Effects of sequential biventricular pacing during acute right ventricular pressure overload

2006 ◽  
Vol 291 (5) ◽  
pp. H2380-H2387 ◽  
Author(s):  
T. Alexander Quinn ◽  
George Berberian ◽  
Santos E. Cabreriza ◽  
Lauren J. Maskin ◽  
Alan D. Weinberg ◽  
...  

Temporary sequential biventricular pacing (BiVP) is a promising treatment for postoperative cardiac dysfunction, but the mechanism for improvement in right ventricular (RV) dysfunction is not understood. In the present study, cardiac output (CO) was optimized by sequential BiVP in six anesthetized, open-chest pigs during control and acute RV pressure overload (RVPO). Ventricular contractility was assessed by the maximum rate of increase of ventricular pressure (dP/d tmax). Mechanical interventricular synchrony was measured by the area of the normalized RV-left ventricular (LV) pressure diagram ( APP). Positive APP indicates RV pressure preceding LV pressure, whereas zero indicates complete synchrony. In the control state, CO was maximized with nearly simultaneous stimulation of the RV and LV, which increased RV ( P = 0.006) and LV dP/d tmax ( P = 0.002). During RVPO, CO was maximized with RV-first pacing, which increased RV dP/d tmax ( P = 0.007), but did not affect LV dP/d tmax, and decreased the left-to-right, end-diastolic pressure gradient ( P = 0.023). Percent increase of RV dP/d tmax was greater than LV dP/d tmax ( P = 0.014). There were no increases in end-diastolic pressure to account for increases in dP/d tmax. In control and RVPO, RV dP/dtmax was linearly related to APP ( r = 0.779, P < 0.001). The relation of CO to APP was curvilinear, with a peak in CO with positive APP in the control state ( P = 0.004) and with APP approaching zero during RVPO ( P = 0.001). These observations imply that, in our model, BiVP optimization improves CO by augmenting RV contractility. This is mediated by changes in mechanical interventricular synchrony. Afterload increases during RVPO exaggerate this effect, making CO critically dependent on simultaneous pressure generation in the RV and LV, with support of RV contractility by transmission of LV pressure across the interventricular septum.

Circulation ◽  
1995 ◽  
Vol 91 (9) ◽  
pp. 2359-2370 ◽  
Author(s):  
Sheng-Jing Dong ◽  
Adrian P. Crawley ◽  
John H. MacGregor ◽  
Yael Fisher Petrank ◽  
Dale W. Bergman ◽  
...  

2001 ◽  
Vol 33 (6) ◽  
pp. A73
Author(s):  
Efren Santos Martinez ◽  
Arturo Gómez ◽  
Oscar Infante ◽  
Tomás Pulido ◽  
Edgar Bautista ◽  
...  

1988 ◽  
Vol 84 (1) ◽  
pp. 157-161 ◽  
Author(s):  
Robert G. Stenberg ◽  
David E. Fixler ◽  
Anne L. Taylor ◽  
James R. Corbett ◽  
Brian G. Firth

1993 ◽  
Vol 72 (15) ◽  
pp. 1179-1182 ◽  
Author(s):  
Jason M. Lazar ◽  
Angel R. Flores ◽  
Donald J. Grandis ◽  
Judith E. Orie ◽  
Douglas S. Schulman

2006 ◽  
Vol 291 (5) ◽  
pp. H2229-H2236 ◽  
Author(s):  
Carol A. Gibbons Kroeker ◽  
Samer Adeeb ◽  
John V. Tyberg ◽  
Nigel G. Shrive

During pulmonary artery constriction (PAC), an experimental model of acute right ventricular (RV) pressure overload, the interventricular septum flattens and inverts. Finite element (FE) analysis has shown that the septum is subject to axial compression and bending when so deformed. This study examines the effects of acute PAC on the left ventricular (LV) free wall and the role the pericardium may play in these effects. In eight open-chest anesthetized dogs, LV, RV, aortic, and pericardial pressures were recorded under control conditions and with PAC. Model dimensions were derived from two-dimensional echocardiography minor-axis images of the heart. At control (pericardium closed), FE analysis showed that the septum was concave to the LV; stresses in the LV, RV, and septum were low; and the pericardium was subject to circumferential tension. With PAC, RV end-diastolic pressure exceeded LV pressure and the septum inverted. Compressive stresses developed circumferentially in the septum out to the RV insertion points, forming an arch-like pattern. Sharp bending occurred near the insertion points, accompanied by flattening of the LV free wall. With the pericardium open, the deformations and stresses were different. The RV became much larger, especially with PAC. With PAC, the arch-like circumferential stresses still developed in the septum, but their magnitudes were reduced, compared with the pericardium-closed case. There was no free wall inversion and flattening was less. From these FE results, the pericardium has a significant influence on the structural behavior of the septum and the LV and RV free walls. Furthermore, the deformation of the heart is dependent on whether the pericardium is open or closed.


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