Dr Hameed is Professor of Clinical Obstetrics & Gynecology, Professor of Clinical Cardiology, Medical Director, Obstetrics, Director, Quality and Safety at University of California, Irvine.
Dr Steller is a third-year resident in the Department of Obstetrics and Gynecology, University of California, Irvine.
Neither author has a conflict of interest to report in respect to the content of this article.
Cardiovascular disease (CVD) complicates 1% of all pregnancies.1 It has surpassed hemorrhage, hypertensive disorders, and embolism to become the leading cause of indirect maternal death in pregnancy, accounting for approximately 26.4% of pregnancy-related deaths.2,3 In the future, the number of pregnant women with CVD is likely to rise as advances in healthcare are simultaneously allowing children with congenital heart disease (CHD) to reach reproductive age and enabling women of advanced maternal age with CVD risk factors to become pregnant.4 Confronting CVD challenges and their associated morbidity and/or mortality requires:
· Foundational knowledge of cardiac physiology and the hemodynamic changes of pregnancy, which can reveal or overwhelm a previously well-compensated defect
· Early identification of cardiac disease regardless of the timing or the manner of presentation
· Early involvement of a multidisciplinary cardiac care team including maternal fetal medicine, cardiology, and anesthesia
Cardiac output is the product of the volume of blood pumped from the left ventricle with each heart beat (stroke volume) and the heart rate. Three major factors that affect stroke volume include:
· Preload: the degree to which the ventricles are stretched prior to contracting; determined primarily by the volume and speed of venous return.
· Contractility: largely affected by sympathetic and parasympathetic interplay.
· Afterload: the aortic pressure during systole (systolic blood pressure); governed by vascular resistance.
Notably, ejection fraction is the fraction of outbound blood pumped from the left ventricle per beat, which is calculated by dividing stroke volume by end-diastolic left ventricular volume.
During pregnancy, the cardiac output increases by 43%. This increase is driven in the first trimester primarily by decreased vascular resistance (-21%), and later in pregnancy by increased plasma volume (+40%–50%) and heart rate (+17%).5,6
Clinical implications during labor and delivery: Hemodynamic changes during Stage I of labor are induced by pain, anxiety, and contractions—all of which increase heart rate, stroke volume, and cardiac output by a further 50%. On the other hand, supine positioning may decrease cardiac output by decreasing preload due to compression of the inferior vena cava. Valsalva during Stage II adds large fluctuations in central venous pressure by increasing preload followed by decreased preload and increased systemic vascular resistance after each push. These fluctuations may effectively be attenuated by adequate pain control, minimization/avoidance of Valsalva, and assisted delivery. Stage III may be complicated by decreased preload secondary to blood loss and/or increased preload by the auto-transfusion of ~500 cc of blood that returns to systemic circulation following delivery of the placenta.5 Therefore, labor, delivery, and early postpartum are vulnerable periods in which decompensations or hemodynamic instability may occur in a patient with significant CVD.