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

We reported a case of 64 year-old female patient of pulmonary tuberculosis associated with ARDS during corticosteroid treatment of Rheumatoid Arthritis. On admission her chief complaints were fever, fatigue and dyspnea. A chest roentgenogram showed diffuse alveolar infiltration consistent with pulmonary edema. Arterial blood gas studies showed severe hypoxemia. We clinically diagnosed so-called ARDS. Smears of sputum for acid fast bacilli were negative, but transbronchial lung brushing by bronchofiberscope revealed many acid fast bacilli. Intensive therapy with anti-tuberculosis drugs (INH, RFP, SM), high dose corticosteroid (methylprednisolone) therapy and mechanical ventilation was started. During the following 2 weeks, the PaO2 rose gradually and the alveolar infiltration on the chest roentgenogram disappeared. The experience of this case to emphasized the importance of suspecting this condition because pulmonary tuberculosis is a potentially curable cause of ARDS and it should also be emphasized that the good treatment effect could be expected with combined use of high dose corticosteroid and mechanical ventilation.
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PMID:[A case of pulmonary tuberculosis associated with adult respiratory distress syndrome during corticosteroid treatment of rheumatoid arthritis]. 221 15

Altitude sickness is a clinical syndrome that occurs with abrupt ascents to altitudes of 3000 metres and above. Symptoms include headache, malaise, fatigue, dizziness, anorexia, nausea and vomiting, and oliguria. At higher altitudes more severe illness resulting from pulmonary oedema or cerebral oedema can occur.
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PMID:Altitude sickness. 232 86

The patient was a 70-year-old male with complaint of macrohematuria at the first visit to our clinic on June 10, 1986. At that time, cystoscopy revealed a thumb sized papillary tumor and a rice sized non papillary tumor, and the biopsy specimen was pathologically diagnosed as undifferentiated carcinoma. But, he refused admission. On January 30, 1987, he came back to our clinic with complaints of dyspnea, general fatigue and weight loss. Moderate lt. gynecomastia was found and the level of serum hCG-beta was detected as high as 101 ng/ml. Excretory urogram and enhanced CT revealed a large mass in the bladder. In the seventeenth day after admission, he died of lung edema and heart failure. The findings of autopsy showed a large light greenish to light brownish tumor of 10 X 10 X 3 cm in the bladder. Distant metastases were observed in internal, common iliac and paraaortic lymph nodes, but without other distant metastasis. In histological and immunohistochemical studies, the final diagnosis is choriocarcinoma of the bladder, containing syncytiotrophoblastic giant cells with hCG-beta granules as an undifferentiated carcinoma. To our knowledge this case is the eighth described in Japan. Herein we report a new case of primary choriocarcinoma of the bladder and make a brief review of the literatures.
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PMID:[Primary choriocarcinoma of the bladder: a case report of autopsy]. 267 66

The efficacy of oral enoximone, a new positive inotropic and vasodilator agent, was assessed in 12 patients with chronic congestive heart failure (New York Heart Association [NYHA] class II or III) in a double-blind randomized crossover comparison with placebo. Duration of each treatment was 6 weeks and the dose of enoximone was 150 mg tid. Efficacy was assessed by exercise tolerance, symptoms, radionuclide angiography for ejection fraction at rest and during exercise, and Holter monitoring. Two patients were withdrawn before completion of the study, one with pulmonary edema after 1 week on placebo and the other for noncompliance with enoximone therapy. Symptom-limited exercise capacity improved with enoximone by 30% and 43% (p less than .01) compared with baseline after 2 and 6 weeks treatment, respectively. Ejection fraction improved at rest (p less than .02) with enoximone but not with placebo. No change was found during exercise. Heart rate and blood pressure remained unaltered. During treatment with enoximone symptoms of exertional dyspnea and fatigue were improved and NYHA class decreased by at least one class for every patient. Holter monitoring revealed an overall increase (NS) in ectopic activity during enoximone therapy. There were no serious adverse effects and laboratory values did not change significantly. The addition of enoximone to the existing therapy of patients with moderately severe congestive heart failure provided clear and sustained subjective and objective benefit when compared with placebo.
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PMID:Double-blind crossover comparison of enoximone and placebo in patients with congestive heart failure. 296 Apr 73

Severe shortness of breath is a prominent symptom in acute heart failure (pulmonary oedema) and is related to left atrial pressure. A reduction of this pressure almost always leads to an improvement in symptoms. Patients with chronic heart failure complain of both shortness of breath and tiredness even when fluid overload has been corrected by the appropriate use of diuretics. Shortness of breath under these circumstances is not related simply to central haemodynamics but is determined more by the interaction of changes in respiratory pattern and the metabolic consequences of reduced perfusion of exercising skeletal muscle. An important clinical consequence is that when such patients are optimally treated with diuretics, further improvement of symptoms would not be expected from drugs which merely alter central haemodynamics without influencing other factors such as skeletal muscle blood flow on exercise, or lung perfusion.
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PMID:The origin of symptoms in patients with chronic heart failure. 304 95

We studied the role of O2 supply and demand factors for producing diaphragmatic failure in a canine model of cardiogenic shock with pulmonary edema. We produced pulmonary edema with oleic acid and then hypotension with cardiac tamponade and followed the animals until respiratory failure began, which was defined by a 50% fall in frequency of breathing and diaphragmatic pressure-time index (PTI; cmH2O.s-1.min-1) with no decrease in the diaphragmatic electromyogram. Regional blood flows were measured with radiolabeled microspheres. Diaphragmatic O2 consumption (VO2 di) (ml.min-1.100 g-1) was determined from the diaphragmatic blood flow (Qdi) and the arterial and phrenic venous O2 contents. With oleic acid-induced pulmonary edema, PTI Qdi, and VO2 di increased from control of 101.7 +/- 31.7, 17 +/- 1.8, and 0.81 +/- 0.11, respectively, to 187.2 +/- 27.6, 42.2 +/- 7.2, and 3.32 +/- 0.35 (P less than 0.05). With tamponade, PTI did not change (186.7 +/- 60.0), whereas VO2 di increased further to 3.98 +/- 0.98 (P less than 0.05) due to increased O2 extraction and no significant change in Qdi (32.8 +/- 4.0). As fatigue developed, VO2 di decreased to 2.30 +/- 0.23 due to the combined effects of small declines in Qdi and the arterial O2 content but remained higher than control even though the energy demands returned to control values. In conclusion, when cardiogenic shock is added to pulmonary edema VO2 di and energy output do not increase further and eventually fall.
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PMID:Diaphragmatic energetics and blood flow during pulmonary edema and hypotension. 339 91

Closing volume was measured by the single breath nitrogen washout test in six normal subjects both before and after inspiratory resistive loading to fatigue. Subjects breathed through an inspiratory resistance until they could no longer maintain the required mouth pressure throughout inspiration. There was electromyographic evidence of diaphragmatic fatigue in all experiments. Closing volume (expressed as a percentage of vital capacity) after resistive loading to fatigue (10.1 +/- 1.9%) was not significantly different from that before resistive loading (10.5 +/- 1.7%). Because pulmonary edema increases closing volume, this study suggests that the very negative intrathoracic pressures generated during resistive loading do not cause pulmonary edema. Therefore, the rapid shallow breathing following inspiratory resistive loading to fatigue is not due to pulmonary edema but is probably a direct consequence of fatigue.
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PMID:Closing volume after inspiratory resistive loading to fatigue. 360 15

A hypertensive urgency should be distinguished from a hypertensive emergency. Although the distinction may not always be obvious, certain guidelines may help the clinician determine which therapeutic approaches are most appropriate for each patient. Hypertensive emergencies include those conditions in which new or progressive severe end-organ damage is present and a delay in appropriate therapy might result in permanent damage, progression of complications, and a poor prognosis. Hypertensive urgencies include those conditions with minimal to no obvious end-organ damage in which blood pressure should be lowered expeditiously. The risk of immediate complications or organ damage is less likely to occur, and thus the immediate prognosis is better, although the ultimate prognosis, if untreated, is poor. There is a marked individual, racial, sexual, and age difference in the ability to tolerate high intraarterial pressure, as evidenced by patients' symptoms and signs of end-organ damage. Patients may have no symptoms of elevated blood pressure until significant intraarterial levels are reached. If symptoms are present, they may include headache, dizziness, blurred vision, shortness of breath (especially with exertion), chest pain, rapid pulse, palpitations, malaise and fatigue, nocturia, or pedal edema. Signs of hypertensive disease vary and depend not only on the level of blood pressure but also include funduscopic changes with arteriolar narrowing, atrioventricular nicking, hemorrhages, exudates or papilledema, central nervous system changes and neurologic abnormalities, cardiac changes with gallop rhythm, cardiomegaly, tachycardia, ectopic ventricular beats, left ventricular hypertrophy or signs of congestive heart failure, pulmonary edema, and signs of renal insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive emergencies and urgencies: pathophysiology and clinical aspects. 394 53

Inspiratory muscle fatigue and pulmonary edema are both known to cause rapid shallow breathing. It has been suggested that exercise tolerance in patients with pulmonary disease and cardiac disease may be limited by the development of inspiratory muscle fatigue and pulmonary edema, respectively, at maximal exercise. If these hypotheses are correct, breathing pattern during recovery from maximal exercise in these patients should be rapid and shallow compared with that during exercise. This study was performed to test these hypotheses. Seven patients with chronic obstructive pulmonary disease (COPD), 8 patients with interstitial lung disease (ILD), 7 patients with cardiac disease (CD) (mitral valve disease or left ventricular dysfunction) and 8 normal (NR) subjects each performed maximal incremental exercise on a cycle ergometer. Exercise breathing pattern was compared with that during recovery by calculating the mean difference in tidal volume (at the same levels of minute ventilation) between exercise and recovery for each subject. Recovery breathing pattern was similar to that during exercise for the COPD, ILD, and NR subjects. In contrast, breathing pattern during recovery was rapid and shallow compared with that during exercise for the CD patients; recovery tidal volume was less than that during exercise for the same level of minute ventilation. The fact that rapid shallow breathing does not develop during recovery from maximal exercise in patients with COPD or ILD suggests that inspiratory muscle fatigue does not limit their exercise tolerance. The relative rapid shallow breathing during recovery from maximal exercise in patients with CD is probably due to the development of pulmonary edema at maximal exercise, but further studies are needed to confirm this.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Breathing pattern during and after maximal exercise in patients with chronic obstructive lung disease, interstitial lung disease, and cardiac disease, and in normal subjects. 396 26


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