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Exercise induced pulmonary vasoconstriction
Insights
Children with congenital heart defects may experience exercise-induced pulmonary vasoconstriction, a concerning rise in pulmonary vascular resistance during physical activity. This may signal developing pulmonary hypertension post-surgery.
Area of Science:
- Pediatric Cardiology
- Cardiovascular Physiology
- Pulmonary Hypertension
Background:
- Pulmonary vascular resistance typically decreases or stays stable during exercise.
- Children with repaired congenital heart defects (ventricular septal defect, truncus arteriosus) were studied.
- Pre-operative pulmonary hypertension was present in the study group.
Purpose of the Study:
- To investigate exercise hemodynamics in children post-congenital heart defect repair.
- To identify abnormal pulmonary vascular resistance responses during exercise.
- To explore potential causes and implications of exercise-induced pulmonary vasoconstriction.
Main Methods:
- Cardiac catheterization during exercise in seven children post-surgery.
- Measurement of pulmonary vascular resistance, cardiac output, and oxygen consumption.
- Analysis of blood gases and left atrial pressure during exercise.
Main Results:
- Postoperative patients showed a 2% rise in total pulmonary vascular resistance during exercise, unlike the normal -18% fall.
- Two patients exhibited significant increases in pulmonary arteriolar resistance during exercise.
- These two patients had limited cardiac output increases despite elevated oxygen consumption, with no abnormal blood gases or left atrial pressure.
Conclusions:
- Exercise-induced pulmonary vasoconstriction may affect 10-25% of survivors of certain congenital heart defect repairs.
- This phenomenon is not linked to abnormal blood gases or left atrial pressure.
- Exercise-induced pulmonary vasoconstriction could be an early indicator of progressive pulmonary hypertension.
Abstract:
Pulmonary vascular resistance normally falls or remains unchanged during exercise. Seven children with pulmonary hypertension were exercised during cardiac catheterisation after operative correction of ventricular septal defect (6) and truncus arteriosus (1). Except for the presence of moderate pulmonary hypertension, resting haemodynamics in these seven children were similar to those of normal children of equal age, but during exercise the postoperative patients showed a rise rather than a fall (+2% vs -18%) in total pulmonary vascular resistance. Two of the seven children had a substantial increase in pulmonary arteriolar resistance during exercise (from 509 to 715 dyne s cm-5 in one patient and from 606 to 828 dyne s cm-5 in the other). These two patients did not differ from normal children in respect of arterial or mixed venous oxygen saturations or of pH with exercise, nor was left atrial pressure related to the rise in pulmonary resistance. These two patients, however, had only a small rise in cardiac output during exercise (6.8% and 43.1%) in spite of a substantial increase in oxygen consumption (121% and 373%). One of the patients with exercise-induced pulmonary vasoconstriction had an 82% increase in resting pulmonary vascular resistance over a five year period subsequent to her first exercise study. Analysis of these data, and those previously reported, suggests that exercise induced pulmonary vasoconstriction may occur in 10 to 25% of patients who survive correction of certain congenital cardiac defects. The vasoconstriction cannot be attributed to abnormal changes in blood gases or left atrial pressure, and may be an early sign of progressive pulmonary hypertension.