The pathogenesis of acute pulmonary edema associated with hypertension.
The pathogenesis of acute pulmonary edema associated with hypertension.
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DOI：
10.1056/nejm200101043440103
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发表时间：
2001-01-04
影响因子：
158.5
通讯作者：
Little, WC
中科院分区：
文献类型：
--
作者：
Gandhi, SK;Powers, JC;Little, WC
背景资料：急性肺水肿患者通常有明显的高血压，但在血压降低后，左心室射血分数正常（大于/等于0.50）。然而，肺水肿可能不是由于孤立的舒张功能障碍，但相反，可能是由于短暂的收缩功能障碍，急性二尖瓣返流，或bounds.Methods：我们研究了38例（14名男性和24名女性，平均[+/-SD]年龄，67+/-13岁）与急性肺水肿和收缩压大于160毫米汞柱。结果：急性发作时平均收缩压为200 ± 26 mmHg，治疗后平均收缩压为139 ± 17 mmHg（P < 0.01），治疗后1 ~ 3d平均收缩压为200 ± 26 mmHg（P < 0.01），治疗后1 ~ 3d平均收缩压为139 ± 17 mmHg（P < 0.01）。
Background: Patients with acute pulmonary edema often have marked hypertension but, after reduction of the blood pressure, have a normal left ventricular ejection fraction (greater/equal 0.50). However, the pulmonary edema may not have resulted from isolated diastolic dysfunction but, instead, may be due to transient systolic dysfunction, acute mitral regurgitation, or both.Methods: We studied 38 patients (14 men and 24 women; mean [+/-SD] age, 67+/-13 years) with acute pulmonary edema and systolic blood pressure greater than 160 mm Hg. We evaluated the ejection fraction and regional function by two-dimensional Doppler echocardiography, both during the acute episode and one to three days after treatment.Results: The mean systolic blood pressure was 200+/-26 mm Hg during the initial echocardiographic examination and was reduced to 139+/-17 mm Hg (P