Pregnancy

Lec 2

Maternal Physiology During

Pregnancy
Dr. Maryam Bakir
Assistant Prof
OBGYN

– Describe the main physiological changes

which occur in a mother during a normal
pregnancy
– Describe how maternal adaptations to
pregnancy and the support of the fetus
influence maternal nutritional requirements
– Describe how the control of maternal blood
glucose is influenced by pregnancy and
describe the potential clinical consequences

Cardiovascular
• System
Blood volume
• Cardiac output
• Stroke volume
• Heart rate
(Remember, CO = HR x SV)
• Blood pressure
Hypotension in pregnancy
T1 and T2 – Progesterone effects on Systemic Vascular Resistance
T3 – Aortocaval compression by gravid uterus. return to the
heart
Clinical aspects of CVS changes:
Breathlessness, edema of extremities, sinus
tachycardia (palpitation), filled and dynamically
pulsating jugular veins, but JVP unchanged,
forcibly beating cardiac apex,
Auscultatory changes:
1)increase loudness of S1, S2.
2)exaggerated splitting of S1.
3)loud S3 by 20 weeks.
4)systolic ejection murmur at left sternal edge
(96%). 5)transient diastolic murmur (20%).
6)continuous murmur due to increase mammary
blood flow(10%).
What are the ECG changes in normal pregnancy?
Urinary System
Renal plasma flow increases as early 6 week
Glomerular Filtration Rate (GFR) increases by 9WK
Filtration capacity intact
Functional renal reserve decreases as GFR increases
Urinary Stasis
Progesteronerelaxes the smooth muscle in the walls
of the renal pelvis & ureters, which can result in
stasis, hydronephrosis, hydroureter, UTIs &
pyelonephritis.
Pyelonephritis can induce pre-term labour.

What are the effects of pregnancy on renin angiotensin

system, prostacyclins & erythropoietein?
Renal hormones
- Renin-angiotensin system: is activated from very early
pregnancy
- Erythropoietin synthesis appears to be stimulated by
hCG& its concentration rises from the first trimester,
peaking in mid-gestation and falling somewhat
thereafter.
- Prostacyclin is a potent vasodilator, synthesized mainly
in the kidney. Concentrations begin to rise rapidly by
8–10 weeks gestation.
 Respiratory
•System is displaced
Diaphragm
• A-P and transverse diameters
of thorax increase
– O2 consumption increases 20%
– Decreases functional residual capacity
– Vital capacity unchanged
– Tidal volume increases
– Respiratory minute volume increased
– Alveolar ventilation rate increased
– Respiratory rate unchanged

Lung
TV TLC Volumes
IRV ERV FRC RV VC IC
 During pregnancy there is a physiological hyperventilation
driven by progesterone, so the mother can blow off the
extra CO2 the fetus produces.
This leads to respiratory Alkalosis, which is compensated for
- carbonic anhydrase in RBC.
-kidneys which compensate for by producing and
reabsorbing less bicarbonate i.ebicarbonate excretion).
Shifting of O2-Hb dissociation curve to the right facilitates
release of O2 from RBC so increase availability of O2 to
tissues (2,3-DPG in RBCs) .

Endocrinological changes in pregnancy

From the beginning of conception there are dramatic increases in
hormones produced by the fetus, placenta & maternal
intrauterine tissues.
 Human chorionic ghonadotrophin:
Chemical structure: hCG is a glycoprotein composed of 2 subunits
α & β-subunits.
• Secretion pattern: Normally hCG rises rapidly as early as 6-8
days post-conception doubles every 2-3 days & reaching a peak
at 9-10 wk gestation. It declines after 12 wk gestation to a
plateau for the reminder of pregnancy
• Biological functions of hCG:
Signals the ovary to maintain corpus luteum & continues
progesterone production.
Regulates fetal testicular testosterone production, which is critical
in the development of male external genitalia
Possesses some TSH-like properties

Detection of hCG in the serum or the urine is the basis of

pregnancy tests.
Serum assays detect pregnacy at 8-12 days of ovulation whereas
urine assays at 14-18 days of ovulation.
After delivery at term hCG can normally be detected in maternal
serum or urine for up to 4 wk.
After first trimester abortion it can be detected for up to 10 days.

The hypothalamus & pituitary gland

The pituitary gland increases in weight by 30% -50%.
The number of lactotrophs is increased and plasma
prolactin secretion is inceased progressively
throughout gestation
The secretion of other anterior pituitary hormones is
unchanged
ACTH concentrations rise during pregnancy, partly
because of placental synthesis of ACTH and of a
corticotrophin-releasing hormone (CRH) and do not
respond to normal control mechanisms.
 The adrenal gland
• Both the plasma total and the unbound cortisol and other corticosteroid
concentrations rise in pregnancy from about the end of the first trimester.
Concentrations of CBG double.

There is marked rise in secretion of the mineralocorticoid aldosterone in

pregnancy.

Plasma catecholamine concentrations fall from the first to the third

trimesters.

Thyroid
• Thryoid-binding globulin(TBG) production increased
• T3 increased
• T4 increased
• Free T4 in normal range due to increased TBG
• hCG has a direct effect on the Thryoid,
stimulating T3 and T4 production
– TSH can be decreased in early normal pregnancies
as a result of negative feedback from T3 and T4
produced due to hCG secretion

Metabolism, nutrition and weight gain in

pregnancy
• The peak energy cost is estimated at 2000 cal/day in late
pregnancy which is fairly easily met and do not require a
major adjustment of calorie intake.

• The only dietary requirements which may

need supplementation are calcium and iron.

• Average total weight gain is 12.5 kg (7-17kg).

Weight gain at around 0.5 kg/wk for the last 20 wk
fetus and placenta (5kg)
increased body fat (3-4kg)
uterus and breasts (1.5kg) blood (1 kg), ECF (1kg).

What is the effect of pregnancy on BMR?

Carbohydrate
Metabolism
• Glucose and amino acid metabolism are altered in
pregnancy to favour nutritional supply to the fetus.
The fat which is laid down in the first half of pregnancy
in the mother helps meet the demands of the fetus
later in the pregnancy when the fetus is most
demanding, metabolically.
• Progesterone stimulates appetite in the first half of
pregnancy and diverts glucose into fat synthesis.
Oestrogen stimulates an increase in prolactin release,
which, along with other hormones, generates a
maternal resistance to insulin. Maternal glucose usage
thus declines and gluconeogenesis increases,
maximising availability of glucose to the fetus.
• In later pregnancy, the mother’s energy needs are met
by metabolising peripheral fatty acids.

• Placental transport of glucose

– Facilitated diffusion
• Pregnancy increases maternal peripheral
insulin resistance after mid-pregnancy
– Mother switches to gluconeogenesis and alternate fuels
• Achieved by Human Placental Lactogen
– Also prolactin, oestrogen / progesterone, cortisol

• Decrease in fasting blood glucose

• Increase in post-meal (post-prandial) blood
glucose
Does the presence of glycosurea during pregnancy
always indicate pathology?

• Maternal insulin is a major factor in controlling the metabolic

response to pregnancy. The rate of secretion of insulin (both basal
and stimulated) normally increases as pregnancy proceeds. The
ability of pancreaticβ-cells to meet this increased demand for
insulin secretion is achieved by β-cell hyperplasia and
hypertrophy as well as the increased rate of insulin synthesis in
the β-cell.

• In some women, the endocrine pancreas is unable to respond to

the metabolic demand of pregnancy and the pancreas fails to
release the increased amounts of insulin required.

• As a consequence there is a loss of control of metabolism, blood

glucose increases and diabetes results (Gestational Diabetes).

• After birth, when the increased metabolic demands of pregnancy

are removed and hormone levels change, the endocrine pancreas
can respond adequately and the diabetes disappears. Women who
experience gestational diabetes are more likely to develop overt
diabetes later in life.
 Lipid Metabolism
• Increase in lipolysis from T2
• Increase in plasma concentration of free
fatty acids on fasting
– Free fatty acids provide substrate for
maternal metabolism, leaving glucose for the
fetus
• Increased utilisation of free fatty
acids increases the risk of
Ketoacidosis
– Combined with pregnancy’s state of
compensated
respiratory alkalosis this can be extremely bad.

Gastrointestinal
• Anatomical Changes (pressure by gravid uterus)
System
• Alterations in the positions of viscera
– E.g. appendix moves from RLQ to LUQ as the
uterus enlarges
• Physiological Changes
• Smooth muscle relaxation by Progesterone
– GI – Delayed gastric emptying, constipation
– Biliary tract – Stasis
– Pancrease – Increased risk of pancreatitis

Why is heartburn is so common during pregnancy

especially at late gestation?
Cholestasis is almost physiological during
pregnancy, how it clinically presents?

Haematology
฀ Pregnancy is a Pro-Thrombotic state
• High amount of fibrin deposition at the site
of implantation
– Increased fibrinogen and clotting factors
– Reduced anticoagulant system & fibrinolysis
• Stasis, venodilation
• Results in Thromboembolic disease in pregnancy
– Cannot give warfarin – Crosses placenta & is teratogenic

฀The total white cell count rises(mainly increased

polymorphonuclear leucocytes)
Hematology
• Plasma volume increases50%
• RBC mass also increases25% , but not to the same
degree
• So there is a state of hemodilution erroneously
called
“physiological anemia of pregnancy”.
– Not a true anaemia, just a mismatch between volume and
rbc mass.
฀ What is the lower normal value of Hb during
pregnancy?

• maternal platelet count usually remains stable

throughout pregnancy, although may be lower than in the
non-pregnant state due to increased aggregation.
Increases in the platelet count have been reported in
the first week postpartum and this may contribute to
the increased risk of thromboembolic complications
in this period
• Normal pregnancy is a hypercoagulable state .Pregnancy is
associated with a dramatic increase in the plasma
concentration of coagulation factors I, V, VII, IX, X, XII & VON
Willebrand factor

ESR rises early in pregnancy due to the increase in fibrinogen

and other physiological changes.

MCV increases secondary to erythropoiesis.

MCHCH remains stable.
Serum iron & ferritin conc decrease due to increased
utilization.
TIBC increased.
Iron requirements increased & there is a moderate
increase in iron absorption.
Serum folate decrease.
Serum vit B12 decrease due to preferential active
transport to the fetus.
there is a reduction in the concentration of protein S and
antithrombin III concentrations while protein C, which
inactivates Factors V and VIII, is probably unchanged in
pregnancy.
Plasma fibrinolytic activity is decreased during pregnancy
and labour, but returns to non-pregnant values within an
hour of delivery of the placenta, suggesting strongly that
the control of fibrinolysis during pregnancy is
significantly affected by placentally derived mediators (
plasminogen activator inhibitor II (PAI-II)).

SKIN CHANGES
Generalized hyperemia & vasodilatation of the skin with increased activity of
the sweat & sebaceous glands.
Skin pigmentation increases e.g chloasma & linea nigra
Spider naevi & palmar erythema may occur (high estrogen)

Striae gravidarum after the 20th week rapid and excessive stretching of the skin
is accompanied by breaking of the underlying connective tissue, giving rise to
the characteristic purplish depressions, these occur in the skin of the lower
abdomen, buttocks , thighs and breasts.
Striae of pregnancy are due to the increased secretion of adrenocortical
hormones which cause a decrease in the collagen and ground substance of
connective tissue and allows the subcutaneous fibrous tissue to rupture
wherever he skin is overstretched.
Following pregnancy the striae become silvery white in
appearance( striae albicans).
 REPRODUCTIVE ORGANS

Uterus: hyperplasia and hypertrophy of the myometrial cells increasing the weight of the
uterus from 50gm prepregnancy to 1000gm by term and increasing its dimensions from
approx.(7.5 *5*2.5 cm) prepregnancy to (28*24*21 cm) at term.

In early pregnancy uterine growth is the result of both hyperplasia and hypertrophy at
this stage it is independent of the growing fetus and occurs even with an ectopic
pregnancy, as gestation increases hypertrophy accounts for most of the increase in
uterine size.

With increasing gestation intercellular gap

junctions develop which allow changes in
membrane potential to spread rapidly from one
cell to another which facilitate myometrial
contraction, in the second half of pregnancy these
are painless contractions that are increasingly
apparent to the woman as pregnancy advances
(called Braxton–Hick’s contractions) and these
subsequently become the coordinated
contractions of labour.

The cervix becomes swollen and softer during pregnancy.

Estradiol stimulates growth of the columnar epithelium of the cervical canal
that becomes visible on the ectocervix called ectropion.
The cervix looks blue during pregnancy due to increased vascularity. There is a
remodeling of cervical collagen towards the end of pregnancy which aids in the
softening of the cervix.

The mucus glands of the cervix become distended and more complex and the
cervical mucus becomes viscous and opaque and fills the endocervix forming a
mucus plug, this has an abundance of leucocytes and acts as an antibacterial
and mechanical barrier.
The vaginal epithelium becomes thicker during
pregnancy with increase rate of desquamation
this leads to increased vaginal discharge
(leukorrhea) which has a more acid pH and may
protect against ascending infection.
The vagina increases in capacity and length and
becomes progressively more distensible in
preparation for delivery.

Immune
• Fetus is an allograft
System
– Genetically different to the mother
• Non-specific suppression of the local immune
response at the materno-fetal interface
• Transfer of antibodies
– IgG crosses the placenta
• Haemolytic disease
– Antibodies for ABO do not cross
– Antibodies of Rhesus do cross
• Graves disease and Hashimoto’s Thyroiditis
– Antibodies will cross the placenta and either stimulate TSH
receptors on or destroy developing fetal thyroid
respectively.

What is the effect of pregnancy on oncotic pressure

& osmotic pressure?
Pregnancy is associated with an increase in the
extravascular fluid by about two litres.
increased fluid shift into the extravascular space may
occur during pregnancy when the intra-capillary
hydrostatic pressure exceeds the opposing influence
of plasma colloid oncotic pressure (COP).
COP fell gradually during the first and second trimesters, lowest
at 30-34 weeks, thereafter it rose. The relationship of COP and
gestational age was best described by the quadratic equation.
The patterns of changes of HCT and STS with respect to
gestational age were similar to COP. MBP and M-C were linearly
correlated to gestational age. The increment in M-C with
advancing gestational age would promote fluid flux from intra to
extravascular space in normal pregnancy.