Background-Postoperative pulmonary hypertension in children after congenita
l heart surgery is a risk factor for death and is associated with severe ac
ute changes in bath pulmonary vascular resistance and lung mechanics.
Objective-To examine the impact of changes in pulmonary blood flow on lung
mechanics in preoperative children with congenital heart disease, in order
to assess the cause-effect relation of pulmonary vascular-bronchial interac
tions.
Design-Prospective, cross sectional study.
Setting-Cardiac catheterisation laboratory, general anaesthesia with mechan
ical ventilation.
Interventions-variation of pulmonary blood flow (QF) by either balloon occl
usion of an atrial septal defect before interventional closure, or by compl
ete occlusion of the pulmonary artery during balloon pulmonary valvuloplast
y for pulmonary valve stenosis.
Main outcome measures-Ventilatory tidal volume (Vt), dynamic respiratory sy
stem compliance (Cdyn), respiratory system resistance (Rrs).
Results-28 occlusions were examined in nine patients with atrial septal def
ect (median age 9.5 years) and 22 in eight patients with pulmonary stenosis
(median age 1.2 Sears). Normalisation of Qp during balloon occlusion of at
rial septal defect caused no significant change in airway pressures and Rrs
, but there was a small decrease in Vt (mean (SD): 9.61 (0.85) to 9.52 (0.9
7) ml/kg; p < 0.05) and Cdyn (0.64 (0.11) to 0.59 (0.10) ml/cm H2O*kg; p <
0.01). These changes were more pronounced when there was complete cessation
of Qp during balloon valvuloplasty in pulmonary stenosis, with a fall in V
t (9.71 (2.95) to 9.32 (2.84) ml/kg; p < 0.05) and Cdyn (0.72 (0.29) to 0.6
4 (0.26) ml/cm H2O*kg; p < 0.001), and there was also an increase in Rrs (2
5.1 (1.7) to 28.8 (1.6) cm H2O/litre*s; p < 0.01). All these changes exceed
ed the variability of the baseline measurements more than threefold.
Conclusions-Acute changes in pulmonary blood flow are associated with simul
taneous changes in lung mechanics. While these changes are small they may r
epresent a valid model to explain the pathophysiological impact of spontane
ous changes in pulmonary blood flow in clinically more critical situations
in children with congenital heart disease.