title: The pathogenesis of acute pulmonary edema associated with hypertension.
abstract: BACKGROUND
  Patients with acute pulmonary edema often have marked hypertension but, after reduction of the blood pressure, have a normal left ventricular ejection fraction (> or =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< 0.01) at the time of the follow-up examination. Despite the marked difference in blood pressure, the ejection fraction was similar during the acute episode (0.50+/-0.15) and after treatment (0.50+/-0.13). The left ventricular regional wall-motion index (the mean value for 16 segments) was also the same during the acute episode (1.6+/-0.6) and after treatment (1.6+/-0.6). No patient had severe mitral regurgitation during the acute episode. Eighteen patients had a normal ejection fraction (at least 0.50) after treatment. In 16 of these 18 patients, the ejection fraction was at least 0.50 during the acute episode.
  
  
  CONCLUSIONS
  In patients with hypertensive pulmonary edema, a normal ejection fraction after treatment suggests that the edema was due to the exacerbation of diastolic dysfunction by hypertension--not to transient systolic dysfunction or mitral regurgitation.
authors.affiliation: Cardiology Section, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1045, USA.
authors.forename: S K
authors.initials: SK
authors.lastname: Gandhi
authors.forename: J C
authors.initials: JC
authors.lastname: Powers
authors.forename: A M
authors.initials: AM
authors.lastname: Nomeir
authors.forename: K
authors.initials: K
authors.lastname: Fowle
authors.forename: D W
authors.initials: DW
authors.lastname: Kitzman
authors.forename: K M
authors.initials: KM
authors.lastname: Rankin
authors.forename: W C
authors.initials: WC
authors.lastname: Little
mesh_terms: D000208:Acute Disease; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D003971:Diastole; D004232:Diuretics / Q000627:therapeutic use; D015150:Echocardiography, Doppler; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008944:Mitral Valve Insufficiency / Q000150:complications; D011654:Pulmonary Edema / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000209:etiology*; D011859:Radiography; D013318:Stroke Volume; D014665:Vasodilator Agents / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000150:complications*; D016277:Ventricular Function, Left
chemical_list: D000959:Antihypertensive Agents; D004232:Diuretics; D014665:Vasodilator Agents