Relationship between mitral valve regurgitant flow and peripartum change in systemic vascular resistance. (Case Report).

Abstract: Mitral regurgitation is usually tolerated well in pregnancy, mainly because of left ventricular unloading due to the physiologic decrease in systemic vascular resistance (SVR). We report the case of a patient with mitral regurgitation who had pulmonary edema soon after delivery, which likely was due to a sudden increase in SVR. The sudden changes in SVR should be added to the differential diagnosis when pulmonary edema occurs after delivery in patients with mitral regurgitation.

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The association between heart failure and pregnancy is well known. It can be due to underlying heart disease before pregnancy or to peripartum cardiomyopathy. (1) The physiologic changes that occur during pregnancy can modify the hemodynamic parameters seen with valvular heart disease. (2) In the case described herein, a patient with mitral regurgitation initially had unilateral pulmonary infiltrates that were seen on x-ray films, and pulmonary edema developed soon after delivery.

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. (4-6) 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 pr egnant 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 progressiv ely 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.

Conclusion

This case illustrates that the hemodynamic changes in the peripartum period, particularly the increase in SVR can be sudden and may occur as long as 8 days after delivery. The sudden changes in SVR should be added to the differential diagnosis when patients with mitral regurgitation have pulmonary edema after delivery. The pathophysiology of this phenomenon remains unknown.

Accepted January 23, 2002.

References

(1.) Homans DC. Pcripartum cardiomyopathy. N Engl JMed 1985;312:l432-1437.

(2.) Robson SC, Hunter S, Boys RI, Dunlop W. Serial study of factors influencing changes in cardiac output during human pregnancy. Am J Physiol 1989;256:H 1060-H 1065.

(3.) Campos O, Andrade JL, Bocanegra J, Ambrose JA, Carvalho AC, Harada K, et al. Physiologic multivalvular regurgitation during pregnancy: A longitudinal Doppler echocardiographic study. Int J Cardiol 1993;40:265-272.

(4.) Roth A, Shotan A, Elkayam U. A randomized comparison between the hemodynamic effects of hydralazine and nitroglycerin alone and in combination at rest and during isometric exercise in patients with chronic mitral regurgitation. Am Heart J 1993;125:155-163.

(5.) Spain MG, Smith MD, Kwan OL, DeMaria AN. Effect of isometric exercise on mitral and aortic regurgitation as assessed by color Doppler flow imaging. Am J Cardiol 1990;65:78-83.

(6.) Hagay ZJ, Weissman A, Geva D, Snir E, Caspi A. Labor and delivery complicated by acute mitral regurgitation due to ruptured chordae tendineae. Am J Perinatol 1995;12:111-112.

RELATED ARTICLE: Case Report

A 24-year-old Asian-American woman (gravida 2, para 1) was admitted to the hospital because of progressive dyspnea associated with cough for 3 days. Her medical history was significant for rheumatic heart disease with mild mitral regurgitation. Seven days before admission, the patient gave birth to a healthy male infant after 37 weeks of gestation. The pregnancy was uncomplicated, with normal vaginal delivery. An echocardiogram obtained during pregnancy showed mild mitral regurgitation with normal left ventricular function. The mitral valve surface area was 2.0 [cm.sup.2] with an atrioventricular gradient of 10 mm Hg. She was discharged from the hospital after 72 hours. Five days later, the patient complained of nonproductive cough associated with progressive exertional dyspnea. She did not seek medical attention until 1 day before admission, when the dyspnea became severe.

At admission, the patient was in mild respiratory distress with blood pressure of 120/70 mm Hg, heart rate 95 beats/mm, and respiratory rate 26 breaths/mm. The patient's body temperature was 37.8[degrees]C. On physical examination, there was neither jugular venous distention nor hepatojugular reflux. The heart sounds were normal without S3 or S4 gallops. A Grade 2/6 to 3/6 apical pansystolic murmur radiating to axilla was heard. Chest examination disclosed mild rales over the right lung base, with normal left lung field. The extremities were normal, and in particular, no peripheral edema was noted. The remainder of the physical examination was unremarkable. Complete blood count at admission showed a white blood cell count of 12,100/[mm.sup.3] (85% granulocytes, 10% lymphocytes), hemoglobin value of 11.5 g/dl, and platelet count of 248,000/[mm.sup.3]. The serum electrolyte; blood urea nitrogen, and creatinine levels were normal. Arterial blood gas values were pH 7.39, [PaO.sub.2] 92 mm Hg, [PaCO.sub.2] 38 mm H g, and [HCO.sub.3] 23 mmol/L. Electrocardiogram showed sinus tachycardia with left atrial enlargement. Chest x-ray film showed right basilar interstitial infiltrates. Blood cultures were obtained, and treatment was started empirically with ceftriaxone and erythromycin for possible pneumonia.

Five hours after admission the patient's respiratory condition began to deteriorate, necessitating administration of oxygen via nonbreather mask. Repeat arterial blood gas revealed a pH of 7.36, [PaO.sub.2] of 55 mm Hg, [PaCO.sub.2] of 45 mm Hg, and [HCO.sub.3] 26 mmol/L. Another chest film showed increased right lung infiltrates with extension to the left lung field. The electrocardiogram was remarkable only for sinus tachycardia at a rate of 100/mm. In the next hour, she became hypotensive, and respiratory distress necessitated endotracheal intubation and mechanical ventilation. Swan-Ganz catheterization showed a mean pulmonary capillary wedge pressure of 27 mm Hg and central venous pressure of 19 mm Hg. Systemic vascular resistance was 1,000 dynes/s/[cm.sub.2] with cardiac output of 5.6 L/min/[m.sub.2]. She was administered furosemide and dopamine intravenously. Repeat echocardiogram showed normal left ventricular function, severe mitral regurgitation with the mitral valve area of 2.6 [cm.sub.2], and atrio ventricular gradient of 14 mm Hg. Moderate left atrial dilation was noted.

Twenty-four hours later, the patient's condition began to improve, and she required less [FiO.sub.2]. She was successfully extubated 3 days after admission. Infiltrates seen on chest films eventually resolved. Microbiologic cultures (blood, urine, and sputum) remained negative. She was discharged on the seventh day of hospitalization and remained free of symptoms after 6 months of follow-up.

Key Points

* Peripartum change in systemic vascular resistance can be sudden.

* Peripartum change in systemic vascular resistance can result in pulmonary edema in the presence of mitral regurgitation.

* The sudden changes in systemic vascular resistance should be added to the differential diagnosis when pulmonary edema occurs after delivery in patients with mitral regurgitation.

From the Division of Critical Care Medicine, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PA.

Reprint requests to Homayoun Khanlou, MD, AHF Foundation, 4835 Van Nuys Blvd., Suite 200, Sherman Oaks, CA 91403.

Copyright [C] 2003 by The Southern Medical Association

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