Related Experiment Videos
Extravascular lung water in children immediately after operative closure of either isolated atrial septal defect or
Insights
Congenital heart disease can cause hydrostatic pulmonary edema. Ventricular septal defects with pulmonary hypertension significantly increase extravascular lung water, unlike atrial septal defects.
Area of Science:
- Cardiology
- Pediatric Cardiology
- Pulmonary Medicine
Background:
- Congenital heart disease (CHD) encompasses structural abnormalities present at birth.
- Pulmonary edema, characterized by excess fluid in the lungs, can be a complication of CHD.
- Accurate measurement of extravascular lung water (EVLW) is crucial for understanding fluid balance in the lungs.
Purpose of the Study:
- To investigate the relationship between specific types of congenital heart disease and extravascular lung water (EVLW) levels.
- To determine if pulmonary artery hypertension in the context of ventricular septal defects (VSD) contributes to increased EVLW.
- To differentiate the impact of atrial septal defects (ASD) versus VSD on EVLW.
Main Methods:
- Extravascular lung water (EVLW) was quantified using the cold green dye, double indicator dilution technique.
- Measurements were performed on 16 patients with various forms of congenital heart disease.
- Patient groups included controls (corrected tetralogy of Fallot), atrial septal defect (ASD), and ventricular septal defect (VSD) with pulmonary hypertension.
Main Results:
- Patients with optimally corrected tetralogy of Fallot (controls) had a mean EVLW of 4.7 +/- 0.5 ml/kg.
- Asymptomatic ASD patients with normal pulmonary artery pressure and increased blood flow showed no significant difference in EVLW compared to controls (5.7 +/- 2.8 ml/kg).
- Patients with VSD, pulmonary artery hypertension, and normal left atrial pressure exhibited significantly elevated EVLW (15.9 +/- 3.8 ml/kg) compared to both control and ASD groups (p < 0.01).
Conclusions:
- Pulmonary artery pressure is transmitted to lung microvasculature in the presence of normal pulmonary vascular resistance, leading to hydrostatic pulmonary edema.
- Ventricular septal defects with pulmonary hypertension are strongly associated with increased extravascular lung water.
- While increased pulmonary blood flow and lymphatic insufficiency may contribute, elevated pulmonary artery pressure is a key factor in VSD-associated pulmonary edema.
Abstract:
Extravascular lung water (EVLW) was measured in 16 patients with congenital heart disease by the cold green dye, double indicator dilution technique. Five patients with optimally corrected tetralogy of Fallot served as controls, and EVLW in this group was 4.7 +/- 0.5 ml/kg (111 +/- 13 ml/m2) (mean +/- standard deviation). In 5 asymptomatic patients with atrial septal defect (ASD), normal pulmonary artery (PA) pressure and increased pulmonary blood flow, EVLW was 5.7 +/- 2.8 ml/kg (132 +/- 63 ml/m2), which was not significantly different from the value of control patients. However, in 6 patients with ventricular septal defect, PA hypertension, normal left atrial pressure and an equivalent left-to-right shunt to ASD patients, EVLW was 15.9 +/- 3.8 ml/kg (270 +/- 60 ml/m2). This was significantly different from values in both control and ASD patients (p less than 0.01). It is concluded that in the face of normal pulmonary vascular resistance, PA pressure is transmitted to the microvasculature, causing hydrostatic pulmonary edema. Other factors that may be implicated in the pathogenesis of pulmonary edema, such as increased pulmonary blood flow and relative lymphatic insufficiency in infants, cannot be excluded.