Cardiac Disease in Pregnancy

The curriculum requires us to describe "The influence of concurrent medical diseases on pregnancy and the management of these patients".

Cardiac disease in the obstetric patient featured as a CRQ in March 2021 (59.8% pass rate); it was considered one of the harder questions on the paper, and examiners noted that "The applied physiology and pharmacology components of the question saw candidates drop the most marks".

This page is an overview of cardiac disease in pregnancy, with separate dedicated pages on arrhythmia, pulmonary hypertension and peripartum cardiomyopathy.

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Cardiac disease remains the leading indirect cause of maternal death in the UK
Globally, cardiovascular disease accounts for around a third of pregnancy-related deaths, and an estimated 68% of these are preventable
The number of pregnancies in women with cardiovascular disease is rising, due to:

Older maternal age
Increasingly prevalent cardiovascular comorbidity
More women with congenital cardiac disease reaching childbearing age

Up to 4% of pregnancies are complicated by cardiovascular disease, rising to 10% if hypertensive disorders are included
In high-income countries the majority is congenital heart disease
Those with congenital heart diseases often undergo pre-conception counselling by cardiologists and obstetricians
Adverse neonatal outcomes occur in around 25% of pregnancies in women with cardiovascular disease

Acquired cardiac disease

Conversely, many women with acquired cardiac disease are unaware of their condition
Risk factors for acquired cardiac disease are as standard, including advanced maternal age, diabetes, essential hypertension and obesity
The commonest acquired cardiac conditions leading to death are ischaemic heart disease and MI (including SCAD)
In the developing world, rheumatic heart disease is also a significant problem

From 6 weeks' gestation:

Stroke volume and cardiac output ↑ 30-50%
HR ↑ 10-20/min
SVR ↓ 20-50%

Atrial and ventricular dimensions increase while ventricular function is preserved
BP and cardiac output increase further during labour
After delivery cardiac output falls rapidly to 15-25% above normal, returning to pre-pregnancy levels by around 6 weeks

In women with heart disease, adaptation may be inadequate, leading to:

Heart failure
Atrial and ventricular arrhythmias (from stretch and hormonal changes)
Aortic dissection in aortopathy
Thromboembolism (pregnancy is hypercoagulable)
Altered drug pharmacokinetics (↑ GFR, plasma volume and hepatic metabolism, ↓ albumin)

The outcome of pregnancy in those with cardiac disease is often predicted by the functional status of a patient e.g. NYHA classification

Class	Description
I	No limitation of physical activity. Ordinary physical activity doesn't cause undue fatigue/palpitations/dyspnoea
II	Slight limitation of physical activity. Comfortable at rest. Ordinary activity leads to fatigue/palpitations/dyspnoea
III	Marked limitation of physical activity. Comfortable at rest but less-than-ordinary activity leads to fatigue/palpitations/dyspnoea
IV	Unable to carry out any activity without discomfort. Symptoms at rest, which worsen during activity

Patients with NYHA class I or II symptoms generally tolerate pregnancy well
Certain conditions make women very high risk even in the absence of symptoms or functional limitation e.g. Marfan's syndrome with aortic root dilatation

Predictors of neonatal complications

Maternal NYHA III/IV or cyanosis
Maternal SpO₂ <90%
Left heart obstruction
Mechanical valve or anticoagulant use
Cardiac medication before pregnancy
Multiple gestation
Maternal cardiac event in pregnancy

Pre-conception

Women with known cardiac disease considering pregnancy should have:

Assessment of disease severity and optimisation of treatment by a cardiologist, including whether intervention is needed before pregnancy
Review of teratogenic medications
Counselling regarding the maternal and foetal risks of pregnancy and delivery
Genetic counselling for inherited conditions (most are autosomal dominant; 50% transmission risk)
Contraceptive advice, starting from adolescence

BNP/NT-proBNP should be considered before pregnancy in heart failure of any cause and levels monitored during pregnancy
A bioprosthetic valve is recommended over a mechanical valve in young women contemplating pregnancy

Risk assessment

All women of childbearing age with cardiovascular disease should be risk-assessed using the modified WHO 2.0 classification
Risk is further individualised using CARPREG II modifiers e.g. prior cardiac event or arrhythmia, NYHA III/IV or cyanosis, mechanical valve, ventricular dysfunction, left-sided obstruction, pulmonary hypertension
Women in mWHO 2.0 class II-III and above should be managed by a Pregnancy Heart Team from pre-conception to the post-partum period

mWHO 2.0 class	Example conditions	Care and delivery
I No detectable ↑ mortality	Isolated ectopics Mild pulmonary stenosis or mitral prolapse Successfully repaired simple lesions (ASD, VSD, PDA)	Local hospital
II Small ↑ mortality	Most supraventricular arrhythmias Unoperated uncomplicated ASD/VSD Repaired ToF	Local hospital
II - III Intermediate ↑ mortality	Mild LV impairment (EF >45%) Uncomplicated HCM Low-risk LQTS/CPVT, Brugada without events Marfan without aortic dilatation; BAV with aorta <45mm Repaired coarctation Mild MS, moderate AS	Shared care with Pregnancy Heart Team
III Significantly ↑ mortality	Moderate LV impairment (EF 30-45%) Previous PPCM with no more than mild residual impairment Sustained VT Mechanical valve Systemic RV with good function; uncomplicated Fontan Moderate MS; severe asymptomatic AS Aortic dilatation 40-45mm (Marfan) or 45-50mm (BAV)	Pregnancy Heart Team; expert centre
IV Extremely high mortality	PAH (any cause), Eisenmenger Severe LV impairment (EF <30% or NYHA III/IV) Previous PPCM with more than mild residual impairment Fontan with any complication Severe MS; severe symptomatic AS Aortic dilatation >45mm (Marfan) or >50mm (BAV); vascular Ehlers-Danlos	Pregnancy Heart Team; expert centre

The 2025 guidelines have moved away from labelling pregnancy in those with Class IV disease as 'contraindicated'
Instead, there should be clear, expert, risk counselling with shared decision-making, including discussion about termination if pregnancy occurs
Follow-up frequency increases with risk class e.g. class III/IV monthly or more

Investigations

ECG: changes in normal pregnancy include:

Sinus tachycardia
15-20° left axis deviation
PR interval shortened by around 20ms
Prominent Q waves in II, III and aVF
Flat or inverted T waves in III, aVF and V_1-3
Atrial or ventricular ectopics

TTE is the first-line imaging tool for any new or unexplained cardiovascular signs or symptoms

Agitated saline contrast is avoided (risk of placental infarction)

BNP/NT-proBNP: a normal value has a strong negative predictive value for heart failure
Troponin: no pregnancy-specific reference ranges, so not used routinely in isolation
CMR is preferred to ionising imaging if further imaging is needed; gadolinium is avoided
CT and CXR should not be withheld if needed; foetal doses are very low (chest CT ~0.02mGy)

Pregnancy alters pharmacokinetics, so doses may need adjustment and monitoring
Beta-blockers should generally be continued, with monitoring of foetal growth
Statins may be continued in established atherosclerotic disease
LMWH is the anticoagulant of choice for most indications; warfarin remain an option in mechanical valves (lower thrombosis risk)

Not recommended in pregnancy

DOACs
ACE inhibitors, ARBs and ARNIs (sacubitril-valsartan)
Mineralocorticoid receptor antagonists
SGLT2 inhibitors
Ivabradine
Endothelin receptor antagonists and riociguat
Amiodarone (unless other agents have failed)

Cardiac catheterisation

May be required to diagnose or treat coronary artery disease; ACS in pregnancy should be managed in the same way as in non-pregnant women
Radiation risk is highest during organogenesis, so where possible procedures are delayed until after 12 weeks
The second trimester (13th - 28th week) is the safest time, because:

Organogenesis is complete
The foetal thyroid is inactive
The foetus is small and further from the field

Foetal dose should be as low as reasonably achievable (preferably <50mGy); radial access by an experienced operator
Abdominal shielding offers limited benefit as foetal exposure is mostly from internal scatter
Maternal safety comes first: necessary procedures should not be withheld

Surgery

Maternal morbidity from cardiac surgery and cardiopulmonary bypass is similar to that of non-pregnant women
There is, however, a high foetal morbidity and mortality
Valve surgery should only be considered when there is a risk of maternal death and other options (e.g. balloon valvuloplasty) have failed

Surgery should ideally be in the second trimester (13th - 28th week) to optimise foetal outcome
For surgery required after 28 weeks, delivery by LSCS usually precedes cardiac surgery

An individualised delivery plan should be agreed in advance by the Pregnancy Heart Team and the woman, and be accessible in the health record
A pre-delivery consultation with the anaesthetic team is required

Goals

Minimise cardiovascular stress by minimising the work of labour and delivery
Monitor and maintain fluid balance
Avoid aortocaval compression
Provide aspiration prophylaxis
Appropriate monitoring

Timing and induction

Induction at 39-40 weeks reduces emergency caesarean section and stillbirth; induction before 39 weeks is reserved for maternal, foetal or obstetric indications
Mechanical methods, misoprostol, slow-release dinoprostone, oxytocin and amniotomy are all considered safe
Mechanical methods (e.g. cervical ripening balloon) may be preferred where a fall in SVR would be harmful

Mode of delivery

Vaginal delivery is advised for most women: less blood loss, infection and VTE
Planned caesarean delivery confers no maternal advantage and may worsen foetal outcomes
Assisted second stage may reduce surges in cardiac output associated with pushing

Caesarean delivery is preferred for:

Obstetric indications
Presentation in labour on a VKA (or VKA within the past 2 weeks): reduces foetal intracranial haemorrhage
High-risk aortopathy
HCM with severe LVOT obstruction (≥50mmHg)
Acute intractable heart failure or severe LV dysfunction (EF <30% and/or NYHA III/IV)
Uncontrolled arrhythmias

The choice of anaesthetic for a LSCS should take into account the underlying cardiac disease and severity, wishes of the mother and anaesthetist's preferences

Monitoring

Pulse oximetry, BP and continuous ECG in significant disease to detect decompensation, arrhythmia or ischaemia early
Arterial lines are reserved for those with, or at risk of, haemodynamic instability
PA catheters are of uncertain benefit and should be avoided in most; minimally invasive cardiac output monitoring is preferable

Uterotonics

PPH is more common in cardiovascular disease and poorly tolerated; active management of the third stage is recommended and anaemia should be treated ante-natally
Oxytocin when given as a rapid bolus can cause marked tachycardia, reduced SVR and hypotension

ESC 2025 regimen: 2 IU by slow IV infusion over 10 minutes after delivery, then 12mU/min for 4 hours
This reduces blood loss with minimal haemodynamic effect

In mWHO III-IV, oxytocin is first line with misoprostol and carboprost second line
Ergometrine is avoided as it causes increased SVR, PVR and coronary vasospasm; it is not recommended in aortopathy
Carboprost can cause bronchospasm and a marked rise in PVR; avoid in pulmonary hypertension and asthma

Planned obstetric interventions, e.g. B-lynch sutures, Bakri balloons, should be used to treat MOH instead

Endocarditis prophylaxis

Previously not recommended; ESC 2025 now states systemic antibiotic prophylaxis may be considered for delivery in women at high risk of endocarditis (e.g. prosthetic valves, previous endocarditis)

Planned delivery

Mechanical valve on VKA: switch to therapeutic LMWH or IV UFH at least 2 weeks before delivery, as the foetus metabolises VKAs slowly
On therapeutic LMWH: one strategy is to switch to IV UFH at least 36 hours before delivery (aPTT ≥2x control)
UFH is stopped 4-6 hours before neuraxial block, caesarean section or anticipated vaginal delivery
Therapeutic LMWH for non-valve indications: omit for 24 hours before; no bridging needed
LMWH and aspirin with a mechanical valve: consider stopping aspirin 4 days before

Urgent delivery on anticoagulation

VKA within 2 weeks: caesarean delivery to reduce foetal intracranial bleeding

Reverse with 4-factor PCC (25 U/kg for INR 2-4) ± vitamin K; FFP if PCC unavailable
The neonate may remain anticoagulated for 8-10 days

Recent heparin: protamine

UFH: 1mg per 100 units
LMWH: 1mg per 1mg enoxaparin if <8 hours, 0.5mg if >8 hours; reversal is less complete

Involve haematology early

Restarting

A balance of bleeding versus thrombosis, agreed by anaesthetic, cardiology, haematology and obstetric teams with the patient
Late obstetric bleeding (>24 hours) is common
UFH or low/intermediate dose LMWH initially; VKAs restarted no earlier than 7-14 days post-partum

Analgesia is crucial in labour to reduce physical stress
Early, incremental, epidural analgesia has several advantages:

Limits increased cardiac output from pain due to analgesic effect
Reduces both preload and afterload
Limits sympathetic block by careful titration of the level of epidural block required
May be topped up for anaesthesia if required, avoiding the airway and other complications of GA

Chosen technique should aim to be cardiovascularly stable/titratable, reliable (good block) and familiar to the anaesthetist
Therefore the technique of choice for operative delivery is typically:

Incremental epidural
Combined CSE with low-dose (<1ml) spinal then incremental epidural boluses
Continuous spinal anaesthetic technique (although unfamiliar to most and associated with high rates of PDPH)

CSE has a faster onset (around 5 minutes vs 15 minutes for epidural) but hypotension and FHR abnormalities occur more quickly and are more pronounced
Women at risk of dural ectasia (e.g. Marfan syndrome) need extra caution and management in an expert centre
Where neuraxial analgesia is contraindicated (e.g. anticoagulation), IV remifentanil PCA is an alternative, accepting the risk of hypoventilation

Vasodilation is a feature and should be controlled with titratable vasopressors

Phenylephrine is preferred in stenotic valve lesions to maintain SVR
Ephedrine is preferred in regurgitant valvular lesions due to its positive chronotropic effect

Advantages	Disadvantages
Reduced maternal anxiety: ↓ catecholamine release and less cardiac work	Those inherent to GA, inc. aspiration, failed I&V, anaesthetic effects on foetus
Stable parameters if 'cardiac anaesthetic' provided	↑ blood loss compared to regional anaesthesia
Suitable in the anticoagulated patient	Cardiac instability due to pressor effects of intubation
	Effect of GA drugs, which are typically cardiac depressants and/or vasodilatory

Monitoring

Association of Anaesthetists standards
Arterial line
Central line may be required, although caution is required with CVP monitoring in the obstetric patient as:

Anatomical variation of the SVC may mean CVC line tip is not where it should be
Irritation by the CVC line may precipitate arrhythmias
Underlying cardiac disease means CVP may not reflect LVEDV
CVP may be a less reliable guide to volume status, especially in PET

TOE may be useful

Conduct

One should aim to avoid tachycardia and large swings in blood pressure
At induction, obtund the hypertensive response to intubation (e.g. alfentanil 25μg/kg, remifentanil 0.5μg/kg) and titrate induction agent carefully
Maintenance is typically with volatile anaesthetic, although addition of remifentanil is useful to:

Reduce volatile requirement and therefore risk of atonic PPH
Reduce chance of hypertension on extubation if continued during emergency

Good analgesia is paramount because pain and tachycardia increase cardiac work; epidural/neuraxial opioids and use of other regional techniques e.g. TAP blocks

Women at the highest heart failure risk, or with heart failure in pregnancy or delivery, should be considered for intensive (cardiac) care for 24-48 hours post-delivery
Mortality due to maternal cardiac disease tends to be post-partum, due to:

Reduced frequency of monitoring compared to ante-natal period
Large fluid shifts in the post-partum period including 500ml autotransfusion at the time of delivery → acute decompensation
Sub-optimal or early withdrawal of analgesia leading to catecholamine surges from pain → worsening cardiac function or arrhythmias

Early mobilisation and thromboprophylaxis to reduce VTE
Hypertensive disorders: BP monitoring for 72 hours after birth and again at 7-10 days
Breastfeeding is encouraged where possible; check drug compatibility
Post-partum depression affects around 1 in 3 mothers with cardiovascular disease (vs 10-20% generally); screen and provide psychological support
Adverse pregnancy outcomes (e.g. pre-eclampsia, gestational diabetes, preterm birth) are markers of future cardiovascular risk and warrant long-term follow-up