1. Correct Answer: C. Cardiac output increased, EF unchanged, LV size increased

Rationale: Cardiac output increases to compensate for an increased circulating blood volume during pregnancy. By the time a parturient is at 36 weeks, echocardiographic changes of LV size and function should be evident. In order to increase cardiac output, LV stroke volume increases, accomplished by increasing LV size, as measured by LV end-diastolic diameter. This increased diastolic size allows for a larger stroke volume but an unchanged EF. Elevation in resting HR also contributes to the increase in cardiac output during pregnancy.

1. Liu, S, Elkayam U, Naqvi T. Echocardiography in pregnancy: part 1. Curr Cardiol Rep. 2016;18(9):92.

2. Correct Answer: C. Increased end-diastolic diameter, increased LV stroke volume

Rationale: During the course of pregnancy, cardiac output undergoes a gradual increase. By the time of delivery, cardiac output has increased by approximately 50% and can increase even more immediately following delivery. This is accomplished by both an increase in HR and stroke volume. In order to increase stroke volume, the LV end-diastolic diameter is increased, resulting in an increased stroke volume but unchanged EF. The images demonstrate an enlarged end-diastolic diameter of 57 mm compared to normal adult females who should have an end-diastolic diameter between 40 and 50 mm. The EF of 68% is not elevated but the stroke volume of 110 mL is also elevated compared to a normal value of 95 mL ± 10 mL. There is also physiologic LV hypertrophy as a result of the increased circulating blood volume. The hemodynamic and echocardiographic changes in pregnancy often resolve within 2 weeks postpartum. The supplemental videos demonstrate increased LV stroke volume and increased end-diastolic diameter.

1. Liu, S, Elkayam U, Naqvi T. Echocardiography in pregnancy: part 1. Curr Cardiol Rep. 2016;18(9):92.

3. Correct Answer: A. Enlarged LV end-diastolic diameter, LVEF estimated at 30 to 35%

Rationale: The European Society of Cardiology working group defines peripartum cardiomyopathy as an idiopathic, dilated cardiomyopathy that presents during the last month of pregnancy or immediately postpartum, with symptoms of heart failure. Peripartum cardiomyopathy affects between 1:1,000 and 1:4,000 live births in the United States. While the underlying cause of peripartum cardiomyopathy is unknown, hypertension during pregnancy may be a risk factor. Peripartum cardiomyopathy is a diagnosis of exclusion, and hypertensive disease, coronary artery disease, and valvular disease must be excluded. Patients with peripartum cardiomyopathy have a reduced LVEF and abnormal contractility. An echocardiogram will reveal an LVEF of less than 45% and both the end-diastolic and end-systolic diameters will be increased. RV function is also affected in peripartum cardiomyopathy, and the TAPSE has been found to be significantly less in peripartum patients when compared to idiopathic dilated cardiomyopathy.

1. Arany Z, Elkayam U. Peripartum cardiomyopathy. Circulation. 2016, 133:1397-1409.

2. Bauersachs J, König T, van der Meer P, et al. Pathophysiology, diagnosis and management of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy. Eur J Heart Fail. 2019;21:827-843.

3. Liu, S, Elkayam U, Naqvi T. Echocardiography in pregnancy: part 1. Curr Cardiol Rep. 2016;18(9):92.

4. Correct Answer: B. Dilated LV with reduced systolic function

Rationale: Peripartum cardiomyopathy is characterized by a dilated left ventricle with a reduction in systolic function. One of the defining characteristics is the onset of heart failure symptoms within the last four weeks of the pregnancy or immediately postpartum. The LV end diastolic diameter increases in size during pregnancy and should measure between 50 and 60 mm in healthy parturients. The images show an increased end-diastolic diameter measuring 66 mm (Figure 66.3B). The increased end-diastolic diameter is accompanied by a calculated end-diastolic volume of 224 mL. The calculated EF seen in Figure 66.3D is 22%, which is below the diagnostic cutoff of 45%.

1. Arany Z, Elkayam U. Peripartum cardiomyopathy. Circulation. 2016;133:1397-1409.

2. Bauersachs J, König T, van der Meer P, et al. Pathophysiology, diagnosis and management of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy. Eur J Heart Fail. 2019;21:827-843.

3. Liu, S, Elkayam U, Naqvi T. Echocardiography in pregnancy: part 1. Curr Cardiol Rep. 2016;18(9):92.

5. Correct Answer: C. Increased LV mass, elevated E/e′

Rationale: The most common cause of nonobstetric death in pregnancy is cardiovascular disease. As discussed in previous questions, there are significant cardiovascular changes that occur during pregnancy. Patients with preeclampsia and gestational hypertension have increased vascular resistance and abnormal LV function. As the pregnancy progresses, cardiac output can fall, which leads to a higher vascular resistance to maintain placental perfusion pressure.

A compensatory response to the increased vascular resistance is for LV hypertrophy to develop. This increase in LV mass results in diminished diastolic relaxation, as evidenced by a decrease in the E/A ratio, and is seen in both preeclampsia and gestational hypertension. E/e′ can be used to differentiate hypertensive cardiomyopathy of preeclampsia from the effects of gestational hypertension. In preeclampsia, elevated LV end-diastolic pressure (LVEDP) is seen as a compensatory mechanism, and E/e′ will be elevated. These changes in diastolic dysfunction are more pronounced in patients that develop early preeclampsia and can often be seen before the clinical diagnosis of preeclampsia is made.

Echocardiographic findings in gestational hypertension include normal LV function and myocardial performance index, and an increase in LV mass resulting from concentric hypertrophy. The LV and LA diameters also increase. The E/A ratio is decreased further than in pregnant patients without hypertension.

Answers A, B and D are all changes found in normal pregnancy.

1. Castleman JS, Ganapathy R, Taki R, Lip GYH, Steeds RP, Kotecha D. Echocardiographic structure and function in hypertensive disorders of pregnancy: a systematic review. Circ Cardiovasc Imaging. 2016;9:e004888.

6. Correct Answer: D. Collapsible IVC with respiratory variation

Rationale: Figures 66.4 and 66.5 show a distended right ventricle that has septal displacement into the left ventricle, which is more pronounced during systole. This finding is caused by both RV pressure and volume overload, in this case as a possible result of an amniotic fluid embolus. In acute volume overload, the right ventricle will cause a leftward septal shift that is most prominent at end diastole because that is when RV volume is the highest and RV end-diastolic pressure exceeds LVEDP. In acute RV pressure overload, the right ventricle contracts against a higher afterload, resulting in high RV systolic pressure and leftward septal shift during systole. The first signs of RV pressure overload will be a loss of septal motion and a flattening of the septum, resulting in a D-shaped left ventricle. As RV pressure rises, a leftward septal shift during systole is seen. Elevated RV pressures prolong RV systole, which also accounts for some of the septal shift. New severe TR is also a sign of RV dilation. With the dilation of the RV and the severe TR that accompanies it, the IVC will become distended and have minimal respiratory variation. Pulsed-wave Doppler of the hepatic vein flow will show systolic flow reversal.

1. McDonnell, NJ, Percival V, Paech MJ. Amniotic fluid embolism: a leading cause of maternal death yet still a medical conundrum. Int J Obstet Anesth. 2013;22:329-336.

2. Sidebotham D. Practical Perioperative Transoesophageal Echocardiography. 3rd ed. Oxford University Press: 2018:209,211,285-288.

7. Correct Answer: D. Dilated LV with systolic and diastolic impairment

Rationale: AFE is a rare but potentially fatal event that can occur in the peripartum period. The incidence ranges between 1:12,000 in the United States and 1:50,000 in the UK. The sentinel event is disruption of the barrier between maternal and placental circulation and the entry of placental, amniotic, or fetal components into maternal circulation via the uterine veins. One theory is that an AFE causes a mechanical obstruction in the pulmonary artery leading to reduced cardiac output. A more recent theory suggests that AFE is an immune-mediated response. Amniotic fluid contains cytokines, vasoactive peptides, and procoagulant factors, which can trigger the immune response that results in pulmonary hypertension. The effect of either mechanical obstruction or pulmonary hypertension is acute RV pressure overload.

The first echo findings seen in AFE is acute RV failure from RV pressure overload. Septal shift can also decrease LV end-diastolic volume and affect LV function. TAPSE is likely to be decreased (<18 mm) with significant RV dysfunction. After the resolution of pulmonary hypertension, LV systolic dysfunction can still be seen; this may be due to ischemia from hypotension or direct myocardial depression from inflammatory mediators. There are also case reports of visualizing transient masses in the RV or pulmonary arteries. It is unclear if these masses are from development of disseminated intravascular coagulation (DIC), amniotic products, or thromboemboli.

AFE does not result in a dilated left ventricle and reduced systolic function, this would be more consistent with peripartum cardiomyopathy.

1. James CF, Feinglass NG, Menke DM, Grinton SF, Papadimo TJ. Massive amniotic fluid embolism: diagnosis aided by emergency transesophageal echocardiography. Int J Obstet Anesth. 2004;13:279-283.

2. Katz J, Shear TD, Murphy GS, et al. Cardiovascular collapse in the pregnant patient, rescue transesophageal echocardiography and open heart surgery. J Cardiothorac Vasc Anesth. 2017;31:203-206.

3. McDonnell, NJ, Percival V, Paech MJ. Amniotic fluid embolism: a leading cause of maternal death yet still a medical conundrum. Int J Obstet Anesth. 2013;22:329-336.

4. Shamshursaz AA, Clark SL. Amniotic fluid embolism. Obstet Gynecol Clin North Am. 2016;43:779-790.

8. Correct Answer: C. This is a Stanford Type A dissection

Critique/Rationale: Half of aortic dissections that occur in patients under the age of 40 occur in a peripartum setting and are less commonly associated with hypertension as compared to non-parturients. In pregnancy, there are hormonal changes that lead to a weakening of aortic tissue and, when combined with an increase in shear stress due to an expansion in blood volume during the third trimester, aortic dissection can occur. Patients at a higher risk for peripartum aortic dissection are those with connective tissue disorders like Marfan syndrome, Ehlers-Danlos syndrome, and Loeys-Dietz syndrome. Management of an acute Type A aortic dissection would include emergent delivery of the fetus and surgical repair.

The diagnosis of aortic dissection can be made with CT angiography or echocardiography. CT angiography has a sensitivity of 100% and a specificity of 98%, and TEE has high sensitivity and specificity for detecting Stanford Type A dissection approaching 100%, as well. In pregnant patients, TEE has the benefit of not requiring ionizing radiation. TEE can also be useful to look for extension of the dissection into the aortic root and, according to one study, up to 79% of patients had severe acute aortic insufficiency.

Differentiating between the true and false lumen is important for surgical repair. This can be done by looking for systolic expansion of the true lumen and more turbulent higher velocity flow based on color flow Doppler within the true lumen. If the origin of the dissection flap is found, color flow can be used to visualize flow directly into the false lumen.

Hypertension is a risk factor for both Type A and Type B aortic dissections. A Stanford Type B dissection originates distal to the left subclavian artery and is often managed medically, while a Type A dissection originates anywhere more proximal and is managed surgically. Traumatic aortic dissections are most commonly seen in the descending thoracic aorta, and most originate where the ligamentum arteriosum tethers the aorta to the chest. TEE can be helpful in diagnosing and determining the origin of Type B dissections; it is also used for guidance during open and endovascular repair.

1. Borhart J, Palmer J. Cardiovascular emergencies in pregnancy. Emerg Med Clin North Am. 2019;37:339-350.

2. Sidebotham D. Practical Perioperative Transoesophageal Echocardiography. 3rd ed. Oxford University Press: 2018: 182-184.

3. Zhu JM, Ma WG, Peters S, et al. Aortic dissection in pregnancy: management strategy and outcomes. Ann Thorac Surg. 2017;103:1199-1206.

9. Correct Answer: C. Acute aortic insufficiency from aortic valve endocarditis

Rationale: Infective endocarditis during pregnancy is a rare but potentially catastrophic occurrence. The prevalence of infective endocarditis during pregnancy is estimated at 0.006%, but as high as 1.2% for patients with preexisting cardiac disease (prosthetic valve or surgically corrected congenital disease). The biggest risk factor for patients without preexisting cardiac disease is IV drug use. Maternal mortality from heart failure or embolic events is 33% and fetal mortality is 29%. Surgery, while high risk, may be required during pregnancy for heart failure symptoms from acute valvulopathy.

Chronic aortic insufficiency results in chronic LV volume overload, which can be well-tolerated because the LV can compensate with hypertrophy and by increasing in size. Acute aortic insufficiency causes rapid LV volume and pressure overload, which can result in an abrupt rise in left atrial and pulmonary pressures, resulting in acute pulmonary edema. The high regurgitant fraction seen with severe aortic insufficiency can result in reduced forward flow leading to cardiogenic shock. The increase in circulating blood volume during pregnancy can exacerbate or unmask underlying aortic insufficiency.

The images above are from a patient who developed sudden severe aortic insufficiency as a result of aortic valve endocarditis.

1. Habib G, Lancellotti P, Antunes MJ, et al. 2015 ECS guidelines for the management of infective endocarditis. Eur Heart J. 2015;36:3075-3123.

2. Sidebotham D. Practical Perioperative Transoesophageal Echocardiography. 3rd ed. Oxford University Press: 2018:155-157.