📚 Guideline basis
2018 ESC guidelines for the management of cardiovascular diseases during pregnancy (Regitz-Zagrosek V, et al., Eur Heart J 2018); ESC Heart Failure Association position statement on peripartum cardiomyopathy; 2025 ESC/EACTS valvular heart disease guidelines; AHA scientific statement on cardiac arrest in pregnancy.
> ⚠️ Reference ranges
> Normal pregnancy changes cardiac structure and function substantially. Applying non-pregnant reference ranges over-diagnoses pathology in this population, and the ASE 2025 diastolic algorithm explicitly states it should not be applied in normal pregnancy.
Normal physiological adaptation
Parameter | Change by the third trimester |
Cardiac output | ↑ 30–50% (early rise in stroke volume, later rise in heart rate) |
Plasma volume | ↑ 40–50%, exceeding the rise in red cell mass — physiological anaemia |
Heart rate | ↑ 10–20 beats/min |
Systemic vascular resistance | ↓ 25–30% |
Blood pressure | Falls in the second trimester, returns toward baseline at term |
LV end-diastolic dimension | Mildly increased; mild eccentric hypertrophy with a ~50% increase in LV mass |
LV ejection fraction | Unchanged or mildly increased |
Left atrial size | Mildly increased |
Valvular regurgitation | Mild mitral, tricuspid and pulmonic regurgitation are normal; new mild AR is less common |
Pericardial effusion | Small effusion is common and benign |
Peak intrapartum output | Further rise during labour and an immediate post-delivery autotransfusion as the uterus contracts |
Consequence: a mildly dilated ventricle, mild multivalvular regurgitation, a small pericardial effusion, and a resting tachycardia are the expected findings, not evidence of disease.
The supine hypotension effect
After roughly 20 weeks, the gravid uterus compresses the inferior vena cava and aorta in the supine position, reducing venous return by up to a third. Every echocardiographic measurement taken supine in the second half of pregnancy systematically misrepresents volume status and cardiac output. Image in the left lateral position, or with manual left uterine displacement, and state the position in the report.
Peripartum cardiomyopathy
Diagnostic criteria
Idiopathic cardiomyopathy presenting with heart failure secondary to LV systolic dysfunction towards the end of pregnancy or in the months following delivery (commonly defined as the last month of pregnancy to five months postpartum), with LVEF < 45%, in the absence of another identifiable cause. The left ventricle may or may not be dilated. It is a diagnosis of exclusion.
Mechanism
The prevailing model implicates oxidative-stress-driven cleavage of prolactin into an antiangiogenic 16 kDa fragment, together with an antiangiogenic environment created by placental sFlt-1. This mechanism underlies the rationale for bromocriptine as adjunctive therapy — supported by a small randomised trial and included as a consideration in ESC guidance, but not established as standard care.
Echocardiographic assessment and prognosis
Finding | Significance |
LVEF < 30% at diagnosis | Adverse; lower likelihood of full recovery |
LVEDD ≥ 6 cm | Adverse |
RV involvement | Adverse |
LV thrombus | Common in severe dysfunction; anticoagulation indicated |
Recovery | A substantial proportion recover LV function within 6 months; recovery is less likely with the adverse features above |
Serial echocardiography guides therapy duration and, critically, counselling about subsequent pregnancy — persistent dysfunction carries a high risk of recurrence and mortality in a future pregnancy.
Pre-eclampsia and hypertensive disorders
The cardiac phenotype is distinct from peripartum cardiomyopathy:
- Concentric remodelling and hypertrophy with increased relative wall thickness
- Diastolic dysfunction with elevated E/e′
- Pulmonary oedema with a preserved ejection fraction — an afterload and diastolic problem, not a systolic one
- Elevated systemic vascular resistance, in contrast to the low SVR of normal pregnancy
Recognising this matters therapeutically: the treatment is afterload reduction and cautious diuresis, not inotropic support.
Amniotic fluid embolism
A biphasic haemodynamic collapse, and echocardiography can capture the phase.
Phase | Timing | Findings | Management |
Phase 1 — acute RV failure | Minutes; often at delivery or immediately after | Severe RV dilatation and dysfunction, septal shift, small underfilled LV, severe pulmonary hypertension | Vasopressor for coronary perfusion, avoid volume loading, pulmonary vasodilators, consider ECMO |
Phase 2 — LV failure | Following the initial phase, over minutes to hours | LV dysfunction, pulmonary oedema, often with disseminated intravascular coagulation | Inotropic support, transfusion and DIC management |
The differential is pulmonary embolism, haemorrhagic shock, anaphylaxis and eclampsia. The combination of acute RV failure with coagulopathy at the time of delivery is characteristic, and echocardiography distinguishes it from haemorrhagic shock (small, hyperdynamic, underfilled chambers) within seconds.
Pre-existing disease decompensating in pregnancy
The physiological output demand of pregnancy is a stress test that unmasks fixed-obstruction lesions.
Lesion | Why pregnancy decompensates it | Management |
Mitral stenosis | The classic lesion. Tachycardia shortens diastole while output demand rises; the fixed orifice cannot accommodate either (Chapter 21) | Rate control with beta-blockade, careful diuresis, balloon valvuloplasty if refractory |
Aortic stenosis | Fixed output against a fall in SVR | Maintain SVR and preload, avoid vasodilatation (Chapter 18) |
Pulmonary hypertension | Historically the highest-risk cardiac condition in pregnancy | Multidisciplinary care in an expert centre |
Mechanical prosthetic valve | Pregnancy is prothrombotic; anticoagulation management is complex | Serial gradients; a rising gradient suggests thrombosis (Chapter 23) |
Marfan / aortopathy | Hormonal and haemodynamic aortic stress | Serial root measurement |
Congenital lesions, Fontan physiology | Limited ability to augment output | Expert centre |
Regurgitant lesions | Generally tolerated well — the fall in SVR reduces regurgitant volume | Supportive |
The pattern: stenotic and fixed-output lesions decompensate; regurgitant lesions are usually tolerated.
Maternal cardiac arrest
Element | Detail |
Left uterine displacement | Manual displacement during CPR after ~20 weeks; do not tilt the whole patient, which degrades compression quality |
Compressions and defibrillation | Standard technique, standard energies; defibrillation is safe |
Resuscitative hysterotomy | Considered within roughly 4 minutes of arrest with delivery by 5 minutes, both to save the fetus and — importantly — to relieve aortocaval compression and improve maternal haemodynamics |
Echocardiography | Same role and same constraints as Chapter 31; do not interrupt compressions. Look specifically for RV dilatation (amniotic fluid embolism, pulmonary embolism), tamponade, and the collapsed chambers of haemorrhage |
Aetiologies | Haemorrhage, amniotic fluid embolism, pulmonary embolism, eclampsia, anaesthetic complications including local anaesthetic systemic toxicity, cardiomyopathy, aortic dissection |
ICU-Specific Limitations
Confounder | Effect | Response |
Supine position after 20 weeks | Aortocaval compression under-represents preload and cardiac output | Left lateral position or manual uterine displacement; state the position |
Non-pregnant reference ranges | Over-diagnosis of chamber dilatation and valvular regurgitation | Use pregnancy-specific expectations |
ASE 2025 diastolic algorithm | Explicitly not applicable in normal pregnancy | Interpret filling pressures descriptively |
Peripartum autotransfusion | Volume state changes abruptly at delivery | Repeat the study after delivery |
Tachycardia | E–A fusion; degraded time intervals | Expected; note it |
Body habitus and displaced diaphragm late in pregnancy | Altered windows; the heart is displaced upward and leftward | Parasternal and apical views are often better than subcostal |
🛑 Critical pitfall: Scanning a woman beyond 20 weeks in the supine position and concluding she is hypovolaemic. Aortocaval compression produces exactly that picture. Reposition and rescan.
🛑 Critical pitfall: Reporting mild mitral and tricuspid regurgitation with a mildly dilated ventricle and a small pericardial effusion as pathology. These are normal findings in late pregnancy.
🛑 Critical pitfall: Treating pre-eclamptic pulmonary oedema as systolic heart failure. The ejection fraction is preserved; the problem is afterload and diastolic stiffness, and inotropes are not the answer.
- 💡 Clinical pearl: Acute RV failure at delivery with coagulopathy is amniotic fluid embolism until proven otherwise. Echocardiography separates it from haemorrhagic shock in seconds — dilated RV versus small, empty, hyperdynamic chambers.
- 💡 Clinical pearl: Mitral stenosis is the lesion that decompensates in pregnancy, and rate control is the single most effective intervention.
- 💡 Clinical pearl: Repeat the echocardiogram after delivery. The autotransfusion from uterine contraction and the loss of the placental circuit change loading abruptly, and the immediate postpartum period is when pre-existing lesions declare themselves.
References
- Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, et al. 2018 ESC guidelines for the management of cardiovascular diseases during pregnancy. Eur Heart J 2018;39:3165–241.
- 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 ESC. Eur J Heart Fail 2019;21:827–43.
- Jeejeebhoy FM, Zelop CM, Lipman S, et al. Cardiac arrest in pregnancy: a scientific statement from the American Heart Association. Circulation 2015;132:1747–73.
- Nagueh SF, Sanborn DY, Oh JK, et al. ASE 2025 diastolic function update. J Am Soc Echocardiogr 2025;38:537–69.
- ESC/EACTS. 2025 Guidelines for the management of valvular heart disease. Eur Heart J 2025;46:4635–.