Physiologic OB

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:

Reference: WILLIAMS OBSTETRICS 23rd Edition

Composed of a dense network of mm fibers

perforated in all directions by blood vessels
Main portion of the uterine wall
consists of a network of vessels & mm cells
Each cell has a double curve so that the
interlacing of 2 muscles forms a figure of eight;
when muscle cells contract they constrict the
penetrating blood vessels
INTERNAL LAYER:
w/ sphincter-like fibers around the fallopian tube
orifices & internal os of the cervix
Uterine Size, Shape & Position
< 12 WEEKS:
PEAR shaped
Pelvic organ
> 12 WEEKS:
Corpus & Fundus: GLOBULAR form to SPHERICAL
Organ more rapidly in length than width & assumes
an OVOID shape
Abdominal organ
Displaces intestines laterally and superiorly, & rises
almost to the liver
As uterus ascends from the pelvis, it rotates to the
RIGHT
Rectosigmoid is at the left of pelvic cavity; hence,
when the uterus enlarges, it tends to rotate to the
right: DEXTROROTATION
Tension is exerted on the broad & round ligaments
Contractility
BRAXTON HICKS CONTRACTIONS:
sporadic, nonrhythmic uterine contractions, may
account for false labor
2nd Trimester: detected by bimanual examination
Varies from 5 25 mmHg
Initially infrequent but during the last 1-2 weeks of
pregnancy
May occur every 10-20 minutes & become
rhythmic , intense & synchronized at term
Uteroplacental Blood Flow
MOTHER IN SUPINE: enlarged uterus can compress the
great vessels, esp. Inferior vena cava & aorta
Uterine arteries are branches of the aorta w/c can be
compressed when mother is in supine; hence,
uteroplacental blood flow is affected with maternal
position
Delivery of substances for fetal growth & metabolism and
removal of metabolic wastes depend on adequate
uteroplacental perfusion, which is dependent on total uterine
blood flow from the uterine and ovarian arteries
Uterine veins has reduced elastin content & adrenergic
nerve density resulting to increased venous caliber and
distensibility thereby increasing uteroplacental blood flow
AT TERM: 450-650 mL
Regulation of Uteroplacental Blood Flow
MATERNAL-PLACENTAL BLOOD FLOW thru
vasodilatation
FETAL-PLACENTAL BLOOD FLOW by growth of
placental vessels.
Uterine artery diameter doubles by 20 wks w/ mead
Doppler velocimetry 8-fold
d/t estradiol & progesterone stimulation
Uteroplacental perfusion, other than maternal position,
is also affected by relationship of blood vessels to your
mms, when uterus is in contraction, it decreases blood
flow to the baby.
Uterine contraction can obliterate blood flow to the
baby; hence depriving fetus from blood flow:
TACHYSYSTOLE if sustained
Contaction should be no longer than 40-60 secs
otherwise will lead to fetal compromise
INCREASED UTEROPLACENTAL PERFUSIONIS BROUGHT
ABOUT BY:
Increased distensibility: Vasodilatation is mediated
principally by estrogen and progesterone

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Physiologic OB
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

Reference: WILLIAMS OBSTETRICS 23rd Edition

large placenta i.e. DM, D-issoimmunization,

multiple fetusus;
chronic renal failure and in hyperthyroidism,;
usually asymptomatic but may cause abdominal
pain and maternal virilization; spontaneously
resolves after delivery
In uncomplicated pregnancy change from exaggerated
ovarian response to Normal hCG
FALLOPIAN TUBES:
Musculature undergoes little hypertrophy
flattening of tubal mucosa epithelium
stromal decidual cells may develop.
VAGINA & PERINEUM
Chadwick Sign: increased vascularity w/ resultant violet color
Hyperemia
Softening of the underlying abundant
Vaginal walls increase in mucosal thickness, assume hobnail
appearance; with hypertrophy of smooth muscle cells, loosening
of CT in preparation for distension during labor
Hyperaemia in skin and muscles of perineum and vulva with
softening of connective tissue
Acidic pH due to increased lactic acid production from glycogen
in the vaginal epithelium
Histopath of vaginal epithelial cells same as Luteal phase
Navicular cells: small intermediate cells seen in pap smear;
ovoid cells with vesicular elongated nucleus
Naked nuclei: vesicular nuclei without cytoplasm seen with
an abundance of lactobacillus.
Areolar and genital pigmentation may be accentuated but
disappear or regress after delivery
Oral Contraceptives produce similar pigmentation
MSH elevated: Estrogen & Progesterone are reported to have
melanocytes stimulating effects
Changes in preparation from distention during labor & delivery
Increase mucosal thickness
Loosening of the CT
Hypertrophy
SKIN:
increased cutaneous blood flow in pregnancy serves to dissipate
heat d/t increased BMR
Abdominal wall:
Striae gravidarum: stretch marks, reddish, slightly
depressed streaks in the skin of the abdomen, breasts and
thighs; previous striae appear glistening or silvery
Diastasis recti: rectus muscle separate in the midline
because the abdominal walls cannot withstand the tension
to which they are subjected
HYPERPIGMENTATION
Linea nigra: linea alba becomes markedly pigmented
Chloasma/melasma gravidarum: mask of pregnancy
irregular brownish patches on the face and neck. Lightens or
disappears following delivery
Areolar & genital pigmentation maybe accentuated but
disappear or regress after delivery d/t melanocyte
stimulating effects of estrogen & progesterone & melanin
stimulating hormone is increased during pregnancy
Oral Contraceptives pro hyperpigmentation
Vascular spiders:
minute, red elevations on arms, the skin of face, neck, upper
chest; with radicles branching out from a central lesion,
designate as nevus, angioma, telangiectasis
Palmar erythema:
of no clinical significance
disappear after pregnancy
most likely due to hyperestrogenemia.
BREASTS:
Breast tenderness and tingling
Increase in size, veins become prominent
Areola becomes broader, more pigmented
Nipple enlarges, more deeply pigmented and erectile
Colostrum: a thick yellowish fluid expressed from the nipples
Glands of Montgomery: hypertrophic sebaceous glands seen
scattered through the areola
Gigantomastia: extensive pathologic breast enlargement that
may be life threatening & require surgical intervention
Pregnancy breast size and volume of milk production do not
correlate.

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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

Reference: WILLIAMS OBSTETRICS 23rd Edition

Electrolyte and mineral metabolism:

Na & K: excretion near nonpregnant range
1000 mEq Na & 300 mEq K retained
Conc in serum is still less d/t expanded plasma hence
conc appears like nonpregnant state
Serum Ca decrease; 200 mg deposited in fetal skeleton/day
rd
in 3 trimester (fetus imposes a significant deman on
maternal calcium homeostasis. This demand is largely met
doubling of maternal intestinal Ca absorption mediated by 1,
25 dihydroxyvitamin D3)
Ionized Ca the same
Mg: decreases
PO2: within nonpregnant range
Fe: increased requirements:
Normal: 2-2.5 g adult, 300 mg young
300 mg: actively transferred to fetus & placenta :
obligatory
200 mg: lost thru excretion in the GIT: obligatory
500 mg: used in creased circulating erythrocytes of
450 ml (1ml RBC contains 1.1 mg Fe)
1000 mg total pregnancy requirement
Obligatory losses occur even when mother is Fe deficient
Amount of Fe from diet together with that mobilized from
stores is insufficient to meet pregnancy demands hence
supplementation. Fe requirement at midpregnancy is 6-7
mg/ day
HAEMATOLOGICAL CHANGES:
Blood volume
Physiologic hypervolemia d/t increase in plasma &
erythrocytes but more plasm leading to hemodilution
Increases beginning 1st trimester, expands most
rapidly in 2nd trimester, slower rate in the 3rd;
expansion results from increase in both plasma &
erythrocytes; plasma increase greater than erythrocyte
increase
Moderate bone marrow erythroid hyperplasia
Reticulocyte count slightly elevated (related to
increased plasma erythropoietin)
Functions of pregnancy; induced hypervolemia:
To meet demands of enlarged uterus with its greatly
hypertrophied vascular system
To protect mother and in turn the fetus vs. The
deleterious effects of impaired venous return in the
supine & erect positions
To safeguard the mother vs. Adverse effects of blood
loss /w parturition.
Hemoglobin: decrease slightly together with hematocrit d/t
increase in plasma thus whole blood viscosity decreases;
average: 12.5 g/dL at term
Hgb concentration below 11g/dL especially late in
pregnancy should be considered abnormal & usually due to
iron deficiency rather than hypervolemia: ANEMIA
Blood loss:
Bleeding form implantation site, episiotomy/lacerations,
lochia;
Must supply iron
Average: 500 mL for singleton NSD (normal spontaneous
delivery): 1000 mL for twins/CS (caesarean section)
IMMUNOLOGICAL & LEUKOCYTE FUNCTION:
suppressed humoral & cell mediated immunological functions to
accommodate the foreign semiallogenic fetal graft
Suppressed T-helper and T-cytotoxic cells decreases secretion of
interleukin-2, interferon-Y, tumor necrosis factor Beta
May explain pregnancy-related remission of some
autoimmune disorders (RA, MS, & autoimmune thyroiditis)
Interferon-alpha is absent
Depressed PMN leukocyte chemotaxis & adherence functions
account for increased susceptibility to infections
Leukocyte count = 5000 to 12 000 / uL, may rise even more
during labor & early puerperium (cause unknown)
If levels are in a non-pregnant woman: severe infection or
sepsis
Normal in pregnancy especially w/vigorous labor; hence,
physiologic
Inflammatory markers are unreliable d/t intrinsically elevated
Leukocyte alkaline phosphatase
CRP
ESR
Complement factors C3 & C4

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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 %

Reference: WILLIAMS OBSTETRICS 23rd Edition

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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

Reference: WILLIAMS OBSTETRICS 23rd Edition

CO in late pregnancy higher in lateral recumbent

position than supine, increase is lost soon after
delivery
IMPORTANT: Blood flow in the legs is retarded with
tendency toward stagnation of blood in the lower
extremity leading to:
dependent edema
varicose veins
haemorrhoids.
Supine hypotensive syndrome:
large pregnant uterus compresses venous system
that returns blood from the lower half of the body
causing arterial hypotension.
All components of the renin-angiotensin-aldosterone
system important in blood pressure maintenance are
angiotensinogen production in fetal & maternal liver
are a result of estrogen level during pregnancy
Normal nulliparas who remained normotensive were
refractory to the pressor effects of Angiotensin II,
those destined to be hypertensive lose this
refractoriness
CARDIAC NATRIURETIC PEPTIDES
ANP: non preganant range despite plasma
volume; ANP-induced physiological adaptations
participate in the expansion of plasma volume
BNP
CNP
PROSTAGLANDINS
Increased PG serves to control vascular tone,
blood pressure & Na balance
PG E2: elevated, presumed natriuretic
PGI2: increased
Prostacyclin (PGI2), the
principal prostaglandin of endothelium, also is
increased during late pregnancy and regulates
blood pressure and platelet function.
Implicated in the angiotensin resistance
characteristic of normal pregnancy.
Ratio of PGI2 to thromboxane in maternal
urine and blood has been considered
important
in
the
pathogenesis
of
preeclampsia
ENDOTHELINS
Endothelin-1: potent vasoconstrictor produced in
endothelial & vascular smooth mm cells &
regulates local vasomotor tone
Production is influenced by:
angiotensin II
AVP
Thrombin
Influence secretion of:
ANP
Aldosterone
catecholamine
Endothelin receptors present in pregnant &
nonpregnant myometrium
Vascular sensitivity to endothelin-1 is not altered
during normal pregnancy
Identified in:
Amnion
amniotic fluid
decidua
placental tissue
NITRIC OXIDE
Potent vasodilator released by endothelial cells
Important for modifying vascular resistance
during pregnancy
Abnormal NO synthesis has been linked to the
development of PREECLAMPSIA
PREGNANCY INDUCED HYPERTENSION:
usually comes in during 2nd trimester
Circulation & BP
BP is lower in lateral recumbent than supine
In supine position: femoral venous pressure rises
steadily, venous flow in the legs is retarded

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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

Increased awareness of a desire to breath interpreted as

dyspnea, w.c may suggest pulmonary or cardiac
abnormalities when none exist: PHYSIOLOGIC
DYSPNEA
d/t tidal volume that lowers PCO2 slightly, w/c
paradoxically causes dyspnea
induced largely by progesterone & to a lesser degree
by estrogen
PROGESTERONE
Act centrally, lowers the threshold & the sensitivity
of the chemoreflex response to CO2
Progesterone (estrogen)
centrally threshold &
sensitivity of chemoreflex response to CO2 (resetting
of sensitivity to CO2)
TV (d/t greater
diaphragmatic excurtion)
physiologic dyspnea
(paradoxic: want to breathe some more)
blood
PCO2 (respiratory alkalosis)
HCO3
BOHR
effect but is counter acted by 2,3 DPG w/c cause
release of O2
Aids CO2 transfer from fetus to
mother & O2 release to fetus
Bohr effect: shift to the left d/t increased affinity
of maternal Hgb for O2 thereby decreasing the
O2 releasing capacity of maternal blood
Increased 2,3 DPG in maternal erythrocytes
counteracts the Bohr effect, facilitating O2
release of the fetus.
Respiratory Disease become more serious during Gestation
GASTROINTESTINAL TRACT & ACCESSORY ORGANS

Functional residual capacity & residual volume

decreased as a consequence of the elevated diaphragm
Peak expiratory flow rates decline progressively w/
increased AOG
Total pulmonary resistance d/t progesterone

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

Reference: WILLIAMS OBSTETRICS 23rd Edition

GIT
Gastric Emptying
Time
(pregnancy)
Gastric Emptying
Time
(labor)
Lower Esophageal
Sphincter Tone
Intraesophageal
Pressure
Intragastric Pressure
Esophageal
Peristalsis wave
speed & amplitude

Unchanged

Appendix displaced upward & laterally & can reach the

right flank
Gastric emptying time unchanged except after analgesia at
labor
MAJOR DANGER: regurgitation & aspiration of
either food-laden or highly acidic gastric contents
Pyrosis (heartburn)
d/t reflux of acid secretions into the lower esophagus
Contributing Factors:
altered position of the stomach
lower esophageal sphincter tone
intraesophageal pressure
intragastric pressure
esophageal peristaltic wave speed & amplitude
Epulis:
focal highly vascular swelling of gums rendering them
hyperaemic, softened & bleed when mildly
traumatized,; spontaneously regress after pregnancy
Hemorrhoids:
caused by constipation & elevated pressure in veins
below the uterus.

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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

reduced contractility leads to stasis hence increased

prevalence of gallstones especially in multigravids
Progesterone GB contraction by inhibiting
cholecystokinin-mediated
smooth
muscle
stimulation w/c is the primary regulator of GB
contraction
Propensity to retained bile salts causing pruritus
gravidarum
Intrahepatic Cholestasis linked to circulating
estrogen w/c inhibit intraductal transport of bile acids

URINARY SYSTEM
KIDNEY
KIDNEY
Size
GFR
Renal Plasma Flow

early

Unchanged

late

Slight increase in kidney size: 1.5 cm longer

GFR 25% by 2nd week after conception & 50% by
2nd trimester
~ 60% of women report urinary frequency
Along w/ renal plasma flow, it is mediated by
relaxin & neuronal NO synthase
Kallikrein
tissue protease synthesized in cells of the distal
renal tubule
increased in several conditions associated with
increased glomerular perfusion in nonpregnant
individuals
increased urinary kallikrein excretion rates in
women at 18 and 34 weeks, but excretion
returned to nonpregnant levels by term.
Late in pregnancy, urinary flow and sodium
excretion average >1/2 the excretion rate in the
supine position compared with that in the lateral
recumbent position. The impact of posture on
glomerular filtration and renal plasma flow is
much more variable
LOSS OF NUTRIENTS
Amino acids & water-soluble vitamins are lost in the
urine in much greater amounts

Reference: WILLIAMS OBSTETRICS 23rd Edition

RENAL FUNCTION
Renal Function

Serum Creatinine
Creatine Clearance

Bile cholesterol

saturation

Unchanged

SERUM CREATININE: 0.7 to 0.5mg/dL

If 0.9 mg/dL, it suggests underlying renal disease
Creatinine Clearance
30% than the 100-115 mL/min in
nonpregnants
Estimate renal function
During the DAY: accumulate water as
DEPENDENT edema
During the NIGHT: mobilization of fluid: nocturia
Urine is more dilute than nonpregnant
Failure to excrete concentrated urine after 18 hrs of
withholding fluids does not signify renal damage
URINALYSIS
GLUCOSURIA:
Not necessarilty abnormal but should not be
ignored d/t
GFR & Impaired tubular reabsorptive
capacity for filtered glucose
PROTENURIA:
slight amounts during or soon after vigorous
labor
albumin excretion from 5 to 30 mg/day, can also
increase w/ preeclampsia
HEMATURIA:
Often Suggest UTI
Common after difficult labor & delivery
URETERS
Ureteral dilatation greater on the right side in 86% d/t
cushioning of sigmoid on (L) ureter
greater compression on right ureter as the
consequence of dextrorotation of the uterus
dilated R ovarian vein complex lying obliquely
over R ureter
dilatation likely d/t Progesterone
Elongation accompanies dilatation & is often thrown
into curves: KINKS
BLADDER
Bladder trigone elevated & thickening of the posterior
or intrauterine margin d/t
uterine size
Hyperaemia that affects all pelvic organs
Hyperplasia of the bladders mm & CT
Urinary Bladder

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.

Reference: WILLIAMS OBSTETRICS 23rd Edition

total triiodothyronine (T3) is more pronounced

up to 18 weeks, and thereafter, it plateaus.
Thyroid-releasing hormone (TRH)
levels are unchanged during normal
pregnancy, but this neurotransmitter does
cross the placenta and may serve to
stimulate the fetal pituitary to secrete
thyrotropin
Approximately a third of women experience
relative hypothyroxinemia, preferential T3
secretion, and higher, albeit normal, serum
thyrotropin levels. Thus, there may be
considerable variability in thyroidal adjustments
during normal pregnancy.
Human Chorionic Gonadotropin (hCG)
alpha-subunits of the two glycoproteins are
identical
beta-subunits, although similar, differ in
their amino acid sequence.
d/t structural similarity, hCG has intrinsic
thyrotropic activity, and thus, high serum
levels cause thyroid stimulation.
thyrotropin levels in more than 80 % of
pregnant women, whereas they remain in the
normal range for nonpregnant women
Normal suppression of TSH during pregnancy
may lead to a misdiagnosis of subclinical
hyperthyroidism.
Of greater concern is the potential failure to
identify women with early hypothyroidism
because of suppressed TSH concentrations.
basal metabolic rate progressively during
normal pregnancy by as much as 25 %, most of
this in oxygen consumption can be attributed to
fetal metabolic activity. If fetal body surface area
is considered along with that of the mother, the
predicted and observed basal metabolic rates are
similar to those in nonpregnant women.
PARATHYROID GLAND
The regulation of calcium concentration is closely
interrelated to magnesium, phosphate, parathyroid
hormone, vitamin D, and calcitonin physiology.
All markers of bone turnover increased during normal
pregnancy and failed to reach baseline level by 12
months postpartum.
calcium needed for fetal growth and lactation may be
drawn at least in part from the maternal skeleton.
Parathyroid Hormone and Calcium
Acute or chronic in plasma calcium or
magnesium stimulate the release of parathyroid
hormone
in calcium and magnesium suppress
parathyroid hormone levels.
The action of this hormone on bone resorption,
intestinal absorption, and kidney reabsorption is
to extracellular fluid calcium and
phosphate.
Parathyroid hormone plasma concentrations
st
during the 1 trimester and progressively
throughout the remainder of pregnancy.
levels likely result from the lower calcium
concentration in the pregnant woman w/c is the
result of:
plasma volume
glomerular filtration rate
maternal-fetal transfer of calcium
Ionized calcium is only slightly, suggest that
during pregnancy a new "set point" is
established for ionized calcium and parathyroid
hormone.
Estrogens also appear to block the action of
parathyroid hormone on bone resorption,
resulting in another mechanism to increase
parathyroid hormone during pregnancy
physiological
hyperparathyroidism
of
pregnancy, likely to supply the fetus with
adequate calcium.
Calcitonin and Calcium

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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

Reference: WILLIAMS OBSTETRICS 23rd Edition

Maternal plasma levels of this potent

mineralocorticosteroid progressively increase
during pregnancy.
plasma levels of deoxycorticosterone rise to near
1500 pg/mL by term, a more than 15-fold
increase
marked elevation is not derived from adrenal
secretion but instead represents increased
kidney production resulting from estrogen
stimulation.
The levels of deoxycorticosterone and its sulfate
in fetal blood are appreciably higher than those
in maternal blood, which suggests transfer of
fetal deoxycorticosterone into the maternal
compartment.
Dehydroepiandrosterone Sulfate
Maternal serum and urine levels of
dehydroepiandrosterone sulfate are decreased
during normal pregnancy.
consequence of increased metabolic clearance
through extensive maternal hepatic 16 alphahydroxylation and placental conversion to
estrogen.
Androstenedione and Testosterone
Maternal plasma levels of both of these
androgens are increased during pregnancy.
Maternal
plasma
androstenedione
and
testosterone are converted to estradiol in the
placenta, which increases their clearance rates.
plasma sex hormone-binding globulin in
pregnant women retards testosterone clearance.
production rates of maternal testosterone and
androstenedione during human pregnancy are
increased.
source of this increased C19-steroid production is
unknown, but it likely originates in the ovary.
little or no testosterone in maternal plasma
enters the fetal circulation as testosterone.
Even when massive testosterone levels are
found in the circulation of pregnant women, as
with androgen-secreting tumors, testosterone
levels in umbilical cord blood are likely to be
undetectable and are the result of the near
complete
trophoblastic
conversion
of
testosterone to 17 beta-estradiol

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.

Reference: WILLIAMS OBSTETRICS 23rd Edition

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