Obstetric cardiology Flashcards
How do the following change in pregnancy:
- blood volume
- cardiac output
- stroke volume
- blood volume -> increase 35%
- cardiac output -> increase 40%
- stroke volume -> increase 30%
How do the following change in pregnancy:
- heart rate
- systemic vascular resistance
- mean arterial pressure
- heart rate -> increases 15%
- systemic vascular resistance -> decreases 15-20%
- mean arterial pressure -> no significant change
How do the following change in pregnancy:
- systolic BP
- diastolic BP
- Central venous pressure
- systolic BP -> decreases 3-5 mmHg
- diastolic BP -> decreases 5-10 mmHg
- Central venous pressure -> no significant change
How do the following change in the pregnancy:
- serum colloid osmotic pressure
- haemoglobin
- serum colloid osmotic pressure -> decreases 14%
- haemoglobin -> decreases 2%
Why does a pregnant woman may seem to be anaemic?
Drop in serum colloid osmotic pressure (due to vasodilatation) -> drop in haemoglobin -> pregnant women may therefore seem to be anaemic
- Define hypertension in the pregnancy
- how many times do you need to measure and when to establish the diagnosis of hypertension?
Hypertension is still defined as 140/90 taken on two separate occasions and at least 4 hours apart
What may be a characteristic and why of ‘booking BP’ in the first trimester of pregnancy?
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
What are the three types of hypertension in pregnancy?
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)
What’s gestational hypertension?
- hypertension that is new and develops after 20th week of pregnancy
- not associated with proteinuria
- normal biochemistry
- normal foetal growth
- Should gestational hypertension be treated?
- What’s the risk of gestational hypertension?
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)
Definition of pre-eclampsia
Pre- eclampsia : Hypertension + proteinuria arising after 20th week of gestation
What are possible complications for babies surviving maternal pre-eclampsia?
risk of long-term complications of:
- intrauterine hypoxia
- pre-maturity,
- heart disease
- diabetes
What are the elements of ‘moderate risk’ of pre-eclampsia?
Moderate Risk:
-nulliparity
- age >40 years old
- maternal BMI >35
- FHx of pre-eclampsia
- pregnancy interval >10 years
- multiple pregnancy
What are the elements of ‘high risk’ of pre-eclampsia?
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)
Pathophysiology of pre-eclampsia
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
What is the classical characteristic of eclampsia?
What effects does it have on the foetus?
- eclampsia: a new onset of tonic- clonicseizurein presence ofpre-eclampsia (hypertension + proteinuria in 20 weeks gestation)
- maternal convulsion -> foetal distress and bradycardia
Signs and symptoms of eclampsia and pre-eclampsia (similar)
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
What is the pathological process behind increased BP in pre-eclampsia/eclampsia?
*hypertension is due to the fact that endothelium is broken, stops producing NO and controlling BP
Possible maternal complications of eclampsia
Materna complicationsl:
- HEELP syndrome (haemolysis, elevated liver enzymes, low platelets)
- DIC
- AKI
- Adult Respiratory Distress Syndrome,
- Cerebrovascular haemorrhage
- CNS damage
- death
Possible foetal complications of pre-eclampsia/ eclampsia
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
Differentials for eclampsia
Differentials: hypoglycaemia, pre-existing epilepsy, head injury, hemorrhagic stroke, meningitis, medication-induced, brain tumour, cerebral aneurysm, septic shock, ischaemic stroke
Investigations and rationale in eclampsia
- 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
Management of eclampsia
Management:
-
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 -
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
- what’s the preferred mode of delivery in eclampsia?
- what happens to mum after delivery?
- what do we need to remember about (baby wise)
- 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
