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Pulmonary vascular-bronchial interactions: acute reduction in pulmonary blood flow alters lung mechanics
I Schulze-Neick1, D J Penny, G P Derrick
1Cardiothoracic Unit, Great Ormond Street Hospital for Children, Great Ormond Street, London WC1 3JN, UK.
Insights
Changes in pulmonary blood flow (Qp) affect lung mechanics in children with congenital heart disease. These findings offer insights into pulmonary vascular-bronchial interactions in critical situations.
Area of Science:
- Pediatric Cardiology
- Respiratory Physiology
Background:
- Postoperative pulmonary hypertension in children post-congenital heart surgery is a significant risk factor for mortality.
- It is linked to acute alterations in pulmonary vascular resistance and lung mechanics.
Purpose of the Study:
- To investigate how variations in pulmonary blood flow (Qp) impact lung mechanics in children with congenital heart disease before surgery.
- To elucidate the cause-effect relationship between pulmonary vascular and bronchial systems.
Main Methods:
- A prospective, cross-sectional study was conducted in a cardiac catheterisation laboratory.
- Pulmonary blood flow (Qp) was manipulated via balloon occlusion of an atrial septal defect or pulmonary artery during balloon pulmonary valvuloplasty.
- Lung mechanics, including ventilatory tidal volume (Vt), dynamic compliance (Cdyn), and respiratory system resistance (Rrs), were measured.
Main Results:
- In atrial septal defect patients, Qp normalization caused minor decreases in Vt and Cdyn, with no significant change in Rrs.
- In pulmonary stenosis patients, complete Qp cessation led to more pronounced reductions in Vt and Cdyn, and a significant increase in Rrs.
- Observed changes in lung mechanics exceeded threefold the baseline variability.
Conclusions:
- Acute alterations in pulmonary blood flow are directly associated with concurrent changes in lung mechanics.
- These findings provide a potential model for understanding the pathophysiological effects of spontaneous Qp changes in critically ill children with congenital heart disease.
Background:
Postoperative pulmonary hypertension in children after congenital heart surgery is a risk factor for death and is associated with severe acute changes in both 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 interactions.
Design:
Prospective, cross sectional study.
Setting:
Cardiac catheterisation laboratory, general anaesthesia with mechanical ventilation.
Interventions:
Variation of pulmonary blood flow (Qp) by either balloon occlusion of an atrial septal defect before interventional closure, or by complete occlusion of the pulmonary artery during balloon pulmonary valvuloplasty for pulmonary valve stenosis.
Main Outcome Measures:
Ventilatory tidal volume (Vt), dynamic respiratory system compliance (Cdyn), respiratory system resistance (Rrs).
Results:
28 occlusions were examined in nine patients with atrial septal defect (median age 9.5 years) and 22 in eight patients with pulmonary stenosis (median age 1.2 years). Normalisation of Qp during balloon occlusion of atrial 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 (0.97) ml/kg; p < 0.05) and Cdyn (0.64 (0.11) to 0.59 (0.10) ml/cm H(2)O*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 Vt (9.71 (2.95) to 9.32 (2.84) ml/kg; p < 0.05) and Cdyn (0.72 (0.29) to 0.64 (0.26) ml/cm H(2)O*kg; p < 0.001), and there was also an increase in Rrs (25.1 (1. 7) to 28.8 (1.6) cm H(2)O/litre*s; p < 0.01). All these changes exceeded the variability of the baseline measurements more than threefold.
Conclusions:
Acute changes in pulmonary blood flow are associated with simultaneous changes in lung mechanics. While these changes are small they may represent a valid model to explain the pathophysiological impact of spontaneous changes in pulmonary blood flow in clinically more critical situations in children with congenital heart disease.