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

This is a prospective study on 24 patients with chronic renal failure. Thirteen of them had evidence of acute uraemic encephalopathy. Of those 9 patients were found to have dilutional hyponatraemia, two patients severe salt and water depletion and one patient septicaemia. Hyponatraemia was associated with pulmonary oedema in 3 patients. Correction of salt and water disturbances and treatment of heart failure improved cerebral functions in 10 (77%) patients. It is therefore concluded that dilutional hyponatraemia probably leading to cerebral oedema is a reversibe major factor in the development of acute uraemic encephalopathy. This, if left uncorrected, may prove fatal especially in tropical countries.
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PMID:Acute uraemic encephalopathy in tropical countries. 70 18

A 35-year-old patient who presented with recurrent chest infection, pulmonary oedema and cardiac failure was found to be grossly hypocalcaemic owing to previously undiagnosed hypoparathyroidism. The cardiac failure was not easily relieved by digoxin and diuretics but it quickly responded when the plasma calcium was restored to normal with dihydrotachysterol. With dihydrotachysterol as sole treatment for more than 2.5 years he had normal exercise tolerance and no features of cardiac failure.
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PMID:Hypocalcaemic cardiac failure. 72 84

Nine patients with acute cardiogenic pulmonary edema were given theophylline intravenously, and its disposition was observed over the next 24 hr. Compared to that in 19 normal subjects, these patients had prolonged plasma half-lifes (mean, 22.9 from 6.7 hr) and decreased plasma clearances of theophylline (mean, 0.041 from 0.062 L [kg-1] hr-1). The intersubject variation in these parameters was 20-fold in patients with pulmonary edema and 4-fold in normal subjects. Since the peak plasma concentrations attained and the apparent volumes of distribution were not different in the two groups, a suitable initial dose can be calculated. A loading dose of 4.5 to 5 mg/kg theophylline (6 mg/kg aminophylline) given over 20 min appears safe. Because of the great variability in the plasma clearance of this drug in patients with heart failure, plasma concentrations and toxicity would be unpredictable after repeated doses or constant infusions.
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PMID:Theophylline kinetics in acute pulmonary edema. 83 50

Three atypical patterns of cardiac failure and pulmonary edema, as frequently seen in chronic obstructive pulmonary diseases, are described; I. regional; II. miliary-like; III. Swiss-cheese like. Their importance in early diagnosis of pulmonary edema is discussed in the light of a review of a series of 98 patients whose pulmonary function was also investigated. Examples and statistical data are drown from this series.
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PMID:[Radiologic patterns of pulmonary edema in chronic pulmonary diseases (author's transl)]. 87 10

On 55 patients with acute myocardial infarction blood gas changes and A-aDO2 while breathing room air were observed for a period of 5 weeks. PaO2 during the 35% O2 inhalation was measured on admission and 5 weeks later for comparisons with the PaO2 while breathing room air. Pulmonary circulatory hemodynamics was measured in 29 cases on admission using Swan-Ganz's right heart flow directed catheter 7F, and the catheter was kept in the pulmonary artery in 13 cases for a maximum of 9 days. The mean PaO2 while breathing room air on admission was 66.7 mmHg in the 55 cases. It was 52.3 mmHg in the heart failure group and 74.9 mmHg in the non-heart failure group, showing prominent hypoxemia in the heart failure group. The mean PaO2 recovered to normal (84.1 mmHg and 87.0 mmHg) 5 weeks later. Inhalation of 35% O2 was performed for 20 minutes on admission and 5 weeks later. The elevation of PaO2 during the oxygen inhalation on admission was smaller than that 5 weeks later, significantly smaller in the heart failure group (P less than 0.001). The mean A-aDO2 on admission was higher in the heart failure group (58.1 mmHg) than in the non-heart failure group (34.8 mmHg). PaO2 showed significant correlations with cardiac index and SvO2. Although it was significantly correlated with PA diast. and TPR, no correlation with CVP was observed. Hypoxemia in acute myocardial infarction is caused by the following process: the onset of myocardial infarction causes low output, leading to left ventricular failure. As the result of elevated left atrial pressure and pulmonary venous pressure, intestinal pulmonary edema develops provoking ventilation-perfusion inequality, intra-pulmonary shunting, and diffusing defect.
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PMID:Studies of hypoxemia and pulmonary hemodynamics in acute myocardial infarction. 93 22

In order to compare the venodilation effect of morphine in normal individuals (22) with that in patients (13) with heart failure morphine sulfate (0.1 mg/kg) was administered to 13 patients with mild pulmonary edema. After morphine congestive symptoms improved and venodilation was induced as determined by two independent techniques: venous pressure fell 10.2 mm Hg by the isolated hand technique and the venous volume of the forearm increased by 0.48 cc/100 ml, measured by equilibration technique. Neither finding differed from those in normal individuals. Reflex venoconstriction noted on the taking of a single deep breath was unaffected by morphine administration and was similar to that observed in normal subjects. Since the drug morphine sulfate does not cause a major pooling of blood in the limbs, the favorable effect of narcotics in patients with pulmonary edema must be caused by other mechanisms such as splanchnic pooling, afterload reduction or reduced breathing effort.
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PMID:The effects of morphine on venous tone in patients with acute pulmonary edema. 93 31

Among 909 patients with acute myocardial inarction treated in an intensive care unit between 1970 and 1974, atrial flutter and (or) fibrillation occurred in 124 (13.6%). The incidence of these arrhythmias rose with increasing age and predominantly in paroxysmal form (78%). The clinic mortality of patients with arrhythmias was 42%, while in the remaining 785 it was only 26% (P less than 0.001). Patients with atrial fibrillation and (or) flutter had a higher mean age, more frequently cardiac failure (P less than 0.001) - especially in the prognostically unfavourable severe forms with pulmonary oedema (P less than 0.05) and combined right and left heart failure (P less than 0.001) - and other disorders of impulse conduction or formation and chronic arterial hypertension (P less than 0.01).
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PMID:[Atrial fibrillation and flutter as a complication of acute myocardial infarction (author's transl)]. 97

The examination was carried out in 787 patients with macrofocal myocardial infarction. The most frequently encountered variant of intraventricular block in males was the right bundle branch block, in females--the left bundle branch block. The rarest variant of intraventricular conductivity disorders in myocardial infarction was the left-posterior hemiblock. The prognostically severest variant of bilateral block consists in a combination of the right bundle branch block with the left-posterior hemiblock. The leading causes of death among the patients with myocardial infarction and intraventricular blocks were acute (cardiogenic shock, pulmonary oedema) and chronic cardiac insufficiency. In patients with bilateral blocks the frequent causes of death were, along with cardiac insufficiency, also arrhythmias (ventricular fibrillation, asystole).
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PMID:[Intraventricular blocks in myocardial infarct]. 97 66

Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to Class III (frank pulmonary edema) patients. Heart rate and pulmonary wedge pressure (Pw) rose and cardiac index declined with increasing severity of heart failure by clinical classification. There was a significant correlation between PEV and Pw independent of clinical class (r = 0.47, p less than 0.01). PaO2 had a negative correlation with Pw (r = -0.28, p less than 0.01) as well as PEV (r = -0.26, p less than 0.02). We conclude therefore that increased pulmonary hydrostatic pressure secondary to pulmonary venous hypertension in patients with acute myocardial infarction is a major determinant of interstitial edema. At higher values of PEV, PaO2 was lower. The mechanism of hypoxemia in the presence of excessive lung water may be due to multiple factors, including small airway dysfunction and intrapulmonary shunting.
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PMID:Hypoxemia and lung water in acute myocardial infarction. 99 75

The administration of a sufficient dose of heterologous antibodies against renal glomeruli in rats produces symptoms of respiratory insufficiency and pulmonary oedema causing death of the animals. Under these experimental conditions the basic pathogenic mechanism appears to be binding of the injected antibodies on the basement membrane structures of pulmonary capillaries resulting in their damage. Such changes are followed by widespread haemorrhagic exsudative changes in the lungs. Localization of the injected antiglomerular antibodies has been studied with the aid of immunohistochemical methods and in addition, by a method using antibodies labelled with radioactive isotopes of iodine, the so-called "paired administration technique". After the administration of a lethal dose of antiglomerular antibodies, they later appeared to be predominantly localized in the lungs. This fact correlates well with the idea of the effect of the antibodies upon pulmonary parenchyma in the present experiment. A remarkable finding was a rather high localization of the injected antibodies in the liver parenchyma which could be explained either by a cross reaction between the antibodies and the antigens of hepatic vascular spaces, or by a shock reaction associated with heart failure and circulatory disturbances.
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PMID:[Experimental administration of a fatal dose of antiglomerular antibodies]. 103 46


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