Hemodynamic Alterations of Acute Pulmonary Thromboembolism

SUMMARY We studied steady state transvascular fluid and protein exchange after uneven obstruction of the pulmonary arteries. In anesthetized sheep, ventilated by positive pressure, we measured pulmonary artery and left atrial pressures, cardiac output, lung lymph flow, and lymph/plasma protein ratios. We calculated pulmonary vascular resistance. In 16 sheep we obstructed the pulmonary arteries with various microemboli or balloons in lobar arteries until pulmonary vascular resistance was 2-3 times baseline. In every experiment, lung lymph flow increased as pulmonary vascular resistance increased. The lymph/plasma protein ratio did not change. In four sheep, we increased left atrial pressure by balloon obstruction of the mitral orifice. Pulmonary artery pressure increased as much as in the embolization experiments and lymph flow increased but the lymph/plasma protein ratio decreased, meaning that the increased fluid and protein flux after embolization cannot be due to high pulmonary artery or pulmonary venous outflow pressures alone. In four sheep we compared obstruction of the lower lobe pulmonary arteries by balloons with that of upper lobe pulmonary arteries. Lower lobe arterial obstruction caused the lymph flow which drains predominantly from the lower lobes to decrease whereas upper lobe artery obstruction increased lymph flow. This means that the increased fluid and protein flux occurred mainly in the open, perfused portion of the microvascular bed. The mechanism of the increased fluid filtration and protein permeability may be related to high vascular pressure and high linear blood flow velocity through a markedly restricted microvascular bed, although release of substances that affect endothelial permeability is not ruled out.IN THE ADULT respiratory distress syndrome, 1 a central feature is the occurrence of interstitial and alveolar edema. Since in pathological sections the edema fluid stains similarly to blood plasma (proteinaceous) and since there are often hyaline membranes in the air spaces, the edema is considered to be of the increased microvascular permeability variety.2 Hemodynamically, features commonly noted are an increase in pulmonary arterial pressure in the face of a normal pulmonary artery wedge pressure or a directly measured left atrial pressure. The calculated pulmonary vascular resistance is elevated. Numerous investigators 3 " 5 have frequently found plugging of pulmonary small arteries and microvessels by various types of microemboli.How is it that obstruction of pulmonary arteries causes pulmonary edema due to increased microvascular permeability? Gibbon and Gibbon 6 made one of the earliest observations on this syndrome. They found that resection of 70% of the lung mass in cats was followed by the development of pulmonary edema, especially if the resection was accompanied by infusions of whole blood or plasma. Although they believed the edema was due to the high pressure in the microvessels, they did suggest that the edema fluid was only slightly diluted plasma (that is, typical of...

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“…Parmley and associates 8 reported pulmonary edema as the immediate cause of death in 8 of 30 dogs given autologous blood clot emboli.…”

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confidence: 99%

Lung fluid exchange after uneven pulmonary artery obstruction in sheep.

Ohkuda¹,

Nakahara²,

Weidner³

et al. 1978

Circulation Research

110

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“…While Souza et al found a significant relationship between the PVS and unilateral PTE, we found a significant relationship between the PVS and bilateral PTE. This may be due to the fact that PTE in the main pulmonary artery or bilateral PTE markedly increases pulmonary artery pressure and pulmonary vascular resistance . However, it does not seem possible to make more comments according to the retrospective analysis in which pulmonary artery pressure and resistance measurements could not be performed.…”

Section: Discussionmentioning

confidence: 99%

A new perspective for pulmonary thromboembolism radiology: ‘Pulmonary vein sign’

Ermin

Çinkooğlu

Susam

et al. 2018

Clinical Respiratory J

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Introduction Pulmonary thromboembolism (PTE) is a clinical condition that can result in sudden death. Computed tomography pulmonary angiography (CTPA) is the most sensitive imaging technique for the diagnosis of PTE. Filling defects in the pulmonary veins, which can be identified in areas adjacent to PTE, have been named the ‘pulmonary vein sign’ (PVS). Objectives The aim of our study is to determine the frequency, sensitivity and specificity of PVS due to the decreased venous drainage in the affected area in PTE patients. Methods Patients who were admitted to the emergency department due to the suspicion of PTE and who underwent CTPA were evaluated retrospectively. The study group consisted of the patients who had an arterial filling defect on CTPA and were diagnosed with PTE. The control group consisted of the patients who had no arterial filling defect on CTPA. Results This study included 286 patients with a mean age of 62(20‐94) years. The PVS was detected in 51(32.7%) of the patients in the study group and in 15(11.5%) of the patients in the control group. The PVS had a sensitivity of 32.69%, a specificity of 88.46%, a positive predictive value of 77.27% and a negative predictive value of 52.27% for PTE. The PVS was significantly more common in the patients having PTE in the bilateral pulmonary arteries or the main pulmonary arteries. Conclusion Despite low sensitivity, the presence of PVS on CTPA is a radiographic marker with high specificity for PTE. To use in practice, there is need for studies with large numbers of patients.

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“…The increase in lung water from uneven obstruction of the pulmonary vasculature ("overperfusion pulmonary oedema") has been studied in animals with a variety of micro emboli,s and has been suggested as a contributing factor in the pulmonary oedema, sometimes seen in pulmonary thrombo-embolism. 9 ,!O The pathogenesis of the oedema may involve "overperfusion" and transmission of high pressures to the unobstructed vasculature, although the release of substances altering endothelial permeability has not been excluded. O'Kuda et al theorise that physical injury to the endotheliun by high velocity and high pressure flow in the patent pulmonary microcirculation may account for the permeability oedema seen.…”

Section: Discussionmentioning

confidence: 99%

The Fulminant Fat Embolism Syndrome

Hagley

1983

Anaesth Intensive Care

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The fulminant form of the fat embolism syndrome is a rare though often fatal complication of injury. Little discussion but much controversy surrounds the subject despite it being of considerable interest to all those managing the early phase of trauma. Recognised presentations of this condition are the fulminating onset, soon after injury, of acute cor pulmonale, respiratory failure and embolic neurological phenomena. I This report describes five cases of the fulminant fat embolism syndrome seen over a period of eight years. Case 1 A 53-year-old man was admitted with a comminuted compound fracture of the tibia and fibula. He was conscious, with a blood pressure of 120/80 mmHg and pulse rate of 90/min. There was no continuing massive blood loss on admission and he was given Stable Plasma Protein Solution 500 ml intravenously. Because he began bleeding profusely from the site of injury an arterial tourniquet was applied and SPPS 500 ml whole blood 1,500 ml and crystalloid solution 2,000 ml given to combat shock. Three and a half hours after injury he was anaesthetised for amputation of the leg. Fifteen

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Hemodynamic Alterations of Acute Pulmonary Thromboembolism

Cited by 45 publications

References 23 publications

Lung fluid exchange after uneven pulmonary artery obstruction in sheep.

Lung fluid exchange after uneven pulmonary artery obstruction in sheep.

A new perspective for pulmonary thromboembolism radiology: ‘Pulmonary vein sign’

The Fulminant Fat Embolism Syndrome

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