course in reducing cardiovascular sequelae in diabetic patients.
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PMID:Diabetes and glucose tolerance as risk factors for cardiovascular disease: the Framingham study. 52 Jan 14

Blood loss of sufficient magnitude to over-ride compensatory mechanisms and result in a lowering of arterial pressure will ultimately lead to irreversible circulatory collapse. Identification of the organ or tissues which may trigger a terminal cascade remains controversial. The weight of evidence supports the view that cardiac performance deteriorates with prolonged oligemic hypotension, although this may not be the initiating or sole reason for irreversible failure of the circulation. Controversy regarding the heart as an important target organ is no doubt in part due to the multiplicity of preparations and protocols, and variety of methods used to characterize cardiac function. We have used ventricular function curves to calibrate LV performance in terms of pump function, while arterial pressure remains at a pre-determined level. With this approach, a progressive decline in stroke volume for a given LV end diastolic pressure is consistently observed in hemorrhagic shock (AP, 30 mmHg). If arterial pressure is briefly re-elevated at 30 minute intervals, permanent deterioration is prevented. However, if the hypotension is sustained for 2 hours, LV performance remains depressed following pressure re-elevation. Among the mechanisms responsible for deterioration of performance, coronary perfusion pressure (CPP) exerts a pivotal role. Thus, no LV depression occurs after 2 hours of shock provided CPP is maintained at normotensive levels. But if myocardial O2 availability falls below 10 ml/min/100 gm of heart, both O2 uptake and extraction decline and this is uniformly accompanied by cardiac failure. This likely reflects mitochondrial damage and impaired aerobic metabolism. These changes are potentiated by the appearance of metabolic acidosis and failure of sympathetic neurohumoral activity. Both factors directly reduce myocardial contractility, but assume much greater importance during shock. While E. coli endotoxin has been shown to reduce cardiac performance, the relative importance of bacterial products which may enter the circulation during hemorrhagic shock in uncertain. Reduced O2 availability, metabolic acidosis and adrenergic failure appear the major determinants of diminished cardiac performance and thereby may contribute to irreversible collapse of circulatory function.
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PMID:Cardiac performance in hemorrhagic shock. 55 6

We compared cardiocirculatory actions of nitroprusside (NP) to prazosin (PZ) in eleven chronic coronary patients with refractory congestive heart failure. Each drug equally lowered systemic arterial pressures mildly while heart rate was unaltered. NP decline (P less than .001) in left ventricular filling pressure (28 to 17 mm Hg) and rise (P less than .005) in cardiac index (2.20 to 2.96 L/min/m2) were similar to PZ (30 to 17) and (2.08 to 3.00). PZ and NP equally enhanced cardiac efficiency of stroke work and myocardial oxygen consumption index. Total systemic vascular resistance declined (P less than .001) the same with NP and PZ. Forearm vascular resistance (FVR) and venous tone (FVT) diminished equally with NP and PZ. Similar FVR/FVT percent changes of 0.88 and 0.64 with NP and PZ indicated relatively balanced systemic arteriovenous relaxation. Sinze PZ effects persisted six hours with symptomatic improvement, oral PZ is the best vasodilator for long-term use, extending in-hospital NP-like actions to ambulatory heart failure therapy.
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PMID:Comparison of effects of nitroprusside and prazosin on left ventricular function and the peripheral circulation in chronic refractory congestive heart failure. 61 83

Nineteen patients, aged 58-80 years, with severe isolated aortic valve stenosis, severely reduced ejection fraction and clinical heart failure underwent aortic valve replacement between January 1970 and April 1977. Ten had concomitant coronary artery disease (all underwent additional coronary bypass surgery), 17 had angina pectoris and four had syncope. Aortic valve area index was 0.32 +/- 0.03 cm2/m2 (mean +/- SEM); left ventricular (LV) end-diastolic volume index was 117 +/- 9 ml/m2 and LV ejection fraction was 0.37 +/- 0.02. There were four operative deaths and one late death. The follow-up time ranged from six to 74 months (38 +/- 6 months). Actuarially determined three-year survival is 74 +/- 10%; the expected five-year survival is the same. One patient had a serious cerebrovascular accident. Of the remaining survivors, seven were initially Functional Class IV and six Class III; currently, six are Class I and seven Class II (New York Heart Association classifications). The cardiothoracic ratio has decreased from 0.54 +/- 0.03 to 0.49 +/- 0.03. Repeat hemodynamic evaluation has been performed in 10 patients, 22 +/- 6 months after surgery. In these 10 patients, the aortic valve gradient decreased from 55 +/- 7 11 +/- 1.3 mm Hg; LV end-diastolic pressure from 22 +/- 2.4 to 9 +/- 1.9 mm Hg; LV end-diastolic volume index from 119 +/- 16 ml/m2 to 107 +/- 11 ml/m2. LV ejection fraction has increased dramatically from 0.34 +/- 0.03 to 0.63 +/- 0.05 and mean velocity of circumferential fiber shortening from 0.57 +/- 0.08 to 1.3 +/- 0.18 circ/sec. The encouraging long-term survival, improved functional class and the marked improvement in left ventricular function that occurred in our patients indicate that all patients with severe aortic stenosis in clinical heart failure should be offered aortic valve replacement.
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PMID:Severe aortic stenosis with impaired left ventricular function and clinical heart failure: results of valve replacement. 66 73

In 85 geriatric premedicated patients haemodynamic effects were investigated following rapid infusion of 500 ml dextrane. The data measured one day preoperative revealed typical age-related changes of the cardiovascular system: decrease of cardiac output, stroke volume and heart rate; increase of peripheral vascular resistance and mean arterial pressure. After infusion of dextran central venous pressure rose by 4.9 mm Hg (mean), mean arterial pressure by 7.5 mm Hg (8.5%) and cardiac output by 1.04 1/min (24.3%). Heart rate alterations were insignificant, but total peripheral resistance decreased significantly by 12.5%. Pulmonary capillary pressure rose to 15.4 +/- 3.4 mm Hg. We conclude that it is possible to increase cardiopulmonary efficiency by extracardiac measures preoperatively even in aged patients. In no case critical left- or right ventricular filling pressure exceeded, so we cannot accept the often expressed warnings against induced hypervolaemia in patients with no cardiac failure except old age.
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PMID:[Haemodynamic effects after rapid infusion of dextrane in geriatric patients (author's transl)]. 67 36

Thirteen patients with severe cardiac failure underwent a single crossover study of dopamine and dobutamine in order to compare the systemic and regional hemodynamic effects of the two drugs. The dose-response data demonstrated that dobutamine (2.5--10 microgram/kg/min) progressively and predictably increases cardiac output by increasing stroke volume, while simultaneously decreasing systemic and pulmonary vascular resistance and pulmonary capillary wedge pressure. There was no change in heart rate or premature ventricular contractions (PVCs)/min at this dose range. Dopamine (2--8 microgram/kg/min) increased the stroke volume and cardiac output at 4 microgram/kg/min. Dopamine at less than 4 microgram/kg/min provided little additional increase in cardiac output and increased the pulmonary wedge pressure and the number of PVCs/min. At greater than 6 microgram/kg/min, dopamine increased heart rate. During the 24-hour maintenance-dose infusion of each drug (dopamine 3.7--4, dobutamine 7.3--7.7 microgram/kg/min), only dobutamine maintained a significant increase of stroke volume, cardiac output, urine flow, urine sodium concentration, creatinine clearance and peripheral blood flow. Renal and hepatic blood flow were not signfiicantly altered by the maintenance dose of either drug. Systemic and regional hemodynamic data suggest that dobutamine has many advantages over dopamine when infused in patients with cardiac failure.
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PMID:Comparative systemic and regional hemodynamic effects of dopamine and dobutamine in patients with cardiomyopathic heart failure. 67 37

Hemodynamic evaluations of 130 patients with acute myocardial infarction were performed by right and/or left heart catheterization. 115 patients were subdivided in six groups by the pulmonary artery mean pressure (PMP)-left ventricular stroke work index (LVSWI) relationship: 1) normal LVSWI in relation to PMP (14.8% of all cases); 2) increased LVSWI in relation to PMP (0.9%); 3) moderately reduced LVSWI with increased PMP (severe heart failure-cardiogenic shock) (7.0%); 5) reduced LVSWI with low or normal PMP (22.6%); 6) normal LVSWI with elevated PMP (reduced left ventricular compliance or high pulmonary vascular resistance) (15.7%). 28 cases were studied by right and left heart catheterization; in 10 cases only left heart catheterization was performed. Discriminant analysis on the values measured at the first stage of hemodynamic monitoring was conducted: this type of mathematical analysis seemed to provide a more useful prognostic index.
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PMID:[Hemodynamic classification of acute myocardial infarction: physiopathological aspects and prognostic implications. Considerations on 130 cases (author's transl)]. 68 Apr 32

Ten patients in severe cardiac failure were treated with dopamine (4 microgram/kg . min) and dobutamine (7.5 microgram/kg.min). Both drugs brought about a similar increase in stroke volume and cardiac output of about 50% and 60%, respectively, accompanied by a fall in peripheral vascular resistance of about 33%. On dopamine the heart rate increased by 12%, but remained unaltered on dobutamine. There was a significant fall in the preload of both ventricles with dobutamine, while ventricular filling pressure during dopamine infusion was only slightly decreased, unchanged or even increased. The pulmonary (wedge) pressure during dopamine infusion averaged 9 mm Hg higher than during dobutamine (P less than 0.001). There is thus the potential danger with dopamine of aggravating pulmonary congestion. Furthermore, the improvement in cardiac function due to dopamine is at the expense of a higher oxygen demand than with dobutamine. Dobutamine is, therfore, preferable to dopamine in the treatment of advanced myocardial failure.
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PMID:[Dopamine and dobutamine in the treatment of severe cardiac failure (author's transl)]. 71 Mar 19


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