Maternal Adaptations To Pregnancy: I
Maternal physiology must adapt in response to
a series of demands attendant to pregnancy (Fig. 20.1). The pregnant woman
needs to increase her circulating blood volume to supply nutrients to the fetus
and to support amniotic fluid production. She must clear fetal waste products
and protect her pregnancy from systemic perturbations, including starvation or
medication ingestion. She must meet fetal and placental nutritional demands for
glucose, amino acids and oxygen. The maternal system must adapt to allow for
timely onset of labor and for protection of the mother from cardiovascular
insults at the time of delivery. It must also prepare to support nourishment of
the infant after delivery. All maternal organ systems are affected to some
degree.
Cardiovascular system
During the first two trimesters
of pregnancy, maternal circulating blood volume increases 40% (3500 cm3
expands to 5000 cm3) with the largest expansion occurring during the
second trimester (Fig. 20.2). The functions of pregnancy-induced hypervolumia
are to meet the demands of the enlarged uterus with its greatly hypertrophied
vascular system, to provide nutrients to the growing placenta and fetus, to protect
both mother and fetus from impaired venous return in certain postures, and to
ensure that the mother does not suffer any adverse effects from the obligatory
blood loss at delivery.
The increase in plasma volume
results from a combination of a modest (10 mOsm/kg) decrease in plasma
osmolality and from water retention through enhanced activity of the
renin–angiotensin system. Placental estrogen increases hepatic production of
angiotensinogen, and estrogen and progesterone together increase renal
production of the proteolytic enzyme, renin. Renin cleaves angiotensinogen to
form angiotensin I, which converts into angiotensin II (AII) in the lung and elsewhere. The increased amounts of
AII act on the zona glomerulosa of the adrenal gland to increase aldosterone
production. Aldosterone promotes volume expansion through sodium and water
retention. Oxygen-carrying capacity must be maintained in the presence of this
increase in circulating blood volume. Iron absorption increases to meet the
demand for increased hemoglobin during volume expansion.
A loss of peripheral vascular
responsiveness to AII accompanies the increase in circulating blood volume. AII
is a potent vasoconstrictor and loss of AII responsivity results in a drop in
maternal blood pressure during the early second trimester. This relative
hypotension is seen in most pregnant women despite elevated AII levels.
Maternal blood pressure slowly rises to prepregnancy levels by the third trimester.
Progesterone promotes overall smooth muscle relaxation and is thereby partially
responsible for alterations in maternal blood pressure. Production of
prostacyclin, the principal endothelial prostaglandin, also increases during
pregnancy and has been implicated in the development of angiotensin resistance.
Immediately following delivery of
the fetus and placenta, a venous “autotransfusion” from the extremities, pelvis
and empty uterus into the right heart occurs. Women with a normal
cardiovascular system tolerate this event well but it is a major challenge for
women with mitral valve stenosis and Eisenmenger syndrome in whom the increased
venous return can result in pulmonary edema and hypoxia.
Respiratory system
An increase in tidal volume,
minute ventilatory volume and minute O2 uptake develops in pregnant
women. These changes allow for increased oxygen delivery to the fetus and the
periphery. They also cause a mild maternal respiratory alkalosis that is compensated for by increased renal
bicarbonate excretion. Progesterone may be responsible for many of these
changes. The decrease in plasma bicarbonate shifts the O2 dissociation
curve to the left and increases the affinity of maternal hemoglobin for oxygen
(the Bohr effect). This decreases the O2 releasing capacity of the
maternal blood which is offset by an increase in 2,3-diphosphoglycerate induced
by the increase in pH. This shifts O2 dissociation curve back to the
right. Fetal hemoglobin binds O2 at a lower partial pressure than
maternal adult hemoglobin. The net result of these changes is to favor transfer
of O2 from mother to fetus within the placenta and to facilitate CO2
(waste) transfer back from the fetus to the mother.
Many pregnant women have the
sensation of shortness of breath in the absence of pathology. This physiologic
dyspnea may be the result of decreased pCO2. It is important to note
that the blood gas pH of a pregnant woman should be in the alkalotic range with
a decrease in pCO2 and bicarbonate and, if not, requires further
investigation.
Kidney and urinary tract
Maternal glomerular filtration
rate (GFR) and renal plasma flow (RPF) begin to increase in early pregnancy. By
midpregnancy, maternal GFR has increased by as much as 50%; it remains elevated
throughout gestation. In contrast, maternal RPF begins to decrease in the third
trimester. As a result, the renal filtration fraction increases during the last
third of pregnancy. Because of the increased GFR, serum creatinine and urea are
lower in pregnancy than in the nonpregnant state. Creatinine clearance is
increased.
A 60–70% increase in the filtered
load of sodium also accompanies the increased GFR. Progesterone appears to
cause some sodium wastage by interfering with normal sodium resorption in the
proximal renal tubule. In response, aldosterone increases proportionately to
levels that are 2–3 times normal. Renal medullary prostaglandin E2
synthesis also increases in late pregnancy, enhancing sodium natriuresis.
The relatively fixed renal
tubular reabsorptive capacity, in combination with an increased GFR, causes a
decrease in the reabsorption of glucose from the proximal tubule of the
pregnant woman’s kidney. Glucose is therefore detectable in the urine of about
15% of healthy pregnant women. Still, any pregnant woman exhibiting glycosuria
should be evaluated for diabetes.
The volume of urine contained in
the renal pelves and ureters can double in the latter half of pregnancy. The
renal collecting system dilates during pregnancy
as a result of mechanical obstruction by the pregnant uterus combined with the
relaxing effects of progesterone upon smooth muscle. This dilatation decreases
the speed of urine passage through the renal system and increases the maternal
risk of developing acute kidney infections.
Hematologic system
Pregnant women are mildly anemic.
Maternal hemoglobin production and total red blood cell mass increase during
pregnancy in response to elevated erythropoietin production. Maternal vascular
volume increases to a greater extent. The result is a mild maternal dilutional
anemia that protects the mother from excess hemoglobin loss at delivery. The
iron requirements of normal pregnancy must satisfy both maternal and fetal red
cell production requirements and total about 1.0
g. Most is needed during the second half of pregnancy. Amounts of iron absorbed
from diet alone, as well as any mobilized from maternal stores, may be
insufficient to meet the demand.
Pregnant women develop a modest
leukocytosis that can become quite marked during labor and postpartum. The
etiology of the mild leukocytosis of early pregnancy is unclear. That seen
during labor, however, resembles the leukocytosis associated with strenuous
exercise, during which previously sequestered white cells re-enter the active
circulation.
Pregnant women are
hypercoagulable. Increased coagulability develops because of the increased
procoagulant synthesis in the liver (Chapter 21). Up to 8% of women will
develop a mild thrombocytopenia (<150 000 platelets/ml). This typically does
not result in a bleeding diathesis. The mechanism by which the thrombocytopenia
develops is unknown.
Skin
Circulating melanotrophic hormone
(MSH) is increased during pregnancy as a result of the increased production of
the precursor molecule proopiomelanocortin (POM-C) (Chapter 18). MSH causes
darkening on the skin across the cheeks (chloasma or pregnancy mask) and
darkening of the linea alba, the slightly pigmented line on the skin that runs
from the navel to the pubis. Hair may also appear to fall out in clumps because
of synchronization of hair follicle growth
cycles during pregnancy.
