From the Guidelines
In patients with ventricular septal defects (VSDs), oxygen saturations in the cardiac chambers change due to left-to-right shunting of blood, resulting in an increase in oxygen saturation in the right ventricle, pulmonary artery, and right atrium compared to normal values. Normally, the right heart contains deoxygenated blood with oxygen saturations of 60-80%, while the left heart contains oxygenated blood with saturations of 95-100% 1. In patients with VSDs, oxygenated blood from the left ventricle passes through the septal defect into the right ventricle, causing an increase in oxygen saturation in the right ventricle, pulmonary artery, and right atrium.
Key Diagnostic Findings
- The "step-up" in oxygen saturation between the right atrium and right ventricle is a key diagnostic finding in VSDs.
- The magnitude of this saturation change correlates with the size of the defect - larger VSDs produce greater increases in right heart oxygen saturations.
- The left heart chambers maintain normal oxygen saturations since the shunt is left-to-right.
Pathophysiology
This abnormal shunting occurs because left ventricular pressure exceeds right ventricular pressure, forcing blood through the defect. In severe cases with pulmonary hypertension, the shunt may reverse (Eisenmenger syndrome), causing deoxygenated blood to enter the left heart and resulting in decreased left heart oxygen saturations and systemic cyanosis, as noted in the 2018 AHA/ACC guideline for the management of adults with congenital heart disease 1.
From the Research
Oxygen Saturation Changes in Cardiac Chambers
- Oxygen saturation changes in the cardiac chambers of patients with ventricular septal defects (VSD) are not directly addressed in the provided studies.
- However, study 2 mentions that pulmonary artery oxygen saturation was significantly higher in patients undergoing correction of complete transposition of the great arteries (TGA) + VSD compared to those with VSD alone.
- Study 3 discusses the improvement in oxygen saturation in patients with atrial septal defect-associated pulmonary arterial hypertension after fenestrated closure, but this is not directly related to VSD.
- Study 4 investigates the nature of heart failure in patients with VSD, but does not provide information on oxygen saturation changes.
- Study 5 reviews the use of ACE inhibitors in pediatric patients with heart failure, including those with VSD, but does not address oxygen saturation changes.
Related Findings
- Study 2 found that patients with TGA + VSD had lower expression of endothelial nitric oxide synthase (eNOS) and matrix metalloproteinases 2 (MMP-2) compared to those with VSD alone, which may affect the progress and reversibility of pulmonary hypertension.
- Study 4 suggests that congestive heart failure (CHF) in patients with VSD results primarily from systolic dysfunction.
- Study 3 demonstrates that fenestrated closure can be safely performed in patients with decompensated heart failure and atrial septal defect-associated pulmonary arterial hypertension, resulting in improved outcomes, including increased oxygen saturation.