4/11 Maternal Adaptation of Pregnancy Flashcards
(40 cards)
Given the fetal/pregnancy need for perfusion, what is the maternal response (generally)?
- Volume expansion
- Vasodilation
- incr cardiac output
Given the fetal/pregnancy need for nutrition and oxygenation, what is the maternal response (generally)?
- Incr respiration
- Increased O2 delivery
- Insulin resistance
- Increased intestinal absorption
Given the fetal/pregnancy need for clearance of waste and toxins, what is the maternal response (generally)?
- Incr renal glomerular filtration
- Incr hepatocellular clearance
Given the fetal/pregnancy need for the mother to survive a potential hemorrhage, what is the maternal response (generally)?
-Increaed coagulation
During pregnancy, by how much does the mom’s plasma volume increase?
What is the mechanism for this?
Plasma vol increases by 50% (incr body water of 6-8 L!)
Mech: RAAS system
Increased angiotensinogen and renin activity -> At I converts to At II
AtII acts on adrenal gland to increase Aldosterone
Aldosterone promotes sodium retention
Sodium retention leads to water retention!

By how much does the mom’s RBC volume increase during pregnancy?
RBC volume increases by ~30%
During pregnancy, how much additional iron does mom’s body require?
At what Hgb level do we worry about iron-deficiency?
(there is increased iron absorption in the gut - duodenum)
Pregnancy requires ~ 1gram additional elemental iron
-Hemoglobin level of <10.5 g/dL anytime during preg is likely iron-deficiency anemia
What is physiologic anemia of pregnancy? How does it occur?
Relative dilution of the cellular component of blood (remember the plasma volume expands ~50% but RBC volume expands ~30%).
Therefore the hematocrit and hemoglobin levels fall
She stressed this: during pregnancy, what hemoglobin level defines iron-deficiency anemia?
Normal level of hemoglobin is >10.5 during all trimesters.
Not iron deficiency anemia unless Hgb is < 10.5
how does the increase in total blood volume (40-50%) help a pregnancy?
- Facilitates maternal and fetal exchange of resp gases, nutrients, metabolites
- Supports production of amniotic fluid (by perfusing uterus/plaenta)
- Buffers postpartum blood loss (women lose 500-1000cc at delivery)
–>Maternal hypervolemia is a normal state of pregnancy.
Pregnancy is a hypercoagulable state: what is the mechanism for this?
Why might this be evolutionarily adaptive?
-Increased amts of coagulation factors (I, VII, VIII, IX, X)
Adaptive: prevents excessive bleeding w delivery
Women are hypercoagulable during pregnancy: what is the downside?
(review: elements of Virchow’s triad?)
10x increased rate of venous thrombo-embolism compared to non-preg women (#2 cause of maternal death)
(Virchow’s is fulfilled: hypercoagulability, venous stasis, vascular trauma [@ delivery])
Maternal immune function during preg: generally what occurs?
Generally pregnancy is an immunocompromised state
The uterus, uterine lymphatics, and placenta adapt their immune response to allow the foreign embryo.
Ex: placenta does not express MHC I or MHC II
What are the risks to mom of altered systemic immune function during preg?
specifically what pathogens do we worry about?
Risk of severe complications from some pathogens.
Viral: Influenza, Varicella (major causes of maternal morbidity/mortality)
Bacterial: Listeria
Parasite: Malaria
What are a few changes to the heart/CV system that mimic cardiovascular disease?
- Dyspnea, SOB
- Fatigue
- Decr exercise tolerance
- Peripheral edema
- Systolic Murmur and S3
- Cadriomegaly on CXR
- Heart placed superior, lateral, and anterior due to uterus
Changes to heart sounds during pregnancy?
2 main changes:
Systolic Ejection Murmur (SEM) & S3
(will hear SEM at left sternal border)
Other changes: S1 louder and widely split, S2 persistent splitting, S4 (uncommon), mammary hum due to incr breast blood flow
by how much does cardiac output increase with pregnancy?
What happens with HR and SV?
incr by 30-50%
HR and SV also increase –> hyperdynamic state
What factors affect cardiac output during preg?
What factors appear near the end of pregnancy?
- increased CO with exertion, labor
- Near end of preg, mom’s posture affects CO: called Supine Hypotension Syndrome.
define Supine Hypotension Syndrome
(aka Inferior vena cava syndrome, aka postural hypotension)
- Huge uterus can compress the vena cava and decrease venous return so CO decreases. can result in bradycardia, hypotension, syncope.
Tx: roll patient on her side to relieve pressure!
- Aortic compression can decrease blood flow to uterus. In this case, the fetal heart rate will change.
What changes take place with the mom’s vasculature during preg?
Overall, vasodilation
- Peripheral vasculature becomes less responsive to vasoconstrictive effects of At II
- Progesterone promotes smooth muscle relaxation
What happens to systemic vascular resistance during preg?
Decreases overall as peripheral vessels relax
Also, placenta acts as a large AV fistula to decrease SVR.
What changes to BP are expected during preg?
What BP levels are never normal in pregnancy?
BP will decrease early, reach lowest point in mid-pregnancy due to decreased SVR.
Will return to near-normal levels by end of preg.
BP >= 140/90 is never normal in pregnancy!

The (normal) systolic ejection murmur often heard during pregnancy: what is the cause? where do we listen for this?
Usual cause of SEM is a flow murmur from pulmonic blood flow.
Heard at LLSB
What explains the sensation of dyspnea that affects 60-70% of preg women?
May be due to progesterone which increases the sensitivity of central CO2 chemoreceptors -> makes you feel out of breath, want to breathe more (works to exhale the fetal CO2)