Key result
Induction of acute pulmonary embolism in pigs immediately increased mean lung attenuation (P < .001) and pulmonary pressures, inducing ground-glass opacification in unobstructed lung zones.
Why the study?
Does acute pulmonary embolism induce ground-glass opacification related to hemodynamic changes in a pig model?
Does acute pulmonary embolism induce ground-glass opacification related to hemodynamic changes in a pig model?
p-value: p=< .001
Acute pulmonary embolism induces ground-glass opacification in unobstructed lung zones on CT, which correlates with elevated pulmonary pressures consistent with pulmonary edema.
Does not support clinical use of GGO-hemodynamic links in PE; leaves open translation from this animal model.
PURPOSE: To investigate the link between acute pulmonary embolism (PE) and occurrence of ground-glass opacity (GGO) and the relationships between this occurrence and hemodynamics in an animal model of acute PE. MATERIALS AND METHODS: In this animal care committee-approved study, PE was achieved by injecting blood clots through a central venous catheter in five pigs. Thin-section computed tomography (CT) and hemodynamic measurements-mean pulmonary arterial pressure (Ppa), systemic and pulmonary cardiac outputs, effective pulmonary capillary pressure (Pc'), right atrial pressure, and occluded Ppa-were obtained before and after PE was achieved. Severity and extent of GGO were assigned scores subjectively, and lung attenuation was measured on each scan. Measurements were performed every 20 minutes after PE was achieved, for a total duration of 60 minutes. Finally, CT pulmonary angiography was performed. Lung attenuation was measured in unobstructed and obstructed zones. Measurements were compared by using analysis of variance and Student t test when appropriate. Correlations were investigated through Spearman rank correlation test. RESULTS: In the unobstructed lung zones, GGO appeared immediately after PE was achieved, with an increased mean lung attenuation (P < .001). Mean Ppa and Pc' increased immediately after PE was achieved, and Pc' reached 23 mm Hg, a value associated with pulmonary edema. Cardiac output did not change (P = .238). Lung attenuation and subjective score assignment for GGO were significantly correlated with Ppa and Pc' (P < .001 to .002). CONCLUSION: Acute PE induces GGO in unobstructed lung zones. Given constant cardiac output, GGO is likely to be related to redistribution of blood flow from obstructed to unobstructed lung zones and occurs at a pressure consistent with pulmonary edema.
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Thoma et al. (2009) studied acute pulmonary embolism (n=5). Injection of blood clots to induce acute pulmonary embolism vs. Baseline (before PE was achieved) was evaluated on Lung attenuation and hemodynamics (mean pulmonary arterial pressure and effective pulmonary capillary pressure) (p=< .001). Induction of acute pulmonary embolism in pigs immediately increased mean lung attenuation (P < .001) and pulmonary pressures, inducing ground-glass opacification in unobstructed lung zones.
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