D. Hoffman et al., LEFT-TO-RIGHT VENTRICULAR INTERACTION WITH A NONCONTRACTING RIGHT VENTRICLE, Journal of thoracic and cardiovascular surgery, 107(6), 1994, pp. 1496-1502
Left ventricular systole is known to contribute to generation of right
ventricular pressure and stroke volume. To study the interactions in
a dilated noncontractile right ventricle after cardiopulmonary bypass
we created a variable volume, neo-right ventricle by excision and repl
acement of the right ventricular free wall with a xenograft pericardia
l patch. We investigated the interactions in eight dogs with neo-right
ventricle, instrumented to measure cardiac pressures and cardiac outp
ut in control conditions (n = 69) and during partial pulmonary artery
occlusion (n = 50). Results: The size of the neo-right ventricle was i
ncreased from original right ventricular volume V-0 to V-1 (V-1 = V-0
+ 54 +/- 23 ml), V-2 (V-2 = V-0 + 124 +/- 85 ml), and V-3 (V-3 = V-0 223 +/- 162 ml). Cardiac output increased with increasing left ventri
cular end-diastolic pressure, indicating that the Frank-Starling mecha
nism was operating in the left ventricle. However, cardiac output decr
eased with increasing neo-right ventricular size (p < 0.001) and durin
g pulmonary artery occlusion (p < 0.001). Maximal neo-right ventricula
r pressure was a linear function of the maximal left ventricular press
ure at each neo-right ventricular size and decreased,vith the increase
in neo-right ventricular size (p < 0.001), both in control conditions
and during pulmonary artery occlusion (p < 0.004), Stroke work of the
neo-right ventricle and left ventricle decreased with increasing neo-
right ventricular size (p < 0.002). The relationship between neo-right
ventricular stroke work and left ventricular stroke work at different
neo-right ventricular sizes was linear both in control conditions and
during pulmonary artery occlusion: in control Y = 0.24X (r = 0.968, n
= 69); in pulmonary artery occlusion Y = 0.35X (r = 0.986, n = 50). I
n both conditions the intercept of the Linear relationship was not sig
nificantly different from zero (p < 0.974 in control; p < 0.614 in pul
monary artery occlusion). The slope was significantly increased in pul
monary artery occlusion (p < 0.001). Conclusion: Left ventricular cont
raction contributes 24% of left ventricular stroke work to the generat
ion of right ventricular stroke work via the septum in the absence of
a contracting right ventricle; this increases to 35% in the face of in
creased pulmonary afterload. This mechanism can maintain adequate glob
al cardiac function in the case of a noncontracting right ventricle wh
ile right ventricular volume is kept small and afterload is not increa
sed. The interventricular interaction of the ventricles must be consid
ered when patients with postbypass right ventricular failure are treat
ed.