Relationship Between Mitral Valve Regurgitant Flow and Peripartum Change in Systemic Vascular Resistance

Homayoun Khanlou, MD, Négar Khanlou, MD, Glenn Eiger, MD

Disclosures

South Med J. 2003;96(3) 

In This Article

Discussion

A pregnant woman can have any type of cardiac disease seen in the nonpregnant woman, but some may have special characteristics such as peripartum cardiomyopathy.[1] The cardiovascular system undergoes profound changes during pregnancy, with an increase in total blood volume and cardiac output and a net progressive fall in SVR until 20 weeks of pregnancy, with no further change until delivery.[2] The aforementioned changes represent an increase above prepregnant values of 12 to 14%.[2] Also, as pregnancy evolves, there is an augmentation of mitral valve regurgitation that is particularly significant by 12 weeks of gestation.[3] Mitral regurgitation is usually well tolerated in pregnancy, mainly because of left ventricular unloading due to a physiologic fall in SVR.[4,5,6] These adaptive mechanisms return to their prepregnant values within 24 hours after delivery to maintain an intact cardiovascular system.[2,3] Thus, this physiologic adjustment must be taken into account in the cardiologic assessment of pregnant women.

Our patient's clinical course presents several important points. It is known that orifice area, heart rate, contractility, preload, and SVR determine the magnitude of the regurgitant flow.[4,5] In fact, the hemodynamic changes observed in our patient behaved like an acute severe mitral regurgitation with decreased left atrial compliance resulting in increased left atrial pressure and subsequent development of pulmonary edema. Her clinical course was not consistent with sepsis or noncardiogenic pulmonary edema, as also evidenced by blood cultures, pulmonary artery catheter values, chest x-ray films, and a rapid response to diuretic therapy. It is reasonable to hypothesize that the development of pulmonary edema with normal systolic and diastolic left ventricle function was possibly due to an increase in mitral regurgitant flow due to sudden augmentation of SVR as evidenced by Swan-Ganz and echocardiographic measurements. It also illustrates that the delay in adaptive mechanisms, which usually occur progressively after delivery, can be sudden and may extend up to several days beyond delivery. The rapid augmentation of SVR and return to prepregnancy mitral valve surface area can provoke an important increase in atrioventricular gradient, resulting in severe pulmonary edema and necessitating mechanical ventilation.

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