PHYSIOLOGIC OBSTETRICS
Topic: Maternal Physiology II
Lecture by: Dr. Estimo
CARDIOVASCULAR SYSTEM
Heart
 Physiological adaptation as early as the First 8 WEEKS of pregnancy
 5th WEEK - ↑ Cardiac output ; ↓ Systemic vascular resistance 
↑ Heart rate  influence ventricular performance
 ↓ Brachial Systolic BP, Diastolic BP & Central Systolic BP
o All are significantly lower 6 to 7 weeks from the last
menstrual period
 Resting pulse rate – ↑ 10 beats/min. during pregnancy
 10th-20th WEEKS – Plasma volume expansion begins, and Preload ↑
 Diaphragm becomes progressively ELEVATED  heart is:
o Displaced to the LEFT and UPWARD
o Rotated to its long axis
o APEX is moved LATERALLY
 Pregnant women normally have some degree of benign pericardial
effusion, which may ↑ the cardiac silhouette
 NO characteristic ECG changes
 Many of the normal cardiac sounds are MODIFIED during pregnancy
Modified Normal Cardiac Sounds
st
1 Heart sound
Exaggerated splitting and increased
loudness
nd No definite changes in the aortic and
2 Heart sound
pulmonary elements
3rd Heart sound Loud and easily heard
During Pregnancy:
 Higher volume of blood is being pumped by the heart per minute 
so women have a higher heart rate
 More blood vessels grow to accommodate this, but the pressure of
the expanding uterus on large veins means blood is more slow at
returning to the heart
 PROGESTERONE relaxes the walls of the blood vessels, so the blood
pressure drops in the 2nd trimester and a woman may feel faint
90% Systolic murmur  intensified during inspiration or
expiration that disappeared shortly after delivery
20% Soft diastolic murmur (transient)
10% Continuous murmurs arising from the breast vasculature
 INCREASE plasma volume – reflected by enlarging cardiac end-
systolic & end-diastolic dimensions
 NO CHANGE in SEPTAL THICKNESS or in EJECTION FRACTION
 Ventricular remodeling – characterized by eccentric left-ventricular
mass expansion averaging 30 to 35% near term
 Ventricular function – NORMAL during pregnancy
Cardiac Output
 There is a ↓ – in mean arterial pressure & vascular resistance
 ↑ - blood volume & basal metabolic rate
 ↑ Cardiac output at rest (lateral recumbent position)
o During late pregnancy, a supine woman – large uterus
compresses venous return from the lower body, and may
compress the aorta  cardiac filling may be REDUCED and
cardiac output DIMINISHED
 Cardiac output at term increase 1.2 L/min – almost 20%- when a
woman was moved from her back onto her left side
 1/3 decrease in uterine blood flow
o Lateral recumbent position – 10% increase
 Standing – cardiac output SAME as non-pregnant woman
 Multiple pregnancies
o Increase CO (20%) = stroke volume (15%) and HR (3.5%)
 Increase Preload
o Increase Left atrial diameter & Left ventricular end-
diastolic diameter
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 ↑ HR and Inotropic contractility  ↓ cardiovascular reserve
1st & 2nd Stage of labor Increase CO
After delivery Decrease CO dependent on blood loss
Hemodynamic Function in Late Pregnancy
 Late pregnancy
INCREASE HR (heart rate), SV (stroke volume), CO
Systemic vascular resistance, Pulmonary vascular
DECREASE
resistance, Colloid osmotic pressure
Pulmonary capillary wedge pressure
NO CHANGE
Central venous pressure
 Normal pregnancy is NOT a continuous “high-output” state
Circulation and Blood Pressure
 Changes in posture affect arterial blood pressure
o Lowest when sitting (compared to lateral recumbent
supine position)
 DIASTOLIC pressure decreases more than systolic
 Antecubital venous pressure remains UNCHANGED
 Supine position – FEMORAL VENOUS PRESSURE ↑ (8 mmHg early in
pregnancy to 24 mmHg at term)
 Venous blood flow in the legs is retarded during pregnancy (EXCEPT
in lateral recumbent position)
o This is due to occlusion of the pelvic veins and inferior
vena cava by the enlarged uterus
 The elevated venous pressure returns to NORMAL when the
pregnant woman lies on her side and immediately after delivery
 These alterations contribute to the dependent edema and to the
development of varicose veins in the legs and vulva, as well as
hemorrhoid. These changes also predispose to deep-vein
thrombosis
Supine Hypotension
 10% of women – supine compression of the great vessels by the
uterus causes significant arterial hypotension, sometimes referred to
as the supine hypotensive syndrome
 When supine, Uterine arterial pressure & blood flow  is
significantly LOWER than that in the brachial artery
Renin Angiotensin II and Plasma Volume
 The renin-angiotensin aldosterone axis is intimately involved in BP
control via sodium & water balance. All components of this system
are INCREASED in normal pregnancy
 Renin is produced by both the maternal kidney and the placenta, and
increased renin substrate (angiotensinogen) is produced by both
maternal and fetal liver
 Elevated angiotensinogen levels result, in part, from ↑ estrogen
production during normal pregnancy and are important in the 1st
trimester blood pressure maintenance
 The vascular responsiveness to angiotensin II may be progesterone
related
Cardiac Natriuretic Peptides
 Atrial Natriuretic Peptide (ANP) and B-type Natriuretic Peptide
(BNP) – are secreted by cardiomyocytes in response to chamber-
wall stretching
 During normal pregnancy, plasma ANP and BNP levels are
maintained in the non-pregnant range despite increase plasma
volume
 BNP levels are increased in SEVERE PREECLAMPSIA
 PHYSIOLOGIC OBSTETRICS
Topic: Maternal Physiology II
Lecture by: Dr. Estimo

Cardiac Natriuretic Peptide continued….. RESPIRATORY TRACT

 In non-pregnant and pregnant patients, levels of BNP and of amino- Anatomically
terminal pro-brain natriuretic peptide (Nt pro-BNP) may be useful in Diaphragm Subcostal angle Thoracic circumference
screening for depressed left ventricular systolic function and Rises at 4 cm Widens appreciably ↑ 6 cm, but not
determining chronic heart failure prognosis as the transverse sufficiently to prevent
 A third species, C-type natriuretic peptic (CNP), is predominantly diameter of the reduced residual lung
secreted by non-cardiac tissues. Among its diverse biological thoracic cage volumes created by the
functions, this peptide appears to be a major regulator of fetal bone lengthens elevated diaphragm
approximately 2 cm
growth

 Diaphragmatic excursion: pregnant > non-pregnant women

Prostaglandins
 Increased prostaglandin production during pregnancy is thought to
Pulmonary Function
have a central role in control of vascular tone, BP, and sodium
 ↓ Functional residual capacity (FRC) – approximately 20-30% or
balance
400-700 mL decrease during pregnancy
 Renal medullary prostaglandin E2 synthesis is increased markedly
o ↓ Expiratory reserve volume (15-20% or 200-300 mL ↓)
during late pregnancy and is presumed to be natriuretic
o ↓ Residual volume (20-125% or 200-400 mL ↓)
 Prostacyclin (PGI2), the principal prostaglandin of endothelium, also
 FRC and residual volume decline due to diaphragm elevation
is increased during late pregnancy and regulates BP and platelet
o Significant reductions are observed by the 6th month with
function
a progressive decline across pregnancy
 ↑ Inspiratory capacity
Endothelin
o Maximum volume that can be inhaled from FRC
 Endothelin 1 is a POTENT VASOCONSTRICTOR
o 5-10% or 200 to 250 mL increase during pregnancy
 Produced in endothelial and vascular smooth muscle cells
 Total lung capacity
 Regulates local vasomotor tone
o Combination of FRC and inspiratory capacity
 Production is stimulated by:
o Unchanged or decreased by 5% at term
o Angiotensin II
 Respiratory Rate – Unchanged
o Arginine Vasopressin
 But there is an ↑ in Tidal Volume (TV) & ↑ Resting Minute
o Thrombin
Ventilation (RMV) as pregnancy advances
 Endothelins, in turn stimulate secretion of ANP, aldosterone, and
↑ Minute ventilation is caused by:
catecholamines
o Enhanced respiratory drive primarily due to the
 Vascular sensitivity to endothelin-1 is not altered during normal stimulatory action of progesterone
pregnancy o Low expiratory reserve volume
o Compensated respiratory alkalosis
Nitric Oxide
 POTENT VASODILATOR  Pulmonary function
 Mediators of placental vascular tone and development o Peak expiratory flow rates ↑ progressively with
 Released by endothelial cells increased AOG
 Implications for modifying vascular resistance during pregnancy o Lung compliance is unaffected by pregnancy
 Abnormal nitric oxide synthesis is inked to PREECLAMPSIA o ↑ airway conductance and ↓ total pulmonary
DEVELOPMENT resistance, possibly because of progesterone
o The maximum breathing capacity and forced or timed
CVS Increase Decrease Unchanged vital capacity are NOT ALTERED appreciably
CO /
HR / Pulmonary Function Increase Decrease Unchanged
Systemic Vascular Resistance / FRC /
Vascular Capacity / Expiratory Reserve Volume /
Vascular Compliance / Residual Volume /
Preload / Inspiratory Capacity /
Plasma Volume / Total Lung Capacity /
Arterial BP / RR /
RAAS / TV & RMV /
PGE2 / Peak Expiratory Volume /
PGI2 / Lung Compliance /
ANP/BNP / Airway Conductance /
Total Pulmonary Resistance /
Maximum Breathing Capacity /
Forced or Timed Vital Capacity /
Oxygen Consumption /

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 PHYSIOLOGIC OBSTETRICS
Topic: Maternal Physiology II
Lecture by: Dr. Estimo

Oxygen Delivery Renal Function Tests

 ↓ Serum Creatinine Levels (mean of 0.7 to 0.5 mg/dL)
Oxygen Delivery Increase Decrease Unchanged
Amount of O2 delivered into the o > 0.9 mg/dL suggests underlying RENAL DISEASE
/  ↑ Creatinine Clearance (averages 30% higher than non-pregnant
lungs
Total Hgb mass / women)
Total O2-carrying capacity / o Useful test to estimate RENAL FUNCTION, provided that
Cardiac Output / complete urine collection is made during an accurately
Maternal arteriovenous O2 timed period
/
difference  During the day, pregnant women tend to accumulate water as
Oxygen consumption / dependent edema, and at night, while recumbent, they mobilize this
fluid with diuresis
 Oxygen Consumption o This reversal of the unusual non-pregnant diurnal
o ↑ 20% - Pregnancy pattern of urinary flow causes nocturia, and urine is more
o 10% - If multifetal pregnancies dilute than in non-pregnant women
o ↑ 40-60% - during labor  Failure of a pregnant to excrete concentrated urine after withholding
fluids for approximately 18 hrs. does not necessarily signify renal
Acid-Base Equilibrium damage
 An increased awareness of a desire to breathe is common even early o In fact, the kidney in these circumstances functions
in pregnancy, which may be interpreted as dyspnea perfectly normally by excreting mobilized extracellular
 The physiological dyspnea: ↑ tidal volume  ↓ blood PCO2  fluid of relatively low osmolality
dyspnea
 This is induced in large part by progesterone and to a lesser degree Urinalysis
by estrogen  Glucosuria during pregnancy may NOT BE ABNORMAL
 Progesterone appears to act centrally, ↓ threshold and ↑ o ↑ GFR + Impaired Tubular Reabsorptive Capacity for
sensitivity of the chemoreflex response to CO2 filtered glucose accounts for most cases of glucosuria
 To compensate for the resulting respiratory alkalosis, ↓ plasma  Hematuria is often the result of contamination during collection; IF
bicarbonate levels (about 26 to 22 mmol/L) NOT, it most often suggests urinary tract disease
 Minimal ↑ in blood pH  shift the oxygen dissociation curve to the o Hematuria is common after difficult labor and delivery
left  ↑ affinity of maternal Hgb for oxygen (Bohr effect)  ↓ because of trauma to the bladder and urethra
oxygen-releasing capacity of maternal blood  Proteinuria
 Slight pH increase  ↑ 2,3-diphosphoglycerate in maternal o Non-pregnant patients: >150mg/day
erythrocytes  shifts the curve back to the right o Because of the aforementioned hyperfiltration and
 ↓ PCO2 from maternal hyperventilation aids carbon dioxide (waste) possible ↓ tubular reabsorption, significant proteinuria
transfer from the fetus to the mother while also aiding oxygen during pregnancy is usually defined as >300 mg/day
release to the fetus
Ureters
URINARY SYSTEM  As uterus rises out of the pelvis  rests on the ureters (displaces
Kidney LATERALLY and COMPRESSES them at the pelvic brim)
 Kidney size - ↑ 1.5 cm o ↑ Intraureteral tonus results
 ↑ GFR (Glomerular Filtration Rate) & RPF (Renal Plasma Flow)  Ureteral dilatation  on the RIGHT side (Progesterone-like effect)
 GFR – Increases 25% 2nd week after conception & Increase 50%  Unequal dilatation may result from:
beginning of the 2nd trimester o Cushioning provided the left ureter by the sigmoid colon
This hyperfiltration is caused by: o Greater right ureteral compression exerted by the
o Hypervolemia-induced hemodilution  DECREASES DEXTROROTATED UTERUS
protein concentration & oncotic pressure of plasma o The right ovarian vein complex, which is remarkably
entering the glomerular microcirculation dilated during pregnancy, lies obliquely over the right
o ↑ Renal plasma flow by 80% before the end of the 1st ureter and may contribute significantly to right ureteral
semester dilatation
 Ureteral elongation accompanies distention, and the ureter is
 ↑ GFR persists until term, even though renal plasma flow ↓ during frequently thrown into curves of varying size, the smaller of which
late pregnancy may be sharply angulated
o As consequence of this ↑ GFR approx.. 60% of women o These so-called kinks are poorly named, because the
report urinary frequency during pregnancy term connotes obstruction
 Relaxin may be important for mediating both ↑ GFR and RBF during
pregnancy Bladder
o Relaxin increases endothelin and nitric oxide production  From 12 weeks onwards, ↑ uterine size, the hyperemia that affects
in the renal circulation  renal vasodilation, ↓ renal all pelvic organs, and the hyperplasia of bladder muscle &
afferent, and ↓ efferent arteriolar resistance  ↑ renal connective tissues elevate the trigone and cause thickening of its
blood flow and ↑ GFR posterior, or intraureteric margin
 One unusual feature of the pregnancy-induced changes in renal  Continuation of this process to the end of pregnancy produces
excretion is the ↑ nutrients lost in the urine marked deepening and widening f the trigone
o Amino acids and water-soluble vitamins are excreted in  NO MUCOSAL CHANGES other than an increase in the size and
much greater amounts totuosity of its blood vessels

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 PHYSIOLOGIC OBSTETRICS
Topic: Maternal Physiology II
Lecture by: Dr. Estimo

Bladder continued….. Liver

BLADDER PRESSURE in Primigravidas
LIVER Increase Decrease Unchanged
During pregnancy Increased from 8 cm H2O
Liver Size /
At term 20 cm H2O
Hepatic arterial & portal venous
/
blood flow
 To compensate for ↓ bladder capacity, absolute and functional Total Alkaline Phosphatase
uretheral lengths increased by 6.7 and 4.8 mm, respectively /
Activity
 ↑ Maximal intrauretheral pressure (from 70 to 93 cm H2O), thus AST (Aspartate Transaminase) /
continence is maintained ALT (Alanine Transaminase) /
o At least half of women experience some degree of GGT (y-glutamyl transpeptidase) /
urinary incontinence by the third trimester Bilirubin /
 Toward the end of pregnancy, particularly in nulliparas in whom the Serum albumin concentration /
presenting part often engages before labor, the entire base of the Total albumin /
bladder is pushed forward and upward, converting the normal Serum globulin /
convex surface into a concavity Leucine aminopeptidase /
 Pressure from the presenting part impairs blood and lymph drainage
from the bladder base, often rendering the area edematous, easily NOTE:
traumatized, and possibly more susceptible to infection  NO INCREASE in liver size
 Pregnancy-induced aminopeptidase has oxytocinase and
GASTROINTESTINAL SYSTEM vasopressinase activity that occasionally causes transient diabetes
Gums insipidus
 During pregnancy, the gums may become hyperemic and softened
and may bleed when mildly traumatized, as with a toothbrush Gallbladder
o This pregnancy gingivitis typically subsides postpartum  During normal pregnancy, ↓ gallbladder contractility  ↑ residual
 Epulis Gravidarum volume
o A focal, highly vascular swelling of the gums  Progesterone potentially impairs gallbladder contraction by
o It is a pyogenic granuloma that occasionally develops but inhibiting cholecystokinin-mediated smooth muscle stimulation,
typically regresses spontaneously after delivery which is the primary regulatory of gallbladder contraction
Stomach & Intestines  Impaired emptying, subsequent stasis, and an increased bile
 As pregnancy progresses, the stomach and intestines are displaced cholesterol saturation of pregnancy contribute to the increased
by the enlarging uterus prevalence of cholesterol gallstones in multiparas
Appendix  Intrahepatic cholestasis has been linked to high circulating levels of
 The appendix is usually displaced UPWARD and somewhat estrogen, which inhibit intraductal bile acid transport
LATERALLY as the uterus enlarges
 It may reach the right flank ENDOCRINE SYSTEM
Tooth Pituitary Gland
 Pregnancy does not incite tooth decay  Enlarges in size by approximately 135%
o Pituitary gland may reach up to 12 mm upon MRI during
PYROSIS (HEARTBURN) the first days of postpartum and involutes rapidly by 6
 Common months postpartum
 Caused by reflux of acidic secretion into the lower esophagus  Pituitary enlargement is caused by estrogen-stimulated hypertrophy
 Lower esophageal sphincter tone is DECREASED and hyperplasia of the lactotrophs and maternal serum prolactin
 INTRAESOPHAGEAL PRESSURE are LOWER levels parallel the increasing size
 INTRAGASTRIC PRESSURE HIGHER in pregnant women
 Esophageal peristalsis has lower wave speed and lower amplitude Gonadotrophs Decline (↓) in number
Corticotrophs & Thyrotrophs Remain CONSTANT
 Gastric Emptying Time SUPPRESSED due to negative feedback by
Somatotrophs the placental production of growth
o Unchanged during each trimester
hormone
o Prolonged during labor and after administration of
analgesic agents
 Clinical Correlations:
o One danger of general anesthesia for delivery is
o Compression of the Optic Chiasm: happens when the
regurgitation and aspiration of either food-laden or
pituitary gland enlarges causing blurring of vision in
highly acidic gastric contents
relation to pregnancy
HEMORRHOIDS
o Prolactinoma: enlargement of the pituitary DURING
 Common
pregnancy
 Caused in large measure by constipation and ↑ pressure in veins
o Macroadenoma: enlargement of the pituitary EVEN
below the level of the enlarged uterus
BEFORE pregnancy
 Both of which results to lactation of the women
involved

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 PHYSIOLOGIC OBSTETRICS
Topic: Maternal Physiology II
Lecture by: Dr. Estimo

Growth Hormone Thyroid Gland

 During the 1st trimester, GH is secreted predominantly from the  Increase production of thyroid hormones by 40-100% to meet
maternal pituitary gland, and concentrations in serum and amniotic maternal and fetal need
fluid are within non-pregnant values of 0.5 to 7.5 ng/mL
 At 8 weeks AOG: GH can be detected in the maternal blood Anatomically
 At 17 weeks AOG: the placenta is the principal source of GH  Thyroid gland undergoes moderate enlargement  by glandular
 Maternal serum values INCREASE SLOWLY from approximately: hyperplasia and increased vascularity
o 3.5 ng/mL at 10 weeks to….  Thyroid volume INCREASE from 12 mL in the 1st trimester to 15 mL
o plateau after 28 weeks at approximately 14 ng/mL at delivery
 At 14-15 weeks AOG: GH in amniotic fluid  Total volume was inversely proportional to serum thyrotropin
 After 36 weeks AOG: slowly declines thereafter to reach baseline concentrations. Such enlargement is NOT PATHOLOGICAL, but
values normal pregnancy does not typically cause significant thyromegaly.
 Placental GH – which differs from pituitary growth hormone by 13 Thus, any goiter should be investigated
amino acid residues- is secreted by syncytiotrophoblast in Physiologically
nonpulsatile fashion  Thyroxine Binding Globulin
 Has some influence on fetal growth as well as preeclampsia o Early in the 1st trimester, levels of the principal carrier
development protein-thyroxine-binding globulin (TBG)- INCREASE,
 Placental GH  major determinant of MATERNAL INSULIN reach their zenith at about 20 weeks and stabilize at
RESISTANCE after mid-pregnancy approximately double baseline values for the remainder
 Maternal serum levels correlate positively with BIRTH WEIGHT but of pregnancy
negatively with FETAL GROWTH RESTRICTION & UTERINE ARTERY o The ↑ TBG concentrations result from both higher
RESISTANCE. That said, fetal growth still progresses in the complete hepatic synthesis rates- due to estrogen stimulation- and
absence of this hormone lower metabolism rates due to increased TBG sialylation
and glycosylation
Prolactin o These ↑ TBG levels INCREASES total serum thyroxine
 Increase concentrations are usually tenfold greater at term- about (T4) and triiodothyronine (T3) concentration, but do not
150 ng/mL affect the physiologically important serum free T4 and T3
 Its increase is correlated with estrogen outburst  stimulates the levels
anterior pituitary lactotrophs  ↑release of prolactin ↑ T4 and T3 but…
 Paradoxically, plasma concentration decrease after delivery even in NO EFFECT on free T4 and T3
women who are breastfeeding. During early lactation, there are
pulsatile bursts of prolactin secretion in response to suckling  Serum Thyroxine (T4)
 Prolactin levels is increased by estrogen, thyroid-releasing hormone,
and serotonin
 In contrast, dopamine (prolactin-inhibiting factor) inhibits its
secretion
 The principal function of maternal prolactin is to 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 increases the number of estrogen and prolactin receptors
in these cells
 Finally, prolactin promotes mammary alveolar cell RNA synthesis,
galactopoiesis, and production of casein, lactalbumin, lactose, and
lipids
 Prolactin is present in amniotic fluid in high concentrations. Levels of
up to 10,000 ng/mL are found at 20 to 26 weeks gestation.
Thereafter, levels decrease and reach a nadir after 34 weeks
 There is convincing evidence that the uterine decidua is the synthesis
site of prolactin found in amniotic fluid. This prolactin impairs water
transfer from the fetus into the maternal compartment, thus,
preventing fetal dehydration

Oxytocin and Antidiuretic Hormone (ADH)

 These are secreted from the posterior pituitary
 Oxytocin – role in parturition and lactation
 Antidiuretic hormone, also called vasopressin – levels DO NOT
CHANGE in pregnancy
 Deficiency  associated with diabetes insipidus

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 PHYSIOLOGIC OBSTETRICS
Topic: Maternal Physiology II
Lecture by: Dr. Estimo
Serum Thyroxine (T4) continued…..
 Serum Thyroxine (T4)
o Total serum T4 increases sharply beginning between 6
and 9 weeks and reaches a plateau at 18 weeks
o Free serum T4 levels rise slightly and peak along with hCG
levels and then they RETURN TO NORMAL
o The rise in total T4 is more pronounced up to 18 weeks,
and thereafter, it plateaus
o The fetus is reliant on maternal thyroxine, which crosses
the placenta in small quantities to maintain normal fetal
thyroid function
o Recall that the fetal thyroid does not begin to concentrate
iodine until 10 to 12 weeks gestation
o The synthesis and secretion of thyroid hormone by fetal
pituitary thyroid-stimulating hormone ensues at
approximately 20 weeks
o At birth, approximately 30% of the T4 in umbilical cord
blood is of maternal origin
 Thyrotropin-Releasing Hormone (TRH)
o Secreted by the hypothalamus and stimulates thyrotrope
cells of the anterior pituitary to release thyroid
stimulating hormone (TSH) or thyrotropin
o TRH levels are not increased during normal pregnancy.
However, this neurotransmitter does cross the placenta
and may serve to stimulate fetal pituitary to secrete
thyrotropin
 TSH and hCG
o The α-subunits of the two glycoproteins are identical
o The ß-subunits, although similar, differ in their amino
acid sequence
o As a result of this structural similarity, hCG has intrinsic
thyrotropic activity, and thus, high serum hCG levels
cause thyroid stimulation
o Thyrotropin levels decrease in more than 80% of
pregnant women, whereas they remain in the normal
range for non-pregnant women
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 Iodine Status
o Iodine requirements INCREASE during normal pregnancy
o DEFICIENY – manifest as low thyroxine and increased
TSH levels
o Iodine deficiency is the most common preventable cause
of impaired neurological development after famine
o Severe deficiency leads to CRETINISM
o Fetus- early exposure to thyroid hormone is essential for
the nervous system
Parathyroid Glands
 The regulation of calcium concentration is closely interrelated with
MAGNESIUM, PHOSPHATE, PARATHYROID HORMONE, VITAMIN D
& CALCITONIN
 All markers of bone turnover increased during normal pregnancy and
failed to reach baseline level by 12 months postpartum
 They concluded that the calcium needed for fetal growth and
lactation may be drawn at least in part from the maternal skeleton
Parathyroid Hormone (PTH)
 DECREASES in calcium & magnesium  stimulate parathyroid
hormone (PTH) release
 Conversely, INCREASE in calcium & magnesium  suppress PTH
levels
 Action of PTH:
o Bone resorption
o Intestinal absorption & Kidney reabsorption is to
increase extracellular fluid calcium concentrations and
decrease phosphate levels
 In most circumstances, increased maternal calcium absorption
provides the additional calcium
 During pregnancy, the amount of calcium absorbed rises gradually
and reaches approximately 400 g/day in the 3rd trimester
 Increased calcium absorption appears to be mediated by elevated
maternal 1,25-dihydroxyvitamin D concentrations. This occurs
despite decreased levels during early pregnancy of PTH, which is the
normal stimulus for active vitamin D production within the kidney
Calcitonin
 Actions of calcitonin is to oppose PTH and vitamin D to protect
maternal skeletal calcification during times of calcium stress
 Pregnancy and lactation cause profound calcium stress  calcitonin
levels are appreciably higher than those in non-pregnant women
 The C cells that secrete calcitonin are deprived 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 hormones – GASTRIN, PENTAGASTRIN, GLUCAGON,
and PANCREOZYMIN- and food ingestion also ↑ Calcitonin levels
Adrenal Glands
Cortisol
 Circulating serum concentration of cortisol is INCREASED, but much
of it is bound to TRANSCORTIN, the cortisol-binding globulin
 The adrenal secretion rate of glucocorticoid is NOT INCREASED and
probably it is decreased compared with that of the non-pregnant
state
 The metabolic clearance rate of cortisol, however, is LOWER during
pregnancy because its half-life is nearly doubled compared with that
for non-pregnant women
 PHYSIOLOGIC OBSTETRICS
Topic: Maternal Physiology II
Lecture by: Dr. Estimo
Cortisol continued……
 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 ACTH (corticotropin), are
REDUCED strikingly
 As pregnancy progresses, ACTH and free cortisol levels rise equally
and strikingly
 The higher free cortisol levels observed in pregnancy result from a
“resetting” of the maternal feedback mechanism to higher levels
 These incongruities may result from an antagonistic action of
progesterone on mineralocorticoids
 Thus, in response to elevated progesterone levels during pregnancy,
an elevated free cortisol is needed to maintain homeostasis
Aldosterone
 As early as 15 weeks AOG, the maternal adrenal glands secrete
considerably increased amounts of aldosterone, the principal
mineralocorticoid
 By the 3rd trimester, approximately 1 mg/day is secreted
 If sodium intake is restricted, aldosterone secretion is elevated even
further
 Levels of renin and angiotensin II substrate normally are increased,
especially during the latter half of pregnancy  increased plasma
levels of angiotensin II, which acts on the zona glomerulosa of the
maternal adrenal glands and markedly elevated aldosterone
secretion
 Increased aldosterone secretion  affords protection against the
natriuretic effect of progesterone and atrial natriuretic peptide
 Play a role in MODULATING TROPHOBLAST GROWTH AND
PLACENTAL SIZE
Androgens
 Androstenedione and Testosterone – INCREASED
 Both androgens are converted to estradiol in the placenta, which
increases their clearance rates
 INCREASED plasma sex hormone-binding globulin (SHBG) in
pregnant women retards testosterone clearance
 Little or no testosterone in maternal plasma enters the fetal
circulation as testosterone
 Dehydroepiandrosterone sulfate – DECREASED
o This is a consequence of increased metabolic clearance
through extensive maternal hepatic 16ß-hydroxylation
and placental conversion to estrogen
MUSCULOSKELATAL SYSTEM
 Progressive lordosis is characteristic feature of normal pregnancy
 Compensating for the anterior positon of the enlarging uterus,
lordosis shifts the center of gravity back over the lower extremities
 Sacroiliac, sacrococcygeal, and pubic joints have INCREASED
MOBILITY during pregnancy
 INCREASED JOINT LAXITY during pregnancy DOES NOT correlate
with increased maternal serum levels of estradiol, progesterone, or
relaxin
 Most relaxation takes place in the first half of pregnancy
 It may contribute to maternal posture alterations and in turn create
lower back discomfort
 Although some symphyseal separation likely accompanies many
deliveries, those greater than 1 cm may cause significant pain
 Aching, numbness, and weakness also occasionally are experienced
in the upper extremities. This may result from the marked lordosis
and associated anterior neck flexion and shoulder girdle slumping,
which produce traction on the ulnar and median nerves
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Strength in knowledge
 Joint strengthening begins immediately following delivery and is
usually complete within 3-5 months
CENTRAL NERVOUS SYSTEM
Memory
 Changes in the central nervous center are relatively few and mostly
subtle
 Women often report problems with attention, concentration and
memory throughout pregnancy and the early puerperium
 Pregnancy-related memory decline, which was limited to the 3rd
trimester
o This decline was not attributable to depression, anxiety,
sleep deprivation, or other physical changes associated
with pregnancy. It was transient and quickly resolved
following delivery
 Pregnant women in late pregnancy performed significantly worse on
tests of verbal recall and processing speed compared with matched
non-pregnant controls
 Attention and memory were improved in women with
PREECLAMPSIA receiving MAGNESIUM SULFATE compared with
normal pregnant women
 Mean blood flow in the middle and posterior cerebral arteries
decreased progressively from 147 and 56 ml/min when non-pregnant
to 118 and 44 ml/min late in pregnancy, respectively. The mechanism
and clinical significance of this decline is unknown
 Pregnancy does not appear to affect cerebrovascular autoregulation
Eyes
 Intraocular pressure DECREASES = INCREASED vitreous outflow
 Corneal sensitivity is DECREASED, and the greatest changes are late
in gestation
 Most pregnant women demonstrate a measurable but SLIGHT
INCREASE in corneal thickness, thought to be due to edema
 Consequently, they may have difficulty with previously comfortable
contact lenses
 Krukenberg spindles  brownish-red opacities on the posterior
surface of cornea
o Hormonal effects similar to those observed for skin
lesions are postulated to cause this increased
pigmentation
 Other than transient loss of accommodation with both pregnancy
and lactation, VISUAL FUNCTION is UNAFFECTED by pregnancy
Sleep
 Beginning as early as approximately 12 weeks gestation and
extending though the first 2 months postpartum, women have
difficulty with going to sleep, frequent awakenings, fewer hours of
night sleep, and reduced sleep efficiency
 Supine position – however, average PaO2 levels were LOWER
 Greatest disruption of sleep is encountered postpartum and may
contribute to postpartum blues or to frank depression
References:
 Williams Obstetrics (25th ed.)
 Lecture Notes