Classification of Heart Disease in Pregnancy
Following are the New York Heart Association (NYHA) functional classifications of heart disease in pregnancy:
• Class I—no signs or symptoms of cardiac decompensation with physical activity
• Class II—no symptoms at rest, but minor limitations with activity
• Class III—no symptoms at rest, but marked limitations with activity
• Class IV—symptoms present at rest, increasing with any physical activity
Signs of Heart Disease
• Any diastolic or continuous heart murmur
• Any systolic murmur associated with a thrill
• Any severe arrhythmias
• Unequivocal cardiac enlargement
General Principles in Pregnancy Management of Rheumatic
Mitral Heart Disease
• Minimize tachycardia.
• Minimize excessive intravascular volume.
Specific Management
• Antepartum. Left lateral rest, 2 g sodium diet, digitalis as indicated, diuretics as indi-cated, avoid strenuous activity, avoid anemia, fetal echocardiogram (if patient has con-genital heart disease).
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Chapter 10 l Medical Complications in Pregnancy
• Intrapartum. Aim for vaginal delivery, left lateral rest, monitor intravascular volume,administer oxygen, reassurance, sedation, SBE prophylaxis, epidural, no pushing, elec-tive forceps to shorten the second stage of labor, possible arterial line and pulmonary artery catheter (if Class III or IV status).
• Postpartum. Watch closely for postpartum intravascular overload caused by suddenemptying of uterine venous sinuses after placental delivery.
Table 10-1. Heart Disease in Pregnancy
| Diagnosis | Problems | Management |
| Rheumatic mitral stenosis | ↓ diastolic filling time | ↓ HR; ↓ IV vol |
| ASD, VSD | Regurgitation | Conservative |
| Tetralogy of Fallot corrected | No problem | Conservative |
| Eisenmenger syndrome | 1 Pulmonary HTN | Avoid hypotension |
| 2 Intracardiac shunt | ||
| Marfan syndrome | Dilated aortic root | Surgical reconstruction |
| External diameter >4 cm | ||
| Peripartum cardiomyopathy | Biventricular | Supportive care |
| cardiac failure | ||
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THYROID DISEASE
A 23-year-old primigravida is at 30 weeks’ gestation. She has lost 4 pounds during the past 2 months. She states her heart “feels like it is racing,” and her resting pulse is 135 beats/min. There is a noticeable tremor when she holds her arms out straight. Her eyes appear prominent and protruding. She is complaining of frequent uterine contractions.
Normal Thyroid Physiology. Increased thyroid blood flow leads to thyromegaly. Increasedglomerular filtration rate (GFR) in pregnancy enhances iodine excretion, lowering plasma iodine concentrations. Estrogen causes an increase in liver-produced thyroid binding globulin (TBG), thus increasing total T3 and T4. However, free T3 and T4 remain unchanged. Fetal thy-roid function begins as early as 12 weeks with minimal transfer of T3 or T4 across the placenta.
Hyperthyroidism
Underlying etiology may be Graves disease, toxic nodular goiter (Plummer disease), hydatidi-form mole, or toxic diffuse goiter.
• If uncontrolled, it is associated with increased spontaneous abortions, prematurity,intrauterine growth retardation (IUGR), and perinatal morbidity and mortality.
• If controlled, pregnancy outcome is not altered. Clinical features include elevated rest-
ing pulse, thyromegaly, exopthalmus, inadequate weight gain or even weight loss, and markedly elevated total and free T4.
• Thyroid storm is a life-threatening hypermetabolic state presenting with pyrexia,tachycardia, and severe dehydration. Management is propylthiouracil (PTU), b-block-ing agents, steroids, and iodine.
OB Triad
Graves Disease
• ↓ TSH level
• ↑ free T4 level
• TSHR-Ab
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USMLE Step 2 l Obstetrics
OB Triad
Hypothyroidism
• ↑ TSH level
• ↓ free T4 level
• Anovulation
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Graves disease
This is the most common kind of hyperthyroidism in pregnancy.
Pathophysiology. It is mediated by autoimmune production of thyrotropin-receptor antibodies(TSHR-Ab) that drives thyroid hormone production independent of thyrotropin (TSH). TSHR-Ab can cross the placenta, potentially causing fetal hyperthyroidism.
Diagnosis. The diagnosis is confirmed by elevated free T4and TSHR-Ab, as well as low TSH inthe presence of clinical features described above.
Management
• Antithyroid medications are the first line of therapy in pregnancy, but can cross theplacenta leading to fetal hypothyroidism. PTU and methimazole are thioamides that block thyroid hormone synthesis. Methimazole is an FDA pregnancy category D so should not be used in the first trimester, though it is acceptable in the second and third. PTU has a risk of liver failure (rare) so it should be used only in the first trimester.
• Subtotal thyroidectomy is primarily indicated when antithyroid medical therapy failsand is ideally performed in the second trimester.
• Thyroid ablation with radioactive iodine (I131) is contraindicated because it can crossthe placenta, destroying the fetal thyroid.
Hypothyroidism
This condition is most commonly a primary thyroid defect and often results in anovulation and infertility. If uncontrolled it is associated with spontaneous abortion; however, if pregnancycontinues, the infant is healthy. If controlled with appropriate thyroid replacement, normal fer-tility and pregnancy outcomes are noted.
Diagnosis. Demonstration of an elevated TSH.
Management. Increase supplemental thyroid hormone by 30% in pregnancy.
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