Study of tracheal dyskinesia impact on the cardiac hemodynamics

Tracheal dyskinesia (TD) was recently recognized as a possible mechanism for acute pulmonary edema (Elamin and Firdose, J Bronchol 2004;11:118-21; Khan and Elamin Eur Respir J 2005;26:319). This study was designed to evaluate possible impact of TD on cardiac hemodynamics.

Patients were prospectively assigned to either study "A" or control "B" groups (TD >50% or <50%, respectively) diagnosed by bronchoscopy or dynamic chest computed tomography. The cardiac hemodynamics was assisted by impedance cardiography (BioZ; CardioDynamics, San Diego, CA) at rest and during coughing. The latter was repeated after 5 minutes of rest.

Thirteen patients were assigned to group A and 14 to group B. There was higher incidence of hypertension, diabetes mellitus, and history of congestive heart failure in group A compared with group B. The percentage of TD was 85% +/- 10.0% versus 25% +/- 2.5%, in the A and B groups, respectively (P < 0.05). Stroke volume index (normal = 35-65 mL/beat/body surface area) was significantly reduced in group A 29.68 [95% confidence interval (CI), 25.557-33.818] compared with group B 38.321 (95% CI, 35.199-41.444; P < 0.05). In addition, the velocity index (representative of aortic blood velocity) was 32.188 (95% CI, 20.841-43.534, P < 0.049) in group A compared with 46.786 (95% CI, 38.209-55.363) in group B, and the left ventricular ejection time measured in milliseconds was 265.813 (95% CI, 246.065-285.560 in group A, P < 0.004) compared with 303.821(95% CI, 288.894-318.749) in group B.

This prospective study demonstrated the importance of recognizing TD as a pathologic entity and the need to consider TD in the workup of acute pulmonary edema especially if other tests were unrevealing.