congenital heart disease in pregnancy for patients
TRANSCRIPT
Hello. I would like to think everyone for coming this morning. I’m going to talk about heart disease in pregnancy.
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I have a few objectives for this talk. First, we’ll review the normal, anticipated chambers of pregnancy. I am going to discuss how you evaluate a pregnant patient with cardiac disease. Brief review of specific cardiac conditions and will conclude on anticoagulation for the pregnant and a few medications.
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There are several anticipated changes with pregnancy including increase in plasma volume and a lesser degree of increase in red blood cell mass resulting in a mild net anemia, diastolic chamber enlargement, hormone mediated changes in the arteries and veins resulting in increased chamber enlargement, increases in heart rate and cardiac output.
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On this graph we have the percent increase in plasma volume on the y‐axis and time on the x‐axis. Plasma volume really starts to increase around 6 to 8 weeks of gestation, peaks at 32. Increases by almost 50% of non‐pregnant values up to a liter to a liter and a half. The exact mechanism is not known but it its thought that it may be impart due nitric oxide mediated vasodilation and changes in vascular compliance leading to stimulation renin‐angiotensin‐aldosterone. This increase is possibly adaptive in reducing hemodynamic instability after blood loss
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On this graph we have the percent increase in plasma volume on the y‐axis and time on the x‐axis. Plasma volume really starts to increase around 6 to 8 weeks of gestation, peaks at 32. Increases by almost 50% of non‐pregnant values up to a liter to a liter and a half. The exact mechanism is not known but it its thought that it may be impart due nitric oxide mediated vasodilation and changes in vascular compliance leading to stimulation renin‐angiotensin‐aldosterone. This increase is possibly adaptive in reducing hemodynamic instability after blood loss
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Histologic and echocardiographic studies indicate that ventricular wall muscle mass and end‐diastolic volume increase in pregnancy without an associated increase in end‐systolic volume or end‐diastolic pressure.[8,9] Ventricular mass increases in the first trimester, whereas end‐diastolic volume increases in the second and early third trimesters.[8,10] This increases cardiac compliance (resulting in a physiologically dilated heart) without a concomitant reduction in ejection fraction, implying that myocardial contractility must also increase. A recent echocardiographic study of left ventricular function during pregnancy suggests that changes in long‐axis performance occur earlier than changes in transverse function and challenges the notion of dominance of circumferential fiber shortening.
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30 year old not pregnant
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33 yo female who is 25 weeks pregnant
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A general softening of collagen occurs in the entire vascular system, associated with hypertrophy of the smooth muscle component. This results in increased compliance of arteries and veins is evident as early as at 5 weeks of the beginning of amenorrhea
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On the vertical axis there we have cardiac output and we can see the overall increase in most notably uterine blood flow both in absolute terms and as a fraction of total cardiac output increasing from 2% in the non‐pregnant state to 15‐20% by the 3rd trimester. There are smaller increases to the skin and breasts as well.
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Maternal posture significantly affects cardiac output. Turning from the left lateral recumbent to the supine position at term can result in a drop in cardiac output by as much as 25% to 30%. This is the result of caval compression by the gravid uterus, which diminishes venous return from the lower extremities, decreasing stroke volume and cardiac output. Although most women do not become hypotensive with this maneuver, up to 8% of women do demonstrate the supine hypotensive syndrome, which is manifested by a sudden drop in blood pressure, bradycardia, and syncope.
[At the bottom of the graph, the changes in systolic (open triangles) and diastolic (closed triangles) blood pressures produced by movement from the left lateral recumbent to the supine position are shown.]
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First stage of labor is early labor. Second stage is the actual delivery of the child. Third is the delivery of the placenta. Because of the severe changes in the second stage, invasive monitoring and assistance is indicated in at risk patients.First stage of labor, CO increases 12‐31%
22% increase in stroke volumeSecond stage of labor, CO increases 49%
Laboring in the left lateral decubitus position or analgesia decreases thisPartially due to painPartially due to painUterine contractions transfer 300‐500 mL of blood from the uterus to the general circulationTransiently increase in SBP (35 mmHg) and DBP (25 mmHg)
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Anxiety, pain, and uterine contractions all alter hemodynamics.
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First stage of labor is early labor. Second stage is the actual delivery of the child. Third is the delivery of the placenta. Because of the severe changes in the second stage, invasive monitoring and assistance is indicated in at risk patients.Rapid increase in ventricular end diastolic volume and end diastolic pressure
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Dyspnea with increased frequency as gestation advances (15% in the first trimester compared with 75% by the third). The mechanism for this is unclear, but it may relate to the exaggerated ventilatory response (perhaps progesterone mediated)
Mild to moderate execise should still be well tolerated
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60% of subjects were randomized to derivation and 40% to validation.
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60% of subjects were randomized to derivation and 40% to validation.
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2006 Article by Paul Kheiry and Michael Lansberg of 90 pregancies of women with CHD at Bringham & Womens Hospital between 98‐2004.
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The modified risk score for cardiac complications during completed (>20 weeks of gestation) pregnancies in women with congenital heart diseaseweeks of gestation) pregnancies in women with congenital heart disease (expressed as % of the total number of completed pregnancies). AV, atrioventricular; AVA, aortic valve area; LHO, left heart obstruction; NYHA, New York Heart Association; PG, peak gradient; Pulm, pulmonary; Syst, systemic.
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ASD, even large defects, generally well tolerated except in pulmonary hypertension or atrial fibrillation. Risk of paradoxic embolism is increased during pregnancy.
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Beta blockers help by increasing diastolic filling time. Council against pregnancy in Severe AS. Balloon valvuloplasty can be considered with shielding of the gravid uterus. Pulmonary stenosis is usually well tolerated unless RV hypertension is present.
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The largest series published retrospectively reviewed 44 women with 70 pregnancies, and 52% of women died in connection with a pregnancy.A smaller more recent series of 12 patients, three spontaneous abortions (early), two still births, Eight born; five premature. Three mothers died. Pulmonary infarct or RV failure.ICU delivery with invasive pressure monitoring, left lateral decubitus positioning may be helpful. Copious LE care for DVT. Low dose heparin is controversial.
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Highly variable risk, most authors estimate 5‐6%Chondrodysplasia punctataLess risk if daily dose <5
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Insert echo or MRI of BAV vs trileaflet
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