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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although gynecologic laparoscopic surgery has recently become a routine and widespread operative procedure in Taiwan, the potential risks and complications in the clinical practice of laparoscopy should not be overlooked. Whilst the incidence of complications are rare, they can sometimes be serious, even life-threatening. This case report presents a woman with ruptured endometrioma, who developed sudden-onset cardiovascular collapse during laparoscopic procedure, in which carbon dioxide was used for insufflation. After resuscitation including cardioversion, her vital functions were restored; pulmonary edema developed soon afterwards but was resolved with conservative treatment. We discuss the possible causes of cardiovascular collapse during laparoscopic procedure and the management of resulting complications.
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PMID:Cardiovascular collapse during gynecologic laparoscopy complicated by pulmonary edema: report of a case. 786 64

We evaluated whether the postexercise reduction of pulmonary diffusion capacity for carbon monoxide (DLco) is influenced by a second bout of rowing and whether it affects arterial O2 tension during maximal exercise. After exercise, DLco was reduced [from a median of 37 (range of 30-44) to 34 (27-40) ml.min-1.mmHg-1; n = 21; P < 0.001], and both the membrane diffusion capacity [from 80 (58-139) to 68 (54-104) ml.min-1.mmHg-1] and the pulmonary capillary blood volume [from 88 (74-119) to 79 (61-121) ml; P < 0.01] were affected. A second bout of exercise did not influence DLco or membrane diffusion capacity (n = 7), but during both bouts arterial O2 tension was reduced [from 105 (91-110) to 91 (77-102) Torr; P < 0.001] and arterial O2 saturation decreased [from 0.98 (0.97-0.99) to 0.95 (0.86-0.96); P < 0.001]. Furosemide (iv) did not affect DLco (n = 7), suggesting that it was influenced by the central blood volume rather than by pulmonary edema.
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PMID:Restricted postexercise pulmonary diffusion capacity does not impair maximal transport for O2. 786 62

The aim of this prospective study was to analyse the contribution of the measurement of alveolar arterial gradients of CO2 during forced expiration in the diagnosis of pulmonary emboli occurring in chronic airflow obstruction (COPD) as a result of smoking. The study was carried out on 178 patients: Group 1: 54 subjects without emboli (14 controls, 33 COPD and 7 patients with chest pain); Group 2: 72 patients with proved emboli (49 non COPD, 23 COPD); Group 3: 52 patients COPD presenting with varied non-embolic broncho-pulmonary pathology (pneumonia, bronchospasm, pulmonary oedema, bronchial neoplasm). The diagnosis of pulmonary emboli was confirmed by scintigraphy in patients with non COPD or angiography (in patients with COPD). The maximal fraction of CO2 was measured using a capnologue during a forced expiration which was long and prolonged until residual volume was achieved. The PaCO2 was measured simultaneously by an analysis of arterial blood gases. The D index was calculated according to the formula [(PaCO2-PEM CO2)/PaCO2] x 100. The D index was significantly lower in Group 1 (3.42 +/- 3.8% p < 0.0001) than in Group 2 (20.8 +/- 10%) and Group 3 (17.6 +/- 11.7%) (not significant between Groups 2 and 3). In patients with COPD the specificity and sensitivity and the predicted positive and negative value were 100% for a D limit of 7%. In COPD patients these values were respectively 82, 95, 75 and 96% for a D limit of 7%; on the other hand for a D below 5% the values were 60, 100, 64 and 100% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The significance of maximal expiratory concentrations of CO2 (MEC CO2) in the negative diagnosis of acute pulmonary embolism in chronic obstructive bronchopneumopathies]. 789 65

Inhalation of smoke containing acrolein, the most common toxin in urban fires after carbon monoxide, causes vascular injury with non-cardiogenic pulmonary edema containing potentially edematogenic eicosanoids such as thromboxane (Tx) B2, leukotriene (LT) B4, and the sulfidopeptide LTs (LTC4, LTD4, and LTE4). To determine which eicosanoids are important in the acute lung injury, we pretreated sheep with BW-755C (a combined cyclooxygenase and lipoxygenase inhibitor), U-63557A (a specific Tx synthetase inhibitor), or indomethacin (a cyclooxygenase inhibitor) before a 10-min exposure to a synthetic smoke containing carbon particles (4 microns) with acrolein and compared the results with those from control sheep that received only carbon smoke. Acrolein smoke induced a fall in arterial PO2 and rises in peak inspiratory pressure, main pulmonary arterial pressure, pulmonary vascular resistance, lung lymph flow, and the blood-free wet-to-dry weight ratio. BW-755C delayed the rise in peak inspiratory pressure and prevented the fall in arterial PO2, the rise in lymph flow, and the rise in wet-to-dry weight ratio. Neither indomethacin nor U-63557A prevented the increase in lymph flow or wet-to-dry weight ratio, although they did blunt and delay the rise in airway pressure and did prevent the rises in pulmonary arterial pressure and pulmonary vascular resistance. Thus, cyclooxygenase products, probably Tx, are responsible for the pulmonary hypertension after acrolein smoke and to some extent for the increased airway resistance but not the pulmonary edema. Prevention of high-permeability pulmonary edema after smoke with BW-755C suggests that LTB4, may be etiologic, as previous work has eliminated LTC4, LTD4, and LTE4.
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PMID:Cyclooxygenase and lipoxygenase inhibition by BW-755C reduces acrolein smoke-induced acute lung injury. 800 44

Smoke inhalation injury in children still represents a significant cause of pulmonary disease and mortality. Carbon monoxide and other toxic products of combustion are major determinants of severity. Early hypoxemia is a contributor to over 50% of deaths. There are several clinical entities: upper airway obstruction, bronchospasm, consolidation, pulmonary edema, ARDS, and late pneumonia. Intensive care has improved outcome from burns, but pulmonary injury is still an important cause of mortality. New therapies such as high frequency ventilation may improve the outcome. Primary prevention is the most important way to reduce the poor outcome from significant exposure.
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PMID:Smoke inhalation injury. 813 78

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

The purpose of this study was to determine the effect of inverse ratio ventilation (IRV) on gas exchanges and circulatory systems in 56 mongrel dogs with oleic acid induced pulmonary edema. The dogs were divided into 9 groups and were ventilated with 9 kinds of ventilatory modes such as I:E ratio of 1:2 (control), 2:1 (2:1 IRV), 3:1 (3:1 IRV), 1:2 with 5 cmH2O PEEP (1:2 PEEP 5), 2:1 with 5 cmH2O PEEP (2:1 PEEP 5), 3:1 with 5 cmH2O PEEP (3:1 PEEP 5), 1:2 with 10 cmH2O PEEP (1:2 PEEP 10), 2:1 with 10 cmH2O PEEP (2:1 PEEP 10) and 3:1 with 10 cmH2O PEEP (3:1 PEEP 10), using a Servo ventilator 900C. IRV could not improve arterial oxygenation in dogs with oleic acid induced pulmonary edema, but PEEP could significantly improve arterial oxygenation depending on PEEP level. Although in the control group, PaCO2 increased gradually, PaCO2 was kept constant for 8 hours in the 3:1 IRV groups. In the 2:1 group, PaCO2 did not change significantly until 6 hours, but in IRV with 10 cmH2O PEEP groups, PaCO2 showed the highest increase. There was no significant alteration in hemodynamics after ventilatory modes were changed to IRV. Although oxygen delivery was the best in the 3:1 IRV group, there was no statistical significance between the 3:1 IRV group and others. It was concluded that IRV did not improve arterial oxygenation but showed a favorable effect for CO2 elimination, in dogs with oleic acid induced pulmonary edema.
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PMID:[Effects of inverse ratio ventilation and positive end-expiratory pressure on gas exchanges in dogs with oleic acid induced pulmonary edema]. 818 79

We report on eight cases of amiodarone pulmonary toxicity. Main clinical symptoms are acute/subacute dyspnea or progression in some cases. Amiodarone responsibility is difficult to ascertain. Several arguments can be presented: clinical symptoms with dyspnea and/or fever and/or cough, interstitial or in diffusing capacity for carbon monoxide, abnormal broncho-alveolar lavage cytopreparation smear with increased percentage of lymphocytes and polymorphonuclear leucocytes in typical cases; trans-bronchoscopic lung biopsy failed to provided information on amiodarone toxicity in the two patients where biopsy were performed. Differential diagnosis is an essential step to eliminate other possible causes ie pulmonary micro-organism infections, cancer or pulmonary oedema secondary to heart failure. In one case acute pulmonary toxicity occurred early, after introduction of amiodarone, with a proposed immuno-allergic mechanism. In other cases, chronic amiodarone deposition in the lungs can explain clinico-radiologic features. In six cases improvement was observed after discontinuation of therapy within a 6-months period.
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PMID:[Pneumopathy caused by amiodarone in internal medicine: 8 cases]. 819 Oct 72

A case of successfully treated multiple venous air embolism occurred in a man aged 41 operated on for cerebellar tumour. Postoperatively exceptionally serious complication developed in the form of neurogenic pulmonary oedema. Attention is called to a number of aetiological factors in this case. The anaesthesiological management in such cases should include careful monitoring of end-tidal CO2 concentration and insertion of catheter into right atrium.
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PMID:[Multiple venous air embolism during cerebellar tumor surgery. Case report]. 823 43

Highly trained athletes (HT) have been found to show arterial hypoxaemia during strenuous exercise. A lack of compensatory hyperpnoea and/or a limitation of pulmonary diffusion by pulmonary interstitial oedema have been suggested as causes, but the exact role of each is not clear. It is known, however, that interstitial pulmonary oedema may result in rapid shallow breathing (RSB). The purpose of this study was therefore twofold: firstly, to determine the exact role of a lack of compensatory hyperpnoea versus a widened in ideal alveolar minus arterial oxygen partial pressure difference [PA(i)-aO2] in the decrease in partial pressure of oxygen in arterial blood (PaO2) and, secondly, to detect RSB during recovery in HT. Untrained subjects (UT) and HT performed exhausting incremental exercise. During rest, exercise testing, and recovery, breathing pattern, respiratory gas exchange, and arterial blood gases were measured. The PA(i)-aO2 and the difference in tidal volume (VT) between exercise and recovery for the same level of ventilation, normalized to vital capacity of the subject [delta VT(%VC)], were then calculated. A large positive delta VT(%VC) was considered to be the sign of RSB. HT showed a marked hypoxaemia (F = 11.6, P < 0.0001), higher partial pressure of carbon dioxide in arterial blood (F = 3.51, P < 0.05), and lower ideal partial pressure of oxygen in alveolar gas (P < 0.001). The relationship between PA(i)-aO2 and oxygen consumption was the same for the two groups. The widening PA(i)-aO2 persisted throughout recovery for both HT and UT. The RSB was observed in HT during recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary gas exchange and breathing pattern during and after exercise in highly trained athletes. 829 15


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