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Maternal Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is the primary/initial cardiovascular adaption to pregnancy?

A

Peripheral vasodilation

  • mediated by endothelium dependent factors
  • oestradiol upregulates nitric oxide synthesis
  • vasodilatory prostaglandins

Leads to a fall in systemic vascular resistance
To compensate for this, the cardiac output increases by approx 40% in pregnancy
- achieved predominantly by increase in SV, but also by an increase in HR

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2
Q

At what gestation is the maximum cardiac output reached?

A

20-28/40

Increases by further 15% in 1st stage and 50% in 2nd stage of labour.

Post partum can increase by 60-80%

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3
Q

At term, turning from the lateral to the supine position may result in a ____ reduction in cardiac output

A

35%

Pressure from the gravid uterus on the IVC causes a reduction in venous return to the heart
And a consequent fall in stroke volume and cardiac output

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4
Q

By how many bpm does the HR increase in pregnancy?

A

10-20bpm

Remains this elevated until term
Unlike SV which increases until 28/40 and then falls a little

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5
Q

How does pulmonary vascular resistance change in pregnancy?

A

Decreases significantly

Like systemic vascular resistance

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6
Q

Why are pregnant women particularly susceptible to pulmonary oedema?

A

Serum colloid osmotic pressure is reduced
Colloid osmotic pressure / Pulmonary capillary wedge pressure gradient is reduced by 30%

Pulmonary oedema will be precipitated if there is an
- increase in cardiac preload (infusion / fluids)
- increased pulmonary capillary permeability (PET)
Or both

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7
Q

How does cardiac output change in labour?

A

Increases by

  • 15% in the first stage
  • 50% in the second stage

Following delivery (third stage)

  • immediate rise in cardiac output due to the relief of IVC obstruction and contraction of the uterus that empties blood into the systemic circulation
  • CO increases by 60-80% followed by a rapid decline to prelabour values within approx 1 hour of delivery
  • transfer of fluid from the extra vascular space increases venous return and stroke volume further
  • This is why women with cardiac disease are most at risk of decompensation during delivery and immediately postpartum.
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8
Q

In labour, what effect do uterine contractions have on the cardiovascular system?

A

Autotransfusion of 300-500mL of blood back into the circulation (increasing SV)

Sympathetic response to pain and anxiety further elevate HR and BP

CO is increased more during contractions, but also between contractions

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9
Q

When are women with cardiovascular compromise most at risk of pulmonary oedema?

A

Second stage of labour

Immediate postpartum period

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10
Q

What are 7 normal findings on examination of the cardiovascular system in pregnancy

A
  1. Bounding / collapsing pulse
  2. Ejection systolic murmur (present in >90% pregnant women)
  3. Loud first heart sound
  4. Third heart sound
  5. Relative sinus tachycardia
  6. Ectopic beats
  7. Peripheral oedema
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11
Q

What are four normal findings on an ECG in pregnancy?

A
  1. Atrial and ventricular ectopic
  2. Q-wave (small) and inverted T wave in lead III
  3. ST segment depression and T-wave inversion inferior and lateral leads
  4. Left axis deviation
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12
Q

In women with cardiovascular disease, what are the factors that determine the ability to tolerate pregnancy?

A
  1. Presence of pulmonary hypertension
  2. Haemodynamic significance of any lesion
  3. Functional class (NYHA)
  4. Presence of cyanosis (arterial oxygenation sats < 80%)
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13
Q

What are the four classes of the NYHA functional classification?

A

Classification for the stages of Heart Failure

I - No breathlessness / uncompromised
II - Breathlessness on severe exertion / slightly compromised
III - Breathlessness on mild exertion / moderately compromised
IV - Breathlessness at rest / severely compromised

Poor pregnancy outcome is more likely if the woman has a poor functional status

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14
Q

What are five cardiovascular conditions that require special consideration in pregnancy?

A
  1. Mitral stenosis - risk of pulmonary oedema
  2. Marfan’s syndrome - risk of aortic dissection or rupture
  3. Pulmonary hypertension - risk of death
  4. Complex congenital heart disease
  5. Mechanical heart valves - risk of valve thrombosis and anticoagulation issues
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15
Q

What are five causes of pulmonary hypertension?

A
  1. Idiopathic pulmonary arterial hypertension
  2. Congenital heart disease - associated pulmonary hypertension
    E.g. ASD / VSD. Includes Eisenmenger’s syndrome (pulmonary HTN with reversed shunt)
  3. Chronic thromboembolic pulmonary hypertension
  4. Lung disease - CF, ILD, hypoxia
  5. Connective tissue disease - scleroderma, SLE
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16
Q

What is the definition of pulmonary hypertension?

A

Non-pregnancy elevation of mean pulmarony artery pressure =/> 25mmHg at rest of 30mmHg on exercise

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17
Q

For most women with Pulm HTN who die as a result of pregnancy, when do they die?

A

Soon after delivery

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18
Q

What are three medical therapies for pulm HTN in pregnancy?

A
  1. Phosphodiesterase inhibitors (sildenafil, tadalafil) - safe to continue
  2. Endothelin receptor antagonists - usually discontinued in pregnancy as they are teratogenic in rats
  3. Prostanoid analogues (prostacyclin) - safe to continue

Additional: VTE prophylaxis with LMWH

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19
Q

What is the recommended mode of delivery for women with Pulm HTN?

A

No evidence that CS vs VD reduces mortality

In most serious cases, delivery has been by CS and is often performed preterm

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20
Q

What are the three most common congenital heart disease in pregnancy?

A

PDA
ASD
VSD

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21
Q

What are the risks of maternal PDA in pregnancy?

A

If corrected - no problems in pregnancy

If uncorrected - usually do well, but risk of congestive cardiac failure

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22
Q

What is the commonest congenital heart defect in pregnant women?

A

Atrial septal defect

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23
Q

What is congenital aortic stenosis associated with?

A

Bicuspid aortic valve

And therefore, a risk of dilation of the ascending aorta

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24
Q

What are the risks with moderate-severe congenital aortic stenosis?

A

Angina
HTN
Heart failure
Sudden cardiac death

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25
Q

In what case is the development of a resting tachycardia a particular concern in pregnancy?

(2)

A

Congenital aortic stenosis
May indicate a failing LV, unable to maintain the increased SV of pregnancy

Mitral stenosis
Diastolic filling of the LV (which is impaired in MS) is further decreased and there is a consequent fall in SV and a rise in LA pressure precipitating pulmonary oedema

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26
Q

What is the treatment of aortic stenosis in pregnancy?

A

Balloon valvotomy

In severe cases

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27
Q

What are the risks of coarctation of the aorta in pregnancy?

A

Angina
HTN
Congestive heart failure

Aortic rupture
Aortic dissection

28
Q

How do you minimise the risk of aortic dissection, in the context of an aortic coarctation in pregnancy?

A

Strict control of blood pressure

Beta-blockade to decreased cardiac contractility

29
Q

What are the three most common types of cardiac involvement in Marfan’s syndrome?

A
  1. MV prolapse
  2. MR
  3. Aortic root dilatation

80% of patients with Marfan’s syndrome have cardiac involvement

30
Q

What are two risk factors for aortic dissection and rupture in Marfan’s syndrome?

A
  1. Pre-existing or progressive aortic root dilatation

2. Positive family history of dissection or aortic rupture

31
Q

In Marfan’s syndrome, at what level of aortic dilation is pregnancy contraindicated due to the risk of aortic dissection / rupture?

A

Aortic root > 4-4.5cm

Patients at high risk (particularly those above) should be offered aortic root replacement prior to pregnancy

El CS is usually recommended for women with aortic roots showing progressive enlargement or > 4.5cm

32
Q

What is the inheritance pattern of Marfan’s syndrome?

A

Autosomal dominant

33
Q

What are 7 extra-cardiac manifestations of Marfan’s syndrome?

A
  1. Increased height
  2. Arm span greater than height
  3. Arachnodactyly - fingers and toes are abnormally long and slender
  4. Joint laxity
  5. Depressed sternum (pectus excavatum)
  6. High arched palate
  7. Dislocation of the lens
34
Q

What are the main causes (2) of cyanotic congenital heart disease?

A

Pulmonary atresia

Tetralogy of Fallot

35
Q

What are four risks for pregnant women (and their fetus) with cyanotic congenital heart disease?

A
  1. Worsening cyanosis - due to increased right-to-left shunting secondary to falling peripheral vascular resistance
  2. Thromboembolic risk increased because of polycythemia (secondary to hypoxaemia)
  3. Increased risk of fetal loss and IUGR. Chance of live birth <20%
  4. Associated pulmonary hypertension
36
Q

What are the two main concerns for a pregnant women with Tetralogy of Fallot?

A
  1. Paradoxical embolism through the right-to-left shunt causing cerebral vascular accidents
  2. Effects of cyanosis and maternal hypoxaemia on the fetus
    - oxygen saturation falls markedly on exercise
    - IUGR
    - increased risk of miscarriage
    - increased risk of spontaneous and iatrogenic prematurity
37
Q

What is a Fontan circulation?

A

Results after surgery for tricuspid atresia, or transposition with pulmonary stenosis?

RV is bypassed
LV provides the pump for the systemic and pulmonary circulations

38
Q

If a pregnant woman has a congenital heart defect, what is the risk of the fetus having one too?

A

2-5%

The level of risk depends on the specific lesion
And is higher for outflow tract lesions
- 18-20% for aortic stenosis
- 5-10% for ASD
If the fetus is affected, it tends to have the same lesion

Women’s it’s congenital heart disease should be referred for a detailed fetal cardiac ultrasound

39
Q

What is the most common acquired heart disease that affects pregnant women?

A

Rheumatic heart disease

40
Q

What is the most common lesion in rheumatic heart disease?

A

Mitral regurgitation (90%)

41
Q

What are symptoms of Mitral stenosis?

A

Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
Cough (productive, pink, frothy sputum or haemoptysis)

May also be asymptomatic

42
Q

What are signs of mitral stenosis?

A

Mitral facies, cold peripheries
Tapping, undisplaced apex beat
Usually in NSR but at risk of atrial flutter and fibrillation
Loud first heart sound, loud pulmonary second heart sound, opening snap
Low-pitched, mid-diastolic rumble
Signs of pulmonary oedema - wheeze

43
Q

What is the effect of pregnancy on mitral stenosis?

A

She can deteriorate quickly

Develop tachycardia, and then pulmonary oedema

44
Q

What is the management of mitral stenosis in pregnancy?

A

Echo
Beta-blockers to slow the HR and allow time for LA emptying
AF - treat aggressively with Dig and beta-blockers
Avoid excessive IVF
Diuretics for pulmonary oedema
Balloon valvotomy and closed mitral valvotomy
Surgical valvotomy - risk of fetal mortality

45
Q

What is the pre-preg management for a woman with severe Mitral Stenosis?

A

Surgery: open / closed / balloon mitral valvotomy or valve replacement
Prior to pregnancy

46
Q

How is regurgitant valve disease tolerated in pregnancy?

A

Well tolerated
Provided there is no significant LV dysfunction
Systemic vasodilation and a fall in the peripheral vascular resistance reduce after-load
And therefore, act to reduce regurgitation

47
Q

What is peripartum cardiomyopathy?

A

Development of heart failure at the end of pregnancy or in the months following delivery

Where no other cause of heart failure is found
Specific to pregnancy

48
Q

What are risk factors for peripartum cardiomyopathy?

A 
Multiple pregnancy
Pregnancy complicated by HTN
Multi parity
AMA
Afro-Caribbean race
49
Q

What are symptoms of peripartum cardiomyopathy?

A 
Dyspnoea
Reduced exercise tolerance
Palpitations
Pulmonary and/or peripheral oedema
Symptoms relating to peripheral or cerebral emboli
50
Q

What are signs of peripartum cardiomyopathy?

A 
Tachycardia, tachypnoea
Pulmonary oedema
Congestive cardiac failure
Arrythmias 
Signs of pulmonary, cerebral and systemic embolisation
51
Q

What are the diagnostic criteria for peripartum cardiomyopathy?

A

LVEF < 45%
Fractional shortening < 30%
LV end-diastolic pressure > 2.7cm / m2

Often, Echo finding: enlarged heart with global dilation of all four chambers and markedly reduced LVF

52
Q

Which women with peripartum cardiomyopathy should be counselled against pregnancy?

A

If LV size or function does not return to normal

There is a significant risk of 
- recurrence
- worsening heart failure
- death
In subsequent pregnancies
53
Q

What blood test do we use to assess effect of Heparin for anti coagulation?

A

Anti-Xa level

54
Q

How can warfarin be reversed?

A

Vitamin K

Prothrombinase complex

55
Q

How can heparin be reversed?

A

Protamine sulphate

56
Q

What are the clinical features of aortic dissection?

A 
Acute severe chest pain
Ripping or tearing
Interscapular radiation
Haw pain
Presence of systolic HTN and/or differential BPs in each arm
57
Q

What is the most common Type of aortic dissection in pregnancy?

A

Type A, involving the ascending aorta

58
Q

What are risk factors for aortic dissection, part from pregnancy?

A 
Marfan’s syndrome
Turner’s syndrome
Ehler’s Danlos Syndrome type IV (vascular)
Aortic coarctation
Bicuspid aortic valve
59
Q

What is the most common arrhythmia encountered in pregnancy?

A

Paroxysmal SVT

60
Q

What is the drug of choice for tachyarrhythmias in the fetus?

A

Flecanide

61
Q

Ergometrine should be avoided in women with

A

Coarctation or risk of aortic dissection
Coronary artery disease

HTN

62
Q

Syntocinon should be avoided in women with

A 
Stenotic lesions (AS / MS)
HCM
63
Q

a. Outline the normal physiological maternal cardiovascular changes that occur during pregnancy to:
i) Blood volume (3 marks)

A

Expansion of blood volume with higher volume of plasma and increase in erythropoeisis

Plasma volume expansion > erythropoiesis- reflected in ‘relative haemodilution of pregnancy- lower haematocrit and haemoglobin

Expansion of blood volume starts in the first trimester and peaks in the middle of the third trimester

64
Q

a. Outline the normal physiological maternal cardiovascular changes that occur during pregnancy to:
ii) Systemic haemodynamics (3 marks)

A
  • Systemic vasodilation occurs (decreased after-load)
  • Expansion of plasma volume is in response to vasodilation, increased plasma volume increases pre-load
  • Stroke volume and heart rate rise to maintain cardiac output in the presence of systemic vasodilation
  • A large amount of blood volume is also directed through the placenta- 30-40% of all blood volume at any time

——–Contractions during labour cause large volumes of blood to be pushed back into the circulation

———Large autotransfusion of blood occurs at delivery when the uterus involutes, the IVC is no longer compressed, and 400-500mls of blood returns to the system- tolerated well by women with normal hearts

  • Blood pressure typically lowers at the end of the first trimester, reaches a nadir in the second trimester, and then rises towards more normal levels in the third trimester, with volume expansion
  • Serum colloid osmotic pressure is reduced, but not pulmonary capillary wedge pressure, so women are at higher risk of pulmonary oedema
65
Q

A 25 year old nulligravid woman with moderate mitral stenosis (MS) is seeing you because she is planning to become pregnant.

b. Name one of the most common maternal cardiac complications that may occur during her pregnancy. (1 mark)

A

Pulmonary oedema

Arrythmias

66
Q

c. Describe 5 important issues specific to her cardiac condition (mitral stenosis) that should be considered at this consultation. (5 marks)

A

Multi-disciplinary team management: obstetrics, cardiology, obstetric physicians, specialist midwifes
NYHA class currently- better prognosis for pregnancy if NYHA class 1 functional capacity, but there can still be decompensation in pregnancy despite good functional capacity
CARPREG score currently- high scores carry very high risk in pregnancy and pregnancy may be contraindicated
Most recent ECHO- important to ascertain if there is any ventricular dysfunction or pulmonary hypertension associated with her MS which may give her a high CARPREG score
ECG- higher risk of atrial fibrillation
If this is present then she is at high risk of rate related pulmonary oedema and failure- she should start a beta blocker and anti-coagulation should be considered
Consider pre-pregnancy surgery for moderate to severe MS pre-pregnancy as the risks are lower after surgery for pregnancy (surgery can also be performed in pregnancy but carries higher fetal risk)
Evaluate medications- ACEi if being used and switch to beta blocker (if no signs acute failure)
Ante-natal considerations
Fetal ECHO essential as baby is at risk of congenital cardiac disease
Will need regular growth scans through pregnancy as her heart condition increases the risk of SGA

67
Q

MITRAL STENOSIS
She asks about delivery.
d. Outline and justify the main issues on how you would optimally manage her delivery. (3 marks)

A

Location of delivery
Should have delivery in tertiary centre with cardiac HDU/ICU due to risk of decompensation during and immediately after labour
Ensure MDT input (as above) available to give optimal advice for management
Experienced midwife caring for her in labour and should labour in a high-dependency obstetric unit
Labour management
Careful fluid balance during labour and careful use of fluids as there is a risk of precipitating pulmonary oedema with fluid overload
IDC in situ to carefully monitor fluid balance
Constant cardiac monitoring labour as has risk of atrial fibrillation in labour
Continuous monitoring of blood pressure, HR, SaO2 (consider arterial line)- tachycardia usually precipitates pulmonary oedema
Consider induction of labour to ensure the right team and location is available for delivery
Use of regional anaesthesia is safe and is recommended as anxiety, pain and exertion can cause tachycardia, which is dangerous in MS as diastolic filling is decreased with a consequent drop in stroke volume and rise in left atrial pressure (precipitating pulmonary oedema)
Avoid supine and lithotomy positions (increases pressure on IVC), aim to stay in left lateral
Delivery
Avoid valsalva as this decreases cardiac output- consider the use of a longer passive second stage and assisted delivery
Consider the administration of a diuretic in the third stage as directed by the MDT to try to reduce the risk of flash pulmonary oedema
Avoid the use of ecbolics which can exacerbate pulmonary hypertension eg carboprost
Avoid the use of IV boluses of oxytocin as these can precipitate hypotension

Maternal Medicine (18 decks)

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