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Maternal Physiology

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MATERNAL PHYSIOLOGY

Chapter 4
Introduction

 Pregnancy induces profound changes in the patient’s anatomy &


physiology
 Changes begin early, even before pregnancy is clinically detected
 Changes are hormonally mediated
 The goal is to optimize maternal conditions for fetal growth, prepare
for delivery and postpartum
CHANGES IN THE REPRODUCTIVE TRACT

I. UTERUS
o With the pregnancy progression, the uterus leaves the pelvis and ascends to abdominal
cavity
o Progressively becomes soft as early as 6 weeks
o Hegar sign: softening of the isthmus
o Dextro-rotation: uterus rotates slightly to the right due to the rectosigmoid on the left
o Endometrium becomes specialized & is called THE DECIDUA
o Changes in the Shape & Size of the Uterus
o Nonpregnant: 70g with 10ml cavity; pyriform or pear shaped
o Becomes globular, thin-walled muscular organ of sufficient capacity to accommodate
the fetus, placenta & amniotic fluid
o The total volume of contents at term averages 5L but may be 20L or more and weighs
nearly 1100g
o At 12 weeks, the gravid uterus becomes palpable above the pubic symphysis and
becomes an abdominal organ
o At 20-34 weeks, the fundic height in centimeters correlates with the AOG in weeks
o Enlargement is due to stretching and marked hypertrophy of muscle cells
o During 1st trimester: hypertrophy is stimulated by estrogen and progesterone
o After 1st trimester: uterine growth is mostly exerted by the expanding products of
conception
B. Uterine Contractility
o Beginning in early pregnancy uterus contracts irregularly and these are perceived as
mild cramps.
o At 2nd trimester: detected by bimanual examination
o Braxton Hicks contractions: infrequent, unpredictable, sporadic, non-rhythmic
contractions which increase progressively as the pregnancy approaches term
C. Uteroplacental Blood Flow
o The delivery of most substances essential for fetal and placental growth,
metabolism and waste removal requires the placental intervillous space to be
adequately perfused.
o Placental perfusion depends on total uterine blood flow.
o Flow rates rise from approx. 450ml/min in the midtrimester to nearly 500 to
750ml/min at 36 weeks gestation
o This results in increased uterine venous caliber and distensibility can result in
uterine vein varices
o The vessels that supply the uterine corpus widen and elongate yet preserve their contractile
function
o Spiral arteries, directly supply the placenta, vasodilate but completely lose contractility
o This vasodilatation allows maternal-placental blood flow to progressively rise during
gestation
o Nitric Oxide (NO): potent vasodilator which has a central role in reduced vascular
resistance
o Normal pregnancy has vascular refractoriness to the pressor effects of angiotensin II,
leading to increased uteroplacental blood flow
o Hormones that augment NO synthesis and production:
o Estrogen
o Progesterone
o Activin
o Placental Growth Factor (PIGF)
o Vascular Endothelial Growth Factor (VEGF)
II. CERVIX
o As early as 1 month gestation, the cervix begins to soften and gain bluish tones
o Goodell sign: softening of the cervix at 6-8 weeks AOG
o Hegar sign: softening of the isthmus
o These changes result from increased vascularity and edema of the entire cervix, from alterations in
collagen network and from hypertrophy and hyperplasia of the cervical glands.
o Rearrangement of this collagen rich tissue aids the cervix in retention of the pregnancy until term, in
dilation to aid delivery and in postpartum repair and reconstitution
o Estradiol stimulates growth of columnar epithelium of cervical canal, leading to ectropion making it
prone to contact bleeding
o The endocervical mucosal cells produce copious amounts of tenacious mucus that obstructs the cervical canal
soon after conception
o Protect the uterine contents from infection
o Mucus plug when expelled results in a bloody show
o Poor crystallization – beading
o Amniotic fluid leakage, ice-like crystals – ferning
o These change are considered to be estrogen induced
o Endocervical gland hyperplasia and hypersecretory appearance – the Arias-stella reactiom
III. Vagina
 Chadwick sign: greater vascularity & hyperemia in the skin & muscles of perineum
 Vagina walls undergo striking changes in preparation for the distention that accompanies labor and
delivery.
 These include considerable epithelial thickening, connective tissue loosening and hypertrophy of
smooth muscle cells.
 Pelvic Organ Prolapse
 Attenuation of anterior vaginal wall support can lead to prolapse of the bladder that is cystocele, associated
with urinary stasis can predispose to infection
 Pregnancy may also worsen existing Stress Urinary Incontinence – urethral closing pressure is insufficient
 Attenuation of posterior vaginal wall support can lead to prolapse of the bladder that is rectocele, and a large
defect may fill with feces
IV. Ovaries
o Ovulation ceased during pregnancy and maturation of new follicles is suspended
o Ovarian hormones play a crucial role during pregnancy
o Corpus luteum (which produces estrogen) persists up to 8 weeks and is completely
obliterated by 20 weeks AOG (luteo-placental shift)
o A single corpus luteum functions maximally during the 1st 6 to 7 weeks of pregnancy
o Removal of corpus luteum before 7 weeks gestation prompts a rapid fall in maternal
serum progesterone levels and spontaneous abortion
o RELAXIN
o Secreted by the corpus luteum, decidua and placenta
o Aid in remodeling of the reproductive tract connective tissue to accommodate labor
o Initiate augmented renal hemodynamics
V. Fallopian tubes

 Myosalpinx – little hypertrophy


 Endosalpinx – epithelium flattens
 May twist during uterine enlargement but more common with comorbid paratubal or
ovarian cyst
CHANGES IN THE BREAST & SKIN

I. BREAST
o Early pregnancy: breast tenderness & paresthesias
o After 2nd month: increase in size and delicate veins are visible just beneath the
skin; nipples become larger, more deeply pigmented and more erectile
o End of pregnancy & early puerperium: colostrum is produced
o Glands of Montgomery: hypertrophic sebaceous glands scattered through
each areola
o Breast size and ultimate volume of breast milk do not corelate
II. SKIN
o Hyperpigmentation in pregnancy: maybe due to estrogen and progesterone increasing
melanocyte-stimulating hormone (MSH) during pregnancy.

CHANGES IN DESCRIPTION
PREGNANCY
Striae gravidarum Reddish, slightly depressed streaks seen in the abdominal skin and over the skin
of breasts and thighs
Diastasis recti Rectus muscles separate in the midline
Due to the muscles of abdominal wall not able to withstand the tension of the
expanding pregnancy
Linea nigra Pigmented skin line in the midline of the anterior abdominal wall
Chloasma or melasma Irregular brownish patches over varying size on the face and mask
gravidarum
Angiomas Minute, red skin papules with radicles branching out from a central lesion;
likely from increased estrogen
Palmar erythema Redness in the thenar & hypothenar eminences of the palms due to increased
estrogen
Telogen effluvium Excessive hair loss in the puerperium
METABOLIC CHANGES DURING PREGNANCY
I. Weight gain
o Average weight gain during pregnancy is 12.5 kg
II. Water metabolism
o There is greater water retention in pregnancy
o Mediated by decreased plasma osmolality of 10mOsm/kg,
relaxin & other hormones
o At term:
o Volumes of fetus, placenta and amniotic fluid is 3.5L
o Expanded maternal volume from uterus and breast
growth 3.0L
o Pitting edema of the ankles and legs due to greater
venous pressure from partial vena cava occlusion by
the enlarging uterus
III. Protein metabolism
o The placenta regulates the amino acid concentrations – it is higher in the fetal than in the
maternal compartment
o Daily requirements of dietary protein intake during pregnancy are increased
o The estimated average requirements of 1.22g/kg/d of protein for early pregnancy and
1.52g/kg/d for late pregnancy
o Non-pregnant 0.88g/kg/d
IV. Carbohydrate metabolism
o Normal pregnancy characterized by:
o Mild fasting hypoglycemia
o Postprandial hyperglycemia
o Hyperinsulinemia
o This is secondary to pregnancy-induced peripheral insulin resistance
o This is needed to ensure sustained postprandial glucose supply to the fetus
o Factors involved: progesterone, placentally derived growth hormone, prolactin, cortisol,
tumor necrosis factor, leptin
o During fasting state, there is lower levels of plasma glucose and some amino acids instead
increase plasma concentrations of free fatty acids, triglycerides and cholesterol
o Switch from glucose to lipid – accelerated starvation
V. Fat metabolism
o Increased concentrations of lipids, lipoproteins &
apolipoproteins in plasma
o Secondary to increased insulin resistance
o Functions of hyperlipidemia in pregnancy:
o Aids in fat metabolism by the fetus
o Preparatory factor in milk production
o Fat storage in pregnancy:
o Functions to protect the mother and the fetus during
times of prolonged starvation of hard physical exertion
o Primarily during mid-pregnancy; in central rather than
peripheral tissues
Leptin
 Peptide hormone primarily secreted by adipose tissue in nonpregnant human
 Plays a key role in body fat and energy expenditure regulation and in reproduction
 Participates in regulating energy metabolism during pregnancy
 Higher leptin levels may be disadvantageous under certain situations such as maternal
obesity
 Abnormally elevated leptin has been associated with preeclampsia, GDM, and fetal
distress
 Lower levels are linked to fetal growth restriction
 VI. Electrolytes & Minerals

REMARKS INCREASED DECREASE


D
Total serum Ca2+ levels • Fetus imposes a significant demand on maternal calcium homeostasis ✔️

Serum Mg2+ levels • Although the GFR is increased, the excretion of Mg, Na, and K are ✔️
unchanged due to enhanced tubular resorption
Serum Na+ levels • The concentration are decreased slightly because of expanded plasma ✔️
volume
Serum K+ levels ✔️

Iron requirement • Iron requirement is increased to meet the expansion of maternal ✔️


hemoglobin mass & the needs of fetal growth
• 300mg iron transferred to the fetus
• 27mg elemental iron

Iodine requirement • Iodine requirement increases because: ✔️


• Maternal thyroxine production increases to maintain euthyroidism and
transfer thyroid hormones to the fetus
• Increase in fetal thyroid hormone
• Increase in iodide glomerular filtration rate
• 220ug/d
CHANGES IN THE HEMATOLOGIC SYSTEM

I. Changes in the blood volume

o 40-45% increase in the blood volume from non-pregnant state at 32-34 weeks
AOG
o Pregnancy-induced hypervolemia serves several functions:
o Meets metabolic demands of enlarged uterus, placenta & fetus
o Provides abundant nutrients and elements to support the rapidly growing
placenta and fetus
o Protects the mother and fetus against the deleterious effects of impaired
venous return in the supine and erect positions
o Buffers against adverse effects of parturition-associated blood loss
II. Blood Cells

o Red Blood Cells


o RBC mass begins to increase at 8-10 weeks AOG and steadily rises
o The increase in RBC mass is smaller than the increase in plasma volume which contributes to the
physiologic anemia of pregnancy
o During pregnancy, total iron requirement increases to 1000mg (iron stores of healthy non-
pregnant woman is 300mg)
o White blood cells
o Pregnancy is associated with leukocytosis and approaches 15,000 to >/25,000/uL during labor and
early puerperium
o Platelets
o Decline as pregnancy progresses, but usually remains in the normal range
o Partly due to hemodilution
III. Coagulation & Fibrinolysis

 Pregnancy is procoagulant (prothrombotic) state


 Most evidence suggest decreased fibrinolytic activity that favors fibrin
formation
 This ensures hemostatic control especially during delivery when blood loss is
expected
CHANGES IN THE CARDIOVASCULAR SYSTEM

I. Hemodynamics
A. The Major Hemodynamic Changes in pregnancy include:
o Increased cardiac output by 30-50%
o Expanded blood volume
o Reduced systemic vascular resistance and blood pressure
o Minimal change in mean blood pressure

B. These changes begin early in pregnancy, peak during the 2nd & early 3rd trimester, & remain relatively
constant until delivery
C. Cardiac output is increased as early as 5th week due to decreased SVR & increased HR
D. Resting pulse rate increases by 10-15 bpm
E. A heart rate >115 bpm may warrant evaluation for pathology
o Components of Hemodynamic Changes

INCREASED DECREASED
Cardiac Output ✔️
Stroke Volume ✔️
Systemic Vascular Resistance or Total ✔️
Peripheral Resistance
Plasma (intravascular) volume ✔️
Cardiac preload ✔️
Arterial pressure ✔️
Brachial and central systolic pressure ✔️
Diastolic pressure ✔️
End Diastolic Volume ✔️
End Systolic Volume ✔️
Resting Pulse Rate ✔️
Renin ✔️
Angiotensinogen ✔️
II. Heart
o As the diaphragm progressively elevated by the uterus in the 3 rd trimester, the heart is displaced to the
left and upward and rotated on its long axis
o Apex is moved laterally, producing larger cardiac silhouette in chest radiograph seen in the latter half of
pregnancy
o Heart sounds
o Exaggerated splitting of S1 and increased loudness of both S1 and S2
o Loud S3
o Systolic murmur in 90% of gravidas that disappear shortly after delivery
o Diastolic murmur are uncommon and many represent pathologic conditions
o Continuous murmurs (mammary soufflé) from breast vasculature in 10% of gravidas
o ECG Changes
o Slight left axis deviation
o Q waves in leads II, III and aVF
o Inverted T-waves in leads III, VI, V1-V3
CHANGES IN PULMONARY SYSTEM
o Physiologic dyspnea is common in pregnancy
o Mainly due to progesterone (and estrogen to a lesser degree)
o Dyspnea is commonly due to upward displacement of the diaphragm manifesting as tachypnea
o Key changes:
o Diaphragm rises +4cm
o The subcostal angle widens appreciably (68.5◦ to 103.5 ◦)
o The transverse diameter of the thoracic cage lengthens by 2cm
o The thoracic circumference increases 6cm
o The diaphragmatic excursion is greater in pregnant than in non-pregnant women
II. Lung volumes
INCREASED DECREASED UNCHANGED
• Inspiratory Capacity • Functional residual • Respiratory rate
• Tidal Volume capacity • Total lung capacity (FRC
• Resting volume o Expiratory reserve + IC)
ventilation volume • Lung compliance
• Peak expiratory flow rates o Residual volume • Maximum breathing
• Airway conductance • Total lung capacity capacity
• Pulmonary resistance • Forced or timed vital
capacity

 Most significant changes are reduction on FRC (along with ERV & RV) and increases in IC & TV
 FRC & RV decreases progressively across pregnancy due to diaphragm elevation
 Enhanced respiratory drive can occur due to stimulatory action of progesterone, low ERV, and compensated
respiratory alkalosis
 O2 delivery in the maternal lungs is increased because of inc. TV, inc. hemoglobin mass, inc. cardiac output
Changes in the Urinary System

I. Overview of Renal Changes


CHANGES CLINICAL CORELATES
Kidney size • Increases to 1-1.5 cm • Returns to normal postpartum
• Resembles hydronephrosis on sonogram
Renal function • GFR & renal plasma flow increase by 50% due to • Increased GFR results in urinary
relaxin frequency and nocturia
Ureter • Displaced laterally and compressed at pelvic brim • Risk of infection due to compression
• Ureteral dilatation (right>left) due to the
dextrorotated uterus & cushioning of the sigmoid
colon on the left
Bladder • Hyperplasia of bladder muscle elevate the trigone • Urinary incontinence (some) by 3rd
• Reduced bladder capacity due to uterine trimester
compression • Risk for infection
II. Changes in Renal Function & Urine
CHANGES IN PREGNANCY
Test of Renal Function
Serum Creatinine • Value usually decreased
• Creatinine >0.9 mg/dL suggest underlying renal disease that warrants further
investigation
Urinalysis
Glucosuria • May be normal due to increased GFR and impaired renal glucose
reabsorption
• Still warrants investigation for diabetes mellitus
Proteinuria • Protein excretion rate increases to 300mg/day
• Increases with gestational age
• Measured using classic dipstick, quantitative 24 hr collection,
albumin/creatinine or protein/creatinine ratio of a single voided urine
specimen
Hematuria • Usually secondary to contamination during urine collection
• May be due to UTI
• Common after difficult labor & delivery due to trauma to urethra & bladder
Changes in Gastrointestinal System
 Stomach & intestines are displaced
 Altered mobility of esophagus, stomach, small intestine, colon and biliary tree
 Impaired function of lower esophageal sphincter
 Decreased gastric acidity
 Altered pancreatic secretion
I. Esophagus
o Heart burn or pyrosis is common in pregnancy due to reflux of acidic secretions into the
lower esophagus from:
• Altered stomach position
• Reduction of LES tone, intraesophageal pressure
• Increased intragastric pressure
• Decreased peristalsis wave speed & amplitude

II. Stomach
o Gastric atony (lack of tone)
o Prolonged gastric emptying
o Stagnation of gastric contents builds up pressure causing gastro-
esophageal reflux
III. Small intestines, Colon and Rectum
o Decreased motility
o Prolonged intestinal transit time
o Constipation & bloating are common, probably due to hormonal changes that affect motility
o Hemorrhoids are common due to constipation and increased pressure in renal veins

IV. Gallbladder
o Progesterone potentially impairs gallbladder contraction by inhibiting cholecystokinin
(CCK)-mediated smooth muscle stimulation, which is the primary mediator of gallbladder
contraction
o Pregnancy may be associated with increased risk of gallstones
CHANGES IN ENDOCRINE SYSTEM

I. Pituitary Gland
 Enlarges by approximately 135%
 Due to estrogen-stimulated hypertrophy and hyperplasia of lactotrophs
 May compress optic chiasm & reduced visual fields
PITUITARY HORMONES REMARKS

Growth hormone (maternal) • 1st Trimester: secreted predominantly from the maternal pituitary gland,
concentrations lie within nonpregnant range
• Serum levels rise slowly at 10 weeks & plateaus after 28 weeks

Growth hormone (placental) • Secreted by syncytiotrophoblasts


• As early as 6 weeks AOG: placental GH becomes detectable
• By 20 weeks: placenta becomes the principal source of GH
• Upregulates insulin-like growth factor 1 (somatomedin) for fetal growth; higher
levels have been linked to preeclampsia
• Fetal growth still progresses in the complete absence of GH

Prolactin • Functions to ensure lactation


• Initiates DNA synthesis and mitosis of glandular epithelial cells and presecretory
alveolar cells of breast

Oxytocin • Increased production of oxytocin close to term as it is needed for uterine


contraction
II. THYROID GLAND

o Hyperplasia and increased vascularity


o Elevation of BMR (basal metabolic rate)
o Pregnancy is a mild hyperthyroid state
A. THYROID HORMONES REMARKS

T3 and T4 • Increase in Total T3 and T4 hormone levels


• Unchanged free T3 and T4. hormone levels
• Increased in TBG
Thyrotropin releasing hormone TRH • Secreted by hypothalamus
• Do not rise during normal pregnancy but can cross the
placenta to stimulate fetal pituitary to secrete TSH
Thyrotropin stimulating hormone (TSH) • Stimulates maternal FT4 secretion
• Does not cross the placenta
B. MATERNAL AND FETAL CHANGES IN
THE THYROID GLANDS
INCREASED UNCHANGED
• Increased throxine-binding globulin , hCG – • The fetus relies on maternal T4 which
increased thyroxine (T4) & triiodothyroxine crosses the placenta in small quantities
(T3) but free T4 & free T3 levels are not • 10-12 weeks: fetal thyroid begins to
affected. concentrate iodine
• FT4 rise slightly and peak with hCG levels • Early exposure to thyroid hormone is
but they return to normal essential for the nervous system.
• Moderate thyroid gland enlargement due to
glandular hyperplasia & greater vascularity;
significant thyromegaly warrants evaluation
• Increased iodine requirements
III. PARATHYROID GLANDS
PARATHYROID REMARKS
HORMONES

Parathyroid Hormones • Raises extracellular calcium concentrations and lowers phosphate


levels; decline in plasma ca or Mg stimulates release of PTH
• PTH levels decline during the first trimester and rises progressively
throughout pregnancy

Calcitonin • Secreted by the C cells (parafollicular cells) in the thyroid glands;


opposes actions of PTH and Vitamin D
• Protects maternal skeleton during times of calcium stress
• Calcitonin levels fall during pregnancy and rise postpartum
IV. ADRENAL GLANDS
ADRENAL DESCRIPTION
HORMONES
Cortisol • Adrenal secretion not elevated but metabolic clearance rate is decreased
• ACTH and free cortisol levels rise equally as pregnancy progresses
• Theories:
• Elevated free cortisol in response to elevated progesterone is needed to
maintain homeostasis
• Higher free cortisol in preparation for stress of pregnancy, delivery and
lactation
Aldosterone • As early as 15 weeks, maternal adrenal secrete increasing amounts
• Increased renin & angiotensin II, promotes adrenal secretion of aldosterone
• Protects against natriuretic effect of progesterone and ANP
• May modulate trophoblast growth and placental size
CHANGES IN NEUROMUSCULAR SYSTEM

I. CENTRAL NERVOUS SYSTEM


o Transient pregnancy-related memory decline limited to 3 rd trimester
o Women often report problems with attention, concentration and memory throughout pregnancy and the
early puerperium.
o Intraocular pressure decreases during pregnancy due to greater vitreous outflow
o Corneal sensitivity is decreased, corneal thickness
o Krukenberg spindles (brownish opacities on posterior surface of cornea) may be seen
o Visual function is unaffected by pregnancy
o Difficulty falling asleep, frequent awakening, decreased sleeping time, reduced sleep efficiency
seen after 12 weeks AOG
o Sleep disruption postpartum may contribute to postpartum “blues” or depression
II. MUSCULOSKELETAL SYSTEM

o Progressive lordosis: characteristic feature of normal pregnancy


o Shift center of gravity dorsally and over the lower extremities
o Sacroiliac, sacrococcygeal, pubic joints; increased mobility
o Joint laxity & discomfort does not correlate with levels of
estradiol, progesterone or relaxin

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