Mk. Karunanithi et al., Effect of acutely increased left ventricular afterload on work output fromthe right ventricle in conscious dogs, J THOR SURG, 121(1), 2001, pp. 116-124
Citations number
30
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objective: To determine the effect of acute increments in left ventricular
afterload on the stroke work output of the right ventricle in vivo.
Methods: After pharmacologic attenuation of autonomic reflexes, left and ri
ght ventricular pressure-volume data were obtained in 9 conscious dogs duri
ng vena caval occlusions performed before and during aortic constriction.
Results: The relationship between right ventricular stroke work and end-dia
stolic volume during vena caval occlusion was highly linear (r = 0.97 +/- 0
.02), but the slope decreased by 20% +/- 13% during aortic constriction suf
ficient to increase left ventricular mean ejection pressure by 25% +/- 14%
(P < .05). The volume-axis intercept remained constant, Similarly, the slop
e of the linear relationship between right ventricular free wall regional s
egment work and end-diastolic segment length declined by 22% +/- 10% during
aortic constriction (P < .05), without significant change in the length-ax
is intercept. The reduction in both global and regional right ventricular s
troke work at any given preload with increased left ventricular afterload w
as due entirely to decreased right ventricular stroke volume and free wall
shortening, because right ventricular mean ejection pressure was unchanged.
Additional experiments were performed in 5 open-chest dogs to produce a gr
eater reduction in left ventricular free wall shortening than observed with
aortic constriction by transient constriction of the left circumflex coron
ary artery. However, this intervention had no effect on right ventricular f
ree wall segment work output.
Conclusion: Increased left ventricular afterload decreases global and regio
nal right ventricular stroke work at any given preload, a direct, negative
systolic ventricular interaction.