28/2/23, 17:01 Physiology, Maternal Changes - StatPearls - NCBI Bookshelf

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Physiology, Maternal Changes

Authors

John M. Kepley1; Kaitlyn Bates2; Shamim S. Mohiuddin3.

Affiliations
1 San Antonio Military Medical Center
2 Central Michigan University College of Medicine
3 Imam Abdulrahman Bin Faisal University, Dammam

Last Update: February 9, 2022.

Introduction
Maternal changes are purely physiological in nature.There are myriad of physiologic changes that occur in the
pregnant patient in response to the growing fetus.During pregnancy period, these all changes are basically an
adaptation process, so that the body of a pregnat female can accomodate the growing embryo as well as the growing
fetus. One obvious factor that affects maternal physiology is the mass effect of the growing fetus and the
ramifications placed on the cardiovascular, pulmonary and gastrointestinal system. As the placenta develops and the
uterus enlarges, these organs receive a greater proportion of blood flow. Other organs such as the kidneys receive
more blood to filter waste from both the fetus and the mother. Hormonal upregulation has downstream effects in
multiple systems as well. The hormone relaxin has a known impact on both vascular tone and connective tissue
(among other areas), whereas, estrogen and progesterone activity have an impact on renal water retention and serum
electrolytes concentrations. These physiologic changes have clinical ramifications that practitioners should be aware
of when caring for the parturient.

Organ Systems Involved

Cardiovascular

There are myriad of physiologic changes that occur to the parturient throughout pregnancy. Each organ system is
affected differently by the demands of the growing fetus. As early as five weeks into the first trimester maternal
cardiac output increases by about 50% by the end of eight weeks.[1] This change is mostly the result of increases in
heart rate; however, stroke volume also increases by about 30% by the start of the third trimester as reflected by an
increase in the velocity of left ventricular muscle fiber shortening.[1][2] This increase in cardiac output directs
towards the uterus, placenta, kidneys, skin, and extremities.Cutaneous and extremity blood flow raises maternal skin
temperature and is a mechanism of maternal thermoregulation.[3] There is as much as an 80% increase in plasma flow
to the kidneys during the second trimester alone.[4] Notably, blood flow to the liver and brain do not increase
throughout pregnancy.

During labor, maternal cardiac output increases by 40% compared to the nonpregnant patient and are followed by an
increase to 75% following delivery.[5] This significant increase in cardiac output is a consequence of greater venous
return and sympathetic tone. During active labor, uterine contractions “auto-transfuse” about 500 mL of blood back
into maternal circulation.[6] Following delivery, cardiac output increases are primarily a result of relief of inferior
vena cava (IVC) compression.

The degree of IVC compression depends on gestational progression and maternal positioning. When a term patient
assumes the supine position, the IVC is almost entirely collapsed, significantly reducing venous return and thus
cardiac output.[7][8] However, the venous return does not suffer complete compromise in the supine position as
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collateral vessels (vertebral veins, and epidural veins) provide a conduit for venous return.[9] Supine hypotension
syndrome can result from parturient supine positioning and is hypotension so severe that the heart cannot compensate
with increased pulse rate and results in concordant bradycardia.[10]

Pulmonary and Respiratory

The mass effect of the gravid uterus not only affects the cardiovascular system. The pulmonary system must adapt to
the growing fetus. Functional residual capacity (FRC) is composed of both expiratory reserve volume and residual
volume. The FRC decreases as much as 10 to 25% as pregnancy progresses. Despite this, tidal volume increases by
about 45%. Minute ventilation increases secondary to this increase in tidal volume.[11] The hormone progesterone
also plays a role as it stimulates respiration.[12] From hyperventilation, the arterial partial pressure of oxygen (PaO2)
increases to 105 mmHg,[13] while the arterial partial pressure of carbon dioxide (PaCO2) decreases to about 30
mmHg.[14] This blood gas change results in a respiratory alkalosis and is metabolically compensated for by a
reduction in serum bicarbonate to approximately 20 mEq/L.[15]

During labor, minute ventilation increases even more by as much as 140% to 200% depending on the stage of labor
leading to an even more pronounced decrease in PaCO2[16]. Metabolic oxygen consumption rises during labor as a
result of uterine contractions, sympathetic activity and maternal Valsalva maneuvers to deliver the fetus. As demand
for oxygen outpaces oxygen delivery during active labor, anaerobic metabolism results and there is lactic acid
production.[17]

Hematologic

Maternal physiology does provide a mechanism to increase oxygen delivery throughout pregnancy. Red blood cell
(RBC) volume increases by about 30% at term gestation.[18] Plasma expansion, however, increases even more than
RBC volume which results in physiologic anemia of pregnancy. Overall, a physiologic hypervolemic state ensues
which helps to meet the nutritional demands of the growing fetus. Both estrogen and progesterone have a role in
retaining sodium and water. Estrogen triggers the renin-angiotensin-aldosterone system (RAAS) while progesterone
activity also leads to the production of aldosterone. This increase in volume status helps to protect against hypotension
respective to patient position. At term, hypervolemia also provides a buffer against blood loss due to delivery. This
propensity for blood loss at delivery also gets mitigated by an increase in coagulation status during pregnancy. Most
coagulation factors (I, II, V, VII, VIII, X, and XII) increase throughout pregnancy.[19][20] Consequently, the pregnant
condition is considered to be a hypercoagulable state. This hypercoagulability places the pregnant patient at almost a
five times higher risk of developing deep vein thrombosis than the nonpregnant female.[21] While coagulation status
increases, the immune system is slightly compromised during pregnancy, which is thought to be one reason why
pregnant patients are more susceptible to infections versus nonpregnant females.[22] Moreover, this is one hypothesis
as to why pregnant patients with coexisting autoimmune disease experience fewer disease exacerbations.

Renal

As previously mentioned, a significant portion of the cardiac output is preferentially directed to the maternal kidneys;
this causes about a 30% increase in renal size.[23] With increased renal blood flow, glomerular filtration rate (GFR)
rises as well about 50% higher than the nonpregnant state.[4] With increased renal plasma flow and GFR, serum
creatinine and blood urea nitrogen (BUN) decrease during pregnancy. In response to the aforementioned respiratory
alkalosis, renal excretion of bicarbonate increases.

Gastrointestinal

The gastrointestinal system is another system that changes due to the mass effect of the growing fetus. The stomach
becomes slightly displaced and rotated during pregnancy. This anatomical change causes a reduction in lower
esophageal sphincter tone, leading to an increased propensity for reflux of gastric contents.[24] Gastric contents
empty at a normal nonpregnant rate throughout pregnancy.[25] Gastric pH is about 20% lower in pregnancy as

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opposed to the nonpregnant female.[26] Intestinal transit times increase in pregnancy, and this can lead to
constipation.[27]

Endocrine

Several other hormonal signaling pathways are activated during pregnancy in addition to estrogen and progesterone.
Relaxin mediates nitric oxide release during pregnancy which allows for systemic vasodilation and decreases in blood
pressure during pregnancy.[28]  Additionally, relaxin accounts for the remodeling of connective tissue throughout the
parturient resulting in laxity of the pelvic girdle. This hormone has implications in pregnancy-related lower back pain.
[29] Thyroid hormone production increases by about 50% during pregnancy but free T3 and free T4 remain
unchanged due to the simultaneous increase in thyroid-binding globulin.[30] Endorphins and enkephalin
concentrations increase in pregnancy leading to an elevated pain threshold to counteract the pain due to labor.[31]
Free cortisol levels are about 2.5 times higher in the pregnant versus nonpregnant state.[32]

Clinical Significance
Maternal physiology changes have an impact on clinical decision making. One area where these changes have a
significant impact is in obstetric anesthesia. The anesthetic implications for the obstetric patient places on the
anesthesia are many. Increased tissue friability and edema can make securing an endotracheal tube more challenging.
Decreased residual capacity coupled with increased oxygen consumption allows little time to place an endotracheal
tube before rapid oxygen desaturation occurs. Decreased lower esophageal tone and lower gastric pH put the
parturient at a higher aspiration risk during general anesthesia. Virtually every organ system is impacted by pregnancy
to some degree, and the anesthetist must know about these physiologic changes to best care for the obstetric patient.

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References
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