Conduit Flow Compensates for Impaired Left Atrial Passive and Booster Functions in Advanced Diastolic Dysfunction.

BACKGROUND: Quantification of left atrial (LA) conduit function and its contribution to left ventricular (LV) filling is challenging because it requires simultaneous measurements of both LA and LV volumes. The functional relationship between LA conduit function and the severity of diastolic dysfunction remains controversial. We studied the role of LA conduit function in maintaining LV filling in advanced diastolic dysfunction. METHODS: We performed volumetric and flow analyses of LA function across the spectrum of LV diastolic dysfunction, derived from a set of consecutive patients undergoing multiphasic cardiac computed tomography scanning (n=489). From LA and LV time-volume curves, we calculated 3 volumetric components: (1) early passive emptying volume; (2) late active (booster) volume; and (3) conduit volume. Results were prospectively validated on a group of patients with severe aortic stenosis (n=110). RESULTS: The early passive filling progressively decreased with worsening diastolic function (P<0.001). The atrial booster contribution to stroke volume modestly increases with impaired relaxation (P=0.021) and declines with more advanced diastolic function (P<0.001), thus failing to compensate for the reduction in early filling. The conduit volume increased progressively (P<0.001), accounting for 75% of stroke volume (interquartile range, 63-81%) with a restrictive filling pattern, compensating for the reduction in both early and booster functions. Similar results were obtained in patients with severe aortic stenosis. The pulmonary artery systolic pressure increased in a near-linear fashion when the conduit contribution to stroke volume increased above 60%. Maximal conduit flow rate strongly correlated with mitral E-wave velocity (r=0.71; P<0.0001), indicating that the increase in mitral E wave in diastolic dysfunction represents the increased conduit flow. CONCLUSIONS: An increase in conduit volume contribution to stroke volume represents a compensatory mechanism to maintain LV filling in advanced diastolic dysfunction. The increase in conduit volume despite increasing LV diastolic pressures is accomplished by an increase in pulmonary venous pressure.

On the sources of drift in a turbine-based spirometer.

A systematic study on the sources of drift in a turbine-based spirometer (VMM-400) is presented. The study utilized an air-tight cylinder to pump air through the spirometer in a precise and programmable manner. Factors contributing to the drift were isolated and quantified. The drift due to imbalance in the electronics and the mechanical blade increased from 1% per breathing cycle to as much as 10% when the flow rate decreased from 0.24 to 0.08 l s(-1). A temperature difference of 16 degrees between the ambient and the air in the cylinder contributed about 3.5%. Most significantly, a difference in the breathing between inhalation and exhalation could produce a drift of 40% per breathing cycle, or even higher, depending on the extent of the breathing asymmetry. The origin of this drift was found to be rooted in the differential response of the spirometer to the different flow rate. Some ideas and suggestions for a correction strategy are provided for future work. The present work provides an important first step for eventual utilization of a spirometer as a stand-alone breathing surrogate for gating or tracking radiation therapy.