Gametes - Maternal Physiology Flashcards
insulin during pregnancy
mothers becomes less sensitive to insulin
Brought about by hCS (also known as Human Placental Lactogen, hPL)
FAs for her own metabolism and glucose spared for baby
Too much insensitivity - gestational diabetes
weight gain expected during pregnancy for each BMI category
underweight BMI (< 18.5) weight gain
28-40 pounds
normal weight BMI (18.5-24.9) weight gain
25-35 pounds
overweight BMI (25-29.9) weight gain
15-25 pounds
obese BMI > or = 30
11-20 pounds
what are obesity and excessive weight gain in pregnancy associated with
gestational diabetes
macrosomia - large baby
pre-eclampsia
caesarean section
post-operative complications
AA essential during pregnancy
leucine
(IGF-1 and IGF-2 also)
distribution of weight during pregnancy
6kg - maternal tissues
5kg - foetal tissues
7kg - water
3kg - fat
1kg - protein
how is weight gain distributed throughout pregnancy
water content at term
foetus + placenta + amniotic fluid = 3.5L
where is this increase in total body water seen
increase in volume of blood, plasma, RBC
when does the increase in TBW start
when does it reach max vol
what is it caused by
increases from week 6/8
max vol@ 32 weeks - 45% increase
→ oestrogen action on renin/angiotensin/aldosterone
pregnancy is a condition of
Chronic Volume Overload
if you’re not pregnant but experience fluid overload, how does your body respond
(ADH stops you getting rid of fluid) → ADH is inhibited
AMP promotes water loss → AMP is increased
⇒ Pressure Diuresis
haemotological changes in pregnancy - RBCs
RBC production is increased by 33% - possibly hormonally mediated
this increases the O2-carrying capacity of blood
the increase in plasma is greater and faster than RBC, so there is no increase in viscosity of blood
⇒ Hb conc falls from 14 g/dL → 12 g/dL
⇒ Dilution Anaemia (Hb and Hct decrease)
[true anaemia = Hb < 12 g/dL, Hct < 32%]
Haemotological changes in pregnancy - leukocytes
WBC count in each trimester and labour
explain the change in WBC count
bone marrow is hyperplastic
peripheral WBC rises progressively during pregnancy
1st trimester - 9500/mm3
2nd and 3rd trimester - 10,500/mm3
labour - 20-30,000/mm3
rise is due to PMNs - polymorphonuclei (eosinophils, basophils etc)
haematological changes in pregnancy - platelets
platelets progressively decline but remain within normal range
likely due to increased destruction
what cells regulate the localised immunity in the uterine environment
T regulatory cells
Haematological changes in pregnancy - coagulation
increase in levels of…
no change in…
decline in levels of…
- increased levels of coagulation factors (more likely to develop embolism) - decreases blood loss at delivery
fibrinogen (Factor I)
Factors VII → X
- no change in prothrombin (Factor II), Factor V and Factor XII
- decline in platelet count, Factor XI and XIII
bleeding time and clotting time are unchanged in normal pregnancy
pregnancy is a
hyper-coaguable state
COAGULATION
increased levels of
fibrinogen - Factor I
Factor VII
Factor X
COAGULATION
no change in
prothrombin - Factor II
Factor V
Factor XII
COAGULATION
decline in
platelet count
Factor XI
Factor XIII
bleeding and clotting time are unchanged in normal pregnancy
clinical implications of the haematological changes in pregnancy
- increased circulatory need of the enlarging uterus and the foeto/placental unit (increase of 45%)
- fills of the ever-increasing venous reservoir
- protects the parturient (woman in labour, about to give birth) from the bleeding at the time of delivery
- parturients become hypercoaguable as the gestation progresses
how long does it take for blood volume to return to normal
8 weeks
CV changes in pregnancy
- increased metabolic demands
- expansion of vascular channels
- increase in steroid hormone
CO =
HR x stroke volume
change in maternal CO
30-40% increase
CO during pregnancy
6-7L/min (to allow for O2 delivery to foetus)
CO remains maximal until delivery/labour
what causes this increase in CO
how long is this increase in CO maintained for
increase in CO ⇒ increase in SBP
fluid and vol increased ⇒ increased CO
oestrogen and progesterone
maintained until 4 days post-partum
what does CO in pregnancy depend on
varies depending on the uterine size + maternal position
haemodynamic parameters during pregnancy
why does CO increase
it facilitates maternal and foetal exchanges of respiratory gases, nutrients and metabolites
it reduces the impact of maternal blood loss at delivery
how does pulse (HR) change during pregnancy
1st trimester - resting pulse increases by 8 beats/min
by term, increased by 15-20 BPM
how does BP change during pregnancy
systolic vs diastolic
systemic BP overall decreased
- systolic BP changes little (even though there’s an increase in CO)
- diastolic reduced by 5-10 mmHg
- Venous pressure in upper body unchanged, venous pressure in the lower body increased
⇒ BP affected by position of mother
what dynamic factor contributes to diastolic BP
peripheral resistance
vessels dilate to ensure you have the blood supply to support the foetus
basis for the haemodynamic changes of pregnancy
increased O2 demand → increased CO
- vasodilation at placenta and increased vascularisation
increased blood flow to foeto-placental unit
decreased systemic vascular resistance (SVR)
- diastolic BP decreases
overview of CVS changes during pregnancy
anatomical and changes of the heart in pregnancy
apex displaced upwards and to the left
heart size is increased by 12%
left axis deviation of 15% (approx) - linked with hypertrophy of ventricle - indicative of heart failure
diaphragm moves upwards by 4cm
ECG changes during pregnancy
benign dysrhythmia
reversal of ST, T and Q waves
left axis deviation
changes in heart sounds in pregnancy
split 1st heart sound - early closure of mitral valve
intensity of 2nd sound may become louder
systolic functional murmurs may develop due to tricuspid regurgitation
peripheral vasodilation during pregnancy
increased blood flow to the skin - especially hands and feet - lead to a feeling of warmth
increased congestion of nasal mucosa leading to nasal congestion (because of peripheral vasoD)
epistaxis is common (increased risk of nose bleeds)
supine hypotension is caused by
compression of inferior vena cava
decreased venous return
decreased cardiac output
lowered BP
movement of diaphragm during pregnancy
at term diaphragm can be elevated up to 4cm
resp system may be compromised - (70% contribution by diaphragm)
diaphragm movement reduces thoracic cavity vol
mobility reduced
respiration becomes mainly thoracic
widened subcostal angle, increasing transverse diameter of the chest
tidal vol during pregnancy
increased by 30-40%
respiration rate during pregnancy
what is it influenced by
increased by 15% at term
influenced by progesterone
minute ventilation during pregnancy
formula
increased at term by 50%
minute ventilation = resp rate x tidal vol
respiration reserve decreases because of anatomical movement upwards
effect of elevation of diaphragm on:
- total lung vol
- residual vol
- FRC - functional residual capacity
- FEV1 or FEV1:forced vital capacity
- total lung vol decreases by 5%
- residual vol decreases by 20%
- FRC decreases by 20%
- no change in FEV1 or the ratio of FEV1 to forced vital capacity
risk of compressed lungs
more susceptible to noxious gases
change in minute ventilation and its subsequent impact on O2 consumption
PA and Pa levels
arterial pH
minute vol increases by 30-40% by late pregnancy
O2 consumption increases only 15-30%
⇒ higher PAO2 (alveolar) and PaO2 (arterial)
⇒ fall in PACO2 (what drives respiration) and PaCO2
arterial pH remains unchanged
increased bicarbonate excretion via kidneys
what causes dyspnea during pregnancy
late 1st or early 2nd trimester
likely due to:
- reduced PaCO2 levels
- awareness of increased tidal vol of pregnancy
