HEART DISEASE IN PREGNANCY

Mortality associated with specific cardiac lesions 1. Low risk of maternal mortality (less than 1%). (a) Septal defects. (b) New York Heart Association classes I and II. (c) Patent ductus arteriosus. (d) Pulmonary / tricuspid lesions. 2. Moderate risk of maternal mortality (5-15%). (a) NYHA classes III and IV mitral stenosis. (b) Aortic stenosis. (c) Marfan’s syndrome with normal aorta. (d) Uncomplicated coarctation of aorta. (e) Past history of myocardial infarction. 3. High risk of maternal mortality (25-50%). (a) Eissenmenger’s syndrome. (b) Pulmonary hypertension. (c) Marfan’s syndrome with abnormal aortic root. (d) Peripartum cardiomyopathy.

Prognosis depending on the functional status  In general, women in NYHA classes I and II lesions usually do well during pregnancy and have a favorable prognosis with a mortality rate of <1%.  Patients in NYHA classes III and IV may have a mortality rate of 5% to 15%. These patients should be advised against becoming pregnant.

Cardiac output begins to rise in the first trimester and continues as steady increase to peak at 32 weeks gestation by 30% to 50% of pre pregnancy level. Causes for increased cardiac output are 1. Increases in stroke volume (early pregnancy) 2. Increase in heart rate (late pregnancy) 3. Decreased peripheral resistance 4. Decreased blood viscosity

The fall in the peripheral resistance is about 20-30% at weeks & returns to normal at term. This fall is due to 1. Due to the trophoblastic erosion of endometrial vessels, the placental bed serves as a large arteriovenous shunt causing lowered systemic vascular resistance 2. There is physiological vasodilatation which is believed to be secondary to endothelial prostacyclin and circulating progesterone.

Physiological changes during labour and puerperium. 1.First stage. Cardiac output increases by15%. Uterine contractions increases venous return, causing increase in cardiac output & can cause reflex bradycardia. 2.Second stage Increase in intra abdominal pressure (valsalva’s) causes inecrease in venous return and cardiac output. 3.Third stage Normal blood loss during delivery (around ml). It leads to a. Decrease blood volume b. Decrease cardiac output.

The clinical features in a normal pregnancy which can mimic a cardiac disease are 1. Dyspnea - due to hyperventilation, elevated diaphragm.. 2. Pedal Edema 3. Cardiac impulse- Diffused and shifted laterally from elevated diaphragm. 4. Jugular veins may be distended and JVP raised. 5. Systolic ejection murmurs along the left sternal border occur in 96% of pregnant women and are believed to be caused by increased flow across the aortic and pulmonary valves.

Criteria to diagnose cardiac disease during pregnancy: 1.Presence of diastolic murmurs. 2.Systolic murmurs of severe intensity (grade 3). 3.Unequivocal enlargement of heart (X-ray). 4.Presence of severe arrythmias, atrial fibrillation or flutter

The indications for Termination of pregnancy: Because of high maternal risks, MTP is indicated in: 1.Eisenmenger’s syndrome. 2.Marfan’s syndrome with aortic involvement 3.Pulmonary hypertension. 4.Coarctation of aorta with valvular involvement. Termination should be done before 12 weeks of pregnancy.

Warfarin use in first trimester can be teratogenic and can cause fetal embryopathy( 15 to 25 % ) which includes · Nasal cartilage hypoplasia, · Stippling of bones, · IUGR and · Brachydactyly.

Risk factors for cardiac failure during pregnancy  Infection  Anemia  Obesity  Hypertension  Hyperthyroidism  Multiple pregnancy

Pregnant women with heart defects to be hospitalized: I in a period of 8-10 weeks, the survey and the issue of the possibility of pregnancy (in the therapeutic department) II at weeks, weeks, hemodynamic load III weeks to prepare and determine the method of delivery

Influence of heart diseases in pregnancy and childbirth  Incomplete pregnancy: abortion and premature birth reach 25-30%.  Intrauterine fetal hypoxia and birth asphyxia, which increase perinatal mortality.  Intrauterine fetal dystrophy.  Congenital heart disease in the newborn.  Perinatal mortality of % (5-10 times higher).  Placental abruption.  Hypogalactia.  Postpartum septic diseases.  Thromboembolism.  Anomalies tribal forces and the sequence and post-natal bleeding.

Delivery The advantage of the natural method of delivery. Compensated vice attempts are not switched off, held cardiotropic therapy, prevention of pulmonary edema with the possibility of arrhythmia - ECG monitoring. Caesarean section is performed in violation of a circulation of 1 degree. the time of delivery, despite treatment with bacterial endocarditis, with AHI, coarctation of the aorta. Cardiotropic therapy - Berglikon or strofantin, with mild hypertension aminophylline, if used during pregnancy anticoagulants - from 37 weeks to go to heparin and in labor to remove it.

In the III stage of labor in pulmonary hypertension and hypervolemia avoid pulmonary edema should not put weight on the belly. Also, when a narrow pulmonary artery, septal defects, OAD. To not develop right ventricular failure and there was no discharge of blood from right to left. With increased cardiac output (aortic, mitral insufficiency) contrary necessary weight on the stomach. Dangerous and the first few hours after birth, and the risk for up to 5 days after birth, so for the prevention of heart failure is assigned to bed rest, limited breastfeeding (even compensated vice). C 7-11 day study on the activity of rheumatism and control of up to a year after childbirth.

Antibiotic prophylaxis consists of a. 2 gm ampicillin IV/plus b. 1.5mg per kg gentamicin /IV prior to the procedure, followed by one more dose of ampicillin 8 hours later. In the event of penicillin allergy 1 gm vancomycin IV can be substituted.