Physiological changes of
pregnancy
Tom Archer, MD, MBA
UCSD Anesthesia
Outline
• Normal changes
–
–
–
–
–
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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 (50%)
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 HCO3Lots 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
in 2008
Genetic
Obesity
Inflammation
Insulin resistance
predisposition
Hyperglycemia
Atherosclerosis
Decreased
insulin output
Nephropathy
Retinopathy
Neuropathy
Pancreatic beta
cell damage
Immune dysfunction
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.
• Case at UTHSCSA of AS, decompensation
with balloon valvuloplasty, emergency AVR,
fetal death, maternal improvement in AS.
For stenotic heart / lung lesions,
highest stress ( highest CO) occurs
immediately after delivery.
Pulmonary
capillaries
LV dilation / hypertrophy
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
capillaries
(edema)
LV failure /
ischemia
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
www.pitt.edu/~super1/lecture/lec9691/018.htm
Volume overload eg
pregnancy or athletics
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 nonpregnant 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 nonpregnant 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/scubaweb.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
Chestnut
At term
PaCO2
Nonpregnant
40
PaO2
100
103
pH
7.40
7.44
HCO3-
24
18
30
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
pregnancy:
Inflammation
Genetic
“Glucotoxicity”
Insulin resistance
predisposition
#1
Placental
hormones
Decreased
insulin output
Hyperglycemia
Placental vascular
damage
#2
Atherosclerosis
Nephropathy
Retinopathy
Pancreatic beta
cell damage
Neuropathy
Immune dysfunction
Poor wound healing
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