Mechanisms leading to lung edema in pulmonary embolization

Kabins, Sherwin A.; Fridman, Jaime L.; Neustadt, Jerome E.; Espinosa, Gerard; Katz, Louis N.

doi:10.1152/ajplegacy.1960.198.3.543

Cited by 16 publications

(3 citation statements)

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“…Indeed pulmonary edema has been suggested as one source of hypoxemia in animals following starch embolism (3,48). In the present study the persistence of the shunting for several weeks after the embolus makes pulmonary edema unlikely as a cause.…”

Section: Discussionmentioning

confidence: 99%

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Hypoxemia in pulmonary embolism, a clinical study

Wilson¹,

Pierce²,

Johnson³

et al. 1971

J. Clin. Invest.

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A B S T R A C T The cause of hypoxemia was studied in 21 patients with no previous heart or lung disease shortly after an episode of acute pulmonary embolism. The diagnosis was based on pulmonary angiography demonstrating distinct vascular filling defects or "cutoffs." It was found that virtually all of the hypoxemia in patients with previously normal heart and lungs could be accounted for on the basis of shunt-like effect. The magnitude of the shunting did not correlate with the percent of the pulmonary vascular bed occluded nor with the mean pulmonary artery pressure. The shunts tended to gradually recede over about a month after embolism. Patients without pulmonary infarction were able to inspire 80-111% of their predicted inspiratory capacities, and this maneuver temporarily diminished the observed shunt. Patients with pulmonary infarcts were able to inhale only to 60-69% of predicted inspiratory capacity, and this did not reverse shunting. These data suggest that the cause of right-to-left shunting in patients with pulmonary emboli is predominantly atelectasis.When the elevation of mean pulmonary artery pressure was compared to cardiac index per unit of unoccluded lung, it fell within the range of pulmonary hypertension predicted from published data obtained in patients with exercise in all except one case. This observation suggests that pulmonary vasoconstriction following embolism is not important in humans, although these data are applicable only during the time interval in which our patients were studied and in patients receiving heparin.

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Section: Discussionmentioning

confidence: 99%

“…(c) The response to foreign body or autologous blood clot emboli may differ from the response to emboli that have existed as thrombi in peripheral veins. (d) There are considerable species differences in the responses to emboli (2)(3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Hypoxemia in pulmonary embolism, a clinical study

Wilson¹,

Pierce²,

Johnson³

et al. 1971

J. Clin. Invest.

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“…24 In experimental pulmonary embolism, pulmonary venous hypertension has also been reported in situations where left atrial pressure remains normal. 25,26 These studies suggest that other mechanisms may be involved.…”

Section: Discussionmentioning

confidence: 89%

Pulmonary embolism as a cause of pulmonary oedema

Montgomery

Marshall

Woolf

et al. 1995

Clinical Intensive Care

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Acute pulmonary oedema is a well-described complication of pulmonary embolism. However, the relationship between these two conditions is not widely appreciated by physicians and the diagnosis of an underlying pulmonary embolism in patients with pulmonary oedema may well be missed. We describe two cases in which pulmonary oedema complicated pulmonary embolism, and discuss the possible factors involved in the development of oedema. These include altered left ventricular (LV) function, increased lung microvascular permeability, overperfusion and reperfusion injury. We also emphasise the importance of considering the possibility of an underlying pulmonary embolism in patients with pulmonary oedema so that appropriate thrombolytic therapy can be given early. Case histories Case oneA 78-year-old male ex-smoker with no previous history of cardiorespiratory symptoms presented with a 10-day history of dyspnoea. This had begun six days after a transurethral resection of a bladder tumour when he was awoken by fleeting sharp chest pain, and breathlessness which persisted until admission. On examination he was in sinus rhythm (80 bpm), with an audible third heart sound, a blood pressure of 145/80 mmHg, a jugular venous waveform visible 3 cm above the sternal angle and bilateral pitting oedema up to the lower thigh. Electrocardiography (ECG) showed occasional runs of 10 beats of atrial fibrillation (160 bpm). Arterial blood gases breathing room air were: pH 7.49, PaO 2 10.7 kPa, PaCO 2 4.3 kPa. Plain posteroanterior chest radiography (CXR) showed upper lobe blood diversion and interstitial shadowing. Routine haematology and biochemistry were normal.Left ventricular failure and paroxysmal atrial fibrillation were diagnosed by the admitting junior doctor, and treated with intravenous heparin, diuretics, and amiodarone. Twentyfour hours later the PaO 2 fell to 4.8 kPa (on room air), and the

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Pulmonary Circulation

Fishman

1985

Comprehensive Physiology

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Mechanisms leading to lung edema in pulmonary embolization

Cited by 16 publications

References 0 publications

Hypoxemia in pulmonary embolism, a clinical study

Hypoxemia in pulmonary embolism, a clinical study

Pulmonary embolism as a cause of pulmonary oedema

Pulmonary Circulation

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