A 30-year-old woman presents to the clinic 17 weeks pregnant and becoming increasingly breathless. The LVEDD is 6.1 cm and the EF is estimated at 25%.
Which one of the following statements is false?
ACE inhibitors are absolutely contraindicated in the second and third trimesters of pregnancy because of the risk of renal defects, oligohydramnios, and limb contractures. Hydralazine and nitrate is a safe alternative. Rest (bed rest in hospital) is likely to be required in this case. The aim would be for the fetus to reach viability without compromising the mother. Termination of pregnancy would be justified in this case as there is a high risk of pulmonary oedema, intractable heart failure, stroke, and fetal loss. Patients with occult left ventricular dysfunction and obstructive valve disease usually present around this point in gestation as this is when their increase in cardiac output and plasma volume during pregnancy begins to peak (apart from in labour). The haemodynamic changes in pregnancy are profound. Hormonally mediated increases in blood volume, red cell mass, and heart rate result in a significant increase in cardiac output. Cardiac output peaks during the second trimester, and then remains constant until term. Circulating prostaglandins and other gestational hormones, and the low-resistance vascular bed of the placenta, result in decreases in peripheral vascular resistance and blood pressure. Blood pressure reaches its nadir in the middle of the second trimester and then begins to rise again towards term.
A 9-year-old woman was born with transposition of the great arteries and had a Mustard repair. She has been well throughout her pregnancy, but presents at 37 weeks with a week of worsening dull central chest pain on exertion, associated with shortness of breath.
Congenital heart disease affects 0.8% of live births and 85% of patients now survive to adulthood. Approximately 70% patients seen in cardiac antenatal clinics are those with congenital heart disease. Patients with atrial switch repair of transposition of the great arteries have a single right ventricle, which does not cope well with the demands of pregnancy. Coronary insufficiency can occur because of a mismatch between myocardial oxygen supply and demand. Short-term conservative treatment is acceptable but delivery should be expedited if possible, and certainly at 37 weeks gestation.
You are called to the labour ward because a 34-year-old woman has become breathless and orthopnoeic 2 hours after delivery. She is pain free. On examination she is tachycardic, tachypnoeic, and has a gallop rhythm. Blood pressure is 136/86 mmHg. On auscultation of her chest she has fine inspiratory crackles to the mid-zones.
What is the most likely diagnosis?
This is a typical picture of peripartum cardiomyopathy (often undiagnosed dilated cardiomyopathy, which decompensates at this time of extreme increase in preload). The largest haemodynamic changes in pregnancy occur in the post-partum period. During labour and delivery, pain and uterine contractions result in additional increases in cardiac output and blood pressure. Immediately after delivery, relief of caval compression and autotransfusion from the emptied and contracted uterus produce a further increase in cardiac output (50–70% more than baseline overall). Most haemodynamic changes of pregnancy resolve by 2 weeks post-partum. Myocardial infarction in pregnancy is generally accompanied by pain, and pulmonary embolus does not result in signs of left heart failure. Tachyarrhythmia in pregnancy is common and is not usually associated with ventricular decompensation. Amniotic fluid embolus is rare and presents with shortness of breath leading to hypotension, cyanosis, and cardiac arrest.
A 27-year-old woman presents at 26 weeks gestation in pulmonary oedema. She recently moved to the UK from Pakistan but was previously well. An echocardiogram showed mitral valve disease. The MV area is 1.0 cm2 , mean gradient is 25 mmHg, and PHT is 220 ms.
What is the most appropriate treatment?
If the patient is already in pulmonary oedema this will continue to worsen through pregnancy, so diuretics etc. will only be a temporary relief. The outcome for a fetus delivered at 26 weeks is poor and therefore delivery is not desirable at this gestation. The treatment of choice is balloon mitral valvuloplasty by a skilled operator. Balloon mitral valvuloplasty is highly effective in pregnancy and safe. If there is severe mitral regurgitation at the end of the procedure this will be much better tolerated in progressing pregnancy than severe mitral stenosis. Note that the increased preload of pregnancy needs to be taken into account when assessing mitral stenosis. Peak and mean gradients will be extremely elevated because of the increase in preload. Cardiothoracic surgery is not the treatment of choice as cardiopulmonary bypass is associated with a 50% risk of fetal mortality. Rheumatic heart disease in pregnancy is common in developing countries and is increasing in the UK because of increased immigration.
A 38-year-old woman presents 34 weeks pregnant to the ED in atrial fibrillation. Blood pressure is 110/62 mmHg. Echocardiograpy and blood test results are normal.
Which of the following is not a good first line of action?
Atrial fibrillation is uncommon in pregnancy. Management needs to focus on treating the arrhythmia and protection from thromboembolic events. Pregnancy is a hypercoagulable state, so full anticoagulation with low molecular weight heparin is recommended until 4 weeks after the restoration of sinus rhythm. If the patient is in AF for a short time this is not required, as with non-pregnant patients. DC cardioversion is safe, but is not recommended unless the patient is compromised. The fetus should be monitored with CTG if this is required. Many antiarrhthymics are relatively safe in pregnancy. Flecainide is FDA Category C (it is effective in medically cardioverting patients in AF and is often used to treat fetal arrhythmias). Beta-blockers can also be used (see Question 5). Digoxin is also Category C and is sometimes used for fetal treatment. The dose may need to be increased in pregnancy because of the increased glomerular filtration rate. Levels need to be checked in case of toxicity, which is dangerous for the fetus. Amiodarone is not safe in pregnancy (Category D). It causes fetal thyroid problems and intra-uterine growth retardation, and is teratogenic.
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