Hematologic System
Maternal blood volume begins to increase early in pregnancy as
a result of changes in osmoregulation and the renin-angiotensin system causing sodium
retention and increasing total-body water to 8.5 L.[14]
By term, blood volume increases by up to 45% whereas red cell volume increases by
only 30%. This differential increase leads
TABLE 58-2 -- Effect of pregnancy on cardiovascular investigations
|
Investigation |
Findings |
|
Chest radiography |
Apparent cardiomegaly |
|
Enlarged left atrium (lateral views) |
|
Increased vascular markings |
|
Straightening of left-sided heart border |
|
Postpartum pleural effusion |
|
Electrocardiography |
Right axis deviation |
|
Right bundle branch block |
|
ST segment depression of 1 mm on left precordial leads |
|
Q waves in lead III |
|
T-wave inversion in leads III, V2
, and V3
|
|
Small decrease in PR and QT interval (heart rate dependent) |
|
Rotation ±15 degrees (QRS axis) |
|
Echocardiography |
Trivial tricuspid regurgitation (up to 43%–93% at term) |
|
Pulmonary regurgitation (up to 94% at term) |
|
Increased left atrial size by 12%–14% |
|
Increased left ventricle end-diastolic dimensions by 6%–10% |
|
Inconsistent increase in left ventricle thickness |
|
Mitral regurgitation (28% at term) |
|
Pericardial effusion (40% postpartum) |
|
Modified from Gei AF, Hankins GDV: Cardiac disease
and pregnancy. Obstet Gynecol Clin North Am 28:465–512, 2001. |
TABLE 58-3 -- Coagulation factors in pregnancy
|
Factor |
Change |
|
II |
Unchanged |
|
VII |
Increased + + + |
|
VII, IX, X, XII |
Increased |
|
XI |
Reduced |
|
Fibrinogen |
Increased + + + |
|
Platelets |
Stable |
|
From Birnbach DJ, Gatt SP, Datta S (eds): Textbook
of Obstetric Anesthesia. New York, Churchill Livingstone, 2000, p 41. |
to "physiologic anemia" of pregnancy with an average hemoglobin and hematocrit of
11.6 g/dL and 35.5%, respectively.[15]
However,
oxygen transport is not impaired by this relative anemia because the mother's body
compensates for it by increased cardiac output, increased partial pressure of arterial
oxygen, and a rightward shift in the oxyhemoglobin dissociation curve.
A state of hypercoagulability exists in pregnancy, with increased
levels of most coagulation factors ( Table
58-3
). Fibrinogen and factor VII are markedly increased, whereas the other
factors increase to a lesser extent. This increase in coagulation factors has been
verified by thromboelastography[16]
and is probably
a protective adaptation to lessen the risks associated with the acute hemorrhage
that occurs at delivery. This hypercoagulable state, however, may lead to thromboembolism,
which remains one of the leading causes of maternal mortality. The platelet count
remains unchanged throughout most of pregnancy, but it may be slightly reduced in
the third trimester with increased activity in vivo. The platelet count increases
in the postpartum period, probably because of activation of hemostasis at the time
of delivery. The incidence of low platelet counts in normal pregnancy is approximately
8%.[17]
However, it appears that mild thrombocytopenia
during the latter part of pregnancy is not associated with adverse sequelae. It
has been suggested that obstetric management of parturients with stable platelet
counts above 50,000 × 109
should be no different
from that of normal parturients.[18]
In addition,
although the cutoff for initiation of neuraxial blocks was considered to be 100,000
× 109
in the past, this level is no longer considered
absolute. Currently, most anesthesiologists feel comfortable initiating a regional
technique with platelet counts above 75,000 × 109
and with counts between 50,000 and 75,000 if the level is stable and clinical laboratory
abnormalities or signs of a coagulopathic state are absent.
 |
