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

Restoration of normal sinus rhythm is usually followed by improved hemodynamics. By contrast, pulmonary edema and cardiovascular collapse have been reported following successful electrical reversion of various tachyarrhythmias to normal sinus rhythm. The mechanism for this adverse reaction is not clear but has been thought to relate, at least in part, to electrical myocardial damage from the countershock. This report describes a patient in whom this complication occurred on two occasions, first following external countershock and subsequently following burst atrial pacing. Thus, conversion to sinus rhythm may be responsible for this phenomenon independent of the method of conversion.
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PMID:Pulmonary edema following conversion of tachyarrhythmia. A case following burst atrial pacing. 394 64

A 2 1/2 year old boy had a sudden, severe, and unexpected anaphylactoid reaction after an otherwise uncomplicated repair of a partial atrioventricular septal defect. The reaction, comprising haemorrhagic pulmonary oedema and peripheral circulatory collapse, followed neutralisation of heparin by protamine. Measurements of serum complement (C3 and C4) concentrations suggested that a pronounced consumption of complement occurred during the adverse response.
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PMID:Complement activation and anaphylactoid response to protamine in a child after cardiopulmonary bypass. 399 75

Sixteen Holstein cattle allotted into 4 groups (4 cattle/group) were each given a single oral dosage of 0.2 g of 3-methylindole (3MI)/kg of body weight. The groups were killed at 12, 24, 48, and 72 hours, respectively, after 3MI administration. Comparison of clinical signs, pathologic pulmonary lesions, and in vitro pulmonary artery responses to pharmacologic stimuli was made between the 4 treated groups and 8 control Holstein cattle of similar age. Clinical signs of pulmonary distress first appeared 8 to 12 hours after 3MI administration. After 20 hours, clinical signs included dyspnea, moderate depression, and a marked expiratory grunt. A partial remission of these clinical signs was seen between 30 and 45 hours after 3MI administration. After remission, the cattle had clinical signs of severe dyspnea and depression and expiratory grunts were more pronounced. Pathologic pulmonary lesions, including heavy rubbery lungs, dilated interlobular septae, and subplural air bullae characteristic of pulmonary edema and interstitial emphysema were observed. The lungs of treated cattle did not collapse when the thorax was incised at necropsy. In vitro pulmonary artery strips contracted dose dependently to norepinephrine (NE). Group I tissues (12 hours after 3MI administration) responded similarly to control samples. Group II tissues (24 hours after 3MI administration) had a significant inhibition (P less than 0.05) in response to NE stimulation as compared with controls.
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PMID:Impairment of sympathetic pulmonary vasoconstriction by 3-methylindole in cattle. 401 39

Fatal air embolism as a complication of legal abortion in a 29-year-old woman is reported. After anesthesia had been induced and dilatation accomplished (Hegar 14), the suction tube was introduced into the uterus. The surgeon felt unusually heavy pressure when the pump was started, and heavy bleeding was observed. Aspiration was discontinued, and the abortion was completed by curettage. Irregular breathing and cardiovascular collapse occurred 4 minutes after the start of the operation, and resuscitation attempts were unsuccessful. Autopsy revealed pulmonary edema, pulmonary emphysema, and air bubbles in many areas of the vascular system, which confirmed the clinical diagnosis of air embolism. The hose of the suction cannula was found to have been attached to the exhaust outlet of the suction pump. It is suggested that the exhaust should be clearly differentiated from the intake valve in order to avoid similar accidents in the future.
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PMID:[Fatal complications by air embolism in legal interruption of pregnancy]. 445 11

The inhalation of toxic gases or vapours is capable of resulting in pulmonary oedema (P.O.), the mechanism of which corresponds, on the basis of a number of hemodynamic studies carried out, to that which characterises the so-called "lesional" pulmonary oedema, which is different from so-called "hemodynamic" oedema. Classically PAP, PCP and P wedge pressure have virtually normal values (normalisation of pulmonary arterial hypertension by correction of hypoxemia). CI and SWILV are normal or increased and pulmonary resistances are virtually normal. The origin of the oedema is thus related to an increase in alveolo-capillary permeability. The inhalation of toxic gases or vapours with a caustic or irritant action, or containing particles, however, usually adds on an obstructive syndrome, similar to a severe asthmatic attack. Under such conditions, the marked reduction in intrathoracic pressure during inspiration definitely favours pulmonary oedema by decreasing intra-alveolar pressure and by the accumulation of blood in the pulmonary circulation, and is capable of masking pulmonary arterial hypertension. Raised pressure, related to expiratory effort, on the contrary, decreases venous return and may result in collapse of the capillaries. Whilst the principal mechanism of PO by the inhalation of toxic gases or vapours is related to an increase in alveolo-capillary permeability, it is nevertheless important not to under-estimate the role of variations in intra-thoracic pressures which may constitute a provoking or at least aggravating element.
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PMID:[Pulmonary edema of toxic origin. Hemodynamic data]. 611 Dec 79

It has been observed that the lung surfactant activity decreased after exposure of the animals to diesel automobile exhaust. This decreased lung surfactant activity could be an important factor in the pathogenesis of pulmonary oedema and collapse seen in our experiments.
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PMID:Diesel automobile exhaust anad lung surfactant activity in an experimental study, in rats. 616 4

In 200 young patients with apparently idiopathic spontaneous pneumothorax, the following radiologic features were analyzed: degree of collapse on the initial chest film, areas of atelectasis, and presence of blebs, apical opacities, fibrous adhesions, pleural effusions, and controlateral shift of mediastinal structures. Confrontation of apical changes with pathologic findings in operative specimens suggests that mesothelial rupture with reactive hyperplasia results in a "pneumatization chamber" visible as a bullous image. Following drainage, homolateral shifts of mediastinum and four cases of pulmonary edema were recorded. Risk factors for pulmonary edema include severe pulmonary collapse with areas of atelectasis, persisting for more than 48 hours and an aspiration which either exceeded 1.5 l. of air or was performed with a depression of more than 30 cm of water.
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PMID:[Radiology of spontaneous pneumothorax in young patients. Apropos of 200 cases]. 632 55

In the anaesthetized rat, injection of the prostaglandin endoperoxide analog, U 44069, in the right ventricle is vasopressor both in the pulmonary and the systemic circulation. When a moderate dose is used, the hypertensive response of the systemic vascular bed changes in an hypotension. The toxicity seems to be cumulative. At high doses, a vascular collapse is observed sometimes with pulmonary oedema. These findings correlate with the EKG pattern typical for an acute cor pulmonale.
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PMID:[Cardiovascular responses of the rat to a prostaglandin endoperoxide analog]. 644 70

Many nonpulmonary diseases may present with respiratory manifestations or may involve the lungs later in the disease course. The mechanisms by which such involvement occurs are almost as diverse as the diseases themselves and include the following. Hematogenous spread of disease is one of the most common mechanisms of lung involvement, for example, lung involvement by metastatic malignant disease. Cytotoxic factors from another anatomic location may be deposited in the alveolar basement membranes and cause pulmonary damage, for example, pulmonary hemorrhage associated with Goodpasture's syndrome. The pulmonary vasculature may prominently manifest generalized disease, as frequently occurs in Wegener's granulomatosis. Toxins accumulated as a result of disease in another organ system may damage the alveolar capillaries and result in pulmonary edema, as can occur in patients with severe azotemia due to renal failure. Depletion of lung surfactant as a consequence of disease in another organ system may produce alveolar collapse and respiratory failure; a disease that can have this effect is acute pancreatitis. The lungs may be the first organs to exhibit, through unknown mechanisms, underlying systemic diseases such as the collagenoses. Humoral factors released in another anatomic site may cause pulmonary problems; for example, bronchospasm may develop in patients with carcinoid of the intestine as a result of serotonin released by the tumor. Injury to another organ system can produce lung damage by complex mechanisms; an excellent example is the occasional development of neurogenic pulmonary edema in patients with trauma to the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory manifestations of systemic disease. 3. Neurologic, skeletal, dermatologic, gynecologic, and gonadal diseases and disorders of pregnancy. 647 14

The clinical syndrome of anaphylaxis may be produced by a number of mechanisms. The life-threatening clinical features are angioneurotic oedema, bronchospasm, cardiovascular collapse and pulmonary oedema. The initial treatment consists of general resuscitation plus adrenaline. In shock, colloid solutions should be used to restore blood volume. The pulmonary oedema that occurs is a membrane oedema, and should be treated with artificial ventilation, positive end expiratory pressure, and volume replacement. After a reaction, all available tests should be used to determine the cause, and the patient should be given a warning letter describing the evidence for attributing his reaction to the determined cause. (This should be done in addition to the provision of any identification bracelet.) Pharmacological pretreatment is a valid preventive manoeuvre, but is not 100% reliable.
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PMID:Anaphylaxis. 648 87


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