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Lecture week III COPY > Obstetric cardiology > Flashcards

Obstetric cardiology Flashcards

1
Q

How do the following change in pregnancy:

  • blood volume
  • cardiac output
  • stroke volume
A
  • blood volume -> increase 35%
  • cardiac output -> increase 40%
  • stroke volume -> increase 30%
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2
Q

How do the following change in pregnancy:

  • heart rate
  • systemic vascular resistance
  • mean arterial pressure
A
  • heart rate -> increases 15%
  • systemic vascular resistance -> decreases 15-20%
  • mean arterial pressure -> no significant change
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3
Q

How do the following change in pregnancy:

  • systolic BP
  • diastolic BP
  • Central venous pressure
A
  • systolic BP -> decreases 3-5 mmHg
  • diastolic BP -> decreases 5-10 mmHg
  • Central venous pressure -> no significant change
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4
Q

How do the following change in the pregnancy:

  • serum colloid osmotic pressure
  • haemoglobin
A
  • serum colloid osmotic pressure -> decreases 14%
  • haemoglobin -> decreases 2%
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5
Q

Why does a pregnant woman may seem to be anaemic?

A

Drop in serum colloid osmotic pressure (due to vasodilatation) -> drop in haemoglobin -> pregnant women may therefore seem to be anaemic

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6
Q
  • Define hypertension in the pregnancy
  • how many times do you need to measure and when to establish the diagnosis of hypertension?
A

Hypertension is still defined as 140/90 taken on two separate occasions and at least 4 hours apart

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7
Q

What may be a characteristic and why of ‘booking BP’ in the first trimester of pregnancy?

A

Booking BP -> at the beginning of pregnancy may be ‘artificially’ low due to peripheral vasodilatation (therefore it’s not unusual to see BPs of 90/60) - normal in 1st trimester of pregnancy

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8
Q

What are the three types of hypertension in pregnancy?

A

Three types of hypertension in pregnancy:

A. Hypertension BEFORE pregnancy (chronic hypertension)

B. Hypertension that develops DURING pregnancy with NO proteinuria (gestational

hypertension)

C. Hypertension that develops DURING pregnancy with proteinuria (pre-eclampsia)

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9
Q

What’s gestational hypertension?

A
  • hypertension that is new and develops after 20th week of pregnancy
  • not associated with proteinuria
  • normal biochemistry
  • normal foetal growth
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10
Q
  • Should gestational hypertension be treated?
  • What’s the risk of gestational hypertension?
A

Gestational hypertension should not be treated- > antihypertensive

drugs would cross the placenta and affect foetus

  • Risk of developing pre-eclampsia (30%) -> there is no way of screening who with gestational hypertension will develop it -> so need to monitor women at risk (with hypertension)
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11
Q

Definition of pre-eclampsia

A

Pre- eclampsia : Hypertension + proteinuria arising after 20th week of gestation

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12
Q

What are possible complications for babies surviving maternal pre-eclampsia?

A

risk of long-term complications of:

  • intrauterine hypoxia
  • pre-maturity,
  • heart disease
  • diabetes
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13
Q

What are the elements of ‘moderate risk’ of pre-eclampsia?

A

Moderate Risk:

-nulliparity

  • age >40 years old
  • maternal BMI >35
  • FHx of pre-eclampsia
  • pregnancy interval >10 years
  • multiple pregnancy
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14
Q

What are the elements of ‘high risk’ of pre-eclampsia?

A

High Risk:

  • chronic hypertension (before pregnancy)
  • Past Hx (HTN, pre-eclampsia, eclampsia in previous pregnancy)
  • pre-existing CKD, DM, autoimmune disease (SLE, anti-phospholipid

syndrome)

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15
Q

Pathophysiology of pre-eclampsia

A

Pathology of pre-eclampsia:

• sort of graft vs host disease

  • spiral artery will not become modified (high resistance, low capacity; normally there will be modifications in SM) -> spiral artery is not remodelle
  • dysregulation of maternal vascular endothelial cells -> multisystem disorder
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16
Q

What is the classical characteristic of eclampsia?

What effects does it have on the foetus?

A
  • eclampsia: a new onset of tonic- clonicseizurein presence ofpre-eclampsia (hypertension + proteinuria in 20 weeks gestation)
  • maternal convulsion -> foetal distress and bradycardia
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17
Q

Signs and symptoms of eclampsia and pre-eclampsia (similar)

A

Signs and symptoms related to end-organ dysfunction e.g. papilloedema

  • headache -> usually frontal
  • hyper-reflexia
  • nausea and vomiting
  • generalised oedema (angioedema, peripheral) -> as endothelial injury -> capillary fluid leaks out
  • RUQ pain +/- jaundice
  • visual disturbance (flushing lights, blurred/ double vision)
  • change in mental status
  • clotting factors abnormalities -> due to vascular endothelium in the liver being destroyed
  • Proteinuria -> due to endothelium being destroyed -> protein leak out
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18
Q

What is the pathological process behind increased BP in pre-eclampsia/eclampsia?

A

*hypertension is due to the fact that endothelium is broken, stops producing NO and controlling BP

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19
Q

Possible maternal complications of eclampsia

A

Materna complicationsl:

  • HEELP syndrome (haemolysis, elevated liver enzymes, low platelets)
  • DIC
  • AKI
  • Adult Respiratory Distress Syndrome,
  • Cerebrovascular haemorrhage
  • CNS damage
  • death
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20
Q

Possible foetal complications of pre-eclampsia/ eclampsia

A

Foetal:

  • IUGR -> as the placenta is hypoperfused
  • pre-mature birth
  • RDS
  • death
  • placental abruption
  • excess skin - decreased adipose tissue
  • ‘head sparing effect’ - head is larger than other parts of the body - as all of the limited nutrient and oxygen are driven there in order to preserve

brain

-small body

21
Q

Differentials for eclampsia

A

Differentials: hypoglycaemia, pre-existing epilepsy, head injury, hemorrhagic stroke, meningitis, medication-induced, brain tumour, cerebral aneurysm, septic shock, ischaemic stroke

22
Q

Investigations and rationale in eclampsia

A
  • FBC -> decreased Hb, decreased platelets
  • U&Es -> assess for kidney damage (elevated: urea, creatinine) and decreased urine output
  • Clotting studies
  • Blood glucose
  • Abdominal USS -> to role out placental abruption
  • CTG monitoring -> foetal distress and bradycardia
23
Q

Management of eclampsia

A

Management:

  1. Resuscitation
    - ABCDE
    - patient should lie on L lateral position, secured airway and oxygen therapy
    - Fluid restriction (max 80ml per hour) -> as we want to avoid pulmonary oedema *even if renal failure -> as pulmonary oedema is more likely to kill
  2. Cessation of Seizures
    - Magnesium sulphate (we do not know how it works, but it does work, probably stabilises cellular membrane)

*Assess for signs of hyper-magnesia (respiratory depression, hyper-reflexia), monitor foetus by CTG

3. Control BP

  • IV anti-hypertensives -> Labetalol and Hydralazine (target MAP <120 mmHg)

*labetalol is an old-fashioned drug, only used nowadays in pre-eclampsia (newer drugs may harm baby)

*rapid decrease in maternal BP -> foetal HR abnormalities -> need for continuous CTG for 30 minutes after IV anti-hypertensives

4. Delivery of baby and placenta

  • to treat eclampsia definitely

*But mum must be stable before delivery - seizures controlled, severe hypertension treated and hypoxia corrected -> this all is regardless of any foetal compromise

24
Q
  • what’s the preferred mode of delivery in eclampsia?
  • what happens to mum after delivery?
  • what do we need to remember about (baby wise)
A
  • CS is recommended mode of delivery

* after delivery, patient required HDU care until stable (well controlled BP, adequate urine output, discontinuation of magnesium sulphate -> usually minimum 24 hours)

  • Post-natal follow up and monitoring are required
25
Q

What is better tolerated in pregnancy: mitral regurgitation or stenosis? Why?

A

Regurgitation is better tolerated than stenosis -> decreased peripheral vascular resistance (in pregnancy) will reduce the degree of regurgitation

* Mitral stenosis is a problem

26
Q

What’s the most frequent valvular lesion associated with Rheumatic Heart Disease?

A

Mitral stenosis

27
Q
  • Possible complications of mitral stenosis in pregnancy
  • What’s the current advice on management of pregnant woman with mitral stenosis
A
28
Q

What’s the prognosis for women with cyanotic and acyanotic CHD in terms of pregnancy?

A
  • Women with acyanotic heart diseases -> should be OK with pregnancy
  • Women with cyanotic heart disease -> poor prognosis, increased risk of

complications

29
Q

What possible complications are there for a pregnant woman with CHD?

A
  • pulmonary hypertension
  • cyanosis
  • severe LV outflow obstruction

*Moreover the baby will be at increased risk (2-10%) of CHD -> therefore need to monitor them closely (to have management plan to be implemented straight after delivery)

30
Q

ASD in a pregnant woman - do we do anything about that?

A
  • We tend not to close ASD while during pregnancy
  • if there is significant L- R shunt or large hole we will close, as this will lead to a significant compromise in oxygen delivery to a baby and mum (as O2 demands are increased)
31
Q

What do we do in VSD in pregnancy?

A

Endocarditis could be more common in pregnancy as there is slight immunosuppression -> give endocarditis prophylaxis

32
Q
  • What’s the most common CHD valve disease among pregnant women?
  • what’s the prognosis for that in relation to pregnancy?
  • what’s possible advice to avoid
  • what to do if symptomatic
A
  • bicuspid aortic valve -> aortic stenosis
  • most will be well tolerated and asymptomatic
  • Advice to avoid: lying flat. epidural. nifedipine (CCB)
  • If symptomatic: bed rest, B-blocker, balloon valvotomy
33
Q

Hypertrophic Cardiomyopathy

  • inheritance pattern
  • diagnosis
  • risk
A
  • 70% Autosomal dominant -> screen baby
  • diagnosis: ECHO, symptoms, murmur
  • Risks: sudden death, endstage HF, fatal CVA,
34
Q

Hypertrophic cardiomyopathy in mum and pregnancy

  • what’s the prognosis
  • what we should avoid/ be cautious about
A
  • Pregnancy may exacerbate the condition -> risk of severe and rapid HF or even death of mum
  • avoid regional anaesthesia - as vasodilation is poorly tolerated
35
Q

What’s prognosis for the pregnancy in women with cyanotic heart disease?

(women and baby wise)

A
  • poor prognosis (due to significant R-L shunting and decreased peripheral vascular resistance)
  • cyanotic HD is very poorly tolerated by the baby = IUGR

*Women who grew up with cyanotic HD may be used to low sats, but developing foetus would not be

36
Q

What do we advice a woman who has Eisnmengers and becomes pregnant? Why?

A

EISENMENGERS -> strong advice to avoid pregnancy due to high mortality rate -> offer TOP

This is because pregnancy can exacerbate R-L shunt (due to fall in peripheral resistance) -> 40% of risk of maternal death (during delivery or 1 week post-partum) due to thromboembolism, PE, hypovolemia

37
Q

When prophylaxis for bacterial endocarditis is recommended in pregnant women?

A
38
Q

Ischaemic heart disease in pregnancy

  • why is it more common?
  • what’s prognosis?
A
  • IHD in pregnant women is increasing due to increase in IVF and

maternal age -> older women get pregnant, there is therefore increase in mums with IHD

  • strain on the heart during later pregnancy and delivery means poor prognosis
39
Q

Possible management of Ischaemic Heart Disease in a pregnant woman

A

aspirin, B-blocker, Heparin, nitrates, angiography, stenting, possible thrombolysis

40
Q

What’s the incidence of cardiac arrest in pregnancy?

  • what’s the prognosis
  • what are the possible causes
A
  • incidence: 1 in 30, 000 women in late pregnancy
  • prognosis: poor chance of maternal survival
  • causes: haemorrhage, placental abruption, PE, eclampsia, drug toxicity
41
Q

Management of cardiac arrest in pregnancy

A
  • L lateral positions -> t decrease strain on vena cava
  • If resuscitation not effective in 4 minutes -> Empty the uterus (delivering baby as it will release vena cava and thoracic compression , improves ventilation - does not matter what stage of gestation is it - needs to save mum’s life)
42
Q
  • What’s Peripartum cardiomyopathy?
  • what are its risk factors?
A
43
Q

What’s clinical presentation of Peripartum Cardiomyopathy?

A
44
Q

Diagnostic criteria for Peripartum Cardiomyopathy

A
45
Q

Prognosis for the outcome of Peripartum Cardiomyopathy

A

Cardiomyopathy in pregnancy: mixed outcomes -> 10% may die, some will get heart transplant, 60% may recover and have fairly normal heart function, 40% may never recover in terms of cardiac function

46
Q

Anti-coagulant use in pregnancy

  • which one are safe
  • which one are not
A

WARFARIN not to be used in pregnancy! -> teratogenic:*chondroplasia punctata -

abnormality of bone and cartilage, optic atrophy, neurodevelopmental delay

Heparin and LMWH

  • are safe for a baby as do not cross

placenta (but not as effective for mum as warfarin)

*factor Xa inhibitors (e.g. Fondaparinux, Apixaban) -> unknown safety in pregnancy (although some studies suggest they do not cross the placenta so perhaps safe)

47
Q

Use of these drugs in pregnancy: recommended or not:

  • antihypertensives
  • B blockers
  • CCBs
  • ACE inhibitors and Angiotensin Receptor Blockers
  • diuretics
A
48
Q
A

Lecture week III COPY (11 decks)

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