Maternal Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

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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
In what case is the development of a resting tachycardia a particular concern in pregnancy? (2)
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
26
What is the treatment of aortic stenosis in pregnancy?
Balloon valvotomy In severe cases
27
What are the risks of coarctation of the aorta in pregnancy?
Angina HTN Congestive heart failure Aortic rupture Aortic dissection
28
How do you minimise the risk of aortic dissection, in the context of an aortic coarctation in pregnancy?
Strict control of blood pressure | Beta-blockade to decreased cardiac contractility
29
What are the three most common types of cardiac involvement in Marfan’s syndrome?
1. MV prolapse 2. MR 3. Aortic root dilatation 80% of patients with Marfan’s syndrome have cardiac involvement
30
What are two risk factors for aortic dissection and rupture in Marfan’s syndrome?
1. Pre-existing or progressive aortic root dilatation | 2. Positive family history of dissection or aortic rupture
31
In Marfan’s syndrome, at what level of aortic dilation is pregnancy contraindicated due to the risk of aortic dissection / rupture?
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
What is the inheritance pattern of Marfan’s syndrome?
Autosomal dominant
33
What are 7 extra-cardiac manifestations of Marfan’s syndrome?
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
What are the main causes (2) of cyanotic congenital heart disease?
Pulmonary atresia | Tetralogy of Fallot
35
What are four risks for pregnant women (and their fetus) with cyanotic congenital heart disease?
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
What are the two main concerns for a pregnant women with Tetralogy of Fallot?
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
What is a Fontan circulation?
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
If a pregnant woman has a congenital heart defect, what is the risk of the fetus having one too?
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
What is the most common acquired heart disease that affects pregnant women?
Rheumatic heart disease
40
What is the most common lesion in rheumatic heart disease?
Mitral regurgitation (90%)
41
What are symptoms of Mitral stenosis?
Dyspnoea Orthopnoea Paroxysmal nocturnal dyspnoea Cough (productive, pink, frothy sputum or haemoptysis) May also be asymptomatic
42
What are signs of mitral stenosis?
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
What is the effect of pregnancy on mitral stenosis?
She can deteriorate quickly | Develop tachycardia, and then pulmonary oedema
44
What is the management of mitral stenosis in pregnancy?
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
What is the pre-preg management for a woman with severe Mitral Stenosis?
Surgery: open / closed / balloon mitral valvotomy or valve replacement Prior to pregnancy
46
How is regurgitant valve disease tolerated in pregnancy?
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
What is peripartum cardiomyopathy?
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
What are risk factors for peripartum cardiomyopathy?
``` Multiple pregnancy Pregnancy complicated by HTN Multi parity AMA Afro-Caribbean race ```
49
What are symptoms of peripartum cardiomyopathy?
``` Dyspnoea Reduced exercise tolerance Palpitations Pulmonary and/or peripheral oedema Symptoms relating to peripheral or cerebral emboli ```
50
What are signs of peripartum cardiomyopathy?
``` Tachycardia, tachypnoea Pulmonary oedema Congestive cardiac failure Arrythmias Signs of pulmonary, cerebral and systemic embolisation ```
51
What are the diagnostic criteria for peripartum cardiomyopathy?
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
Which women with peripartum cardiomyopathy should be counselled against pregnancy?
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
What blood test do we use to assess effect of Heparin for anti coagulation?
Anti-Xa level
54
How can warfarin be reversed?
Vitamin K | Prothrombinase complex
55
How can heparin be reversed?
Protamine sulphate
56
What are the clinical features of aortic dissection?
``` Acute severe chest pain Ripping or tearing Interscapular radiation Haw pain Presence of systolic HTN and/or differential BPs in each arm ```
57
What is the most common Type of aortic dissection in pregnancy?
Type A, involving the ascending aorta
58
What are risk factors for aortic dissection, part from pregnancy?
``` Marfan’s syndrome Turner’s syndrome Ehler’s Danlos Syndrome type IV (vascular) Aortic coarctation Bicuspid aortic valve ```
59
What is the most common arrhythmia encountered in pregnancy?
Paroxysmal SVT
60
What is the drug of choice for tachyarrhythmias in the fetus?
Flecanide
61
Ergometrine should be avoided in women with
Coarctation or risk of aortic dissection Coronary artery disease HTN
62
Syntocinon should be avoided in women with
``` Stenotic lesions (AS / MS) HCM ```
63
a. Outline the normal physiological maternal cardiovascular changes that occur during pregnancy to: i) Blood volume (3 marks)
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
a. Outline the normal physiological maternal cardiovascular changes that occur during pregnancy to: ii) Systemic haemodynamics (3 marks)
- 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
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)
Pulmonary oedema | Arrythmias
66
c. Describe 5 important issues specific to her cardiac condition (mitral stenosis) that should be considered at this consultation. (5 marks)
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
MITRAL STENOSIS She asks about delivery. d. Outline and justify the main issues on how you would optimally manage her delivery. (3 marks)
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
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