Physiological

Adaptation during
pregnancy, labor and
early postpartum
period
Shinta Prawitasari
 Highlight
• Understand the physiological adaptation during
pregnancy and its impact on mother’s body

• Understanding the physiological adaptation during

labor and its impact on mother’s body

• Understanding the phyiological adaptation during

early postpartum period and its impact on mother’s
body
NORMAL PHYSIOLOGICAL
ADAPTATION DURING PREGNANCY
• Physiologic adaptation:
– Cardiovascular
– Respiratory
– Hematologic
– Endocrine
– Urinary
– Gastrointestinal

• Pregnancy as a “stress test for life”  Underlying

disease  manifest during pregnancy
 Cardiovascular Adaptation

– Increased blood volume / red blood cell

mass
– Decreased HCT and viscosity
– Increased cardiac output (CO)
– Reversible cardiac hypertrophy (50%)
• Blood volume increased by 45%.
• RBC volume increased by 15%.
• Hct falls blood viscosity fall
• The Impact: Pregnant woman may tolerate
hemorrhage better than non-pregnant
woman, before showing fall in BP.
 Cardiac output

• Increase O2 demand Increased Cardiac Output (CO).

• Increased CO achieved by slight increase in heart rate

and increase in stroke volume (SV).

CO = HR x SV

• But why does the blood pressure remain stable with

increased CO?  Decreased systemic vascular
resistance (SVR).
 Stroke volume ( 30%)
 Heart rate ( 15%)
 SVR ( 5%)
 Systolic BP ( 10 mmHg)
 Diastolic BP ( 15 mmHg)
 Mean BP ( 15 mmHg)
 O2 ( 20%)
Consumption
 ECG Changes
• Increased heart rate ( 15%)

• 15° left axis deviation.

• Inverted T-wave in lead ІІІ.

• Q in lead ІІІ & AVF

• Unspecific ST changes
 The impact of increased CO

• Increased CO in pregnancy increases

symptoms from stenotic heart lesions or
pulmonary hypertension
 Pulmonary LV dilation / hypertrophy
capillaries
Tricuspid
Aortic
stenosis

Pulmonic Mitral

Aortic stenosis at rest

Cardiac output not sufficient to cause
critically high LV intracavitary pressure /
LV failure.

Resistance arterioles
 Hematologic Adaptation at term

• Fibrinogen increased.
• PT, PTT shortened 20%.
• Increased platelet
turnover.
• Increase in coagulation
factors,
• immobilization and
aorto-caval
compression all
increase risk of DVT.
 Mom
4 ml O2 / kg / min

Feto-placental unit
12 ml O2 / kg / min

Mother is consuming and delivering

oxygen for two!

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Respiratory Adaptation
 Pulmonary Function
• The functional residual
capacity (FRC) and the
residual volume of air are
decreased due to the
elevated diaphragm.

• Lung compliance remains

unaffected.

• Airway conductance is
increased and total
pulmonary resistance is
reduced, possibly as a
result of progesterone
action.
 Pulmonary Function
• The respiratory rate is little
changed.

• Tidal volume, minute

ventilatory volume (MVV),
and minute oxygen uptake
increase significantly as
pregnancy advances.

• T V by about 40% lead to

MVV from 7.25 liters to 10.5
liters.
 Physiological changes
of pregnancy at term:
• Maternal-fetal O2 consumption increases 40-50% over non-
pregnant state.

• Cardiac output increases by 50%.

• Functional residual capacity (apneic reserve of O2) is reduced

to 80% of non-pregnant value by term.
• FRC of pregnant woman in supine position is 70% of that in
sitting position.

Pregnant patient has diminished capacity to tolerate apnea!

Chestnut chap. 53
• Functional residual
capacity (FRC) is our “air
tank” for apnea.
• Pregnant Mom has a
smaller “air tank”.

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/blog/images/scuba-
web.jpg
 Endocrinologic Adaptation
• Pregnancy is “diabetogenic”  Placental
hormones plus obesity may overwhelm
adaptive capacity of pancreatic insulin
output.
 Gestational DM:
• Appears in 4% of pregnancies. Possibly due to
inability to make enough insulin to counteract the
“counteregulatory hormones” which increase in
pregnancy—placental lactogen, placental Growth
Hormone, cortisol and progesterone.

• Gestational DM tends to recur in subsequent

pregnancies. Gestational DM increases risk for
type 2 DM later in life.
 Pregestational DM:
Insulin requirements increase rapidly after the
26th week of gestation. Insulin requirement at
term is about 50% more than pre-pregnant
requirements.
 Urinary Tract Adaptation

• Glomerular Filtrate Rate increases, normal

creatinine falls.
• “Normal” creatinine may show disease!
• Progesterone relaxes ureters
• Compression of ureters at pelvic brim due to
enlarged uterus  further obstruction
infection
 Urinary system
• Its impact:
• Ureteral obstruction with hydropnephrosis
and pyelonephritis is common.
• 1/200 pregnancies will have urolithiasis
Gastrointestinal adaptation

• Reduced motility in small intestine lead to increase time

of absorption.

• Reduced motility of large intestine lead to increase time

for water absorption that predisposes to constipation.

• Its impact: Gastroesophageal Reflux Disease (GERD) is

common
 Hepatobiliary
• Serum AST,ALT, bilirubin levels are slightly
lower than non pregnant normal values.

• Serum concentration of albumin decreases.

• Decrease in albumin to globulin ratio occurs

due to combined reduction in albumin
concentration & slight increase in serum
globulin levels.
 Gallbladder changes
• Reduced contractility of the gallbladder  Due to high levels
of estrogen as well as increased progesterone & genetic
factors  leads to stasis cholesterol saturation of
pregnancy  cholesterol stone in multiparous.

• Its impact: Pregnancy causes intrahepatic cholestasis

&pruritus gravidarum from retained bile salts.
PHYSIOLOGIC ADAPTATION DURING
LABOR
 Labor and Delivery

– Pain / Anxiety – can increase CO by 50-61%

– Uterine contraction – 300-500 mL infusion into central
venous system

Elkayam U et al. Cardiac Problems in Pregnancy. 1990. 16.

Cardiocirculatory effects of uterine contraction

Parameter Change Comments

Blood Volume Increase 300-500 mL

Cardiac Output Increase 30-60% increase

Heart Rate Increase or Decrease

Blood Pressure Increase SBP and DBP

Peripheral Unchanged
Resistance
O2 Consumption Increase 100% increase
– Hemodynamic
changes of pregnancy
less dramatic in lateral
position

– Maneuvers in delivery
position depending on
cardiac pathology
Anaesthesia consideration during
labor
– Epidural anesthesia – systemic vasodilation that
can reduce SV
• Poorly tolerated in patient who cannot increase SV,
fixed CO
– Cesarean section – with General Endotracheal
Anaesthesia (GETA)
• Reduced maternal metabolic needs and stabilization of
blood volumes
 Gastrointestinal
• Gastric emptying time is
unchanged during
pregnancy,but during
labor and with
administration of
analgesics prolonged
that lead to aspiration.
PHYSIOLOGIC ADAPTATION DURING
EARLY POSTPARTUM PERIOD
 Hemodynamic Changes Postpartum
Parameter Change Comment
Blood Volume Decrease Blood loss
CO Increase 60-80% immediate
increase followed by rapid
decrease, returns to normal
levels in few weeks
SV Increase
HR Decrease
BP Unchanged
SVR Increase Loss of low resistance
placenta
• CO highest right after delivery (release of
aorto-caval compression) and uterine
contraction (autotransfusion).

• For stenotic heart / lung lesions, highest stress

( highest CO) occurs immediately after
delivery.
 Pulmonary LV failure /
capillaries ischemia
(edema)
Tricuspid Aortic
Stenosis

Pulmonic Mitral

Aortic stenosis with

increased cardiac output /
arteriolar vasodilation:
Decreased SVR Fall in systemic BP and
/ or increase in LV intracavitary pressure
ischemia or LV failure.

Resistance arterioles– decreased SVR

 References
• Tom Archer, MD, MBA
• ROBAB DAVAR M.D.
Thank You