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

The pericardium is largely responsible for displacement of the left ventricular diastolic pressure-volume curve observed after acute volume loading in dogs. Likewise the pericardium has been considered likely to play a role in displacement of the curve in patients with acute cardiac failure and in shifts following manipulation of afterload. This study was designed to examine the influence of the pericardium on the diastolic pressure-volume relation of the left ventricle when volume load is more sustained, a setting relevant to observations made in patients with heart failure. We measured left ventricular pressure and volume in six conscious dogs with sustained volume overload (mean left ventricular end-diastolic pressure 21 mm Hg, left ventricular end-diastolic volume 149% of the upper limit of normal for our laboratory) produced by aortocaval shunt created 7 to 29 days earlier. Simultaneous left ventriculograms and pressures were obtained before and during nitroprusside infusion with the pericardium intact and in four dogs the studies were repeated 7 to 15 days after pericardiectomy. In all six dogs with intact pericardium, nitroprusside displaced the entire pressure-volume curve downward whereas after pericardiectomy, the pressure-volume data points obtained before and during nitroprusside infusion fell on a single curve. These results were similar to those previously reported for acute volume overload. Nitroprusside did not alter the time course of left ventricular pressure fall during the isovolumic period of diastole either before pericardiectomy (28.8 +/- 10.2 sec,-1, 28.4 +/- 11.9 sec-1) or after (28.8 +/- 6.7 sec-1, 26.1 +/- 7.2 sec-1). These data indicate that in dogs subjected to volume overload sustained for periods of up to 29 days, the pericardium affects the left ventricular diastolic pressure-volume curve and contributes to the elevation of left ventricular filling pressure through upward displacement of this curve.
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PMID:Influence of the pericardium on left ventricular diastolic pressure-volume curves in dogs with sustained volume overload. 685 47

Despite the high incidence of sudden death in pregnant patients with primary pulmonary hypertension (PPH) and heart failure, no data are available that thoroughly elucidate the peripartum hemodynamic alterations occurring in these patients. The present report describes the clinical course of a pregnant patient with PPH and provides data regarding peripartum hemodynamic alterations. Hemodynamic parameters were stable during labor and delivery, but pulmonary vascular resistance rose gradually while cardiac output fell after parturition. Dobutamine caused a modest but unsustained increase in cardiac output. Nitroprusside produced a significant sustained augmentation of cardiac output from 3.5 to 5.0 liters/min due to reduction of systemic and pulmonary vascular resistances, and permitted restoration of hemodynamic stability and resolution of heart failure. The authors believe that pregnant patients with PPH and severe heart failure in whom abortion is not possible should have complete hemodynamic monitoring during parturition and for several days thereafter. Segmental epidural anesthesia and lateral positioning of the patient minimize hemodynamic alterations during labor and delivery. Nitroprusside and dobutamine may be effective for treatment of congestive heart failure.
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PMID:Peripartum heart failure due to primary pulmonary hypertension. 687 14

The hemodynamic effects of acute intravenous administration of nitroprusside, dobutamine, enalaprilat, and digoxin was investigated in a canine model of chronic heart failure (CHF) produced by multiple sequential intracoronary microembolizations. Dobutamine (4 micrograms/kg/min) increased cardiac output (2.4 +/- 0.1 vs. 4.0 +/- 0.4 l/min; p < .001) and LV ejection fraction (LVEF; 26 +/- 1 vs. 30 +/- 4%; p < .01), and decreased systemic vascular resistance (SVR; 3620 +/- 170 vs. 2470 +/- 190 dynes sec cm-5; p < .001). Nitroprusside (3 micrograms/kg/min) acted as a venodilator; it decreased pulmonary artery wedge pressure (16 +/- 1 vs. 13 +/- 1 mmHg; p < .01) and SVR (3730 +/- 440 vs. 3210 +/- 280 dynes sec cm-5; NS) but had no effect on cardiac output. Enalaprilat (1.875 mg) produced a significant increase of cardiac output (3.0 +/- 0.5 vs. 3.8 +/- 0.5 l/min; p < .001) and LVEF (22 +/- 1 vs. 30 +/- 1%; p < .01), and decreased SVR (3280 +/- 400 vs. 2450 +/- 250 dynes sec cm-5; p < .01). Intravenous digoxin at a cumulative dose of 0.75 mg increased LVEF (23 +/- 2 vs. 31 +/- 2%; p < .01) but had no effect on SVR. These data indicate that this canine model of CHF responds to acute pharmacologic intervention in a manner comparable to that seen in patients with CHF. Accordingly, this model may be a useful tool for the preclinical evaluation of new drugs targeted toward the treatment of CHF and for investigating the mechanisms of action of drugs currently used for the treatment of this disease state.
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PMID:Hemodynamic response of a canine model of chronic heart failure to intravenous dobutamine, nitroprusside, enalaprilat, and digoxin. 839 76

Baroreceptor-heart rate reflex sensitivity is decreased in congestive heart failure. The reflex control of heart rate and sympathetic nerve activity in rats with chronic volume overload, an established model for moderate heart failure, is still unknown. Therefore, we investigated the regulation of humoral and neuronal sympathetic activity and the baroreflex control of heart rate and sympathetic nerve activity in conscious, unrestrained rats with aortocaval shunt. Rats with aortocaval shunts had larger hearts (388 +/- 11 vs. 277 +/- 4 mg/100 g body wt), elevated central venous pressures (14 +/- 4 vs. 4 +/- 3 mmHg), and higher atrial natriuretic peptide plasma levels (87 +/- 16 vs. 25 +/- 3 pmol/l) than controls but had similar systemic blood pressure and heart rate values. Plasma epinephrine (0.63 +/- 0.16 vs. 0.21 +/- 0.08 pmol/l, P < 0.05) and norepinephrine concentrations (0.27 +/- 0.03 vs. 0.16 +/- 0.02 pmol/l, P < 0.05) were elevated in shunted rats compared with controls. Nitroprusside-induced hypotension led to a significantly greater increase in efferent splanchnic sympathetic nerve activity in shunted rats than in controls (0.9 +/- 0.1 vs. 2.6 +/- 0.6 microV, P < 0.05), whereas the heart rate responses were not different between the groups. These results indicate that the regulation of the autonomic nervous system is altered in chronically volume-overloaded rats. The arterial baroreflex control of efferent splanchnic sympathetic nerve activity was dissociated from the control of heart rate. Therefore, analysis of the activation of sympathetic nervous system assessed by direct measurements of efferent sympathetic nerve activity appears to be more sensitive for the detection of altered autonomic nervous system function than the analysis of baroreflex control of heart rate.
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PMID:Effect of chronic volume overload on baroreflex control of heart rate and sympathetic nerve activity. 943 90

In children with large left-to-right shunts secondary to congenital heart defects the imbalance between the pulmonary and systemic perfusion may lead to circulatory congestion with clinical signs similar to those of heart failure. The circulatory function in this state was evaluated by using the invasive measurements performed during cardiac catheterisations in n = 64 young patients with ventricular septal defect (n = 56) or complete atrioventricular septal defect (n = 8) aging 0.1-23.7 years (median 1.1 years). The mean shunt ratio was Qp/Qs = 2.4 (range 1-8). With increasing shunt ratio the pulmonary perfusion raised (r = 0.84), but the systemic output dropped significantly (r = -0.77) while the total cardiac output (Qp + Qs) increased slightly not exceeding 141/min/m2. In infants, the systemic hypoperfusion affects the hemoglobin content: Hb = 14.9-1.01 x Qs, r = 0.63, p < 0.01. This may be due to the diminished oxygen extraction reserve of 46%. With dropping systemic output, the vascular resistance increases and the mean aortic pressure (MAP) remains normal. The actual pressure values layed near to the curve of the normal aortic pressure calculated as MAP = Qs x Rs. This pressure-flow-resistance diagram was used to interpret the effects of vasodilators established by 7 studies: ACE-Inhibitors, Hydralazine, and Na-Nitroprusside reduce the vascular resistance effectively but induce hypotension, because the systemic output fails to increase. In the chronic circulatory congestion secondary to a large intracardiac left-to-right shunt the pulmonary perfusion increases with the shunt ratio but the systemic output decreases and the total cardiac output is limited to a maximum of 141/min/m2. In this state vasodilators cause systemic hypotension thus offering no acceptable therapeutic option.
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PMID:[Circulatory failure in children with left-to-right shunt in the framework of congenital heart defects: pathophysiology and therapeutic results]. 1081 53

Acute heart failure is a rapidly growing clinical problem in the United States. There are few randomized clinical trials to guide treatment; however, important observational data are now emerging from the Acute Decompensated Heart Failure National Registry regarding the demographics and treatment of these patients. Management consists largely of identification and treatment of precipitating factors, correction of comorbid conditions, and IV diuretics and vasodilators. Nitroprusside is a valuable treatment, but its use is usually restricted to patients in the intensive care unit who are undergoing hemodynamic monitoring. Nesiritide is being increasingly employed. Specialized strategies such as dialysis, continuous venous-venous hemodialysis, extra-corporeal membrane oxygenator, left ventricular assist device, and heart transplantation are employed in a small subset of patients. Although recovery is the rule, the in-hospital mortality for acute heart failure is high and the readmission rate is very high. Prevention of acute heart failure by avoiding factors known to precipitate decompensation remains the most cost-effective strategy.
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PMID:Acute heart failure: patient management of a growing epidemic. 1553 70

Most patients with acute heart failure present with increased left ventricular filling pressure and high or normal blood pressure; only a minority present with cardiogenic shock. In this context, therapy with vasodilators in the acute setting can improve both hemodynamics and symptoms. Vasodilators are usually given in conjunction with diuretics, although much of the acute effect of loop diuretics may be due to venodilation. Currently available agents include nitroglycerin, nitroprusside, and nesiritide. Nitroglycerin relieves pulmonary congestion primarily through direct venodilation, but may dilate coronary arteries and increase collateral blood flow at higher doses, an effect desirable in patients with ischemia. Tachyphylaxis may develop, necessitating incremental dosing. The major adverse effects of nitrates are hypotension and headache. Nitroprusside is a balanced arterial and venous vasodilator with a very short half-life, facilitating rapid titration. Afterload reduction lowers blood pressure and can increase stroke volume. The major complications of nitroprusside therapy are hypotension, and toxicity from accumulation of cyanide or thiocyanate, usually in patients with renal insufficiency treated for more than 24 h. Nesiritide, a recombinant form of human B-type natriuretic peptide (BNP), is a venous and arterial vasodilator that may also potentiate the effect of concomitant diuretics. Hypotension is the most common side effect. In addition, meta-analyses have suggested that nesiritide may worsen renal function and decrease survival at 30 days compared to conventional therapies. Resolution of these concerns awaits completion of appropriately powered prospective clinical trials. Angiotensin-converting enzyme (ACE) inhibitors have vasodilatory effects, but intravenous infusion of enalapril within 24 h of ischemic chest pain is not recommended. Oral ACE inhibition may be used to reduce afterload in other settings if blood pressure permits. Use of calcium antagonists in acute heart failure is not recommended.
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PMID:Vasodilators in acute heart failure. 1744 37

OPINION STATEMENT: Treatment goals of acute decompensated heart failure are to decrease congestion, afterload, and neurohormonal activation in order to improve hemodynamics and symptoms and, perhaps, reduce in-hospital events, re-hospitalizations, and mortality while avoiding toxicities of therapy such as hypotension, arrhythmias, and renal dysfunction. Relief of congestion through intravenous loop diuretics is a mainstay of therapy. In cases where diuretics are not effective, ultrafiltration may be used to achieve euvolemia. Beta-blockers should be continued or reduced in dose at admission but should not typically be held. In patients with normotensive or hypertensive heart failure, afterload reduction with vasodilators should be instituted at presentation. Choice of a particular agent such as nitroglycerin, nitroprusside, or nesiritide depends on patient characteristics such as presence of ischemia, degree of congestion, and renal function. Nitroprusside may be preferable in patients with congestion and low cardiac output, but with caution in patients with significant hypotension. Intravenous inotropes/inodilators, such as dobutamine and milrinone, should be limited to hypotensive patients with evidence of poor tissue perfusion. Milrinone may be preferable in patients who have significant pulmonary venous hypertension. In patients who do not respond to initial medical therapy and who are candidates for either cardiac transplantation or destination left ventricular assist device, mechanical circulatory support should be considered early, prior to the development of end-organ damage.
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PMID:Update on the Management of Acute Decompensated Heart Failure. 2197 29


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