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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In acute and chronic left heart failure peripheral resistance is elevated due to increased sympathetic tone. This should compensate the decrease in stroke volume. In the diseased left ventricle however the augmentation of afterload leads to further reduction of stroke volume and to increase of heart size and myocardial oxygen consumption. This vitious cycle may be interrupted by vasodilators. Drugs like nitroglycerin, mainly acting on the venous system, reduce preload and thereby relieve symptoms of pulmonary congestion (backward failure). Phentholamin on the other hand primarily reduces afterload by an action on the resistance vessels and thereby increases cardiac output (forward failure). Nitroprusside has effects on both, the capacity and resistance vessels. So nigroglycerin is the remedy of choice in acute pulmonary edema. Nitroprusside in leftf heart failure in acute myocardial infarction and Phentolamin in acute left ventricular failure due to critical rise in blood pressure. For long term treatment of chronic left heart failure (coronary heart disease, cardiomyopathy, rheumatic heart disease) hydralazin or prazosin may be used as well as long acting nitrates.
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PMID:[Progress in the therapy of acute and chronic cardiac insufficiency by means of systemic vasodilators. Studies with prazosin and nitroglycerin]. 12 80

Two types of vasodilators are used for treatment of acute myocardial infarction: Nitrates on the one hand with predominant venodilation and agents like Phentolamie and Nitroprusside on the other hand with venodilation as well as arteriolar vasodilation. Different opinions exist with respect to indication of these vasodilators. They are used for reduction of arterial blood pressure, for reduction of left ventricular filling pressure and for increase of cardiac output. A marked decrease in ejection fraction is the hemodynamic basis of application of vasodilators in the latter indication. By reduction of peripheral vascular resistance emptying of the left ventricle in these patients is enhanced.) As a working hypothesis in clinical situation elevated filling pressure indicates a decreased ejection fraction. The first part of this investigation deals with relation of left ventricular and diastolic pressure to ejection fraction. A good correlation between these two parameters was found in 717 patients with coronary artery disease. However variability was so wide that regression from enddiastolic pressure to ejection fraction in the individual seemed impossible. In 26.6% of patients with ejection fraction over 0.6%, filling pressure was 20 mm Hg or more. On the other hand, in 34.7% of patients with ejection fraction below 0.3% filling pressure was 20 mm Hg or less. As a consequence of practical value, reduced ejection fraction has to be assumed, if a patient presents elevated filling pressure and reduced cardiac output. In the second part, the hemodynamic effects of Phentolamine in 12 patients with acute myocardial infarction and elevated filling pressure (PCV resp. PADP greater than 18 mm Hg) are described. Maximal effects on hemodynamic variables were: reduction of peripheral vascular resistance by 31.4%, of left ventricular filling pressure by 16.2%, and of mean arterial pressure by 17.0%. Cardiac output increased by 25.8% and heart rate rose by 14.8%. At optimal efficacy, stroke volume increased by 23.7%. Further increase of infusion rate with concomitant fall of peripheral vascular resistance resulted in decrease of stroke volume and tachycardia. Most serious side effects consisted in sudden fall of blood pressure. Therefore intraarterial monitoring of blood pressure is demanded. The third part deals with hemodynamic effects of nitrates (Isosorbiddinitrate 10 mg p.o.) in patients with acute myocardial infarction and elevated filling pressure. One hour after application peripheral vascular resistance decrease by 16.5%, filling pressure by 20.8%, and mean arterial pressure by 9.0%. Cardiac output stroke volume and heart rate did not change significantly. No side effects were observed with Isosorbiddinitrate although two cases of nitrate syncope occurred with Nitroglycerin, resulting in bradycardia and hypotension. Indications for vasodilator therapy therefore has to be handled as follows: Nitrates should be given to patients with elevated filling pressure and normal cardiac output...
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PMID:[Hemodynamic guidelines in the treatment of acute myocardial infarction by means of vasodilators]. 16 46

The systemic hemodynamic effects of deep hypotension (MAP: 38 +/- 6 mm Hg) induced by sodium nitroprusside (S.N.) were studied in 20 patients who underwent surgery for cerebral aneurysm. The hemodynamic measurements were performed four times.: (1) during the preoperative period, (2) during stable anesthesia just before hypotension, (3) during stable hypotension, (4) 20 minutes after stopping nitroprusside. All patients were mechanically ventilated with a constant tidal volume and rate. Parameters for acid-base balance and Pa O2 were also recorded. Nitroprusside produces arterial and venous dilatation which results in a decrease of afterload and preload. The mean dosage of S. N. was 18 mcg/kg/mn. Systemic vascular resistances decreased by 62 p. cent. Mean arterial pressure decreased by 53 p. cent; it reached 40 mm Hg. Fall in preload resulted in a decrease in pulmonary wedge pressure by 28 p. cent. This fall in preload produced a decrease in stroke index according to Frank-Starling's mechanisms. However tachycardia allowed a rise in cardiac index by 20 p. cent. Increase of pulmonary wedge pressure at 8-10 mm Hg by blood volume expansion maintains stroke index at control level. Under these conditions the elevation of cardiac index is due to tachycardia. Cardiac rhythm disorders (wandering pace-maker, nodal rhythm) are observed in 5 patients after having stopped nitroprusside.
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PMID:[Deep hypotension induced by sodium nitroprusside in neurosurgery. I.--Systemic hemodynamic effects (author's transl)]. 48 87

Myocardial performance in the immediate postoperative period was studied 49 cardiac surgical patients treated with nitroprusside alone. With a thermodilution catheter positioned in the pulmonary artery, cardiac output was calculated and cardiac index, systemic vascular resistance index, and stroke work index were derived before after treatment with nitroprusside. The drug was a administered to all patients because of elevated systemic vascular resistance index. Based on their mean arterial pressure and cardiac index before treatment, the patients fell into two groups. Group I patients (N = 25) had elevated mean arterial pressure and normal cardiac index. Group II patients (N = 24) had normal mean arterial pressure and subnormal cardiac index. Nitroprusside administration resulted in a significant reduction of systemic vascular resistance index in all patients. In Group I the mean arterial pressure was lowered significantly while cardiac index increased only slightly. In Group II there was no change in arterial pressure, but cardiac index improved significantly. The results not only confirm that nitroprusside is effective in managing postoperative hypertension, but also demonstrate that in patients with postoperative left ventricular failure, the drug can improve cardiac output by reducing systemic vascular resistance without significantly lowering arterial blood pressure.
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PMID:Improved myocardial performance in postoperative cardiac surgical patients with sodium nitroprusside. 64 13

In the presence of regional myocardial ischemia, a 20% decrease in systemic arterial pressure following nitroprusside caused a 25% decrease in coronary perfusion pressure in animals with normal left ventricular end-diastolic pressures. This pressure decrement resulted in a significant decrease in the shortening of the regionally ischemic segment during the ejection phase of systole. A comparable arterial pressure drop of 21% with nitroprusside infusion during ischemia in the animals with elevated diastolic pressures caused a similar 28% decrease in coronary perfusion pressure, but resulted in a simultaneous increase in regional shortening. For the entire group there was no significant change in stroke volume. Even in the 11 animals where stroke volume increased, systolic regional shortening increased in only 4. An increase in stroke volume cannot be used to infer a parallel increase in the performance of a regionally ischemic segment. Nitroprusside appears to improve regional performance only in the presence of severe failure.
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PMID:Effects of sodium nitroprusside on function of regional ischemic myocardium. 75 85

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.
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PMID:Hemodynamic effects of nitroprusside infusion during coronary artery operation in man. 99 24

Nitroprusside was used to reduce afterload in 13 patients with isolated, severe aortic regurgitation. The drug significantly lowered mean aortic pressure, pulse pressure, left ventricular end-diastolic pressure and left ventricular volume. Total ventricular, or angiographic, cardiac index was generally unaffected, but forward cardiac index was improved significantly in 8 of 13 patients. Augmentation of forward cardiac index was seen in patients with subnormal resting forward cardiac index, in patients with decidedly elevated end-diastolic pressure, and in those with depressed resting ejection fractions. Regurgitant fraction fell with nitroprusside in six patients and remained unchanged in seven. Total stroke work index was diminished in all patients. These data show that afterload reduction in patients with severe aortic regurgitation may improve hemodynamics by reducing aortic regurgitation or by improving ventricular pump function. The lowered total stroke work, reduced ventricular size and improved forward cardiac index imply that afterload reduction may benefit left ventricular failure and delay progressive ventricular dysfunction in patients with aortic regurgitation.
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PMID:Hemodynamic consequences of afterload reduction in patients with chronic aortic regurgitation. 126 Sep 93

Nitroprusside was infused intravenously (20, 40, 80 and 200 mug/min) in nine patients with pulmonary hypertension due to mitral stenosis (group I), nine with precapillary pulmonary hypertension associated with primary lung disease (group II) and nine with normal pulmonary-arterial pressures (group III). The mean pulmonary-arterial pressure was markedly reduced at a rate of 20 mug/min in group I and II, while higher doses were necessary in group III to produce a similar effect. Mean arterial pressure was decreased in all three groups and was dose-related. Heart rate rose, stroke volume fell during nitroprusside administration, while cardiac output remained unchanged. Pulmonary vascular resistance was reduced on 20 mug/min in group I, but only on 200 mug/min or more in group II, and unchanged at all dosages in group III. Peripheral vascular resistance declined in all three groups on nitroprusside infusion, which is apparently of value in the short-term lowering of pulmonary hypertension.
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PMID:[Lowering of pulmonary-arterial pressure with nitroprusside in mitral stenosis and cor pulmonale (author's transl)]. 126 32

The effects of unloading a depressed heart were assessed in terms of optimal coupling between the ventricle and arterial system. To assess the effects of preload on ventricular load coupling, preload was reduced with a lower body negative pressure of -20 mm Hg. Nitroprusside was used to evaluate the effects of afterload on the coupling under the condition that preload reduction was comparable to that with lower body negative pressure. In 13 patients with heart failure (ejection fraction 32 +/- 3%, mean +/- SE), direct arterial pressure was simultaneously recorded with the left ventricular echocardiogram as the pressure was elevated by phenylephrine. Left ventricular contractile properties were defined by the slope (Ees) of the end-systolic pressure-volume relation. The effective arterial elastance (Ea) was expressed by the slope of the end-systolic pressure-stroke volume relation. Left ventricular external work, end-systolic potential energy and work efficiency, defined as external work per pressure volume area (external work + potential energy), were determined. Baseline ventricular load coupling in these patients was characterized by an increase in the ratio of arterial elastance to ventricular elastance (Ea/Ees) (1.96 +/- 0.31). This ratio decreased significantly, to 1.45 +/- 0.22, with nitroprusside, and increased to 2.37 +/- 0.34 with lower body negative pressure. Therefore, end-systolic potential energy was decreased by nitroprusside but was unaltered by lower body negative pressure while external work was comparably decreased by both manipulations, indicating that work efficiency was significantly augmented with nitroprusside but declined with lower body negative pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventricular load optimization by unloading therapy in patients with heart failure. 198 27

The authors investigated the cardiovascular effects of low doses of nitroprusside, dobutamine, and phenylephrine and a beta-adrenergic blocking dose of propranolol in conscious, healthy horses with and without prior atropine administration. A parasympathetic blocking dose of atropine produced significant increases in heart rate and arterial pressures, and decreased stroke volume, ejection fraction, pulse pressure, and right-ventricular end-diastolic pressure and volume. Cardiac output was not changed by atropine administration. Nitroprusside reduced arterial pressures to a greater extent in atropinized horses but increased heart rate in both atropinized and non-atropinized horses. Dobutamine increased mean arterial pressure in both non-atropinized and atropinized horses but increased heart rate, diastolic arterial pressure, and systemic vascular resistance only in atropinized horses. Propranolol did not affect any of the hemodynamic variables that were measured. Phenylephrine, in the presence of beta-adrenergic blockade, increased mean arterial pressure and reduced cardiac output. This study showed that low doses of nitroprusside, dobutamine, and phenylephrine produce significant hemodynamic effects in conscious, healthy horses and that these effects are modified by prevailing parasympathetic tone.
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PMID:Hemodynamic effects of atropine, dobutamine, nitroprusside, phenylephrine, and propranolol in conscious horses. 206 69


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