Right ventricular function in respiratory distress syndrome and subsequentpartial liquid ventilation - Homeometric autoregulation in the right ventricle of the newborn animal
Rhl. Cardozo et al., Right ventricular function in respiratory distress syndrome and subsequentpartial liquid ventilation - Homeometric autoregulation in the right ventricle of the newborn animal, AM J R CRIT, 162(2), 2000, pp. 374-379
Infant respiratory distress syndrome (IRDS) and subsequent partial liquid v
entilation (PLV) cause increased pulmonary vascular resistance, thus raisin
g afterload. In nine newborn lambs the effects of IRDS and subsequent PLV o
n right (RV) and left ventricular (LV) contractility and systolic pump func
tion were assessed using indices derived from RV and LV pressure-volume rel
ations, obtained by micromanometric and conductance catheters during transi
ent inferior vena cava occlusion. Pulmonary function deteriorated during IR
DS with a significant decrease in the ratio of arterial oxygen pressure to
fraction of inspired oxygen (Pa-O2/F-lO2) whereas pulmonary artery pressure
(Ppa) showed a significant increase and pulmonary vascular resistance show
ed a substantial though not significant increase. Cardiac output (Q), strok
e volume (SV), and end-diastolic volume (EDV) did not change. RV contractil
ity showed a significant increase during IRDS: the slope of the end-systoli
c pressure-volume relation (RV-E,) increased whereas its volume intercept a
t 5 kPa (RV-V-5) decreased. The preload-corrected time derivative of ventri
cular pressure (RV-dP/dt(max)), however, did not change significantly. LV p
ump function and contractility were unchanged. During PLV pulmonary functio
n showed a recovery but Ppa and pulmonary vascular resistance remained high
; indices for RV contractility showed a sustained significant increase comp
ared with baseline conditions whereas indices for LV pump function and cont
ractility remained unchanged. These results show that the right ventricle o
f the newborn heart, in the face of increased pulmonary vascular resistance
, is able to maintain cardiac output through homeometric autoregulation.