disease | Pregnancy-related Heart Disease |
Cardiac disease during pregnancy can be divided into two main categories. The first category includes pre-existing heart diseases, predominantly rheumatic and congenital heart diseases, with hypertensive heart disease, mitral valve prolapse, and hypertrophic cardiomyopathy being less common. The second category comprises pregnancy-induced heart diseases, such as pregnancy-induced hypertension-related heart disease and peripartum cardiomyopathy.
bubble_chart Clinical Manifestations
1. Heart failure: In patients with heart disease, if cardiac function is already impaired or barely compensated, pregnancy can lead to further decompensation of cardiac function. In pregnant women with rheumatic heart disease, cardiac insufficiency manifests as: ① Pulmonary congestion: More common in mitral valve disease, patients experience dyspnea, worsening after exertion, with fine moist rales at the lung bases. X-ray shows interstitial edema. ② Acute pulmonary edema: More common in grade III mitral stenosis, caused by increased pulmonary capillary pressure due to hypervolemia. Patients suddenly experience dyspnea, inability to lie flat, cough, frothy sputum or hemoptysis, and scattered wheezing or moist rales in both lungs. ③ Right heart failure: Common in older patients with significant cardiac enlargement, atrial fibrillation, preexisting reduced exercise tolerance, or a history of heart failure. In pregnant women with congenital heart disease, conditions such as patent ductus arteriosus, atrial septal defect, or ventricular septal defect with pulmonary hypertension often lead to right heart failure; pulmonary stenosis or tetralogy of Fallot, due to excessive right ventricular pressure load, also frequently presents as right heart failure; aortic stenosis can lead to left heart failure due to excessive left ventricular pressure load.
2. Infective endocarditis: Both rheumatic and congenital heart diseases can complicate infective endocarditis due to bacteremia. If not controlled in time, it may trigger heart failure and be fatal.3. Hypoxia and cyanosis: In cyanotic congenital heart disease, hypoxia and cyanosis are already present at baseline. During pregnancy, peripheral resistance decreases, worsening cyanosis. In pregnant women with non-cyanotic, left-to-right shunt congenital heart disease, a drop in blood pressure due to blood loss or other reasons can cause temporary reverse shunting (right-to-left shunt), leading to cyanosis and hypoxia.
4. Embolism: During pregnancy, the blood is in a hypercoagulable state, and the increased venous pressure and venous stasis associated with heart disease predispose to embolism. Thrombi may originate from the pelvis, causing pulmonary embolism, which increases pulmonary circulation pressure, triggering pulmonary edema or reversing a left-to-right shunt to a right-to-left shunt. In congenital heart disease with communication between the left and right heart chambers, thrombi may pass through the defect and cause peripheral arterial embolism.
If organic heart disease is known before pregnancy, there is of course no diagnostic issue, but some patients may have no subjective symptoms and thus do not seek medical attention. The series of functional changes in the cardiovascular system caused by pregnancy can lead to symptoms such as palpitations, shortness of breath, and edema, and may also be accompanied by signs like grade I cardiac enlargement, heart murmurs, as well as X-ray and electrocardiogram changes, thereby increasing the difficulty of cardiac diagnosis. However, if the following abnormalities are detected, the presence of organic heart disease should be considered.
1. A grade III or higher, harsh systolic murmur.2. A diastolic murmur.
3. Severe arrhythmias, such as atrial fibrillation or flutter, atrioventricular block, etc.
4. X-ray films showing significant cardiac enlargement, especially marked enlargement of individual atria or ventricles.
5. Echocardiography revealing lesions of the heart valves, atria, or ventricles.
bubble_chart Treatment Measures
Monitoring of Pregnant Women with Heart Disease
1. Indications for terminating pregnancy: Whether women with pre-existing heart disease can tolerate pregnancy depends on various factors, such as the type of heart disease, the severity of the condition, cardiac function status, and the presence of complications. When assessing a pregnant woman's ability to tolerate pregnancy, careful consideration must be given to the potential for pregnancy to increase cardiac burden and endanger life, while also avoiding excessive caution that might deprive capable individuals of the opportunity to bear children. Generally, pregnancy is not advisable and should be terminated early under the following conditions: ① Severe cardiac lesions, cardiac function grade III or above, or a history of heart failure; ② Rheumatic heart disease with pulmonary hypertension, chronic atrial fibrillation, advanced atrioventricular block, or recent bacterial endocarditis; ③ Congenital heart disease with significant cyanosis or pulmonary hypertension; ④ Coexisting severe conditions such as nephritis, grade III hypertension, or pulmonary nodules. However, if pregnancy has exceeded 3 months, termination is usually not considered, as the risk to the diseased heart at this stage is comparable to continuing the pregnancy. If heart failure has already occurred, timely termination of pregnancy is still advisable.
2. Monitoring during continued pregnancy: Heart failure is the most critical threat to pregnant women with heart disease, and the increased cardiac load due to physiological changes such as expanded plasma volume and metabolic demands, along with diminished compensatory function, are key factors leading to heart failure. Therefore, the goal of enhanced prenatal monitoring is to prevent heart failure, with specific measures focusing on reducing cardiac burden and improving cardiac compensatory function.(1) Reducing cardiac burden: The following aspects should be considered:
1) Limit physical activity. Increase rest time, ensuring at least 10–12 hours of sleep daily. A left lateral position is recommended to enhance cardiac output and maintain stable venous return.
2) Maintain emotional calm and avoid agitation.
3) Adopt a high-protein, low-fat, vitamin-rich diet. Restrict sodium intake to 3–5g of salt daily to prevent edema. Ensure balanced nutrition and control weight gain to no more than 0.5kg per week and 10kg for the entire pregnancy.
4) Eliminate factors that impair cardiac function, such as anemia, hypoalbuminemia, vitamin deficiencies (especially B1), infections, and pregnancy-induced hypertension syndrome.
5) If transfusion is needed, administer small, frequent doses (150–200ml); if fluid replacement is required, limit to 500–1,000ml/day at a drip rate of <10–15 drops per minute.
(2) Improving cardiac compensatory function: This includes the following:
1) Cardiovascular surgery: For severe conditions with cardiac function grade III–IV, uncomplicated procedures with low anesthesia requirements can be performed during months 3–4 of pregnancy. Emergency mitral valve commissurotomy (for acute pulmonary edema due to pure mitral stenosis) can be performed pre-delivery. Patients with patent ductus arteriosus who develop heart failure or ductal infection during pregnancy are candidates for surgery.
2) Digitalization: Pregnant women with heart disease who show no signs or symptoms of heart failure generally do not require digitalis therapy, as it is ineffective in such cases. Moreover, digitalis use during pregnancy does not guarantee prevention of heart failure during delivery, and adverse reactions may complicate medication adjustments. Rapid digitalization can take effect within minutes, and close monitoring allows timely control of early heart failure. Thus, digitalis is typically reserved for pre-heart failure symptoms, early heart failure, or cardiac function grade III at 28–32 weeks (before the peak hemodynamic load of pregnancy). Due to lower tolerance and higher toxicity risk in pregnant women, rapid-acting preparations like deslanoside (Cedilanid) or strophanthin K are preferred. Maintenance therapy uses digoxin, which is excreted more quickly, usually continued until 4–6 weeks postpartum when circulation normalizes.
In addition, pregnant women with cardiac function class I or II should increase the frequency of prenatal check-ups. Before 20 weeks, they should be examined by a cardiologist and obstetrician at least every two weeks, and then weekly thereafter, with home follow-ups if necessary. Apart from monitoring obstetric conditions, the focus should be on assessing cardiac compensatory function and various symptoms. Regular electrocardiograms and echocardiograms should be performed to comprehensively evaluate the condition. If abnormalities or early signs of heart failure are detected, immediate hospitalization is required. Admission two weeks before the expected due date allows for adequate rest and facilitates monitoring. Those with cardiac function class III or heart failure should be hospitalized and remain under medical supervision until childbirth.
Management during childbirth and puerperium periods
1. Choice of childbirth method: The method of childbirth for pregnant women with heart disease primarily depends on cardiac function status and obstetric conditions.
(1)Cesarean section: Cesarean section can conclude childbirth in a shorter time, thereby avoiding hemodynamic changes caused by prolonged uterine contractions and reducing cardiac load from fatigue and pain. Additionally, during the procedure under continuous epidural anesthesia, changes in maternal blood pressure, mean arterial pressure, and heart rate are smaller compared to vaginal childbirth. However, surgery increases the risk of infection and bleeding, and the procedure itself is also a burden. Therefore, when obstetric indications exist (such as abnormal fetal position, large fetus, etc.), the criteria for cesarean section can be appropriately relaxed, but selective cesarean section is only performed in cases of cardiac function class III–IV, active rheumatic fever, pulmonary arterial hypertension or pulmonary congestion, aortic stenosis, etc. Preoperative, intraoperative, and postoperative cardiac monitoring, as well as postoperative anti-infection measures, are essential for ensuring surgical safety.
(2)Vaginal childbirth: For those with cardiac function class I–II, vaginal childbirth is the principle unless obstetric complications arise. The average duration of labor for pregnant women with heart disease does not significantly differ from that of normal pregnant women, but close monitoring by dedicated personnel is mandatory. Antibiotics should be administered at the onset of labor to prevent infection, with the laboring woman placed in a semi-recumbent position and given oxygen. If contractions are strong and pain is unbearable, meperidine (Demerol) 50–100mg can be administered intramuscularly; continuous epidural anesthesia may also be used to alleviate pain and facilitate management during the second stage of labor. Heart rate and respiratory rate should be closely monitored—hourly during the first stage of labor and every 10 minutes during the second stage. If the heart rate exceeds 100 beats per minute during the contraction interval or fine moist rales appear at both lung bases accompanied by grade I dyspnea, these are signs of impending grade III heart failure, and digitalization should be initiated immediately with intravenous deslanoside or strophanthin K. Once the cervix is fully dilated and the fetal head is at an appropriate station, operative delivery should be performed to shorten the second stage of labor. Patients with congenital heart disease and left-to-right shunting should particularly avoid the Valsalva maneuver. After delivery of the fetal anterior shoulder, administer 10mg morphine intramuscularly and 10 units of oxytocin. After placental delivery, place a sandbag (1kg) on the abdomen. Closely monitor blood pressure, pulse, and uterine contraction, and record vaginal bleeding volume.
2. Key points of puerperium management: With enhanced monitoring during pregnancy and childbirth, most patients can pass through safely. However, neglecting puerperium monitoring may lead to failure at the last hurdle. Statistics show that 75% of maternal deaths due to heart disease occur in the early puerperium.
(1)Continue antibiotics to prevent infection and avoid subacute bacterial endocarditis.
(2)Postpartum women with a history of heart failure should continue taking cardiac medications.
(3)Monitor temperature, pulse, respiration, blood pressure, uterine involution, and bleeding.
(4)Postpartum bed rest for 24–72 hours; women with severe heart disease should adopt a semi-recumbent position to reduce venous return and receive oxygen. If no signs of heart failure are present, encourage early ambulation. For those with heart failure, leg exercises should be performed during bed rest to prevent thrombophlebitis.
(5)Women with cardiac function class III or above should not breastfeed. Lactation increases metabolic demands and fluid requirements, potentially worsening the condition.
(6)Postpartum hospitalization for at least 2 weeks is required, and discharge should only occur once cardiac function improves. After discharge, adequate rest and limited activity are necessary, along with strict contraception.
Diagnosis and treatment of heart failure
Heart disease is the basis for the occurrence of heart failure. From the perspective of the hemodynamic changes during pregnancy, childbirth, and the puerperium period and their impact on the heart, the 32nd to 34th week of pregnancy, the childbirth period, and the first 3 days of the puerperium period are the most dangerous times for patients with heart disease, as they are highly prone to heart failure. The left heart is more likely to develop heart failure faster than the right heart under excessive volume load, while the right heart is more likely to develop heart failure faster than the left heart under hydrostatic pressure load.
Primary left heart failure is seen in mitral valve disease, aortic valve disease, and left-to-right intracardiac shunts caused by patent ductus arteriosus or ventricular septal defects. The clinical manifestations result from pulmonary congestion and elevated pulmonary capillary pressure: dyspnea, orthopnea, cough, hemoptysis, pulmonary rales, accentuated second heart sound in the pulmonary valve area, and decreased vital capacity with normal venous pressure. Acute left heart failure presents as paroxysmal dyspnea and acute pulmonary edema.
Right heart failure usually occurs secondary to left heart failure. Primary right heart failure is seen in pulmonary hypertension, pulmonary stenosis, etc. The clinical manifestations mainly arise from systemic venous congestion and elevated venous pressure: superficial vein engorgement, subcutaneous edema, hepatomegaly with tenderness, cyanosis, ascites, pleural effusion, pericardial effusion, and renal, gastrointestinal, and neurological disturbances.
1. Early diagnosis: The classification of cardiac compensatory function corresponds to the grading of heart failure: cardiac function class II = grade I heart failure; cardiac function class III = grade II heart failure; cardiac function class IV = grade III heart failure.
Early symptoms of heart failure include: unexplained fatigue, chest tightness and shortness of breath after mild exertion, waking up at night due to breathlessness and/or needing to elevate the head, distending pain in the liver area, and lower limb edema. Early signs include: resting heart rate >120 bpm, respiratory rate >24 bpm, enhanced jugular venous pulsation, wet rales at the lung bases, pulsus alternans, diastolic gallop rhythm, reduced urine output, and weight gain. The ECG V 1 P-wave terminal vector (PTF-V 1 ) is positive (-0.03 mm·s or deeper). Serial chest X-rays (upright position) show thickening of pulmonary venous markings in the middle and upper lung fields.
2. Treatment principles: The treatment principles for heart failure in pregnancy are similar to those for non-pregnant individuals.
(1) Cardiotonic: Rapid-acting digitalis preparations are used to improve myocardial function. Deslanoside is the first choice, administered as 0.4 mg with 20 ml of 25% glucose solution via slow intravenous injection. If needed, an additional 0.2–0.4 mg can be given after 2–4 hours, with a total dose up to 1.2 mg. Strophanthin K can also be used, with 0.25 mg in 20 ml of 25% glucose solution via slow intravenous injection, followed by 0.125–0.25 mg after 2–4 hours if necessary. The appropriate digitalization dose is 0.5 mg. After efficacy is achieved, switch to the faster-excreting digoxin for maintenance. Pregnant women have poorer tolerance to digitalis cardiotonics, so close monitoring for toxicity symptoms is required.
(2) Diuresis: Furosemide 40–60 mg is commonly administered intravenously to promote diuresis, reduce circulating blood volume, and alleviate pulmonary edema. It can be repeated, but electrolyte balance must be monitored.
(3) Vasodilation: In heart failure, peripheral vasoconstriction is often heightened, increasing cardiac afterload. Vasodilators can act as "internal bloodletting." Options include isosorbide dinitrate 5–10 mg, captopril 12.5 mg, or prazosin 1 mg, three times daily.
(4) Sedation: A small dose of morphine (5 mg) diluted and administered intravenously not only provides sedation, analgesia, and suppression of the overexcited respiratory center but also dilates peripheral vessels, reducing cardiac preload and afterload. It also has antiarrhythmic effects and is commonly used in acute left heart failure and pulmonary edema emergencies.
(5) Reducing venous return: Apply tourniquets to the limbs, releasing one limb every 5 minutes in rotation. A semi-recumbent position with legs dangling can achieve the same effect.
(6) Antiarrhythmic: Arrhythmias can be caused by heart failure or can induce or worsen heart failure. Severe cases should be promptly corrected. For rapid atrial ectopic rhythms, electrical cardioversion is safe and effective, and quinidine or procainamide can also be used. Rapid ventricular ectopic rhythms are often treated with lidocaine, mexiletine hydrochloride, or phenytoin sodium, with the latter being particularly suitable for digitalis toxicity. High-grade or complete atrioventricular block generally requires temporary pacemaker implantation, or intravenous infusion of isoproterenol.