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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 21 month old female had voluntarily ingested 0.5-1.51 of isotonic sports drink daily from 10 months of age. She developed hyponatremia and beriberi heart disease, which resulted in metabolic acidosis and cardiogenic shock (shoshin beriberi). Mechanical ventilation was applied for pulmonary edema. Right heart failure was improved after administering vitamin B1. However, 5 days after the shock, hypoxemia and diffuse radiographic infiltrates progressed, and a diagnosis of adult respiratory distress syndrome (ARDS) was made. After the occurrence of an air leak, the patient died of respiratory failure. The cardiogenic shock and pulmonary edema due to cardiac beriberi may have triggered the ARDS.
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PMID:Cardiac beriberi (shoshin beriberi) caused by excessive intake of isotonic drink. 141 37

Deadspace is defined in terms of the efficiency of the lung in eliminating carbon dioxide. The airway deadspace is the volume of the airway in which gas moves chiefly by convection. The alveolar deadspace is caused by ventilation/perfusion inequalities at the alveolar level. The commonest causes of increased alveolar deadspace are airways disease--smoking, bronchitis, emphysema, and asthma. Other causes include pulmonary embolism, pulmonary hypotension, and ARDS. In addition, right-to-left shunting (cyanotic heart disease, atelectasis) causes an apparent or virtual deadspace, which, although not representing non-perfusion of any compartment, nevertheless reduces the efficiency of ventilation.
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PMID:Deadspace during anaesthesia. 229 89

During the winter of 1986-1987, 64 children with respiratory syncytial virus (RSV) infection were admitted to our hospital. The diagnosis was made by direct immunofluorescent antibody technique. Twenty-three children (36%) needed intensive care treatment. Nearly 11 (52%) had a preexisting disease state, identified as a risk factor i.e., prematurity (n = 8), bronchopulmonary dysplasia (n = 2), congenital heart disease (n = 1). Twelve patients (50%) were intubated and ventilated. Conditions for intubation and ventilation were repetitive apnea with or without bradycardia (n = 4), clinical deterioration (n = 3) or hypercarbia (n = 5). Seventy-five percent of the patients who needed intensive care management were under three months of age compared to 34% of the children who were admitted to the clinical ward. The mean age for ventilated patients was 7.9 weeks. The mean duration of ventilation was 5.5 days. Volume controlled ventilation was initially applied to all patients. Pulmonary complications (atelectasis, pneumonia, pneumothorax or adult respiratory distress syndrome) were present in 15 (65%) IC patients. Nine (39%) of them also had symptoms of inappropriate antidiuretic hormone secretion (IADHS). Only two patients had symptoms of IADHS and two others had convulsions. Three children (5%) died as a result of respiratory insufficiency. Two of these infants belonged to the risk group.
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PMID:Respiratory syncytial virus infections in children admitted to the intensive care unit. 281 76

The volume of extravascular lung water is currently measured in vivo from the difference in mean transit times of the extrapolated first-pass dilution curves of two indicators, one diffusible and the other confined to the intravascular space. To overcome the limitations of this method, one can prolong the measurement interval, introduce a highly diffusible indicator, or both. In the first case, recirculating indicators are measured and included in the computation by deconvolution of the mean transit time through the lung. In the second case, heat is used as the water indicator. In the third case, not yet explored, recirculating heat would be measured and long thermal transit times uncovered. In view of the complexity of the deconvolution method and the pitfalls of the thermal dilution method, a radiographic score of pulmonary edema may be more useful clinically to assess the volume of extravascular lung water in patients with heart disease or adult respiratory distress syndrome.
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PMID:Theoretical and practical considerations of measuring extravascular lung water. 329 81

A quasi steady-state noninvasive, radioisotopic technique for measuring regional lung water distribution in man is described. The method depends upon the dilution principle. 123I labelled human serum albumin (HSA) and sodium iodide (NaI) were injected intravenously, allowed to mix completely within the body fluids and then counted externally over the chest. The size of each compartment to which the markers are confined was calculated from the external count rate and the isotopic concentration of the marker in plasma. 123I-HSA was used to estimate intravascular water and 123I-NaI extracellular water. Ratio analysis of the differential attenuation of the two photoenergies of 123Iodine (29 keV, 159 keV) by the lung and chest wall was used to estimate the absolute amount of isotope in the lung, independent of chest wall contribution, after validation by phantom studies. Regional pulmonary plasma (PPVr) and interstitial (PIVr) fluid volumes in normal subjects were 7.1 +/- 1.4 and 7.6 +/- 1.3 ml.100 cm-3 lung (mean +/- SD; n = 13) at mid-tidal volume, respectively. In patients with the adult respiratory distress syndrome, PPVr and PIVr were 7.0 +/- 2.9 and 15.9 +/- 4.6 ml.100 cm-3 lung (n = 18), respectively. The pulmonary artery wedge (Paw) pressure was normal (12.5 +/- 2.5 mmHg; n = 5). In patients with pulmonary oedema due to left heart disease, PPVr and PIVr were 7.2 +/- 2.7 and 12.1 +/- 3.7 ml.100 cm-3 lung (n = 8), respectively. The mean Paw pressure in this group was high (28.5 +/- 3.9 mmHg).
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PMID:Noninvasive measurement of regional lung water distribution in healthy man and in pulmonary oedema. 369 23

Fluid movement from the pulmonary capillaries into the interstitial space occurs continuously and is drained by the lymphatics. With increased leakage or decreased clearance, excessive extravascular lung water accumulates, initially as interstitial edema and subsequently as alveolar edema. The most common cause of pulmonary edema is an increase in microvascular hydrostatic pressure. An increased permeability of the capillaries is the other mechanism of production of pulmonary edema. An acute, critical reduction in colloid osmotic pressure may play a contributory role in pulmonary edema even at normal hydrostatic pressures. Dyspnea, diaphoresis, and anxiety characterize the clinical picture. A history of heart disease and congestive heart failure may be present in CPE, whereas evidence of an inciting event or disease process suggests NCPE. Hypoxia, decreased lung compliance, and increased shunt fraction are seen in both types of pulmonary edema, but the duration of pulmonary edema tends to be more severe and prolonged in NCPE. Evidence of increased permeability in NCPE distinguishes it from CPE. Clinically, this is assumed when pulmonary edema is demonstrated at normal PCWP and when edema fluid protein concentration and COP are close to those of plasma. The management of pulmonary edema consists of the improvement of gas exchange by methods that range from supplemental oxygen administration to mechanical ventilatory support with PEEP, depending on the severity of the disturbance in lung function. Improvement in myocardial function and a decrease in pulmonary congestion are accomplished with diuretics and morphine; in those patients who do not respond to this therapy, manipulation of preload, afterload, and myocardial contractility by vasodilators and inotropic agents may be required. In acute pulmonary edema, intravenously administered agents with a short half-life and rapid onset of action are preferred. The role of colloids in the treatment of pulmonary edema is controversial. The indications for the use of corticosteroids in ARDS are controversial, and an optimum dose has not been determined. Many clinicians tend to choose steroids to treat these patients, but the value of these agents in this setting awaits the results of controlled trials now under way.
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PMID:Acute pulmonary edema. 644 44

The radiographic findings of a series of infants of diabetic mothers and a review of the literature are presented to illustrate the wide spectrum of abnormalities that may be seen with this condition. Congenital anomalies of the spine and skeletal, genitourinary, and cardiovascular systems and visceral situs inversus are significantly more frequent among infants of diabetic mothers than normal. The most specific anomaly is sacral agenesis. Renal vein thrombosis and adrenal hemorrhage are also more common and may be diagnosed by sonography. Over one-half of the cases of the small left colon are associated with maternal diabetes and may be diagnosed and treated with a contrast enema. The incidence of the respiratory distress syndrome is higher in infants of diabetic mothers than other premature infants, and the disease may occur in the presence of reliable indicators of lung maturity. Other common causes of dyspnea include cardiomyopathy, congenital heart disease, wet lung syndrome, hyperviscosity syndrome, and persistence of fetal circulation. Echocardiography is the most valuable adjunct in differentiating cardiac from pulmonary problems.
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PMID:Infants of diabetic mothers: radiographic manifestations. 678 62

Activations of leukocytes and platelets have been considered to be one of the major harmful factors related to Adult Respiratory Distress Syndrome (ARDS). As a hypothesis of the present study, similar events may exaggerate the post perfusion lung syndrome following the cardiopulmonary bypass (BPB). Since platelet activating factor (PAF) is a strong activator of leukocytes and platelets, we measured the kinetics of PAF level, number of leukocytes and platelets in 20 anesthetized dogs. beta-TG and PF4 were also measured in patients with organic heart disease before and after CPB. We also studied the preventive effects of PAF antagonist (CV-3988) on the postperfusion lung injury in dogs. The PAF activities increased twice 5 minutes after the beginning of CPB, then it was progressively increased to a level 4.5 times at the end of CPB. Circulating numbers of leukocytes and platelets depleted sharply after the CPB, and then decreased gradually. Such depletion was not modified by PAF antagonist, CV-3988. Accumulation of leukocytes at the pulmonary circulation, and the microscopic evidence of leukocyte sequestration in pulmonary capillary beds were noted in cases without PAF antagonist. Rapid increases of beta-TG and PF45 minutes after the beginning of CPB also showed that activation of platelets occurs immediately. Adhesion of activated leukocytes or platelets to the pulmonary capillary bed in dog cases may suggest the ensuring damage to the vascular beds by releasing free radicals, lysosomal enzymes, or other chemical mediators. Restriction of inflow rate of activated leukocytes to the lung or the heart before aortic clamping may attenuate harmful effects of leukocytes on the respiratory function related to the CPB.
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PMID:[Participation of platelet activating factor in the pulmonary injury during cardiopulmonary bypass]. 847 89

Persistent or recurrent acute allograft rejection (AR) refractory to high-dose steroid therapy can adversely affect long-term outcomes of heart-lung (HLT), bilateral-lung (BLT), and single-lung (SLT) transplantations. The use of total lymphoid irradiation (TLI) for the management of refractory acute AR in six transplant recipients (two men, four women; mean age, 29.8 +/- 3.8 years) is detailed. There are two HLT (primary pulmonary hypertension [PPH], cystic fibrosis [CF]), 1 BLT (pulmonary hypertension postventricular septal defect repair), and 3 SLT (sarcoid, PPH, congenital heart disease with atrial septal defect) recipients. Refractory AR is defined as persistent rejection unresponsive to high-dose steroid therapy in all cases. The BLT and SLT recipients had at least two moderate and one mild AR events per patient. The HLT recipients had at least two moderate acute heart and one severe and one mild asynchronous acute lung rejection events per patient. A total of 800 cGy of total lymphoid irradiation (TLI) was administered over a 5-week period. Mild and transient leukopenia was the only observed side effect. The patient with PPH received TLI 313 days after HLT for recurrent AR at another institution and died of ARDS 4 weeks after completing TLI. The patient with CF received TLI 707 days after HLT and died 457 days after TLI of severe obliterative bronchiolitis (OB) with multiorgan failure. The patient with BLT received TLI 176 days after transplant and died 372 days after TLI of respiratory failure related to severe rejection. One patient with SLT received TLI 78 days after transplant and died 679 days after TLI of severe acute AR. The two remaining patients with SLTs have been free from acute AR for more than 4 years. The patient with sarcoidosis received TLI 37 days after SLT following a clinical rejection event and two severe acute AR events. He is alive with normal lung function 5 years later. The patient with PPH received TLI 108 days after SLT following three moderate acute AR events and is alive with stable OB 4 years later. These limited preliminary results suggest that TLI has merit for the treatment of intractable acute AR following HLT and lung transplantation.
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PMID:Total lymphoid irradiation for refractory acute rejection in heart-lung and lung allografts. 862 53

Pregnancy increases the risk for respiratory failure from to numerous pulmonary diseases. Adult respiratory distress syndrome, aspiration, venous air embolism, asthma, thromboembolism, and heart disease are etiologies shared by non-pregnant women. However, their management is complicated by complex physiologic changes during pregnancy. Amniotic fluid embolism and tocolytic-induced pulmonary edema are unique to pregnancy and must be added to the list of causes of respiratory failure. Diagnostics and supportive care is difficult and must be directed with the mother and the fetus in mind. This dictates a thorough understanding of maternal physiology, and the safety of drug use during pregnancy.
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PMID:Acute respiratory failure in pregnancy. 863 95


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