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

The effect of hypoxemia on total vascular compliance was studied in anesthetized dogs using a venous bypass technique. Cardiac output was kept constant with an extracorporeal pump and respiration controlled to maintain normocapnia. When nitrogen was added to the respired gas to produce an arterial PO2 approximately 45 mm Hg, total vascular compliance was rapidly and significantly reduced to 0.93 ml (mm Hg)(-1) kg(-1) with incomplete recovery to baseline values of 1.30 plus or minus 0.06 ml (mm Hg)(-1) kg(-1) during subsequent ventilation with 100% oxygen. Acute heart failure was induced by gradual aortic constriction. Ventilation with 100% oxygen failed to prevent a gradual reduction in total vascular compliance to 0.86 ml (mm Hg)(-1) kg(-1) from a baseline value of 1.23 plus or minus 0.06 ml (mm Hg)(-1) kg(-1). Ventilation with 100% oxygen following the reduction in vascular compliance during acute heart failure also failed to significantly alter this parameter. Thus, improvement of arterial oxygen tension in patients with acute heart failure would be beneficial in providing greater oxygen delivery to the tissues without abolishing a compensatory mechanism of reduced vascular compliance which attempts to maintain a cardiac filling gradient of pressure.
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PMID:Oxygen and effective vasular compliance in acute heart failure. 23 27

Myocardial protection, in two parallel series of 100 consecutive valvular patients operated upon between June 1972 and July 1973 in Broussais Hospital, was afforded in two different ways: one withh hypothermic ischemia (H.I.) as it was advocated by N. Shumway, the other with coronary perfusion (C.P.) of a beating heart with consecutive ischemic periods limited to 20 minutes. Three parameters were used to evaluate the quality of protection: death with primary cardiogenic shock, post-operative myocardial infarction and acute cardiac insufficiency making it necessary to use post-operative inotropic support. Death was 1% (H.I.) and 5% (C.P.). Infarctions were 5% (H.I.) and 8% (C.P.). Acute cardiac insufficiency was: with cardiogenic shock 0% (H.I.) and 4% (C.P.), without cardiogenic shock 8% (H.I.) and 2% (C.P.). Peculiar aspects of myocardial infarction in each series are analyzed, and apparent absence of correlation between aortic cross-clamp time and ischemic complications is discussed. A "myocardial intrinsic factor" seems to be part of each valvular group and appears also to be an important factor in producing ischemic complications.
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PMID:Selective cardiac hypothermia versus coronary perfusion. A study of ischemic complications in two series of 100 consecutive valvular patients. 115 Jul 30

General considerations in planning therapy of heart failure include identification of the cause, rapidity of onset, and the age of the patient. Neonates and young infants with acute onset heart failure frequently develop acidaemia, respiratory compromise or failure, and metabolic derangements such as hypoglycaemia, hypocalcaemia or hypomagnesaemia. These complications require early recognition and urgent therapy. The diagnosis of heart failure in neonates with ductal dependent congenital cardiac lesions (such as coarctation of the aorta, hypoplastic left heart syndrome or pulmonary valve atresia) allows the early institution of alprostadil (prostaglandin E1) therapy to maintain patency of the ductus arteriosus, which stabilises these infants before surgical therapy. Classic therapy for infants with heart failure due to a large left-to-right shunt consists of salt restriction, diuretics and digoxin. If this treatment is inadequate an angiotensin converting enzyme (ACE) inhibitor (e.g. captopril) is added to therapy. The question then arises whether captopril and diuretics should be the initial therapy and digoxin added if this treatment fails. Acute heart failure may occur in the immediate postoperative period after cardiac surgery or may complicate acute overwhelming infections. Therapy consists of volume loading, vasodilator or inotropic agents. Heart failure due to various forms of chronic dilated cardiomyopathy usually responds to treatment with salt restriction, diuretics, digoxin and captopril. Acute deterioration requires treatment with vasodilators and/or inotropic agents. Heart failure in fetuses may occur from sustained supraventricular tachyarrhythmias, and may respond to treatment of the mother with antiarrhythmic agents such as digoxin or procainamide.
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PMID:New drug approaches to the treatment of heart failure in infants and children. 218 7

Complications and causes of death in patients with transplanted heart were analyzed in various intervals after operation. They comprised early deaths in the first week, short-time survival until one year, and long-time survival over one year. Acute heart failure of varied nature prevailed in early deaths as well as in long-time survival. In short-time survival, there were different causes of death in addition to heart failure.
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PMID:[Complications and causes of death in heart transplantation]. 220 29

Two patients suffering from dilated Cardiomyopathy (CMP) had to undergo orthotopic heart transplantation (HTX). In both cases, the postoperative period was without any complications. The immunosuppression consisted of Cyclosporin-A and Azathioprine including a one week prophylactic treatment with Antithymocyte Globuline (ATG). Four months postoperatively, they developed clinical signs of heart failure. The endomyocardial biopsies showed rejection at stage I according to Billingham's grading plus a fine interstitial fibrosis. Therefore, the Cyclosporin treatment was suspended and replaced by conventional immunosuppression consisting of Prednisolone and Azathioprine. Acute heart failure was managed by catecholamines in combination with aggressive diuretic therapy. After three weeks, both patients recovered. 12 weeks later, one died because of an acute rejection episode. The other is in good condition, with conventional immunosuppression at the present time. A vascular process caused by Cyclosporin-A as the pathogenic mechanism is considered. The absence of rejection signs in the biopsies as well as the remarkable improvement of heart failure after withdrawal of Cyclosporin-A support this possibility.
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PMID:Cyclosporin-A induced heart failure after orthotopic heart transplantation. 244 Jan 40

42 patients with isolated mitral valve defect were divided into two groups: without cardiac complications -- and with acute myogenic heart failure, after implantation of a mitral valve prosthesis. In the first postoperative hours, a decrease in cardiac output and pulmonary hypertension were observed in both groups. By the end of the 1st postoperative day, cardiac output reached in both groups the initial level, but in patients of group 2 only thanks to catecholamine administration. The poor functional state of the heart before surgery is consequently the main cause of the fact that surgical intervention is not immediately followed by normalization of haemodynamics. Acute heart failure occurs in the early postoperative period in patients with an extremely impaired left ventricular pump function and with depleted myocardial reserves. In these patients, special attention must be given during surgery to myocardial protection.
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PMID:Early haemodynamic effects of mitral valve prosthesis in patients with acquired heart disease. 648

A 6-year-old girl suffering from idiopathic hypoparathyroidism and being treated with anticonvulsive drugs developed acute heart failure due to hypocalcemia. Acute heart failure is a rare complication of hypocalcemia. The probable role of anticonvulsive drugs in provoking this complication is discussed.
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PMID:Idiopathic hypoparathyroidism and anticonvulsive treatment as possible cause for cardiac failure. 744 Feb 33

Low heart stroke volume syndrome is clinically manifested with hypoperfusion of all body systems. Inotropic or mechanical support is applied. Acute heart failure is one of the most important complications after open heart surgery. Catecholamines have been up to non considered as a therapy of choice for the acute heart failure. Effectiveness of catecholamines could be limited with some side effects. Phosphodiesterase inhibitors promise a new therapeutic approach. PDE III primary act through phosphodiesterase inhibition which leads to a rise of aAPM levels. Thus they show positive inotropic and lusitropic effects, which could be monitored by occlusive pulmonary capillary pressure values. Amrinone is obviously superior to inotropic catecholamines.
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PMID:[Hemodynamic effects of amrinone, dobutamine and dopamine in the cardiac low output syndrome following open-heart surgery]. 864 47

The relationship between stressed and total blood volume, total vascular capacitance, central blood volume, cardiac output (CO), and pulmonary capillary wedge pressure (Ppcw) was investigated in pacing-induced acute and chronic heart failure. Acute heart failure was induced in anesthetized splenectomized dogs by a volume load (20 mL/kg over 10 min) during rapid right ventricular pacing at 250 beats/min (RRVP) for 60 min. Chronic heart failure was induced by continuous RRVP for 2-6 weeks (average 24 +/- 2 days). Total vascular compliance and capacitance were calculated from the mean circulatory filling pressure (Pmcf) during transient circulatory arrest after acetylcholine at three different circulating volumes. Stressed blood volume was calculated as a product of compliance and Pmcf, with the total blood volume measured by a dye dilution. Central blood volume (CBV) and CO were measured by thermodilution. Central (heart and lung) vascular capacitance was estimated from the plot of Ppcw against CBV. Acute volume loading without RRVP increased capacitance and CO, whereas after volume loading with RRVP, capacitance and CO were unaltered from baseline. Chronic RRVP reduced capacitance and CO. All interventions, volume +/- RRVP or chronic RRVP, increased stressed and central blood volumes and Ppcw. Acute or chronic RRVP reduced central vascular capacitance. Cardiac output was increased when stressed and unstressed blood volumes increased proportionately as during volume loading alone. When CO was reduced and Ppcw increased, as during chronic RRVP or acute RRVP plus a volume load, stressed blood volume was increased and unstressed blood volume was decreased. Thus, interventions that reduced CO and increased Ppcw also increased stressed and reduced unstressed blood volume and total vascular capacitance.
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PMID:Vascular capacitance and cardiac output in pacing-induced canine models of acute and chronic heart failure. 878 19

Acute cardiac insufficiency is often the result of acute or chronic overloading of the heart due to arterial hypertension, coronary heart disease and/or a reduction in ventricular muscle mass following myocardial infarction. Whenever possible, treatment should be causal (e.g. treatment of hypertension, operative correction of valvular disease). While the incidence of heart failure continues to increase, morbidity and mortality associated with the disease process have remained essentially unchanged. About 30% of the patients die within the first 12 months. The prognosis and outcome of heart failure patients strongly correlate with markers of neuroendocrine activation. While numerous drugs are capable of improving hemodynamics at rest or physical performance, they fall to prolong survival. It is hoped, that new pathophysiological information might lead to the development of new, effective therapeutic approaches.
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PMID:[Therapy of heart failure. I. Definition, pathophysiology, therapy of acute heart failure]. 928 Jul 46


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