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Mitral stenosis, atrial septal defects, aortic insufficiency, and other maternal complications can challenge obgyns, but the mode of delivery for CHD patients should be dictated by obstetric issues, not the presence of a defect.
In the past, women with CHD were often told to avoid or even terminate their pregnancy. Today, however, surgical technique has significantly improved clinical outcomes in this patient population. Of course, ideally surgical repair should be performed before conception occurs, especially if a woman is already experiencing cyanosis.3 And while other cardiac problems that occur in pregnancy may not warrant immediate attention-the majority of mild systolic murmurs and T wave abnormalities, for instance-symptoms such as chest pain and exertional syncope or dyspnea should be investigated, as undiagnosed lesions may exist.4
ASDs are the most common shunt defects found in adults. In the asymptomatic patient, women with these defects are no more likely to suffer adverse pregnancy outcomes than women with normal hearts. However, if a woman with an atrial septal defect shows evidence of pulmonary hypertension, chronic atrial fibrillation, or right ventricular dysfunction, pregnancy is contraindicated.4
Muscular ventricular septal defects usually close spontaneously early in life, but if they persist, the patient will be asymptomatic. Membranous VSDs, on the other hand, pose more of a threat because they don't close spontaneously, and the severity of disease depends on the size of the lesion. If there is no evidence of pulmonary hypertension, then the outcome for VSDs is similar to that of mild ASDs, but keep in mind that Eisenmenger syndrome-explained below-is a possibility with large VSDs.4
PDA is a shunt lesion in which the ductus arteriosus does not close after birth. It is generally recognized and repaired in childhood. Depending upon the size of the defect, it may persist without serious compromise into adulthood.4 If a large lesion is left untreated, however, the patient may develop Eisenmenger syndrome.
Technically, VSD, PDA, and ASD can all lead to this condition, but VSD is the most common cause.4 An understanding of the pathophysiology of Eisenmenger's provides the basis for appropriate care. Initially, a structural lesion (e.g., VSD) allows formation of a left-to-right shunt, where blood from the systemic circulation is forced across the defect into the pulmonary circulation. If untreated, this leads to increased pulmonary vascular resistance, pulmonary hypertension, right ventricular hypertrophy, and eventually to cyanosis due to a reversal of shunting to a right-to-left shunt.