Cardiovascular

Question 1

Normal ECG findings in pregnancy

Answer 1

Partly related to changes in the position of heart
- Slight left axis deviation due to altered heart position
Sinus tachycardia
Atrial and ventricular ectopics
Q-wave (small) and inverted T wave in lead III
ST segment depression and T wave inversion - inferior and lateral leads
QRS axis leftward shift

Question 2

Normal cardiovascular examination findings in pregnancy

Answer 2

Bounding / collapsing pulse
Ejection systolic murmur (in >90% of pregnant women)
Loud first heart sound
Third heart sound
Relative sinus tachycardia
Ectopic beats
Peripheral oedema

Question 3

CXR features in pregnancy

Answer 3

Heart is enlarged and pushed up by growing uterus
The aorta unfolds and the heart is rotated upwards and outwards
CXR may show heart displaced into a horizontal position, rotating to the left, with increased transverse diameter
Increased pulmonary vascular markings
Pulmonary venous distension
Elevated right hemidiaphragm

Question 4

CV changes in pregnancy (physiology)

Answer 4

Drop in systemic vascular resistance - from peripheral vasodilation
Increase plasma volume
Increase stroke volume by 10-30%
HR increases from normal 70 to 80-90bpm
Cardiac output rises from 4L/min at week 10 to 6L/min at week 24 (~40% in pregnancy)

Question 5

BP changes in pregnancy

Answer 5

Before the increase in CO can adequately compensate for the fall in SVR, BP begins to decrease in early pregnancy
Continues to decrease in second trimester until the nadir in SBP and DBP is reached by about 22-24 weeks’ gestation
From then on, there is a steady rise to pre-pregnancy levels until term
Post-partum - BP falls immediately after delivery, although tends to rise subsequently reaching a peak 3-6 days postpartum
- This may relate to return of normal vascular tone and a period of vasomotor instability while normal, and non-pregnant vasoregulation is re-established

Question 6

Describe the New York Heart Association classification

Answer 6

Functional system based on symptoms

Class I
No breathlessness / uncompromised
No limitation on physical activity

Class II
Breathlessness on severe exertion / slightly compromised
Ordinary activity –> symptoms

Class III
Breathlessness on mild exertion / moderately compromised
Asymptomatic at rest
Less than ordinary activity –> symptoms

Class IV
Breathlessness at rest / severely compromised

Question 7

Cardiac lesions that limit the ability to increase CO appropriately:

Answer 7

• Valvular stenosis - especially AS and MS
• Ventricular systolic impairment
• Cyanotic heart disease
• Ischaemic heart disease
• Dilated aortic root - increased risk of dissection
• Pulmonary artery HTN - a/w the highest risk of maternal mortality

Question 8

Class IV of WHO classification

Answer 8

Conditions a/w extremely high risk of mortality or severe morbidity
Pregnancy is contraindicated

Severe MS
Symptomatic severe aortic stenosis
Bicuspid aortic valve with ascending aorta diameter >5cm
Marfan’s with aorta >45mm
Severe systemic ventricular systolic dysfunction with LVEF <30%
NYHA III-IV
Native severe coarctation
Fontan circulation with complications
Significant pulmonary arterial HTN
Previous peripartum cardiomyopathy with residual impairment

Question 9

Antibiotic prophylaxis with heart disease

Answer 9

Current UK recommendations (NICE): antibiotic prophylaxis against infective endocarditis is not required for childbirth

Consider cover only for patients deemed to be at high risk of developing IE (e.g. previous IE) and for those who have the poorest outcome (e.g. cyanotic congenital heart disease)
Amoxicillin 2g IV + gentamicin 1.5mg/kg IV at onset of labour / ROM or prior to C/S

Question 10

Maternal mortality of pulmonary HTN

Answer 10

Was 40% but more recent data suggest this may have fallen to 10-25%

Fixed pulmonary vascular resistance (PVR) means that these women cannot increase pulmonary blood flow to match the increased CO and they tolerate pregnancy poorly

High risk scenarios:

• Right to left shunt in Eisenmenger’s syndrome
• Right heart failure
• Escalating pulmonary HTN with pulmonary hypertensive crises

Question 11

Diagnosis of pulmonary HTN

Answer 11

Non-pregnant elevation of mean (non-systolic) pulmonary artery pressure > 22mmHg at rest or 30mmHg on exercise in the absence of left to right shunt

If there is pulmonary HTN in the presence of a left to right shunt, the diagnosis of pulmonary vascular disease is particularly difficult and further investigation including cardiac catheterisation to calculate PVR is likely to be necessary

Question 12

Causes of pulmonary HTN

Answer 12

Idiopathic pulmonary arterial hypertension (PAH)
Congenital heart disease-associated pulmonary hypertension - E.g. ASD / VSD with PAH - includes Eisenmenger’s syndrome
Chronic thromboembolic pulmonary HTN
Lung disease
- E.g. cystic fibrosis, interstitial lung disease, hypoxia
Connective tissue disease - E.g. scleroderma, SLE

Question 13

Antenatal management of pulmonary HTN

Answer 13

MDT
Review meds re. safety in pregnancy
PAH-targeted therapies should be continued
- Sildenafil (aka VIAGRA) - safe to continue
Thromboprophylaxis
Elective admission for best rest, O2 therapy and escalation of targeted therapies

TOP should be considered
- TOP itself is associated with maternal mortality up to 7% (less than the risk of pregnancy continuing)

Question 14

Intrapartum management of pulmonary HTN

Answer 14

MDT discussion and planning of delivery
No evidence that C/S vs. vaginal delivery, or regional anaesthesia vs. GA reduces mortality
In most case series delivery has been by C/S, often preterm
Telemetry
ICU
Avoid:
- Hypovolaemia (maintain preload)
- Acidosis
- Thromboembolism (heparin bridging)
- Pulmonary artery catheters (carry a risk of thrombus)
Systemic vasodilation (caution with regional anaesthesia, syntocinon - slow bolus)

Aggressive diuresis post-partum

Question 15

Impacts of ecbolics - pulm HTN

Answer 15

Syntocinon - causes vasodilation, therefore give in slow bolus or infusion

Ergometrine - increases SVR (and pulmonary)

Carboprost - increases pulmonary vascular resistance –> pulmonary oedema

Misoprostol - safe

Question 16

Post-delivery changes in CV physiology

Answer 16

Increased CO 60-80% due to relief of IVC obstruction and uterus emptying blood into the systemic circulation
~500-600ml blood from uterine circulation returns ~ autotransfusion (increases pre-load)
Then rapid decline to prelabour values within 1 hour of delivery
Transfer of fluid from extra-vascular space increased VR and SV
CO returns to pre-pregnancy levels 2 weeks after delivery

Question 17

Impact of patent ductus arteriosus on pregnancy

Answer 17

Aorta to pulmonary artery
Left to right shunt, some oxygenated blood into pulmonary circuit
Most cases encountered would have been repaired in childhood (corrected cases) - Pose no problems in pregnancy
Uncorrected cases do well but are at risk of congestive cardiac failure

Question 18

Impact of ASD on pregnancy

Answer 18

Commonest congenital heart defect in women
Usually well tolerated in pregnancy
If unrepaired:
- Potential risk of paradoxical embolism - low risk (Passage of thrombus from a vein to an artery)
- Atrial arrhythmia

If increase in left to right shunt following blood loss at delivery may deteriorate –> hypotension –> drop LVEF

Question 19

Impact of VSD in pregnancy

Answer 19

Small (<1.25cm) or repaired defects - low risk during pregnancy
Increased volume load of left ventricle
Usually well tolerated in pregnancy unless Eisenmenger’s syndrome

Question 20

Management of coarctation of the aorta

Answer 20

Usually corrected if diagnosed pre-pregnancy
Risks if uncorrected:
- Angina
- HTN
- Congestive heart failure
- Aortic rupture
- Aortic dissection 

Ideally have MRI pre-pregnancy to exclude any aneurysm of post-stenotic dilatation around the repair site
Minimise risk of aortic dissection with strict BP control and beta-blockade to decrease cardiac contractility

Question 21

What is Marfan’s syndrome?

Answer 21

Connective tissue disorder
Autosomal dominant disorder
80% have cardiac involvement (usually mitral valve prolapse, mitral regurgitation, aortic root dilatation)
Those with cardiac lesions tend to have offspring with cardiac abnormalities 
Other features of Marfan's
- Increased height
- Arm span > height
- Arachnodactyly
- Joint laxity
- Depressed sternum
- High arched palate
- Dislocation of the lens

Question 22

Risk of aortic dissection in pregnancy with Marfan’s?

Answer 22

1% if <4cm

Predictors for dissection and rupture:

• Pre-existing or progressive aortic root dilatation (10% if root >4cm)
• Positive FHx of dissection or aortic rupture

Question 23

Management of Marfan’s in pregnancy

Answer 23

Genetics referral
BP check
Beta blockers shown to reduce the rate of aortic dilatation and the risk of complications in Marfan’s
- Serial growth scans if on beta blocker
Regular ECHO to assess aortic root diameter
Elective C/S - if aortic roots show progressive enlargement or >4.5cm
- Deliver in hospital with cardiothoracic support available

Question 24

4 features of ToF

Answer 24

1. VSD
2. Pulmonary artery stenosis
3. Overriding aorta
4. RV hypertrophy

Question 25

Pregnancy impact on ToF

Answer 25

Majority of women will have undergone surgical correction - Main issue is RV dysfunction that can deteriorate in view of pulmonary regurgitation resulting from earlier surgery If unoperated, those without pulmonary vascular disease may negotiate pregnancy successfully Two main concerns: - Paradoxical embolism through right to left shunt --> CVA - Effects of cyanosis (from increased right to left shunt due to fall in SVR) and maternal hypoxaemia on fetus FGR, miscarriage, spontaneous and iatrogenic prematurity

Question 26

Important considerations for post-op congenital heart disease

Answer 26

- The risk of ventricular failure (particularly when the RV is acting as the systemic pumping chamber) - Any residual pulmonary HTN

Question 27

Fontan circulation

Answer 27

Characterised by a single functioning ventricle Increases in venous pressure may cause hepatic congestion and oedema, but sufficient volume loading is required to ensure adequate perfusion of the pulmonary circulation Risks of HF, VTE (blood flows slowly through the lungs) HTN dangerous as quickly cyanotic Risks with pregnancy: - Miscarriage (30%) - Premature birth - FGR - Neonatal death

Question 28

Genetic counselling

Answer 28

Risk of fetus having congenital heart disease is higher if the mother rather than the father has congenital heart disease - Risk is 4% (50% same defect) Level of risk depends on the specific lesion In women with ASD, risk in fetus ~5-10% Refer women for detailed fetal echo

Question 29

Cause of Eisenmengers

Answer 29

VSD > ASD > PDA Syndrome where is a long standing left to right shunt due to a congenital heart defect --> pulmonary HTN and eventual reversal of shunt into a cyanotic right to left shunt

Question 30

Pregnancy implications of Eisenmengers

Answer 30

Preload of the RV increases Afterload of the LV decreases Shunting, and therefore cyanosis, increases MATERNAL Mortality 20-50% VTE - because of erythrocytosis Maternal cyanosis ``` FETAL Chance of livebirth <50% if sats <90% PTB Stillbirth IUGR Increased risk of CHD ```

Question 31

What is rheumatic heart disease?

Answer 31

RF - caused by an immunological reaction to a streptococcal infection Damage to heart valves may remain once the acute episode has resolved Cardiac inflammation results in fibrosis of the valves and they are either stenotic or insufficient Mitral stenosis accounts for 90% of RHD in pregnancy If get another strep bacteraemia, then bacteria land on damaged valve --> endocarditis and more damage to heart Antibiotic prophylaxis is crucial after acute RF episode (as per local guidelines)

Question 32

Effect of pregnancy on MS

Answer 32

Can deteriorate quickly and develop pulmonary oedema, even if asymptomatic at start of pregnancy 40% increase in preload in pregnancy - can't travel through stenotic valve Tachycardia --> diastolic filling of the LV is further decreased from fall in SV and a rise in left atrial pressure --> pulmonary oedema Secondary pulmonary HTN can occur --> RV failure Most women who develop complications do so in the late second or third trimester, or peripartum period - Second trimester because preload and CO peak Poor prognostic features for development of pulmonary oedema: - Severe MS - valve area <1cm2 - Presence of moderate to severe symptoms prior to pregnancy

Question 33

Antenatal management of MS in pregnancy

Answer 33

MDT Beta-blockers - Slow the heart rate, allows time for left atrial emptying Treat AF aggressively with digoxin or beta-blockers VTE prophylaxis if AF, periods rest, or LA dilation Baseline ECHO If pulmonary oedema, admit to hospital Can consider balloon valvotomy and closed mitral valvotomy Surgical open valvotomy associated with fetal mortality rate 15-35% (compared with 5-15% for closed)

Question 34

Intrapartum management of MS

Answer 34

Tertiary centre Avoid supine and lithotomy positions - Could decrease preload Avoid excessive IV fluids - keep women on the dry side - May need to give frusemide (risk of pulmonary oedema) - Abrupt increase in preload at delivery may --> increase in RA pressure and pulmonary oedema Good analgesia Telemetry Short second stage +/- instrumental

Question 35

Aortic stenosis in pregnancy

Answer 35

Causes: - Congenital (usually bicuspid valve) - Rheumatic HD Narrow aortic valve --> LV hypertrophy and LA dilatation Can restrict blood flow to brain and heart muscle Preconception functional status provides good estimate of pregnancy risk - if asymptomatic well tolerated

Question 36

Management of AS

Answer 36

Maintain adequate preload to maintain SV - Hypotension and tachycardia are poorly tolerated Optimise volume status Avoid hypotension - Maintenance of left uterine displacement - Aggressive treatment blood loss Arterial line monitoring Third stage: - Oxytocin infusion for third stage - bolus can ---> severe intractable hypotension - Mechanical methods (bimanual) and misoprostol - If haemodynamically significant haemorrhage, can use syntometrine

Question 37

Regurgitant valve disease

Answer 37

Systemic vasodilation and fall in PVR reduce after load and therefore act to reduce regurgitation MR and AR are well tolerated in pregnancy, provided there is no significant LV dysfunction Women with heart failure can be safely treated with diuretics, digoxin and hydralazine and / or nitrates as vasodilators to 'offload' the LV

Question 38

Mechanical vs. graft tissue heart valves

Answer 38

Mechanical (metal) - Life long anticoagulation - Last longer - 10-15y - High risk of thrombosis on valves - Warfarin issues in pregnancy Graft tissue (bioprosthetic) - No anticoagulation - Better choice for women of childbearing age? - Accelerated deterioration throughout pregnancy - Surgery should be one year before pregnancy

Question 39

Management if mechanical heart valve

Answer 39

Warfarin - Lowest risk of thrombosis (0-4%) and haemorrhagic complications - Associated with increased risk of teratogenesis, miscarriage, stillbirth and intracerebral bleeding - highest risk time of warfarin is 6-12 weeks, consider clexane for first trimester, then switch depending on how high risk the valve is - All women should discontinue warfarin for 10-14 days prior to delivery to allow clearance by the fetus, cover with LMWH or heparin LMWH - Safe for fetus - Associated with a higher risk of thrombosis for the pregnant woman - Doses should be adjusted according to anti-factor Xa levels - 2 weeks after starting and every trimester - Low dose aspirin should be added as adjunctive antithrombotic therapy

Question 40

Hypertrophic cardiomyopathy in pregnancy

Answer 40

~70% are familial, autosomal dominant Mostly well tolerated because of an increase in LV cavity size and the SV is usually able to increase Beta-blockers should be continued or started for those with symptoms Caution with regional anaesthesia to avoid hypotension with consequent increased LV outflow tract obstruction - Hypovolaemia will have the same effect

Question 41

Define PERIPARTUM CARDIOMYOPATHY

Answer 41

Rare condition, specific to pregnancy Defined as the development of heart failure at the end of pregnancy or in the months (up to 5/12) following delivery, where no other cause of heart failure is found On echocardiography: - LVEF <45% Often, echo shows enlarged heart with global dilation of the four chambers and markedly reduced LV function

Question 42

Risk factors of peripartum cardiomyopathy

Answer 42

``` Multiple pregnancy Pregnancy complicated by HTN Multiparity Advanced maternal age Afro-Caribbean race Obesity ```

Question 43

Management of peripartum cardiomyopathy

Answer 43

Elective delivery if antenatal Thromboprophylaxis Conventional heart failure treatment - Diuretics, vasodilators, beta blockers, digoxin, inotropes - After delivery - ACE inhibitors Immunosuppressive therapy may be considered in cases with myocarditis (confirmed with endomyocardial biopsy) that fail to improve within 2 weeks Bromocriptine has been suggested in view of the link with a pathogenic form of prolactin Intra-aortic balloon pumps and left ventricular assist devices may provide temporary support Cardiac transplantation Follow up in clinic LARC

Question 44

Prognosis of peripartum cardiomyopathy

Answer 44

Mortality much lower than previous suggested, 10% ~50% make a spontaneous and full recovery Prognosis depends on normalisation of LV size and function within 6 months of delivery - Mortality increased in those with persistent LV dysfunction Counsel against further pregnancy if LV size or function does not return to normal - Otherwise significant risk of recurrence, worsening heart failure (50%) and death (25%) in subsequent pregnancies If cardiomyopathy resolves, recurrence is not known but appears to be lower (? u to 25%)

Question 45

Work up of tachycardia in pregnancy

Answer 45

Investigations: - ECG - look for WPW - Bloods - TFTs, electrolytes, Hb, iron studies Consider 24 hour Holter monitor if history suggests frequent and troublesome arrhythmias If diagnose arrhythmia, should do echo to exclude structural heart disease

Question 46

Prevalence of hypertensive disorders of pregnancy

Answer 46

HTN complicates 10-15% of pregnancies PET 3-5% Severe PET 1% Eclampsia 0.03%

Question 47

Placental growth factor (PlGF)-based testing

Answer 47

Has a high sensitivity and negative predictive value in diagnosing pre-eclampsia that requires delivery within 14 days

Question 48

Chronic HTN | If first presentation in early first trimester, exam/investigate for clues to a possible secondary cause...

Answer 48

``` Essential HTN (90%) Secondary causes (10%) ``` - Femoral pulses - radiofemoral delay suggests coarctation of the aorta - Renal bruit - possible renal artery stenosis - Urinalysis - proteinuria or haematuria suggests renal disease - Serum creatinine - to exclude renal impairment - Electrolytes - hypokalaemia may suggest hyperaldosteronism / Conn’s syndrome - Serum calcium - to exclude hyperparathyroidism - Urinary catecholamines - phaeochromocytoma

Question 49

Outcomes with chronic HTN

Answer 49

22% will get PET - 10% <34/40 50% will have a CS 27% will have SGA if get PET, 50% will have PTB

Question 50

Diagnostic criteria of PET

Answer 50

New onset of HTN (SBP >140 or DBP >90) after 20/40 and the coexistence of 1 or more of the following new onset conditions: - Proteinuria - PCR >30 mg/mmol, or - Renal insufficiency, Cr >90 micromol/L - Liver involvement - ALT or AST >40 IU/L with or without RUQ or epigastric pain - Neurological complications - Eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, persistent visual scotomata - Haematological complications - thrombocytopenia (plt <150,000/microlitre), DIC, haemolysis - Uteroplacental dysfunction - FGR, abnormal umbilical artery doppler waveform analysis, stillbirth - Pulmonary oedema

Question 51

Aetiology of PET

Answer 51

Abnormal trophoblast invasion --> spiral arterioles fail to become high capacitance and low resistance vessels --> inadequate perfusion --> uteroplacental ischaemia Placenta unable to optimise blood supply from maternal uterine vessels

Question 52

Pathogenic mechanisms of PET and clinical sequalae

Answer 52

Impaired trophoblast differentiation and invasion with failure of spiral arteries to remodel --> Uteroplacental unit fails to become a high capacitance, low resistance circulation --> increased placental resistance and ischaemia, and fetal hypoxia, IUGR Increased pro-inflammatory cytokines --> Widespread microvascular damage / endothelial dysfunction --> HTN, liver and renal impairment. Increased VTE risk Placental hypo-perfusion --> increased trophoblastic breakdown --> Hyperuricaemia Increased anti-angiogenic factors with resultant inhibition of angiogenic factors (e.g. VEGF and PlGF) --> Poor placental blood flow Endothelial cell activation --> Increased capillary permeability - peripheral oedema, cerebral oedema. Increased platelet activation and vascular tone - HTN Immunological factors -Exposure to paternal and fetal antigens protects against PET. Increased PET in nulliparous women / women who change partners / use barrier contraception Genetic predisposition - Maternal genes involved - e.g. increased risk in primigravid with FHx or PET in previous pregnancy

Question 53

Doses of MgSO4

Answer 53

Loading dose: 4g IV over 5-15 mins Maintenance dose: 1g / hour for 24 hours If eclamptic fit, continue for 24h after last fit Recurrent fit: further dose of 2-4g IV over 5-15 mins

Question 54

Reasons to treat HTN in pregnancy

Answer 54

No difference in neonatal outcomes between DBP 85 vs. 100 (CHIPS) Does not prevent PET or adverse outcome Decreases incidence of severe HTN

Question 55

Treatment tips for antihypertensives - antenatal

Answer 55

LABETALOL - serial growth scans with beta blockers, CI: asthma METHYLDOPA - CI: depression, switch postnatal (by day 2) - slow onset of action over 24h NIFEDIPINE - calcium channel blocker, ADR: headache, flushing. CI: aortic stenosis

Question 56

PET - Counselling for future pregnancies

Answer 56

Overall risk of recurrence is ~1 in 5 Advise aiming BMI within health range to lower risk of PET If PET <34/40, recurrence 25% - 55% if <28/40 If prev gest HTN, risk of PET 2-7%

Question 57

Monitoring in HTN of pregnancy

Answer 57

Chronic HTN - Assess for proteinuria each visit - PET bloods if new proteinuria or change in BP - Early dating - Third trimester growth, repeat as indicated Gest HTN - assess for proteinuria 1-2 times per week - PET bloods weekly - USS 3-4 weekly from time of diagnosis PET - assess for proteinuria at time of Dx, repeat daily if negative - PET bloods twice weekly, more frequent if unstable - growth USS at time of diagnosis, 2 weekly - CTG twice a week

Question 58

Acute BP lowering medications

Answer 58

BP 170/110 - Level where cerebral autoregulation is overcome - Risk of haemorrhage and hypertensive encephalopathy MDT ICU / HDU Aim for gradual and sustained lowering of BP - Precipitous fall may impair placental perfusion Given concurrent long-acting and short-acting agent Labetalol - 20-80mg IV over 2 mins Max effect 5 mins after dose Repeat every 10 mins Nifedipine Hydralazine - 10mg IV bolus Onset of action: 20 mins First dose 5mg if fetal compromise

Question 59

Indicators for high risk of developing eclampsia:

Answer 59

- Persistent headache - Hyperreflexia with clonus - Liver involvement - Severe HTN

Question 60

Principles of management of eclampsia

Answer 60

Resuscitation - Seizures are self-limiting - Ensure patent airway, oxygen, IV access Prevention of further seizures - MgSO4 4g loading dose over 20mins - Maintenance: 1g/hr for 24h - If second seizure on maintenance, give further 2-4g over 10 mins - Don't monitor Mg levels unless renal function is compromised - In AKI same loading dose but half maintenance Control of HTN Delivery

Question 61

Aspirin for PET prophylaxis

Answer 61

Before 16/40 Corrects imbalance between circulating prostaglandins, inhibits platelet aggregation, dilates blood vessels and anti-inflammatory effect NNT for high risk women = 19 10-20% reduction in women at moderate to high risk of PET 14% reduction in stillbirth 10% reduction in SGA No increased bleeding risk

Question 62

Calcium for PET prophylaxis

Answer 62

Low Ca stimulates parathyroid hormone and renin release --> increases intracellular Ca in vascular smooth muscle --> vasoconstriction Reduces risk of PET in high risk women and those with low dietary intake