Chapter 5
Maternal Physiology I
Dr. Rebecca Brillantes
ADAPTATIONS TO PREGNANCY:
Physiological
perceived as abnormal in the nonpregnant woman
CVS changes during pregnancy normally include
in blood volume & CO, w/c may mimic
thyrotoxicosis
Can lead to ventricular failure if there is
underlying heart disease
Anatomical
Biochemical
Remarkable changes begin soon after fertilization & continue
throughout gestation & most occur in response to physiological
stimuli provided by the fetus & placenta
Can unmask or worsen pre-existing dse
Hypervolemnia of pregnancy can unmask heart disease
Changes can alter appreciably criteria for diagnosis & treatment
of disease
REPRODUCTIVE TRACT
UTERUS
Non-pregnant: almost solid structure weighing 70 g w/ a cavity of
10 ml
Pregnant: thin-walled muscular organ w/ capacity to
accommodate fetus, placenta, & amniotic fluid
End of pregnancy: uterus capacity has reached 500 1000x
greater than non-pregnant state
Total volume at term: ave ~5 L (can be 20L or more)
Organ wt: ~ 1100 g
Uterine enlargement involves the following w/c ensures that the
uterine wall is strengthened, stimulated by estrogen &
progesterone
stretching and hypertrophy of muscle cells
Limited production of new myocytes
Uterine Hypertrophy:
< 12 WEEKS pf PREGNANCY: not entirely in
response to mechanical distension by the
products of conception because similar changes
occur in ectopic pregnancy
> 12 WEEKS of PREGNANCY: in uterine size
is R/T pressure exerted by the expanding
products of conception.
20 WEEKS AOG: level of umbilicus
Stimulating HORMONES:
chiefly ESTROGEN
perhaps progesterone
accompanied by accumulation of fibrous tissue
particularly in the external mm layer
most marked in the FUNDUS
elastic tissue
Uterine Corpus: walls are considerably thicker during the first
few months of pregnancy but thin gradually as gestation
advances
By term: 1-2 cm thick
Changed into muscular sac w/ thin, soft, readily indentable
walls through w/c the fetus can be palpated
Attachment of Fallopian Tubes & the Ovarian & Round
Ligaments
EARLY PREGANCY: slightly below apex of fundus
LATE PREGNANCY: slightly above middle of the uterus
Position of Placenta
Influences the extent of uterine hypertrophy in that the
portion of the uterus surrounding the placental site enlarges
more than the rest
placenta implants at the fundus; hence, fundus has the
most enlargement
Arrangement of Muscle Cells
Uterine muscles arranged in 3 layers:
OUTER HOOLIKE LAYER:
arches over fundus & extends into the various
ligaments
MIDDLE LAYER:
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Vascular refractoriness to pressor effects of angiotensin II
serves to increase uteroplacental blood flow
Endothelial cells secrete Nitric oxide: or endothelium
derived relaxing factor; vasodilator released by
endothelial cells; abnormal synthesis linked to
development of preeclampsia.
CERVIX
Undergoes softening and cyanosis due to increased vascularity &
edema, hypertrophy & hyperplasia of cervical glands
Soft d/t edema
Cyanosis during speculum examination
Endocervical glands are hypertrophied & hyperplastic w/c
produces tenacious mucus
Endocervical mucosal cells produce copius tenacious mucus rich
in immunoglobulins & cytokines that act as an immunological
barrier to protect the uterine contents against infection coming
from the vagina into the intrauterine environment. During cervical
dilation, blood may get admixed w/ mucous creating bloody
show.
Bloody show: expulsion of mucus plug before or at onset of
labor. Can occur 2 or 3 weeks before onset of labor
especially for primiparas.
Beading: crystallization of cervical mucus, result from
presence of progesterone.
Ferning: arborization of the crystals, result of amniotic fluid
leakage. On assessment is cervical mucus is admixed w/
amniotic fluid
PAPS SMEAR: screening tool for cervical cancer for every
sexually active woman annually. Result in pregnancy is less than
optimal; hence, difficult to identify CA cells during pregnancy.
Arias Stella Reaction: endocervical gland hyperplasia &
hypersecretory
Estrogen induces basal cells near the squamocolumnar junction
to undergo changes in size, shape and staining qualities hence
pap smear in pregnant woman is less-than-optimal
OVARIES:
Ovulation ceases; maturation of new follicles suspended
Only a single corpus luteum can be found in pregnant women
Corpus luteum functions maximally during first 6 to 7 weeks (4 to
5 weeks postovulation) thereafter contributes little to progesterone
production
Progesterone is important for maintenance of pregnancy on
1st 7 wks
If corpus Luteum is removed before 6-7 wks: ABORTION
After 6-7 wks, placenta takes over the production of
progesterone
Decidual reaction on & beneath surface may be observed
Decidual reaction also occurs in ovaries & fallopian tubes
Ovarian vascular pedicle increases in diameter
Generalized vasodilatation
Clinical significance: wait postpartum when doing any
surgery because if you do surgery on a pregnant woman,
there is increased blood loss w/ dilated blood vessels
Relaxin:
Secreted by heart, brain & kidney
secreted by corpus luteum, decidua, placenta
protein hormone similar to insulin & insulin-like GF I & II
major biological action: remodelling of CT of reproductive
tract especially the cervix; implicated in pre-term birth due to
effect on myometrial contractility.
2 OVARIAN CYSTS ASSOCIATED W/ PREGNANCY: benign,
can cause maternal virilisation
Luteoma of pregnancy:
solid ovarian tumor
exaggerated luteinisation reaction of the ovary
regress after delivery but may recur
androgen secreting; hence, may result in maternal
virilisation (mother looks like a male d/t high androgen
content) but not the fetus because of the protective
role of the placenta w/c converts androgens to
estrogen.
Theca-Lutein Cyst:
cystic, benign ovarian lesion due to exaggerated
physiological follicle stimulation (hyperreactio
luteinalis)
usually bilateral.
Associated with markedly elevated serum HCG
found in
GTD
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Physiologic OB
METABOLIC CHANGES:
By 3rd trimester, maternal BMR increases by 10-20%
weight gain in pregnancy is attributable to the uterus & its
contents, the breast, increased blood volume, increased
extravascular extracellular fluid and increased cellular water &
deposition of new fat & protein (maternal reserves); average of
12.5 kg (27.5 lbs)
Water metabolism:
Increased water retention due to a fall in plasma
osmolality demonstrated as pitting edema of ankles & legs
Resetting of osmotic threshold for thirst & vasopressin
secretion fall in plasma osmolality edema ankles &
legs
Decrease in interstitial colloid osmotic pressure favors
edema
Edema also attributed to compressing effect of heavy uterus
on blood vessels thereby obstructing venous return on vena
cava, hence edema most prominent at the end of the day
Pitting edema of the ankles
Minimum amount of extra water accrued during pregnancy =
6.5 L (water contents of the fetus, placenta, amniotic fluid,
increase in the maternal blood volume & in the size of the
uterus & breast)
Maternal body water rather than fat contributes more to
infant birthweight.
Protein Metabolism:
products of conception, uterus, maternal blood are rich in
protein
At term:
Fetus + placenta =
500 g
Uterus (contractile Protein)
Breast (glands) =
500 g
Maternal blood (hgb & plasma) -------------total
1000 gram
nitrogen balance increased with gestation suggesting a
more efficient use of dietary protein
amino acid concentrations higher in the fetal than in
the maternal compartment
Pregnancy is associated with nitrogen conservation,
because we need protein to supply the demands of
fetal growth
Breakdown of maternal muscle is not required to meet
demands of growing maternal & fetal tissue, unlike in
calcium
Carbohydrate metabolism:
Normal pregnancy is characterized by mild fasting
hypoglycemia, post prandial hyperglycemia and
hyperinsulinemia
Pregnancy induces a state of peripheral resistance to insulin
to ensure sustained supply of glucose to the fetus; mediated
by E & P (estrogen and progesterone)
Increased plasma levels of:
placental lactogen: aid in insulin resistance, a protein
hormone with growth hormone-like action that
increases lipolysis with liberation of free fatty acids
thereby increasing tissue resistance to insulin
Accelerated starvation: pregnancy induced switch in fuels
form glucose to lipids during fasting, as evidence by higher
plasma concentrations of FFA, triglycerides and cholesterol
Can occur in early labor where patient is NPO
Prevented by administering D5W fluids
When fasting is prolonged in the pregnant woman,
ketonemia rapidly appears
Fat metabolism:
Plasma lipids, lipoproteins, and apolipoproteins increase
Storage of fat occurs at midpregnancy; fat is deposited in
central rather than peripheral sites
It becomes available for placental transfer during 3rd
trimester
Progesterone hypothalamic lipostat energy storage
(protects mother & fetus)
Maternal Hyperlipidemia
As fetal nutritional demands increase, maternal fat storage
decrease
Lactation increases fat loss
LDL-C & HDL-C increase believed to be mediated by
estrogens & progesterone
Lactation speeds the rate of fat decrease
Leptin & Ghrelin: a peptide hormone secreted by adipose
tissue and placenta; role in body fat regulation and energy
expenditure; increased during pregnancy, help regulate fetal
growth
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Physiologic OB
Leukocyte alkaline phosphatise which is seen in a wide variety of
conditions i.e. inflammatory state, is increased.
C-reactive protein, ESR elevated thus cannot be used reliably to
diagnose inflammation during pregnancy
Complement factors C3 & C4 also significantly elevated.
Cervical mucus increase:
COAGULATION
(contraceptive pill create the same effect; hence, risk for
thromboembolism during surgery)
In activated state
Increased concentrations of all clotting factors, except XI & XIII
Percentage of high molecular weight fibrinogen is unchanged
resulting to increase ESR
Clotting time same
Platelet count decreases slightly due to hemodilution but may also
be due to increased platelet consumption hence greater
proportion of younger, larger platelets
Thromboxane A2
which induces platelet aggregation
progressively increases
Fibrinolytic activity reduced due to increased plasminogenactivator inhibitors
Antithrombin levels are constant.
REGULATORY PROTEINS
Inhibitors of coagulation decreased during pregnancy
SPLEEN
Enlarge by 50 %
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Physiologic OB
CHAPTER 5
Maternal Physiology II
Dr. Rebecca Brillantes
CARDIOVASCULAR SYSTEM
Most important changes in cardiovascular function occur in
1st 8 weeks of pregnancy
CO as early as 5th week HR & systemic vascular
resistance
Ventricular performance influenced by systemic vascular
resistance & changes in pulsatile arterial flow
Vascular Capacity: d/t vascular compliance d/t
restructuring of bv walls
Systemic Vascular resistance + increased HR =
increased CO
preload due to plasma volume at 10 to 20 weeks
Resting pulse rate by 10 beats/min
CVS
Cardiac Output
HR
Systemic Vascular
Resistance
Vascular Capacity
Vascular
Compliance
Preload
Plasma Volume
Arterial BP
RAAS
PGE2
PGI2
ANP
Unchanged
HEART
Diaphragm progressively elevated
Displaced to the left & upwards & rotated on its long
axis
CXR: Increase in size of cardiac silhouette in
radiographs
Heart apex is moved somewhat laterally from its
usual position d/t elevated of diaphragm displaces
heart to the left & upwards on its axis
With some degree of BENIGN PERICARDIAL
EFFUSION adding to increase silhouette (difficult to
identify moderate cardiomegaly)
ECG: slight L axis deviations
Why do you think this is a physiologic
phenomenon in a pregnant patient?
Its not pathologic
d/t alteration and rotation of the heart
On ECG, you can pick it up b/c there is a
slight left axis deviation
Altered cardiac sounds:
Murmurs: NORMAL or does not necessarily
point out as cardiac pathology especially when
auscultating by the chest or breast, you might end
up auscultating the vein and mistake it as
murmurs.
Exaggerated splitting of S1 w/ loudness of both
components
No definite changes in the aortic & pulmonary
elements of the S2
Loud, easily heard S3
90% Systolic murmur heard thats intensified
during inspiration or expiration & disappears
shortly after delivery
20% Soft Diastolic Murmur
10% Continuous Murmurs arising from breast
vasculature
Little change in inotropic state of the myocardium
Greater CO in Multifetal pregnancies because of
greater stroke volume & HR
Sustained cardiac changes similar to acute changes in
moderate to strenuous exercise
Normal pregnancy: arterial blood pressure & vascular
resistance while basal metabolic rate
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Physiologic OB
Tendency toward stagnation of blood in the LE
d/t occlusion of pelvic veins & IVC thus:
Dependent edema
Varicose veins in legs & vulva
Haemorrhoids
DVT
SUPINE HYPOTENSIVE SYNDROME
Large pregnant uterus compress venous system
that returns blood from the lower half of the body
causing arterial hypotension
Uterine arterial pressure decreased > blood flow
decreased > fetal HR pattern
Also occurs in Hge & spinal anesthesia
RAAS
Intimately involved
High level of estrogen: angiotensinogen
production by maternal & fetal liver
RESPIRATORY TRACT
Diaphragm rises 4 cm
Subcostal angle widens as transverse diameter of thoracic
cage increases ~ 2 cm
Thoracic circumference about 6 cm but not significantly
to prevent a reduction in the residual lung volume created
by elevated diaphragm
Increased in RMV is caused by:
Enhanced respiratory drive d/t stimulatory effect
of progesterone
Low expiratory reserve volume
Compensatory respiratory alkalosis
PULMONARY FUNCTION
Pulmonary
FUNCTION
Respiratory rate
Tidal Volume
Resting Minute
ventilation
FRC
Residual Volume
Peak expiratory
flow rate
Lung Compliance
Airway
Conductance
Total Pulmonary
Resitance
Maximum
Breathing Capacity
Forced or Timed
Vital Capacity
Oxygen
Requirements
Critical Closing
Volume
Unchanged
OXYGEN DELIVERY
Unchanged
Oxygen delivery
Amount of Oxygen
Delivered into the
Lungs
Total Hgb Mass
Total O2-carrying
capacity
CO
Maternal
Arteriovenous O2
Difference
ACID-BASE EQUILIBRIUM
Acid-Base
Equilibrium
Desire to breathe
PCO2
Plasma HCO3
Blood pH
2,3 DPG
(compensatory)
Unchanged
GIT
Gastric Emptying
Time
(pregnancy)
Gastric Emptying
Time
(labor)
Lower Esophageal
Sphincter Tone
Intraesophageal
Pressure
Intragastric Pressure
Esophageal
Peristalsis wave
speed & amplitude
Unchanged
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Physiologic OB
LIVER
Total serum alkaline phosphate activity almost
doubles mostly d/t heat stable placental alkaline
phosphatase isoenzymes
Decrease in serum albumin to 3.0 (N: 4.3g/dL)
Decrease albumin-globulin ratio similar to that seen in
hepatic diseases
Leucine Aminopeptidase is usually increased in liver
disease but is normally increased in pregnancy
LIVER
Liver Size
Hepatic Blood Flow
Portal Vein Diam
Alkaline Phosphatase
AST
ALT
GGT
Bilirubin
Serum Albumin
Total Albumin
Serum Globulin
Leucine
Aminopeptidase
Unchanged
GALLBLADDER
GALLBLADDER
Contractility
Residual Volume
Bile cholesterol
saturation
Unchanged
URINARY SYSTEM
KIDNEY
KIDNEY
Size
GFR
Renal Plasma Flow
early
Unchanged
late
RENAL FUNCTION
Renal Function
Serum Creatinine
Creatine Clearance
Bile cholesterol
saturation
Unchanged
Unchanged
Mucosa
Blood vessels
Bladder
Bladder Capacity
Urethral length
Intraurethral
Pressure
Bladder pressure (8 cm H2O to 20 cm H2O) w/c is
assessed via URETHROCYSTOMETRY
Urethral length to compensate for reduced bladder
capacity
Maximal intraurethral pressure increased from 70 to
93 cm H2O, and thus continence is maintained.
Half of women experience some degree of urinary
incontinence by the third trimester w/c is always
considered in the differential diagnosis of ruptured
membranes.
Toward the end of pregnancy in nulliparas, entire
base of the bladder is pushed forward and upward,
converting the normal convex surface into a
concavity.
The pressure of the presenting part impairs the
drainage of blood and lymph from the bladder base,
often rendering the area edematous, easily
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Physiologic OB
traumatized, and probably more susceptible to
infection.
ENDOCRINE SYSTEM
PITUITARY GLAND
Enlarges to 135%
Can compress the optic chiasma & reduce visual
fields
Decreased calcium & magnesium stimulates increase
in parathyroid
Maternal pituitary gland is not essential for
maintenance of pregnancy
GROWTH HORMONE
produced by maternal pituitary as well as by the
placenta,
GH in fetal circulation is not a major regulator of
fetal growth: placental GH correlates more to
fetal growth rate
PROLACTIN
markedly increased; 150 ng/mL at term
decrease after delivery even in breastfeeding
women
pulsatile bursts occur in response to suckling
estrogen stimulation increases the number of
anterior pituitary lactotrophs and may stimulate
their release of prolactin
Thyroid-releasing hormone also acts to cause an
increased prolactin level in pregnant compared
with nonpregnant women, but the response
decreases as pregnancy advances
Serotonin also is believed to increase prolactin
Dopaminepreviously known as prolactininhibiting factorinhibits its secretion.
Principal function: ensure lactation.
Early in pregnancy, prolactin acts to initiate
DNA synthesis and mitosis of glandular
epithelial cells and presecretory alveolar
cells of the breast.
Prolactin also increases the number of
estrogen and prolactin receptors in these
cells.
Prolactin promotes mammary alveolar cell
RNA synthesis, galactopoiesis, and
production of casein, lactalbumin, lactose,
and lipids
Prolactin is present in amnionic fluid in high
concentrations
Levels of up to 10,000 ng/mL are found at
20 to 26 weeks.
Decrease and reach a nadir after 34 weeks.
Uterine decidua is the site of prolactin
synthesis found in amnionic fluid
Prolactin impairs water transfer from the
fetus into the maternal compartment, thus
preventing fetal dehydration.
THYROID GLAND
Thyroidal stimulatory factors of placental origin
produced in excess
production of thyroid hormones by 40 to 100 % to
meet maternal and fetal needs
Undergoes moderate enlargement during pregnancy
caused by glandular hyperplasia and vascularity.
Mean thyroid volume from 12 mL in the 1st trimester
to 15 mL at delivery.
1st trimester:
principal carrier proteinthyroxine-binding
globulin:
& reaches its zenith at about 20 weeks
stabilizes at approximately double baseline
values for the remainder of pregnancy. d/t
estrogen
Total serum thyroxine (T4)
sharply beginning 6 and 9 weeks and
reaches a plateau at 18 weeks.
Free serum T4
levels slightly and peak along with hCG
levels, and then they return to normal.
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Physiologic OB
The calcitonin-secreting C cells are derived
embryologically from the neural crest and are
located predominantly in the perifollicular areas
of the thyroid gland.
Calcium and magnesium increase the
biosynthesis and secretion of calcitonin. Various
gastric
hormonesgastrin,
pentagastrin,
glucagon,
and
pancreozyminand
food
ingestion also increase calcitonin plasma levels.
actions oppose those of parathyroid hormone
and vitamin D to protect skeletal calcification
during times of calcium stress.
Pregnancy and lactation cause profound calcium
stress, and during these times, calcitonin levels are
appreciably higher than those in nonpregnant women
Vitamin D and Calcium
After its ingestion or synthesis in the skin,
vitamin D is converted by the liver into 25hydroxyvitamin D3.
This form then is converted in the kidney,
decidua, and placenta to 1,25-dihydroxyvitamin
D3, serum levels of which are increased during
normal pregnancy.
Although its control is unclear, the conversion of
25-hydroxyvitamin D3 to 1,25-dihydroxyvitamin
D3 is facilitated by parathyroid hormone and by
low calcium and phosphate plasma levels and is
opposed by calcitonin.
ADRENAL GLANDS
In normal pregnancy, the maternal adrenal glands
undergo little, if any, morphological change.
Cortisol
The serum concentration of circulating cortisol is
increased, but much of it is bound by
transcortin, the cortisol-binding globulin.
The rate of adrenal cortisol secretion is not
increased, and probably it is compared with
that of the nonpregnant state.
The metabolic clearance rate of cortisol,
however, is lower during pregnancy because its
half-life is nearly doubled over that for
nonpregnant women
Administration of estrogen, including most oral
contraceptives, causes changes in serum cortisol
levels and transcortin similar to those of
pregnancy
During early pregnancy, the levels of circulating
corticotropin (ACTH) are reduced strikingly. As
pregnancy progresses, the levels of ACTH and
free cortisol rise.
Higher free cortisol levels observed in pregnancy
are the result of a "resetting" of the maternal
feedback mechanism to higher levels.In response
to elevated progesterone levels during
pregnancy, an elevated free cortisol is needed to
maintain homeostasis.
Aldosterone
As early as 15 weeks, the maternal adrenal
glands secrete considerably increased amounts
of aldosterone.
third trimester, about 1 mg/day is secreted. If
sodium intake is restricted, aldosterone
secretion is elevated even further
renin and angiotensin II substrate normally are
increased, especially during the latter half of
pregnancy. This scenario gives rise to increased
plasma levels of angiotensin II, which by acting
on the zona glomerulosa of the maternal adrenal
glands, accounts for the markedly elevated
aldosterone secretion.
increased aldosterone secretion during normal
pregnancy affords protection against the
natriuretic effect of progesterone and atrial
natriuretic peptide.
Deoxycorticosterone
MUSCULOSKELETAL SYSTEM
compensatory lordosis shifts the center of gravity back over
the lower extremities
Sacroiliac, sacrococcygeal & pubic joints have increased
mobility contributing to alteration in posture, in turn to
lower back discomfort
Aching, numbness & weakness in the upper extremities
result from marked lordosis with anterior neck flexion &
slumping of the shoulder girdle causing traction on ulnar
& median nerve
Relaxation of pelvic bones & ligaments particularly the
Symphysis pubis.
EYES
Intraocular pressure decreases due to increased vitreous
outflow
Corneal sensitivity decreases
greatest changes are late in gestation.
Most pregnant women demonstrate a measurable but slight
increase in corneal thickness, thought to be due to edema.
may have difficulty with previously comfortable contact
lenses.
Brownish-red opacities on the posterior surface of the
corneaKrukenberg spindles
Hormonal effects similar to those observed for skin lesions
are postulated to cause this increased pigmentation.
transient loss of accommodation reported with both
pregnancy and lactation, visual function is unaffected by
pregnancy.
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Physiologic OB
CNS
Transient pregnancy related memory decline seen in the 3 rd
trimester
Difficulty going to sleep, frequent awakenings, fewer hours
of sleep, reduced sleep efficiency
Greatest sleep disruption occurs post-partum and may
contribute to pospartum blues.
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