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

Fibrosing alveolitis is a rare, diffuse lung disease characterized by varying combinations of two histological features: thickening of alveolar walls and the presence of large mononuclear cells in the alveolar spaces. Clinical details of 10 children with fibrosing alveolitis are reported. The main symptoms in children are tachypnoea or dyspnoea, cough, poor weight gain, and cyanosis. The condition is similar to that in adults, but it is usually a more acute illness, and if untreated, more predictably fatal. Respiratory failure, pulmonary hypertension, and cardiac failure are the major complications. Less commonly, superimposed bacterial infection and pneumothorax occur. Chest x-rays often show a sequence of changes with a ground-glass appearance and fine mottling in the early stage of the disease, progressing to a picture of mainly hilar linear markings in those children who recover. The histological features at lung biopsy or necropsy are described; these correlated poorly with the radiological features, steroid responsiveness, and clinical course. Lung function tests in 3 older children showed evidence of markedly reduced lung volumes in 2. Static lung compliance in 4 children in the acute stage of the illness was normal in 3 and diminished in one. The response to steroid therapy was analysed in cases from the literature and the 10 reported cases. No spontaneous remissions occurred, all the survivors having been treated with corticosteroids. In children fibrosing alveolitis is almost always a corticosteroid-responsive disease. An appropriate course of prednisolone would be of at least 4 week's, but preferably of 8 weeks' duration, at a minimum daily dose of 2 mg/kg. After improvement the steroid withdrawal should be cautious and protracted, comprising at least a year's continuous treatment.
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PMID:Fibrosing alveolitis in infancy and childhood. 83 51

Five children (four boys and one girl) with chronic renal failure (CRF) developed congestive heart failure 0.5 to 11 years after the onset of the disease. Their ages were from 4 to 13 years old. They noticed tachypnea, tachycardia, cough, chest anxiety, general fatigue and their chest X-rays showed cardiomegaly with cardio-thoracic ratio (CTR) of from 55 to 63% and pulmonary congestion. Their echocardiograms showed no cardiomuscular hypertrophy, but the dilatation of left ventricular diastolic diameter (LVDd), and the decreased ejection fraction (EF) were observed. They were treated with water restriction, antihypertensive agents, cardiotonics and dialysis. Their clinical symptoms improved promptly, but their cardiomegary and echocardiographic findings improved gradually. The causes of heart failure in these patients seemed to be due to uremia, fluid overload and hypertension. The echocardiographic examination was useful for the management of the children with CRF in heart failure.
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PMID:[Echocardiographic assessment of cardiac function in the children of chronic renal failure with cardiomegary]. 129 69

A Japanese black calf with cyanosis, tachycardia, tachypnea and systolic murmur died of hypoxemia and cardiac insufficiency on the 38th day after birth. We could not establish the diagnosis during it's life. However, anatomically corrected malposition (ACM) with ventricular septal defect was confirmed at autopsy. There was situs solitus of the viscera and atria with atrio-ventricular discordance and ventriculo-arterial concordance. The ventricles demonstrated l-loop, i.e. on the right-sided ventricle there was a markedly enlarged morphologic left ventricle, and on the left-sided ventricle there was a hypoplastic morphologic right ventricle with a stenotic tricuspid valve and Ebstein-like deformity. The right posterior aorta originated from the left ventricle. The pulmonary artery arose from the left-sided right ventricle via infundibulum. There was a fibrous continuity between the aortic and mitral valve. We considered that this is the first reported case of bovine ACM.
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PMID:Anatomically corrected malposition (ACM) with subpulmonary infundibulum in a calf: clinico-morphologic case report. 142 May 62

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice and are time-consuming, expensive, and stressful to the animal. Acute loss of 20-25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7-12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five per cent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10-20 ml/kg, recipient weight, is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10-15 ml of blood/kg body weight at 2-4 week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood crossmatching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 ml of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 ml) intravenously or (4 to 5 ml) intramuscularly if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of blood and blood products. 217 38

Eight children with human immunodeficiency virus (HIV) infection had symptomatic cardiac dysfunction. The median age was 1.4 years (range 0.2 to 7.9 years). All had hepatosplenomegaly, fever, pneumonia with tachypnea, and tachycardia ascribed to infection and anemia. An S3 gallop was present in six of eight. All had normal creatine phosphokinase values. Chest x-rays did not aid in the diagnosis of cardiac dysfunction. ECG showed flattened T waves in five of eight with left ventricular hypertrophy, right ventricular hypertrophy, or both in seven of eight. Results of echocardiography showed decreased left ventricular function in all eight, despite anemia, with dilated left ventricular myopathy in six, concentric left ventricular wall thickening in two of eight, an enlarged right ventricle in two, and pericardial fluid in three. Medical therapy improved cardiac function in all. All patients subsequently died of noncardiac causes. Results of autopsies on four of eight patients showed focal myocarditis in two (with cytomegalovirus inclusions in one) and dilated cardiomyopathy in two others. We conclude: (1) Preexistent hepatosplenomegaly, fever, infection, and anemia result in physical findings that mimic findings of heart failure, thereby masking the occurrence of cardiac dysfunction; (2) an S3 gallop may indicate the presence of impaired heart function when other clinical signs are masked; (3) confirmation of cardiac compromise may be accomplished by noninvasive evaluation with echocardiography and (4) medical therapy can improve cardiac dysfunction in HIV-infected children.
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PMID:Symptomatic cardiac dysfunction in children with human immunodeficiency virus infection. 252 16

Twenty-five infants with transient tachypnoea of the newborn (TTN) were examined by serial echocardiography during the first 4 days of life. The infants could be divided clinically into two groups: group 1 (n = 19) babies with mild classical TTN requiring less than 40% oxygen, and group 2 (n = 6) babies with severe TTN needing greater than 60% oxygen. Apart from amount of oxygen these two groups differed in that those with severe TTN had lower Apgar scores and arterial pH soon after birth. Echocardiography showed that the babies with classical TTN had increased left ventricular pre-ejection period to ejection times (LPEP/LVET) during the first day of life. Initial LPEP/LVET ratio correlated with duration of treatment with oxygen. The babies with severe TTN increased LPEP/LVET and right ventricular pre-ejection period to ejection times ratios (RPEP/ RVET) during the first 3 days of life. There was no correlation between systolic time intervals and duration of oxygen treatment. These findings suggest that there may be two distinct types of TTN: mild or classical type resulting from mild left ventricular failure, and a severe type associated with generalised myocardial failure, pulmonary hypertension, and right-to-left shunting.
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PMID:Transient tachypnoea of the newborn: two distinct clinical entities? 725 52

Persistent fetal circulation ("PFC") is a condition characterized by perduring after birth of fetal hemodynamic pattern: persistence of high pulmonary vascular resistance then occurs. "PFC" is a high mortality syndrome recently recognized as a cause of severe cyanosis and tachypnea in full-term newborns. Perinatal hypoxia, hyperviscosity, acidosis etc, may be also responsible of a persistence of high pulmonary vascular resistance. The increased right heart pressures cause a right to left shunt across the ductus arteriosus and foramen ovale not yet completely closed at birth. In this paper the clinical and angiographic evaluation of two full-term newborns, males, 5 days and 5 months old, are described, who presented with tachypnea, cyanosis and heart failure. Moreover we want to make a critical review of medical literature about this subject. The electrocardiogram of both patients showed right ventricular hypertrophy and myocardial ischemia. The chest roentgenograms showed cardiac enlargement and increased pulmonary vascular markings. Lung and central nervous system disorders were excluded by clinical and instrumental exams. Both patients underwent cardiac catheterization and angiocardiography in order to exclude a congenital heart disease. There was just evidence of pulmonary vascular resistance and right to left shunt at ductal and atrial level. O2 100% administration in one patient determined a decrease in pulmonary resistance and the shunting abolition. Clinical and hemodynamic patterns of this syndrome are very different. There are "simple forms" with normal myocardial function and "complex" higher mortality forms with evidence of cardiac involvement. It is often difficult to distinguish such forms from the other causes of central cyanosis and/or cardiac failure in the newborn as transposition of the great arteries, total anomalous pulmonary venous connection: the individualization of the syndrome then may be impossible without cardiac catheterization. A correct diagnosis for a precocious and reasonable treatment are extremely important for the survival of such critical newborns.
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PMID:[Persistence of fetal circulation. Clinical and angiographic evaluation of two cases. Review of the literature (author's transl)]. 734 16

The effects of angiotensin-converting enzyme (ACE) inhibitors in high-output heart failure have not yet been well established. We evaluated the effects of lisinopril (3 mg/kg/day) on hemodynamics, neurohormones, and survival in 10-week-old spontaneously hypertensive rats (SHR) with aortocaval fistula. Sham-operated treated and untreated SHR served as controls. Cardiac output (CO) was determined by thermodilution method, and renal blood flow (RBF) was assessed by laser-Doppler flowmetry. In sham-operated SHR, 2-week treatment with lisinopril decreased blood pressure (BP), left ventricular (LV) weight, and total peripheral resistance (TPR) (p < 0.01 each) and increased RBF and plasma renin activity (PRA) (both p < 0.05); CO and LV end-diastolic pressure (LVEDP) were unchanged. Fistula creation induced biventricular hypertrophy and high-output heart failure [increased LVEDP, CO, pulse pressure, and plasma norepinephrine (NE) and decreased RBF] with congestive signs (ascites, tachypnea). Lisinopril decreased LVEDP (p < 0.01), increased RBF, prolonged survival (both p < 0.05), and prevented ascites (0 vs. 46%) and increased PRA (p < 0.05) and attenuated the increase in plasma NE. Heart weight, BP, and CO were not affected by lisinopril. Thus, lisinopril ameliorated congestion and improved survival in SHR with fistula without compromising cardiorenal hemodynamics. Venous and renal dilatation and attenuation of vasoconstrictive systems may have contributed to the beneficial effects.
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PMID:Converting enzyme inhibition improves congestion and survival in hypertensive rats with high-output heart failure. 751 28

A major determinant of survival in patients with advanced viral or bacterial infection, or following severe trauma or burns complicated by multiple organ failure, is the combination of clinical signs termed the systemic inflammatory response syndrome (SIRS). SIRS is characterized by hypotension, tachypnea, hypo- or hyperthermia and leukocytosis as well as other clinical signs and symptoms, including a depression in myocardial contractile function. Heart failure complicating systemic sepsis or other causes of SIRS is usually not accompanied by coronary artery ischemia due to hypotension, myocardial necrosis, or marked cardiac interstitial inflammatory infiltrates, and thus the cause of cardiac contractile dysfunction in this syndrome has remained unclear. However, recent evidence has implicated an endogenous nitric oxide (NO) signalling pathway within cardiac myocytes and other cellular constituents of cardiac muscle, including the microvascular endothelium, as a possible contributor to the pathogenesis of heart failure in this syndrome. Cardiac myocytes are now known to express both constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities. Activation of cNOS appears to modulate cardiac myocyte responsiveness to muscarinic cholinergic and beta-adrenergic receptor stimulation. Induction of iNOS by soluble inflammatory mediators, including cytokines, causes a marked depression in myocyte contractile responsiveness to beta-adrenergic agonists. Thus, inappropriate activation of cNOS or excessive or prolonged induction of iNOS in the myocardium may contribute to cardiac dysfunction complicating SIRS.
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PMID:Myocardial contractile dysfunction in the systemic inflammatory response syndrome: role of a cytokine-inducible nitric oxide synthase in cardiac myocytes. 753 82

One hundred and three hospitalised urban pre-school Nigerian children aged 2 weeks to 4 years with various acute lower respiratory tract infection (ALRI), were studied prospectively over a 9- month period (August 1985 - April 1986). Overlapping seasonal peaks, corresponding to the rainy/early harmattan months of August through November were most noticeable for the two major viral ALRI syndromes namely, bronchiolitis and croup. The overall M:F ratio was 1.1:1, but a corresponding ratio of 1.6:1 was recorded in the infants. The commonest ALRI symptoms were cough, breathlessness and fever while chest wall retraction, nasal flaring, tachypnoea and auscultatory crepitations were the most frequently recognised physical findings. Grunting respiration was recognised in 26 patients, majority of whom had pleural effusion and/or severe bronchopneumonia. Bronchopneumonia was the single commonest ALRI diagnosis, recorded alone or in combination with another lower respiratory syndrome, in 64 (61.2%) of the 103 cases. The croup:bronchiolitis: pneumonia ratio was 1:2.3:8.3. Nasopharyngitis was recorded in 42 (40.7%) of cases, and was frequently associated with the presumably viral ALRI syndromes of croup and bronchiolitis. Pleural effusion, frequently purulent, was the commonest respiratory complication, while heart failure and anaemia were the most frequently recognised associated conditions, found predominantly in patients with pneumonia and bronchiolitis. There was an overall ALRI case-fatality of 7.8%, representing 8 deaths, in 3 of whom measles was a co-morbid condition. All the 8 deaths had a final diagnosis of pneumonia with or without other ALRI syndromes/associated complications. While subjects with complicating pleural effusion recorded the longest mean duration of hospitalisation, those with bronchiolitis had the shortest duration of hospitalisation and no death. The epidemiologic, as well as the diagnostic and therapeutic implications of our observations are discussed.
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PMID:Acute lower respiratory infections in hospitalised urban pre-school Nigerian children: a clinical overview. 762


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