Physiological changes of

pregnancy

Tom Archer, MD, MBA

UCSD Anesthesia
 Outline
• Normal changes
– CV
– Respiratory
– Hematologic
– Endocrine
– Urinary
– GI

• Implications for pathological conditions.

• Pregnancy as a “stress test for life”
– Unveils problems that will appear later.
 Outline
Cardiovascular changes:

To meet increased metabolic demand.

Increased blood volume / RBC mass

Decreased Hct and viscosity

Increased cardiac output deterioration in symptoms from

stenotic heart lesions or pulmonary hypertension.
 Outline
Cardiovascular changes:

Reversible cardiac hypertrophy (30%?)

Valvular incompetency / conduction changes

All murmurs are not “flow murmurs”! But most

are innocent.
 Outline
Hematologic changes:

Increased clotting tendency

Increased fibrinogen

Decreased PT / PTT

Stasis in legs DVT

Increased platelet turnover.

 Outline
Respiratory changes:

Increased O2 consumption / CO2 production

Decreased PaCO2 and venous HCO3-
Lots of normal saline will cause hyperchloremic
metabolic acidosis.
Increased work of breathing
Decreased FRC (“airtank” reserve)
Decreased tolerance for apnea or hypoventilation.
Airway swelling.
 Outline
Endocrine (insulin) changes:

Pregnancy is diabetogenic due to placental hormones

(Placental lactogen, HGH, cortisol, progesterone).

Insulin requirement increases during pregnancy.

Insulin requirement falls abruptly after delivery.

RAAS probably influences cardiac hypertrophy and

increased RBC mass.
Type II DM Obesity
in 2008 Inflammation

Genetic Insulin resistance

predisposition

Hyperglycemia
Atherosclerosis
Decreased Nephropathy
insulin output
Retinopathy
Neuropathy
Pancreatic beta Immune dysfunction
cell damage
Poor wound healing
 Outline
Urinary changes:

GFR increases, normal creatinine falls.

“Normal” creatinine may show disease!

Ureteral obstruction with hydropnephrosis and

pyelonephritis is common.

1/200 pregnancies will have urolithiasis

 Outline
GI changes:

GERD is common

Gastric emptying is impaired during labor

assume full stomach

Routine “triple Rx” before C/S? Bicitra,

metoclopramide, famotidine.
 Mom
4 ml O2 / kg / min

Feto-placental unit
12 ml O2 / kg / min

Mother is consuming and delivering

oxygen for two!

www.studentlife.villanova.edu
 CV in pregnancy– Big Picture

• Increase O2 demand Increased CO.

• Stable BP with increased CO means

decreased SVR.

• Slight increase in HR, Increase in SV.

 Cardiac output increases
• 35% by 12 weeks

• 50% for rest of pregnancy

• 60%-100% during labor

• CO highest right after delivery (release of

aorto-caval compression) and uterine
contraction (autotransfusion).
Increased CO in pregnancy increases
symptoms from stenotic heart lesions
or pulmonary hypertension

• May need interventional procedure (balloon

mitral valvuloplasty, AVR) or termination of
pregnancy.
 For stenotic heart / lung lesions,
highest stress (highest CO) occurs
immediately after delivery.
 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
 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

 Eccentric cardiac hypertrophy
in pregnancy

• Due to increased activity of RAAS?

Non-pregnant vs late pregnant mouse hearts. Note hypertrophy and conduction
disturbance (QRS prolongation) in LP mouse heart.

Eghbali M (Trends Cardiovasc Med 2006;16:285–291)

 Pressure overload eg AS Volume overload eg
pregnancy or athletics

www.pitt.edu/~super1/lecture/lec9691/018.htm
Hematologic changes at
term:
Blood volume increased by 45%.
RBC volume increased by 15%.
Hct falls blood viscosity falls

Pregnant woman may tolerate

hemorrhage better than non-
pregnant woman, before showing
fall in BP.
 Average blood loss at delivery:

• 600 ml with vaginal delivery.

• 1000ml with C/S.

Hematologic changes 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.
 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)

decreases by 20%

Pregnant patient has diminished capacity to tolerate

apnea!
Chestnut chap. 53
Functional residual capacity (FRC) is our “air tank” for apnea.

www.picture-newsletter.com/scuba-diving/scuba... from Google images

Pregnant Mom has a smaller “air tank”.

Non-pregnant
woman

www.pyramydair.com
/blog/images/scuba-
web.jpg
 Pregnant woman: a respiratory
disaster waiting to happen
• Lung Volumes and implications:
• FRC is reduced to 80% of non-pregnant value by term.
• FRC of pregnant woman in supine position is 70% of that in sitting
position.
• Regional anesthesia further decreases the FRC!
• HENCE: SUPINE, PREGNANT PATIENT WITH A REGIONAL
BLOCK HAS A TRIPLY DIMINISHED FRC!!!
• OBESITY IS A FOURTH FACTOR DECREASING FRC!
• Anesthetic implication: VERY rapid desaturation in pregnant patients
after apnea due to rapid sequence induction or seizure.
• YOU MUST DO A GOOD PRE-OXYGENATION PRIOR TO
INDUCTION OF GA!
• YOU MUST HAVE ALL OF YOUR AIRWAY SUPPLIES
IMMEDIATELY AVAILABLE!
 At term, mother has respiratory alkalosis with
metabolic compensation (less HCO3- buffer).

ABGs Non- At term

pregnant
PaCO2 40 30

PaO2 100 103

pH 7.40 7.44

HCO3- 24 18

Chestnut
Compared to non-pregnant state, pregnant
woman has less tolerance for:

• Apnea

• Acidosis
 Vascular congestion

• Swelling of respiratory mucosa (nose, rest

of airway).

• Don’t put anything through the nose if you

can avoid it  prevent bad nose bleed.
 Pregnancy is “diabetogenic”.
Why?

• Placental hormones plus obesity may

overwhelm adaptive capacity of pancreatic
insulin output.
Two vicious cycles Obesity
of type II DM in
Inflammation
pregnancy:
“Glucotoxicity”
Genetic Insulin resistance
predisposition
#1
Placental
Hyperglycemia
hormones
Placental vascular
damage
Decreased Atherosclerosis
insulin output #2
Nephropathy
Retinopathy
Pancreatic beta Neuropathy
cell damage Immune dysfunction
 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 GH,
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.

Insulin requirements fall during first stage of labor,

but rise during second stage of labor.

Insulin requirement falls up to 40% the day after

delivery. Placental hormones are “diabetogenic”.
 Urinary system
• Renal infections increase in incidence.

• Progesterone relaxes ureters

• Compression of ureters at pelvic brim

obstruction infection
 GI tract

• Decreased gastric emptying

• Increase GERD

• Full stomach precautions

 Avoid aorto-caval compression: use
left uterine displacement (LUD)

• LUD helps venous return. C/S as part of

resuscitation?
• LUD decreases chance of DVT
• LUD increases O2 delivery to fetus:
– Increases uterine artery pressure and decreases uterine
venous pressure.

•Why we don’t do it: It doesn’t look right!

Colman-Brochu S 2004
Chestnut chap. 2
The End