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

In the treatment of arterial hypertonia with calcium antagonists good use is made of the vasodilatory effect, which is in the chronic therapy not accompanied by water and volume retention. In three clinical studies it was investigated, which patients could be given a single drug treatment with calcium antagonists. Older patients with a high basal blood pressure and a slight activation of the renin system seem to respond most favourably. Single drug therapy with calcium antagonists is also advantageous for the various illnesses accompanying hypertonia, such as coronary heart disease, cardiac insufficiency, obstructive lung disease or diabetes mellitus.
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PMID:[Calcium antagonists in the treatment of arterial hypertension. Attempt at a differential therapy]. 647 15

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

A program of respiratory muscle sparing in 9 patients with late stage Duchenne muscular dystrophy is presented. Results indicate that regular efficient night-time support by body respirator provides a constant significant improvement in daytime gas exchange for periods averaging up to 2 years following the occurrence of moderately severe respiratory failure. Until now, the longest survival is more than 4 years at the age of 28. the average PaCO2 and PaO2 before night ventilation were 60.8mmHg and 59.3mmHg, respectively. The levels after the program was begun were 45.5 (PaCO2) and 74.6 (PaO2). These arterial blood gas levels are acceptable for good cardiopulmonary homeostasis. There have been no deaths or episodes of cardiac failure since the program began. The ease of integrating the program into the patient's lifestyle and home are important advantages. Cost of equipment is discussed. The view that these patients are terminal must be qualified. A case is also made for early aggressive conservative measures including body respirators, postural drainage, chest physiotherapy with abdominal assisted coughing, intratracheal suctioning and bronchoscopy to combat respiratory infection, and decreasing the need of tracheostomy and volume ventilators which can be so disabling to the chronic restrictive lung disease (CRLD) patient. Research and development into better design of body respirators is vitally needed. Acute care hospitals must prepare themselves for such patients who now attain more independent living and longer lifespan. For this reason there is a growing need for these facilities to acquire tank ventilators for handling such patients who may need hospitalization for acute medical complications.
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PMID:Night ventilation by body respirators for patients in chronic respiratory failure due to late stage Duchenne muscular dystrophy. 678 53

Hypoxemia, hypercarbia, and cor pulmonale ultimately occur in most patients with chronic lung disease. Although oxygen therapy may reduce or delay the development of pulmonary hypertension and myocardial failure in these patients, its use is thought to lead to CO2 narcosis and apnea. The effect of O2 administration during sleep has been examined in 12 patients (seven with cystic fibrosis, three with bronchopulmonary dysplasia, one with bronchiolitis obliterans, and one with severe hypersensitivity pneumonitis) using skin surface O2 (Roche) and CO2 (Radiometer) electrodes. Both electrodes were calibrated over wet gas and applied at 44 C. Ten patients had chronic hypercarbia (PaCO2 62 +/- 19 torr; range 46 to 103 torr) when awake. Humidified oxygen was administered by nasal cannula, Venturi mask, or head hood. Oxygen flow was increased every 20 minutes from 80 minutes or until the patient awoke. In eight of ten patients with hypercarbia and in the two normocarbic patients, skin surface carbon dioxide tension (PsCO2) increased by 10% or less as the skin surface oxygen tension (PsO2) was increased. In the remaining two patients with hypercarbia (both had cystic fibrosis) PsCO2 increased 18% and 24% as PsO2 was increased. These last two patients with depressed responsiveness to CO2 could not be separated from the other patients by clinical or laboratory criteria. It is concluded that the skin surface blood gas tensions are a simple and reproducible method for adjusting oxygen therapy in patients with chronic lung disease, and although the response to oxygen varies from patient to patient, most patients with chronic hypercarbia retain their central responsiveness to CO2 during sleep and for them O2 therapy is probably safe.
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PMID:Effect of oxygen administration during sleep on skin surface oxygen and carbon dioxide tensions in patients with chronic lung disease. 678 98

Nitroglycerin (Ng) is a potent and short-acting coronary and systemic vasodilator, widely used in anginal pain treatment. When given to patients with pneumonia or chronic lung disease, Ng was found to cause a further decrease in arterial oxygen tension (PaO2) by increased perfusion of poorly ventilated territories in the lungs. In order to investigate the potential hazard in Ng decreasing the PaO2 in ischemic heart disease patients, who develop acute pneumonia, we administered 0.4 mg Ng sublingually to 11 patients who suffered concomitantly from ischemic heart disease and acute pneumonia. Arterial blood gases were monitored before, 2, 5 and 10 min following Ng administration, as well as a standard 12-lead electrocardiogram that was monitored as the same time. 8 out of the 11 patients showed a decrease in PaO2 which was mild to moderate, during the study period of time, none of them showed an increase, and there was tendency for the lower (less than 60 mm Hg) initial PaO2 to show a lesser decrease in the PaO2 in comparison to the higher (greater than 60 mm Hg) initial PaO2. There was no statistical significant correlation between the decrease in PaO2 and patients' age, sex, coexisting chronic obstructive lung disease and severity of systemic heart failure. Our conclusion is that the hazard in lowering PaO2 by Ng in ischemic heart disease patients who develop acute pneumonia is minimal, but the drug should be used with caution.
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PMID:Arterial hypoxemia following the administration of sublingual nitroglycerin in patients with ischemic heart disease and pneumonia. 679 69

The effects of oxprenolol on blood pressure levels, pulmonary ventilatory function, myocardial contractility and myocardial oxygen consumption are described in 66 patients with essential hypertension and no clinical evidence of obstructive lung disease of heart failure. Two groups of patients were treated with medication for a total of 16 weeks. Group 1 received oxprenolol and diuretics for the first eight weeks and a placebo plus diuretics for the second eight weeks. Group 2 received the same drugs in reverse order. The results of the study indicate that oxprenolol is an effective antihypertensive drug that does not hamper lung volume capacity or myocardial contractility and markedly reduces myocardial oxygen consumption, although it may cause a mild increase in airway resistance.
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PMID:Effect of oxprenolol on blood pressure, pulmonary ventilatory function and myocardial contractility in hypertensive patients. 739 73

Seven patients with late sequelae of allergic bronchopulmonary aspergillosis (ABPA) are described. All seven had significant chronic symptoms from asthma. At the time of diagnosis of ABPA all patients had marked irreversible pulmonary function abnormalities; symptoms of chronic bronchitis were present in all. Pulmonary fibrosis was present in six of seven patients. Three patients have died from irreversible lung disease with terminal cardiac failure. Despite the difficulty in establishing an early diagnosis of ABPA, its importance must be emphasized in order to attempt to prevent progression of the disease to severe irreversible and potentially fatal end-stage lung disease.
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PMID:Late sequelae of allergic bronchopulmonary aspergillosis. 741 34

Inspiratory muscle weakness has been demonstrated in ambulatory, stable chronic heart failure (CHF) and may contribute to dyspnea during daily living. However, the mechanisms underlying this weakness are unknown. Malnutrition and electrolyte depletion are recognized complications of CHF that may impair skeletal muscle function, and limb muscle weakness and myopathic changes have also been demonstrated in CHF. We examined whether nutrition and electrolyte status contribute to the reduced skeletal muscle strength and whether inspiratory muscle weakness in CHF is part of general skeletal muscle weakness. We measured maximum inspiratory and expiratory mouth pressures as indices of respiratory muscle strength, maximum hand-grip strength as an index of limb muscle strength, anthropometric indices, serum albumin, and total lymphocyte count as indices of nutritional status, and serum electrolytes in 15 stable patients with chronic cardiac pump failure who had no evidence of primary lung disease, and in 15 age-and-sex-matched healthy controls. As compared with the matched controls, the CHF patients had reduced inspiratory muscle strength (p < 0.0025), but their expiratory and limb muscle strength were not significantly reduced. CHF patients were not malnourished; they were heavier than matched controls because of increased body fat (p < 0.05). Serum sodium was significantly lower in the CHF patients than in the controls (p < 0.01), but was within the normal range in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inspiratory muscle weakness in chronic heart failure: role of nutrition and electrolyte status and systemic myopathy. 769 38

A retrospective review was carried out of the radiographic features of 1016 adults admitted to hospital with acute asthma over a 4-year time period. The radiographic features were classified into five groups: (I) normal, 536 patients (52.9%); (II) features compatible with obstructive lung disease, 323 patients (31.8%); (III) complications of asthma including infection, segmental or greater atelectasis, one case of pneumomediastinum and one case of pneumothorax, 83 patients (8.2%); (IV) unimportant incidental findings, six cases (0.6%); and (V) important incidental findings including tuberulosis, heart failure, and bronchial neoplasm, 68 cases (6.7%). We conclude that in this large series of patients presenting with asthma symptoms severe enough to merit admission there is an incidence of clinically significant radiographic abnormalities of approximately 15%. Admission chest radiography is therefore indicated in adults who are hospitalized with acute asthma.
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PMID:Radiographic features in 1016 adults admitted to hospital with acute asthma. 789 9


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