Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patterns of breathing at night were recorded in 4 patients with heart-failure. 2 had periodic breathing while awake and in 2 it developed after they fell asleep. In all 4 the phase of hyperventilation disturbed sleep. These cases also illustrate other problems caused by periodic respiration in heart-failure, which range from tiredness during the day to an inability to sleep for more than a few minutes. Nocturnal waking in the hyperventilation phase of Cheyne-Stokes breathing should be differentiated from paroxysmal nocturnal dyspnoea caused by episodes of pulmonary oedema at night.
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PMID:Paroxysmal nocturnal dyspnoea and periodic respiration. 9 69

Two cases of acute pulmonary distress following very shortly after irradiation of the upper half of the body are described. The first occurred one hour and forty minutes after irradiation and led to the patient's death three hours after irradiation. The second occurred 15 minutes after irradiation and was successfully treated with hydrocortisone and Frusemide. The features are the sudden onset of dyspnoea and cyanosis associated with pyrexia. Auscultatory evidence of pulmonary oedema was not apparent initially. The response to steroid alone is transitory. High single-dose pulmonary irradiation causes transudation of extracellular fluid and diapedesis of red cells from the alveolar capillaries. The supervention of these effects on severly compromised pulmonary function can well prove dangerous.
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PMID:Acute pulmonary distress following high-dose irradiation of the upper half of the body. 11 68

A primigravida was induced for PET, the liquor was meconium stained; she was put on oxytocin in-fussion and developed hypertonic uterine action. She then had an amniotic fluid embolism which presented clinically as profound shock, dyspnoea, tachycardia, cyanosis, hypotension and pyrexia. The patient was delivered by vacuum extraction. The picture was further complicated by pulmonary oedema intravascular microcoagulation and anuria. She deteriorated rapidly and died despite treatment with double strength plasma (in the absence of fibrinogen), massive hydrocortiosone therapy, blood transfusion amd sub-total hysterectomy. Post mortem findings in the lungs confirmed amniotic fluid embolism.
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PMID:Case report: a fatal case of amniotic fluid embolism. 12 35

Of 22 patients with the classical clinical signs of pulmonary oedema (orthopnoe, cyanosis, sweating and rales heard at a distance) 15 (Group A) were observed clinically, while seven (Group B) underwent haemodynamic studies. Those in Group A were given 0.8-2.4 mg nitroglycerin sublingually one to six times at 5--10 minute intervals. Within five minutes of nitroglycerin administration 7 of the 15 had their first signs of clinical improvement. In 11 patients the rales had disappeared after 15--20 minutes or had regressed. In the remainder the dyspnoea had decreased so that at this point in 14 of the 15 patients various degrees of improvement had occurred. Four patients were completely without clinical signs after 30 minutes. The increased arterial blood pressure and heart rate had fallen markedly. In the seven patients of Group B mean left ventricular filling pressure fell within ten minutes of nitroglycerin administration (1.6 mg) from 33 +/- 10 to 24 +/- 8 mmHg, cardiac output rising sifnificantly from 3.3 +/- 0.8 to 3.7 +/- 0.8 1/min. Such favourable results with nitroglycerin are to be expected only if the pulmonary oedema is of cardiac origin.
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PMID:[Effect of nitroglycerin sublingually in the emergency management of "classical" pulmonary oedema (author's transl)]. 40 57

A 32-year-old man with a long history of grand mal seizures but otherwise good health had recurrent episodes of postictal pulmonary edema when he failed to take anticonvulsant medication regularly. This case illustrates most of the features observed in other reported cases of postictal pulmonary edema. Symptoms include dyspnea and cough with production of various quantities of mucoid fluid that may be copious and frankly hemorrhagic. Blood pressure is normal, and temperature may be normal also but is frequently elevated to 100 or 101 F. No cardiac irregularities are heard on auscultation, and the ECG is often normal, but a wide range of abnormalities may be seen. Considerable arterial hypoxemia may occur, and leukocytosis (11,000 to 14,000 cells per cubic millimeter) is common. Rales and rhonchi are audible, and chest films often show bilateral upper and middle lobe infiltrates. The patient is usually clinically improved within 24 hours and the pulmonary edema completely cleared in three to five days.
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PMID:Case report: Recurrent postictal pulmonary edema. 41 95

In 15 patients with left ventricular failure, ten with recent myocardial infarction and five with old infarct a highly significant fall in pulmonary-artery pressure occurred within 3-5 minutes of sublingual administration of nitroglycerine, 0.8 and 1.6 mg. End-diastolic pulmonary-artery pressure, as an expression of left ventricular filling pressure, fell from 25 plus or minus 8 to 17 plus or minus 8 mm Hg (P smaller than 0.001). In some patients cardiac output rose markedly, while arterial blood pressure fell only slightly (not statistically significant). In six patients with pulmonary oedema there was a decrease in dyspnoea within a few minutes. Left-ventricular filling pressure fell markedly in all cases, in one patient from 50 to 27 mm Hg. This study indicates that nitroglycerine can be effective in the treatment of left-ventricular failure of various causes.
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PMID:[Effect of nitroglycerine in acute myocardial infarction: I: Sublingual nitroglycerine in the treatment of left-heart failure and pulmonary oedema (author's transl)]. 80 40

Thirty-four cats with primary myocardial disease were studied. The cats were divided into two groups, depending on the clinical, hemodynamic, angiocardiographic, and pathologic findings. Group A consisted of those cats with hypertrophic cardiomyopathy and Group B consisted of those cats with congestive cardiomyopathy. Similarity in the characteristics of cardiomyopathy in the human cat was found. Both Group A and Group B consisted predominantly of mature adult male cats. The most common presenting signs were dyspnea and/or thromboembolism, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (Group A) or without (Group B) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (Group A) or left ventricular dilatation (Group B). Some cats in Group A also had evidence of left ventricular outflow obstruction. The principal pathologic findings in these cats were left atrial dilatation, symmetric hypertrophy or asymmetric septal hypertrophy of the left ventricle (Group A), and dilatation of the four cardiac chambers (Group B). Aortic thromboembolism was commonly observed in both groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat is similar to the two most common forms of cardiomyopathy in the human (hypertrophic cardiomyopathy, with and without obstruction, and congestive cardiomyopathy).
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PMID:Primary myocardial disease in the cat. A model for human cardiomyopathy. 84 11

Two patients with chemical pneumonitis secondary to inhalation of an epoxy curing material used in the coating of pipes had similar patterns of cough, hemoptysis, and dyspnea associated with diffuse bilateral alveolar infiltrates shortly following the exposure. Pulmonary function studies showed a volume-restrictive defect with severe hypoxemia, but an elevated diffusing capacity. All lung function studies returned toward normal within 1 month of exposure. One patient underwent an open lung biopsy which showed changes consistent with a nonspecific injury to the alveolar wall. This epoxy curing material, trimellitic anhydride, represents another cause of diffuse lung injury that can result in pulmonary edema.
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PMID:Chemical pneumonitis secondary to inhalation of epoxy pipe coating. 88 55

A rebreathing technique was utilized to assess changes in diffusing capacity (DCO), pulmonary capillary blood volume (Vc), pulmonary parenchymal tissue volume (Vt), and cardiac output (Qc), after infusion of 2 liters of 0.9% saline intravenously in 13-25 min in five healthy subjects. Blood hemoglobin concentration decreased an average of 17%. Vc increased strikingly in all five subjects. No significant changes in Vt, or in Vt per unit lung volume were observed. Radiographic evidence of interstitial pulmonary edema was present in four of the five subjects. Radiographic total lung capacity was reduced significantly in four of the five subjects. Significant reductions in forced vital capacity (FVC), forced expiratory volume in 1.0 and 3.0 s, and mean forced expiratory flow during the middle half of the FVC occurred in three of the five subjects. No dyspnea, cough, or physical examination abnormalities of lungs or heart occurred. This noninvasive, ventilation-limited, rebreathing technique appears capable of detecting early changes in pulmonary congestion, at a time when definitive radiographic changes and changes in the physical examination are absent. It appears capable of detecting the increase in Vc associated with hypervolemia in man.
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PMID:Rebreathing pulmonary capillary and tissue volume in normals after saline infusion. 89 78

A case of a non-hemolytic transfusion reaction with pulmonary infiltration secondary to leukocyte antibodies is described, and previously reported cases are reviewed. This type of reaction can be diagnosed at the bedside when a patient develops fever, hypotension and dyspnea within a few hours following transfusion of whole blood or a plasma product. The roentgenogram of the chest shows pulmonary infiltrates with a normal cardiac silhouette constituting non-cardiac pulmonary edema. To provide laboratory confirmation of this reaction, it is essential to search for leukocyte antibodies by both leukoagglutinin and cytotoxic technics, as well as to determine HL-A phenotypes of both donor and recipient. As the plasma products involved usually come from multiparous women, donor parity should be a routine question in the donor interview in transfusion services. To prevent this reaction, which may prove fatal, blood donated by women who have two or more children should be used for packed cells only.
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PMID:Transfusion reaction with pulmonary infiltration associated with HL-A-specific leukocyte antibodies. 96 28


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