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

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the newborn lung. 676 Oct 39

Contrast echocardiography was used to detect atrial right-to-left shunts in 20 term infants; there were 10 cyanosed infants who had severe respiratory distress and signs of cardiac failure but no apparent congenital heart disease and 10 noncyanosed infants with no respiratory distress and no signs of cardiac failure who underwent exchange transfusion for hyperbilirubinemia. All of the venous contrast echocardiograms in the cyanosed infants showed an atrial right-to-left shunt with a dense contrast effect in the left atrium and aorta but little in the right ventricle. A sparse effect in the left atrium and a dense one in the right ventricle were recorded in infants with resolving respiratory distress and in three infants from the control group. The other seven infants in the control group showed no right-to-left shunt. Conventional M-mode echocardiograms showed no evidence of congenital heart disease in any of the 20 infants. This contrast echocardiographic technique was useful for demonstrating an atrial right-to-left shunt in cyanosed term infants with neonatal respiratory problems and signs of congestive failure but no apparent congenital heart disease.
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PMID:Atrial right-to-left shunt in infants with respiratory and cardiac distress but without congenital heart disease. Demonstration by contrast echocardiography. 706 22

A case is presented in which a fatal acute respiratory distress syndrome, associated with disseminated intravascular coagulation, developed immediately after the insertion of a peritoneovenous shunt for management of refractory ascites. The absence of left-sided heart failure or fluid overload was established by (a) lack of diuresis from intravenous furosemide; (b) repeatedly normal pulmonary wedge pressures; and (c) autopsy findings. The nature of the toxic effect of this patient's ascites upon the alveolar membrane remains obscure.
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PMID:Acute respiratory distress syndrome after peritoneovenous shunt. 706 30

Two new cases of type B congenital interruption of the aortic arch are described. Both had other congenital cardiovascular malformations as well as absence of the thymus and parathyroids. They were newborn male and female, their parents were young and healthy, admitted in our institution because of feeding difficulty, respiratory distress and cyanosis with signs of heart failure. Both were diagnosed at necropsy. According to the site of the interruption of the aortic arch, three types (A, B and C) of absence of the aortic arch are recognized. In our patients as in the majority of reported cases, the interruption of the aortic arch was associated with patent ductus arteriosus, ventricular septal defect and atrial septal defect, and other cardiovascular anomalies. The association of Di George syndrome with cardiovascular anomalies is commented.
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PMID:[Steidele complex (author's transl)]. 708 60

Nine infants with episodic or continuous chaotic atrial rhythm (CAR) are presented. In addition to 3 or more different P-wave contours, atrial rates greater than 100 per minute, variable PP, RR, and PR intervals, and a discrete isoelectric baseline, findings included atrial rates that varied from a low of 50 to 120 to a high of 140 to 270 per minute, ventricular rates that varied from a low of 40 to 50 to a high of 180 to 270 per minute, and periodic sinus arrest with junctional escape rhythm. Except for the arrhythmia, all had a normal cardiac examination, ECG, chest x-ray film, and echocardiogram. Six infants were otherwise normal; one had an orbital rhabdomyosarcoma; one had neonatal asphyxia; and one had respiratory distress, bronchopulmonary dysplasia, and an intraventricular cerebral hemorrhage. The CAR persisted from 3 days to 20 months; it spontaneously reverted to normal sinus rhythm in 8 infants and persists in 1 infant at age 7 months. Digoxin (4 patients), propranolol hydrochloride (3 patients), quinidine sulfate (2 patients), and lidocaine (1 patient) did not alter the CAR. No patient had heart failure secondary to the CAR, although three also had episodes of sustained atrial tachycardia, which while present caused heart failure. All patients are functioning normally at home and have normal findings on cardiac examination and have normal ECGs at ages 3 to 38 months. Seven are in normal sinus rhythm, one has rare atrial premature contractions, and one has persistent CAR. We conclude that specific treatment was not necessary in these infants with CAR, except in those with associated sustained atrial tachycardia, which itself may cause heart failure.
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PMID:Multifocal or chaotic atrial rhythm: report of nine infants, delineation of clinical course and management, and review of the literature. 711 Oct 53

Seven patients who became pregnant after valve replacement with a Hancock bioprosthesis were followed up during 8 pregnancies. Six had undergone isolated mitral valve replacement, and 1 had mitral and aortic valve replacement. Their age at the time of operation ranged from 14 to 31 years (average 24); delivery occurred 21 to 88 months (average 51.3) after valve replacement. All women were in sinus rhythm at the time of gestation, and administration of oral anticoagulants was avoided in all. No embolic episodes occurred either after operation or during pregnancy, labor, or puerperium. The only major complication during pregnancy was cardiac failure in 1 patient, associated with onset of atrial fibrillation. Four women had vaginal delivery and 3 required cesarean section. All but 1 delivered a normal, healthy baby. One premature infant died soon after birth because of respiratory distress. No maternal or fetal hemorrhagic complications were observed. One patient died 3 months after delivery in severe heart failure caused by diffuse calcification of both mitral and aortic xenografts. Another women underwent successful reoperation soon after the second pregnancy because of calcific stenosis of the mitral porcine valve. It is concluded that (1) bioprosthetic valves can be considered the most suitable devices employed in women of childbearing age because anticoagulants can be avoided, therefore eliminating the risks related to inappropriate administration of oral anticoagulants as well as the hazards associated with the potential teratogenic effect of coumarin drugs; and (2) pregnancy might favor calcification of porcine heterografts, leading to bioprosthetic failure. Until further data are available to support this suspicion, close clinical and echocardiographic follow-up study of these patients is recommended after pregnancy.
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PMID:Pregnancy in patients with a porcine valve bioprosthesis. 713 31

At the Laennec Hospital in Paris, between 1976 and 1980 twenty-two children with Truncus Arteriosus Communis (TAC) underwent primary total repair during the first twenty-four months of life, according to the technique described by McGoon in 1968. All infants operated before the age of three months (group A: 7 patients) were in severe cardiac insufficiency with respiratory distress. Eleven patients (group B) were electively operated between four and nine months of age. Only four patients (group C) underwent surgical treatment after twelve months and before twenty-four months of age. The hospital mortality was very high in group A, because of the severity of the preoperative conditions. In three patients who underwent total repair at eight and eighteen months of age respectively, irreversible pulmonary hypertension (stage IV according to Edwards classification) was the cause of death. In our experience, severe postoperative myocardial ischemia was often associated with complete atrio-ventricular block (BAV): the possible causes are discussed. Furthermore, all patients, to a variable extent, had some manifestations of left ventricular (LV) insufficiency, which was always reversible after medical treatment. For several days, almost systematically, mechanical ventilation is necessary after a total repair of TAC. The result in the nine surviving patients is excellent: they had a strictly normal life, without any therapy. In conclusion, we believe that elective surgery for TAC can be performed more safely between six and nine months of age: if medical treatment cannot control heart failure, surgery must be performed urgently in order to avoid severe ventilatory disturbances. After twelve months of age, total repair is performed only if a pulmonary biopsy confirms the possibility of regression of the pulmonary vascular lesions.
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PMID:[Surgery of truncus arteriosus in the first 2 years of life. Analysis of a consecutive series of 22 patients]. 718 11

Fetal and neonatal biophysical and biochemical changes were studied in four preterm infants who developed cardiogenic shock as a result of severe perinatal asphyxia. Fetal distress was documented by the presence of severe late and variable decelerations associated with decreased fetal heart rate variability. Severity of fetal acidosis was decumented by scalp and umbilical cord blood pH. Apgar scores at 1, 5, and 10 minutes were all equal to or less than 5. Although the clinical findings shortly after birth resembled respiratory distress syndrome, it was possible to make a primary diagnosis of cardiac failure with the recognition of cardiomegaly, hepatomegaly, electrocardiographic changes of myocardial hypoxia, decreased myocardial contractility, elevated central venous pressure, and severe lactic acidosis. The treatment of heart failure, including use of inotropic agents, resulted in rapid improvement in the clinical condition, with reversal of the abnormal findings within 24 to 36 hours. Concomitant with this improvement, the increase in arterial blood pressure was paralleled by increase in peripheral (toe) temperature.
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PMID:Cardiogenic shock associated with perinatal asphyxia in preterm infants. 718 61

Varying degrees of respiratory distress developed in 3 dogs in which hyperadrenocorticism was diagnosed. The respiratory distress was attributed to pulmonary artery thrombosis. Radiography revealed pleural effusion, increased diameter and blunting of the pulmonary arteries, lack of perfusion of the obstructed pulmonary vasculature, and overperfusion of the unobstructed pulmonary vasculature. Thrombosis was confirmed by nonselective angiocardiography in each case. In 1 case, selective angiocardiography showed marked reduction of the transit time of contrast medium from the right atrium to the aorta. Hypertension proximal to the site of thrombosis was confirmed in 2 cases by showing increases in the right ventricular systolic pressures (80 mm of Hg in one case and 54 mm of Hg in the other case). In 3 cases, there was moderate hypoxemia with hypocapnia, suggesting a ventilation-perfusion mismatch. Clinical findings other than respiratory distress included hepatomegaly, ventral edema, orthopnea, and a jugular pulse. Pulmonary artery thrombosis, as it occurred in these 3 cases, was compared with the disease in man. It was concluded that pulmonary artery thrombosis should be suspected in cases of intractable dyspnea, right-sided heart failure of unexplained origin, and acute unexplainable death.
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PMID:Pulmonary artery thrombosis in three dogs with hyperadrenocorticism. 723 99


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