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

Thrombosis of the great vessels, and especially of the aorta, is rare in neonates. We report a case with thrombosis of the ascending aorta, aortic arch, brachiocephalic trunk and subclavian artery. Clinically, severe heart failure occurred on the 1st day of life and the diagnosis was confirmed by echocardiography and cardiac catheterization, including angiocardiography. Left ventricular function was found to be extremely depressed. An infusion with prostaglandin E1 was initiated in order to improve the systemic circulation by dilating the arterial duct. The infant died of neurological complications prior to surgery.
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PMID:Complete thrombotic obliteration of the ascending aorta and the aortic arch as a cause of acute heart failure in a newborn. 319 27

In neonates with isolated coarctation of the aorta presenting with acute neonatal heart failure refractory to classical treatment, emergency surgery is associated with a 30% death-rate. We rather suggest to add to treatment a perfusion of prostaglandin E1 in order to dilate the ductus arteriosus and thereby the aortic isthmus. This was performed successfully in 9 of 12 neonates aged 5 to 16 days: coarctation was relieved and heart failure disappeared. As soon as the left ventricle became hyperkinetic again (2 to 6 days later), prostaglandin was discontinued. Coarctation reappeared with either chronic heart failure (3 cases) or severe arterial hypertension (5 cases). Eventually one child recovered without surgery and the other 11 were operated on at an average age of 24 days, with only one death.
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PMID:[Treatment by prostaglandin E1 of isolated coarctations in newborn infants with acute cardiac failure]. 356 40

Seventeen neonates received an intravenous infusion of prostaglandin E1 for an average of 39 days (range 8 to 104). Seven (group 1) had transposition of the great arteries with no ventricular septal defect or a small one; eight (group 2) had ductus-dependent pulmonary flow (pulmonary atresia or stenosis in six and tricuspid atresia in two); and two (group 3) had aortic coarctation, one with no ventricular septal defect, the other with ventricular septal defect, isthmus hypoplasia and descending aortic flow supplied mainly by the ductus. An increase in the arterial partial pressure of oxygen (PO2) was seen in groups 1 and 2. Six patients from group 1 and two from group 2 developed heart failure; cortical hyperostosis of long bones was seen in three patients from group 1 and three from group 2; one from group 1 had refractory diarrhea. Other side effects seen at the beginning improved as the rate of infusion diminished. In group 3, the patient with complex coarctation had a decrease in blood pressure in the arms, an increase in pressure in the legs and restoration of renal function; in the patient with no ventricular septal defect, heart failure worsened during therapy. Histologic changes seen in three ductus were attributed to the closing process. When delaying surgery in selected ill infants with heart defects is deemed advantageous, long-term infusions of prostaglandin E1 are feasible.
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PMID:Long-term prostaglandin E1 therapy in congenital heart defects. 653 55

An elderly woman with a history of cardiac failure treated with digitalis had both abdominal pain and dehydration. Parenteral fluid and electrolyte support failed to alleviate abdominal pain. Superior mesenteric arteriography combined with "spillover" method of estimating blood flow revealed an intestinal nonocclusive ischemic state which was treated successfully with 44-hour intraarterial infusion of prostaglandin E1. Laparotomy performed during the drug infusion revealed viable intestine.
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PMID:Nonocclusive intestinal ischemia treated with intraarterial infusion of prostaglandin E1. 720 Aug 29

Prostaglandin E1 (PGE1) has been used prior to operation in 28 neonates (0 to 30 days) with congenital heart disease (CHD). The patients were divided into two groups. Group I consisted of 19 neonates with CHD resulting in marked cyanosis. Thirteen patients had pulmonary atresia, three had tetralogy of Fallot, and three had complex defects with pulmonary stenosis. All patients were markedly hypoxemic. The average oxygen saturation was 41%. PGE1 infusion, 0.1 mcg/kg/min, was successful in 17 of 19 patients, as it resulted in an increase in oxygen saturation from 41% to 79%, average increase 38%. Two patients did not respond to PGE1 infusion. One was 30 days of age and the other had no patient ductus arteriosus. All of the patients underwent a palliative shunt procedure. There were three hospital deaths in this group. No patient died of hypoxemia. Group II consisted of nine patients whose CHD was predominantly that of aortic obstructive disease with clinical manifestations of cardiac failure, hypoperfusion, and acidemia. Six of these patients had complicated coarctation of the aorta. Three patients had interruption of the aortic arch. The pH of these patients averaged 7.19. PGE1 infusion resulted in improvement of the pH to average of 7.37, improvement of congestive heart failure, and reappearance of femoral pulses. One patient failed to respond. All patients in Group II underwent operation. There were three hospital deaths in this group. No patient died intraoperatively. PGE1 infusion is a valuable aid to surgical treatment of desperately ill neonates with both cyanotic and acyanotic forms of CHD.
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PMID:Prostaglandin E1 as an adjunct to emergency cardiac operation in neonates. 745 32

To investigate the impact of staged therapy for advanced heart failure on therapeutic endpoints, 236 consecutive patients (coronary artery disease/dilated cardiomyopathy in 61/175 patients, left ventricular ejection fraction 14% +/- 5%, New York Heart Association Class II/III/IV in 102/79/55 patients, respectively) with advanced heart failure were prospectively followed. One hundred thirty-seven patients enrolled from January 1989 to December 1991 were treated conventionally with digoxin, furosemide, and low dose angiotension converting enzyme (ACE) inhibition. Patients refractory to this therapy underwent urgent heart transplantation. Ninety-nine patients enrolled from January 1992 to August 1993 underwent staged therapy: stage 1: maximal tolerated ACE inhibition; stage 2: therapy with PGE1 for pre- and afterload reduction to achieve hemodynamic stabilization; or stage 3: refractory patients bridged to heart transplantation with continuous outpatient dobutamine. Sudden death was defined as death within 1 hour of symptoms if heart failure symptoms remained stable over the previous 7 days. Conventionally treated patients were followed for 10 +/- 9 months; patients who underwent staged therapy for 9 +/- 5 months. In the group of patients that underwent standard therapy, 39 of 137 (28%) patients died: 5 (13%) deaths occurred suddenly, and death due to progressive pump failure occurred in the remaining 34 (87%) patients. In the group of patients that underwent staged therapy, 25 of 99 (25%) patients died: 13 (52%) deaths occurred suddenly, and 12 (48%) deaths occurred due to progressive pump failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sudden death and staged therapy for hemodynamic stabilization in patients enrolled in a heart transplantation program. 772 90

In this work we analyze the renal and systemic factors involved in the sodium retention in two conditions: in extracellular volume depletion and in edema forming states, particularly liver cirrhosis with ascitis. In this paper we accept that the volume loss of body fluids stimulates the "effective arterial blood volume" (VAE). This term results from a decrease in the arterial blood volume secondary to a fall in cardiac output or a peripheral arterial vasodilatation. The reduction in the VAE stimulates: the high pressure baroreceptors (carotid sinus and aortic arch); the intrarrenal mechanisms, such as the yuxtaglomerular apparatus and the renin angiotensin aldosterone system; the sympathetic adrenergic system; the non osmotic release of antidiuretic hormone; prostaglandins (PGE1, Tromboxane) and endothelin; and inhibits the atrial natriuretic peptide. We also describe the sodium transport mechanisms along the nephron during physiological conditions and after volume depletion, and in edema formation states, specially hepatic cirrhosis with ascitis. We speculate that the intrarenal mechanisms are more important and persistent than the systemic mechanisms. It is possible that the sodium retention of these states might be the result of direct stimuli of the tubular sodium transport mechanisms in the different segments of the nephron, mediated by the co and counter transports, ATPase activity or by the second messengers cyclic AMP and cyclic GMP. The clonation and structural characterization of the different sodium transports may help us to establish, more precisely, the intracellular tubular mechanisms responsible for the tendency of the body to retain sodium. The amount of information generated in the future may help us to demonstrate, with more precision, the mechanisms responsible for the sodium retention and excretion in normal and pathological conditions, particularly the edema forming states such as cardiac failure, nephrotic syndrome and hepatic cirrhosis with ascitis.
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PMID:[Renal and extra-renal mechanisms of sodium and water retention in cirrhosis with ascites]. 777 18

Paediatric cardiac transplantation (pHTX) has gained widespread acceptance as a therapy in end-stage myocardial failure and some forms of congenital heart disease, particularly hypoplastic left heart syndrome (HLHS). The major problems to the anaesthesiologist in these patients are induction of anaesthesia in infants with HLHS and treatment of pulmonary hypertension in the early post-bypass period. PATIENTS AND METHODS. Anaesthesia for pHTX was performed in 15 children < 1 year of age (4-237 days); 12 suffered from HLHS, 2 from endocardial fibroelastosis, and 1 from dilatative cardiomyopathy. Induction of anaesthesia in patients with HLHS IS a challenge to the anaesthesiologist, as he has to maintain the delicate balance between pulmonary and systemic blood flow. Anaesthesia was induced with fentanyl (10-15 micrograms/kg) and pancuronium (0.2-0.4 mg/kg) and maintained with fentanyl (total dosage 70-100 micrograms/kg). Modification of ventilatory parameters such as FiO2, PaCO2, and airway pressure (PEEP, I:E ratio) was used to influence systemic and pulmonary blood distribution in the pre-bypass period according to changes in haemodynamics (target: O2 saturation approximately 75%-80%, PaCO2 45-50 mmHg). Treatment of pulmonary hypertension in the weaning and early post-bypass period consisted of respiratory (PaCO2 < 30 mmHg) and metabolic alkalinisation (pH 7.45-7.55, BE > +3 mmol/l), the use of prostaglandin E1 (3-6-12 micrograms/kg.h), and the phosphodiesterase inhibitor enoximone (10-15 micrograms/kg.min). Additional positive inotropic support was achieved with dobutamine (5-10 micrograms/kg.min), adrenaline (0.1-0.5 micrograms/kg.min), and/or orciprenaline (0.1-0.2 micrograms/kg.min) and calcium chloride (25-100 mg/kg). RESULTS. Two children died intraoperatively and 1 on the 1st postoperative day from overwhelming pulmonary vascular resistance and right ventricular failure. Three children died between 3 and 4 weeks postoperatively, 1 from cytomegalovirus infection, 1 from sepsis, and 1 from acute rejection. Nine patients survived and are well up to 5.5 years after transplantation. CONCLUSION. Pulmonary hypertension in the weaning and early post-bypass period is the main anaesthesiological problem of pHTX, particularly in children with HLHS. A polypragmatic approach to this problem consisting of alkalinisation, pulmonary vasodilatation, and inotropic support is presented and seems to be effective. Further improvements in concepts of pHTX are limited by the lack of donor organs. Though the experience with pHTX in neonates and infants is growing slowly, it might be a routine procedure from the anaesthesiological point of view within a few years in some selected centres.
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PMID:[Anesthesia for heart transplantation in newborn and suckling infants. Special aspects of the hypoplastic left heart syndrome]. 778 53

We recently encountered a patient with mitral insufficiency, accompanied by PN (polyarteritis nodosa), who developed a cardiac rupture immediately after a mitral valve replacement. The patient was a 60-year-old woman. After she was diagnosed as having mitral stenosis and insufficiency in 1968, the patient developed congestive heart failure and underwent repeated hospital admissions and discharges. In 1989, she was diagnosed as having PN and began to receive a high-dose steroid therapy (prednisolone; total dose 5245 mg). Because of transient brain ischemia and exacerbation of the symptoms of heart failure, the patient underwent mitral valve replacement on December 19, 1991. For anesthesia, oxygen, fentanyl, midazolam and vecuronium were administered. During surgery, catecholamine, nitroglycerin and prostaglandin E1 were continuously infused intravenously. The patient was weaned smoothly from the cardiopulmonary bypass. The operation was completed in about 6 hours. Her postoperative course was satisfactory until she suddenly developed left ventricular rupture and died 6 hours after surgery. The rupture seemed to be attributable to a weakening of the myocardial wall following long-term, high-dose steroid therapy, and to myocardial degeneration caused by PN-associated necrotizing vasculitis of myocardial arterioles.
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PMID:[Anesthetic management of a patient with polyarteritis nodosa who suddenly developed cardiac rupture after valve replacement]. 790 39

A 61-year-old male with coma and undiagnosed dilated cardiomyopathy received emergency cerebral aneurysm surgery. Anesthesia was induced with thiamylal, fentanyl and vecuronium and maintained with 66% N2O and 1.0% isoflurane. Five hundred ml of 20% mannitol was infused in 30 min. At the end of the infusion, hypotension occurred. Immediately after the injection of ephedrine, acute brain swelling was observed. The operation was switched to external decompression. Post-operative echocardiography revealed the presence of dilated cardiomyopathy (DCM). The ejection fraction was 34%. Two weeks later, the second operation was scheduled. The anesthesia was induced with fentanyl, midazolam and vecuronium and maintained with N2O and 0.7% isoflurane. Nitroglycerine, lidocaine, PGE1, dopamine and dobutamine were infused throughout the operation. Five hundred ml of 20% mannitol was infused in 60 min. There were no considerable hemodynamic changes and no episode of brain expansion during operation. We conclude that the rapid infusion of mannitol can trigger acute cardiac failure and brain edema in patients with DCM.
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PMID:[Acute brain expansion during emergency neck clipping surgery for cerebral aneurysms in a patient with dilated cardiomyopathy]. 875 74


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