6.1 part 2 Maternal Adaptations to Pregnancy Flashcards
What are the main maternal CVS changes seen during pregnancy? (4)
- increase plasma volume, CO, SV and HR
- decrease serum albumin and colloid osmotic pressure
- increase in coagulation factors and fibrinogen
- compression of IVC by uterus
What is pre-load and after-load and how are these affected during pregnancy?
In what instance may this not be the case?
Pre-load is the volume of blood returning to the heart through RA
After-load is the resistance to blood flow exiting the LV
In pregnancy pre-load increases as there is increased blood volume and after-load decreases due to decreased TPR
Sometimes in late pregnancy when women is lying down, uterus can compress vena cava, decreasing return to the heart (pre-load) and resulting in vasovagal syncope
What are the changes in cardiac size/position during pregnancy?
The heart is enlarged by both chamber dilation and hypertrophy.
Upward displacement of the diaphragm by the enlarging uterus causes the heart to shift to the left and anteriorly.
Give 3 maternal changesto the renal system during pregnancy?
1) Increase in renal blood flow
2) IncreaseGFR ➞ functional renal reserve decreases and serum creatinine decreases
3) filtration capacity intact
List the specific changes tobladder and ureter during pregnancy?
Why can this cause problems and 3 consequences of this
Bladder capacity doubles and there is dilation of the ureters due to progesterone
Can cause urinary stasis which can lead to:
1) hydroureter
2) obstruction
3) predispose women to UTI, specificallypyelonephritis
As a result of pyelonephritis, contractions may be stimulate which can result inPre-term labour
What is the main maternal changeseen in the liver during pregnancy?
changes in oxidative liver enzymes eg. cytochrome P450
Give 4 maternal GI changes seen during pregnancy?
1) nausea and vomiting
2) delayed gastric emptying
3) prolonged small bowel transit time(SM relaxation by
4) gastrointestinal reflux
What are the changes in BP (systolic and diastolic) during pregnancy? What condition can this lead to and why?
Systolic BP is NEVER increased in pregnancy (normally)
Women may experience hypotension:
T1 & T2 – progesterone effects on SVR
T3 – Aortocaval compression by gravid uterus
What happens to the endothelium of BV’s and the plasma during pregnancy?
How do these changes differ in a a pre-eclamptic pregnancy, why may this occur and what 3 things may this result in?
Normal pregnancy = Vasodilation (due to decreased TPR) and plasma-expanded
Pre-eclamptic pregnancy:
Vasoconstricted + plasma-contracted due to increased vascular permiability (lots of fluid leakage) and dailure of spiral artery remodelling causes insufficient blood flow. These can lead to…
1) Defect in placentation
2) Poor uteroplacental circulation
3) Widespread endothelial dysfunction
What are the anatomical chest wall changes that occur during pregnancy?
Why do these increase?
The subcostal angle, the anterior-posterior, transverse diameters and the chest wall circumference all INCREASE
These changes compensate for the 4-cm elevation of the diaphragm so that the total lung capacity is not significantly reduced
What changes occur to the following and why?
functional residual capacity (FRC) tidal volume(TV) vital capacity andtotal lung capacity (TLC) alveolar ventilation/minute RR
FRC is decreased due to the elevation of the diaphragm
TV increases due to the increase in the AP and transverse diameter
Vital capacity and TLC are unchanged
Alveolar ventilation/minute is Increased
RR is unchanged
Why does pregnancy result in overall respiratory alkalosis and how is the compensated?
What is the hormone responsible for these changes
Due to physiological hyperventilation:
Increased metabolic CO2 production ➞increasedrespiratory drive ➞respiratory alkalosis ➞ compensated by increased renalHCO3 excretion
All controlled by Progesterone
How does maternal carbohydrate metabolism ensure that glucose is used for the foetus? (incl hormones - CHOP)
What risk does this pose to the mother?
Glucose is preferential to the foetus. In order to ensure glucose is used by foetus and not by mother there is an increase in maternal peripheral insulin resistance. This means the mother will switch to gluconeogenesis and use alternative fuels for herself (lipolysis in T2)
Hormones involved are➞ cortisol, HPL, oestrogen/progesterone, prolactin
Risk: mother can become keto acidotic because lipolysis results in FA production which are metabolised in the liver to produce ketone bodies (decrease pH)
How do blood glucose levels vary in pregnancy?
- Decrease in fasting blood glucose
* Increase in post-prandial blood glucose
Give 4 risk factors for gestational diabetes? (F-POP)
- pre-existing diabetes
- obesity (BMI > 30)
- family history
- previous GD
- ethnicity (asian/African)
- previous child with fatal macrosomia (weight <4.5kg)
Give 3 risks to the foetus if GD is controlled poorly and why?
- Macrosomic fetus
- Stillbirth
- Increased rate of congenital defects
Why does Macrosomia occur with uncontrolled GD?
Give 2 significant neonatal risks/consequences?
What tests would be done?
In GD, the large amounts of glucose in blood cross placenta to foetus. Foetus pancreas responds by producing large amounts of insulin. As insulin stimulates storage of glucose it causes increased growth of baby ➞ macrocosmic
Neonatal risks
1) shoulder dystocia, can get stuck during birth and lead to fractures ➞ damage to brachial plexus can result in Erb’s or Klumpke’s palsy
2) metabolic problems: hyperglycaemia, hyperkalemia, hyperbilirubinemia
Oral glucose tolerance test required
What is the effect of pregnancy on thyroid metabolism?
Pestrogen increases production of thyroid binding globulin which increases amount of T3 and T4 overall.
BUT remember 99% of T3 and T4 are bound hence the free T4 remains in normal range
What is Hyperemesis gravidarum?
A pregnancy complication caused by increase hCG concentrations
It is characterised by severe nausea, vomiting, weight loss, and dehydration.
How can Hyperemesis gravidarum lead to biochemical hyperthyroidism?
Due to the increased concentration of hCG.
hCG has an α subunit very similar to TSH, hence hCG can mimic TSH causing increased thyroid hormones in pregnancy.
Note: because of increased T3 and T4 by hCG the overall TSH level will slightly drop (due to negative feedback)
What are the anatomical changes that occur in pregnancy?
Alterations in the disposition of the viscera
e.g. Appendix moves to RUQ as uterus enlarges
Describe the haematological state during pregnancy
- Pregnancy is a pro-thrombotic state
- increased fibrin deposition at the implantation site
- Increased fibrinogen and clotting factors
- Reduced fibrinolysis
- Stasis due to venodilation
What do the Haematological changes in pregnancy increase the risk of?
How would you treat?
Thromboembolic disease (increased risk of clotting -DVT)
Treatment: LMWH (low molecular weight heparin). Do NOT use Warfarin, as this crosses the placenta and is teratogenic
List 4 clinical presentation signs of a PE in pregnancy
1) dyspnoea
2) palpitations
3) pleuritic chest pain
4) hemopytisis
5) tachycardia
6) cyanosis
