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7/10/2018 Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes - UpToDate
Official reprint from UpToDate®

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Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes
Author: Michael R Foley, MD

Section Editors: Charles J Lockwood, MD, MHCM, Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editor: Kristen Eckler, MD, FACOG
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2018. | This topic last updated: Oct 10, 2017.
INTRODUCTION — The major pregnancy-related hemodynamic changes include increased cardiac output,
expanded blood volume, and reduced systemic vascular resistance and blood pressure. These changes contribute
to optimal growth and development of the fetus and help to protect the mother from the risks of delivery, such as
hemorrhage. Knowledge of these cardiovascular adaptations is required to correctly interpret hemodynamic and
cardiovascular tests in the gravida, to predict the effects of pregnancy on the woman with underlying cardiac
disease, and to understand how the fetus will be affected by maternal cardiac disorders.
The cardiovascular changes associated with normal pregnancy will be reviewed here. The management of specific
cardiac disorders, such as acquired and congenital heart disease, heart failure, and arrhythmias, are discussed
separately.
● (See "Acquired heart disease and pregnancy".)
● (See "Pregnancy in women with congenital heart disease: General principles".)
● (See "Pregnancy in women with congenital heart disease: Specific lesions".)
● (See "Management of heart failure during pregnancy".)
CHANGES RELATED TO PREGNANCY
Timeline of cardiovascular changes — These changes begin early in pregnancy, reach their peak during the
second and early third trimester, and then remain relatively constant until delivery (figure 1 and figure 2) [1].
● First trimester (conception to 13+6 weeks of gestation) – Maternal systemic vasodilation begins at
approximately 5 weeks of gestation [2]. Systemic vascular resistance (SVR) progressively drops by
approximately 35 to 40 percent and nadirs in the mid-second trimester while cardiac output begins to rise.
● Second trimester (14 to 27+7 weeks of gestation) – The reduction in SVR that began in the first trimester ends
in a plateau in the middle of the second trimester [2]. Cardiac output continues to rise, but in a nonlinear
fashion.
● Third trimester (28 weeks of gestation to delivery) – Cardiac output peaks in the early third trimester [2]. Heart
rate, which rises throughout gestation, peaks in the late third trimester at an average of 16 beats per minute
(24 percent) above nonpregnant values. Supine positioning reduces cardiac output and stroke volume and
increases heart rate due to compression of the aorta and vena cava from the enlarging uterus. Placing the
woman in the left lateral decubitus position shifts the uterus off the aorta and vena cava, which in turn
increases blood flow to the heart and results in increased cardiac output and stroke volume. Blood pressure
returns to prepregnancy levels during the third trimester.
● Intrapartum – Cardiac output increases by 15 percent above prelabor levels in early labor and 25 percent
during the active phase. During pushing in the second stage, cardiac output rises by 50 percent (figure 3). With
epidural anesthesia, the baseline increase in cardiac output is attenuated; however, the increases associated
https://www.uptodate.com/contents/maternal-adaptations-to-pregnancy-cardiovascular-and-hemodynamic-changes/print 1/15
with uterine contractions persist. Position changes from supine to lateral decubitus during labor increases
cardiac output. This effect is more pronounced during labor, suggesting that cardiac output during labor may
be more dependent on preload.
● Postpartum – Following birth, heart rate and blood pressure returns to non-pregnant values and remains
unchanged throughout the postpartum period [2].
Changes in blood volume
Timeline — Expansion of the plasma volume and an increase in red blood cell mass begin as early as the
fourth week of pregnancy, peak at 28 to 34 weeks of gestation, and then plateau until parturition [3-5]. Plasma
volume expansion is accompanied by a lesser increase in red cell volume (figure 4) [6]. As a result, there is a
modest reduction in hematocrit, with peak hemodilution occurring at 24 to 26 weeks. Compared with the blood
volume (65 to 70 mL/kg) in nonpregnant women, the blood volume in pregnant women at term is increased to 100
mL/kg [7].
Plasma volume — Plasma volume increases by 10 to 15 percent at 6 to 12 weeks of gestation [8-10], expands
rapidly until 30 to 34 weeks, and then plateaus or falls slightly (figure 4). The mechanisms of plasma expansion are
presented in detail in a related topic review. (See "Maternal adaptations to pregnancy: Hematologic changes",
section on 'Plasma volume'.)
Red blood cell mass — Red blood cell mass begins to increase at 8 to 10 weeks of gestation and steadily
rises, in women taking iron supplements, by 20 to 30 percent (250 to 450 mL) above nonpregnant levels by the end
of pregnancy [5,11-14]. Among women not on iron supplements, the red cell mass may only increase by 15 to 20
percent [15]. Increased plasma erythropoietin induces the rise in red cell mass, which partially supports the higher
metabolic requirement for oxygen during pregnancy [16]. (See "Maternal adaptations to pregnancy: Hematologic
changes", section on 'Red blood cells'.)
Physiologic anemia — A greater increase in intravascular volume compared with red cell mass results in the
dilutional or physiologic anemia of pregnancy. This becomes most apparent at 30 to 34 weeks of gestation when
plasma volume peaks in relation to red cell volume. Assuming normal renal function, blood volume and
constituents return to nonpregnant values by eight weeks postpartum, a result of diuresis. Hemoglobin begins to
increase from the third postpartum day [7].
The physiologic effects of hypervolemia and anemia during pregnancy have several benefits:
● Decreased blood viscosity (from greater increases in plasma volume than red cell volume) results in reduced
resistance to flow, facilitating placental perfusion and lowering cardiac work.
● Total intravascular volume increases to approximately 50 percent above nonpregnant values near term to
provide some reserve against the normal blood loss during parturition (about 300 to 500 mL for vaginal
delivery, 600 to 1000 mL for cesarean delivery) and peripartum hemorrhage [4,5]. During delivery, as much as
500 mL of blood sequestered in the uteroplacental unit is autotransfused to the maternal circulation, thereby
minimizing adverse circulatory effects from blood loss at delivery.
● Most of the increase in cardiac output is distributed to the placenta, kidneys, and skin to provide nutrients to
the fetus, excrete maternal and fetal waste products, and assist maternal temperature control, respectively.
The increases in renal blood flow and glomerular filtration rate during pregnancy are largely mediated by the
ovarian hormone relaxin, the release of which is increased by human chorionic gonadotropin [17]. (See
"Maternal adaptations to pregnancy: Renal and urinary tract physiology".)
The absence of physiologic anemia appears to be harmful [18,19]. A population-based, case-control study using
data from the Swedish Medical Birth Register reported that women with a hemoglobin concentration of 14.6 g/dL or
higher at the first prenatal visit were at increased risk of stillbirth (odds ratio [OR] 1.8), antepartum stillbirth without
malformations (OR 2.0), and preterm and small for gestational age nonmalformed stillbirth (OR 2.7 and 4.2,
respectively) [18]. The elevated risk persisted despite a subsequent fall in hemoglobin concentration and after
excluding women with preeclampsia. It is hypothesized that high blood viscosity increases the risk of thrombosis in
the uteroplacental circulation.
Changes in systemic hemodynamics — Maternal and fetal metabolic requirements increase as pregnancy
progresses. A change in the rate and distribution of cardiac output (the product of stroke volume and heart rate)
occurs during pregnancy to meet these demands (figure 5).
Heart rate — During normal pregnancy, the resting heart rate begins to rise in the first trimester, with an
average increase of 10 to 30 beats per minute (71 +/- 10 bpm) having been reported [20-22]. In one meta-analysis,
heart rate peaked in the late third trimester at an average of 16 bpm (83 +/- 10) (24 percent) above nonpregnant
values [2]. The maximum heart rate occurs in the third trimester and returns to baseline quickly postpartum. The
upper limit of resting heart rate is typically not greater than 95 bpm. Thus, pregnant women with resting heart rates
>100 bpm are generally considered to have tachycardia and warrant further evaluation [22].
Cardiac output
● Physiology – The cardiac output, calculated as the heart rate x the stroke volume, rises 30 to 50 percent (1.8
L/min) above baseline during normal pregnancy. The elevation in cardiac performance results in part from
changes in three important factors that determine cardiac output [20]:
• Preload is increased due to the associated rise in blood volume
• Afterload is reduced due to the decline in systemic vascular resistance
• Maternal heart rate rises (see 'Heart rate' above)
In early pregnancy, increased cardiac output is primarily related to the rise in stroke volume; one meta-analysis
reported an 8 percent increase (6 mL) in stroke volume in the first trimester [2]. In late pregnancy, heart rate
change is the major factor contributing to increased cardiac output. The ejection fraction is unchanged from
normal nonpregnant values, making it a reliable indicator of left ventricular function during pregnancy, although
the direct effect of pregnancy on left ventricular contractility remains controversial [23]. Although changes in
blood volume during pregnancy affect right ventricular preload, central venous pressure remains in the normal
nonpregnant range throughout pregnancy due to the reduction in cardiac afterload induced by the substantial
decrease in both systemic vascular resistance and pulmonary vascular resistance (ie, afterload to the left and
right heart, respectively) [24].
Regardless of the mechanism, the stress induced by the increase in cardiac output can cause women with
underlying and, in some cases, asymptomatic heart disease to decompensate during the latter half of
pregnancy. (See "Management of heart failure during pregnancy".)
● Cardiac function – The inherent contractility of the myocardium is stable to slightly improved in pregnancy
[25,26]. This stable to improved function may be a result of increased left ventricular mass, with the greatest
change, an increase of an average of 40 g (34 percent) above baseline, noted in the early third trimester [2].
Pulmonary capillary wedge pressure and pulmonary artery systolic and diastolic pressures remain in the
normal nonpregnant range since the hypervolemia of pregnancy is balanced by the fall in pulmonary vascular
resistance.
● Timing – About one-half of the increase in cardiac output occurs by eight weeks of gestation [20,27-30]. The
slope of increase in cardiac output slows in the late second trimester and drops in the late third trimester,
although it remains above prepregnancy levels until postpartum [2]. Increased venacaval compression by the
uterus, increased blood flow to the uteroplacental circulation, or both have been a proposed as the cause of
the late third trimester drop.
● Impact of maternal posture – The degree of change is acutely influenced by posture, as the cardiac output is
higher when the pregnant woman is in the left lateral decubitus position, particularly after 20 weeks of
gestation [6,31,32]. By comparison, assumption of the supine position can lower the cardiac output by as much
as 25 to 30 percent due to compression of the inferior cava by the gravid uterus, leading to a substantial
reduction in venous return to the heart. Changes in maternal heart rate, stroke volume, and cardiac output
during pregnancy measured in the lateral and supine positions are demonstrated in the figure (figure 5). (See
'Postural hypotensive syndrome' below.)
● Multiple gestation – The cardiovascular changes in women carrying twins are greater than those described
above for singleton pregnancies. Two-dimensional and M-mode echocardiography of 119 women (in the left
lateral position) with twins suggested that cardiac output was 20 percent higher than in women carrying
singletons, and peaked at 30 weeks of gestation [33]. This increase was due to a 15 percent increase in stroke
volume and 3.5 percent increase in heart rate.
Blood pressure and vascular resistance — Systolic and diastolic blood pressure (BP) typically fall early in
gestation and are about 5 to 10 mmHg below baseline in the second trimester, declining to a mean of about 105/60
mmHg [20,21,34-38]. In the third trimester, blood pressure gradually increases and may normalize to nonpregnant
values by term.
The fall in BP is induced by a reduction in systemic vascular resistance (SVR), which in pregnancy appears to
parallel changes in afterload [39]. A meta-analysis of 39 studies reported that the SVR progressively dropped
throughout pregnancy, with the lowest value (396 dyne s/cm6) being 30 percent below the nonpregnant baseline
and occurring in the early third trimester [2]. Both creation of a high flow, low-resistance circuit in the uteroplacental
circulation and vasodilatation contribute to the decline in vascular resistance [20]. The factors responsible for the
vasodilatation are incompletely understood, but one of the major findings is decreased vascular responsiveness to
the pressor effects of angiotensin II and norepinephrine [40-42]. Several additional mechanisms for the fall in
vascular resistance have been proposed:
● Increased endothelial prostacyclin [43]
● Enhanced nitric oxide production [44]
● Reduced aortic stiffness [45]
The possible role of humoral agents, such as estrogens, progesterone, and prolactin, in mediating the vasodilation
remains to be established [46]. In animals, as an example, estrogen and prolactin can both lower vascular
resistance and raise cardiac output [6].
Postural hypotensive syndrome — Uterine enlargement beyond about 20 weeks' size can compress the
inferior vena cava (IVC), which markedly reduces cardiac preload. This occurs in normal, healthy pregnant patients
primarily in the supine position or with prolonged standing. It is generally relieved by displacing the uterus to the left
and off the IVC by having the patient positioned in the left lateral decubitus position or manually displacing the
uterus to the left side. Other, less common, causes of supine hypotension include aortic compression and
neurogenic etiologies.
The reduction in preload can result in maternal hypotension, usually within 3 to 10 minutes, associated with one or
more signs and symptoms of reflex autonomic activation and/or reduced cardiac output (table 1) [47,48]. The
earliest sign of developing supine hypotension is an increase in maternal heart rate and a decrease in pulse
pressure indicating significantly reduced venous return [47]. Although these alterations are the best indicators of an
impending attack, many women remain asymptomatic.
In addition, a reduction in placental perfusion may result in nonreassuring changes in the fetal heart rate with no or
minimal decrease in upper extremity maternal blood pressure [49]. Therefore, it is important to position the
parturient in the left lateral tilt position for procedures (eg, labor and delivery, surgery, nonstress test, ultrasound)
and to avoid the supine position, even in symptom-free women.
Changes to blood vessels and blood flow — The vascular system is more compliant during pregnancy.
Although not consistently found, specific changes have been reported in the aortic media of pregnant women. [50].
These include fragmentation of reticular fibers, a decrease in acid mucopolysaccharides, loss of normal corrugation
of elastic fibers, and hypertrophy and hyperplasia of smooth muscle cells [51]. In addition, a small increase in the
aortic diameter occurs, which increases its compliance [52].
Systemic changes in the vascular system during pregnancy contribute to the following:
● Aortic dissection – Aortic dissection is rare in normal young women, but when dissection occurs it usually
does so during pregnancy [53-55]. Dissecting aneurysm may result, in part, from the alterations described
above and the occasional coincidence of pregnancy and a clinically isolated connective tissue disease such as
Marfan syndrome or a bicuspid aortic valve.
● Increased uterine artery blood flow – Uterine artery blood flow has been reported to increase from 50 to 60
mL/minute in the late first trimester, to 185 mL/minute at 28 weeks, and to 450 to 750 mL/minute at term
[56,57]. Cardiac output and uterine artery diameter also increase with advancing gestation. In early pregnancy,
the uterus receives 3 to 6 percent of cardiac output; at term, the proportion is about 12 percent [56,58].
● Increased cerebral blood flow – In addition, several studies have reported a small increase in cerebral blood
during normal pregnancy, accompanied by a progressive decrease in cerebral vascular resistance [59-62].
Utero-placental circulation — Pregnancy facilitates the growth and development of both the uterus and uterine
vessels through a combination of sex steroids, growth factors, and cytokines. Uterine vascular change consists of
(1) vascular growth with decidualization, and (2) vascular remodeling that occurs in response to trophoblast
invasion [63]. By five weeks of gestation, the uterine arteries have grown both in length and diameter, and by 20
weeks of gestation the uterine artery diameter has doubled [63,64]. By six to eight weeks after implantation, human
trophoblasts have invaded maternal tissues and begun placental development, which continues until approximately
19 to 20 weeks of gestation [63]. Abnormalities of vascular remodeling likely contribute to pregnancy-related
complications. The depth of trophoblast invasion has been reported as more shallow in women with preeclampsia,
growth restriction, and preterm birth compared with unaffected pregnant women [65-68].
Changes in vascular tone that enhance uteroplacental blood flow also occur. These changes are due to a variety of
factors (eg, nitric oxide, endothelin, renin-angiotensin, estrogen, progesterone, prostacyclin). Estimation of utero-
placental blood flow is difficult because there is no technique that concurrently measures blood flow in the placenta
and uterine, ovarian, and collateral vessels. Both invasive and noninvasive measures have estimated
uteroplacental blood flow between 450 and 750 mL/minute at term [69]. For comparison, approximately 5000
mL/minute flows through the entire circulation of a nonpregnant woman.
Changes in coagulation — Pregnancy is associated with changes in several coagulation factors that result in a 20
percent reduction of prothrombin and the partial thromboplastin times [70-72]:
● Resistance to activated protein C increases in the second and third trimesters [72]
● Free protein S decreases [73]
● Factors I, II, V, VII, VIII, X, and XII increase [73-75]
● Activity of the fibrinolytic inhibitors PAI-1 and PAI-2 increases, although total fibrinolytic activity may not be
impaired [76,77]
The net effect of these pregnancy-induced changes is to produce a hypercoagulable state, which is a double-
edged sword of protection (eg, hemostasis contributing to reduced blood loss at delivery) and risk (eg,
thromboembolic phenomenon) [73]. (See "Maternal adaptations to pregnancy: Hematologic changes".)
Venous thrombosis in pregnancy occurs in approximately 0.7 per 1000 women, and is three- to fourfold higher in
the puerperium than during pregnancy [74,78]. The risk is increased in women with underlying inherited
thrombophilia (eg, factor V Leiden or the prothrombin gene mutation) [79-81]. The risk, pathophysiology,
prevention, and treatment of thrombosis and thrombophilia in pregnancy are presented in detail elsewhere:
● (See "Deep vein thrombosis in pregnancy: Epidemiology, pathogenesis, and diagnosis".)
● (See "Deep vein thrombosis and pulmonary embolism in pregnancy: Prevention".)
● (See "Deep vein thrombosis and pulmonary embolism in pregnancy: Treatment".)
● (See "Inherited thrombophilias in pregnancy".)
Arrhythmias and palpitations — The exact mechanism of increased arrhythmia burden during pregnancy is
unclear, but has been attributed to hemodynamic, hormonal, and autonomic changes related to pregnancy. (See
"Supraventricular arrhythmias during pregnancy" and "Ventricular arrhythmias during pregnancy".)
Palpitations occur frequently during pregnancy and are a common indication for cardiac evaluation during
pregnancy. The differential diagnosis of palpitations is extensive and the diagnostic evaluation of pregnant women
with palpitations does not differ from nonpregnant women. (See "Overview of palpitations in adults".)
CHANGES RELATED TO LABOR AND DELIVERY — Normal labor and delivery is associated with significant
hemodynamic changes due to anxiety, exertion, pain, uterine contractions, uterine involution, and bleeding.
Cardiovascular effects also occur in some women due to infection, hemorrhage, or the administration of anesthesia
or analgesia.
Increased cardiac output — Blood from the uterine sinusoids is forced into the systemic circulation with each
uterine contraction, thereby increasing preload during labor (figure 3).
● Cardiac output increases by 15 percent above prelabor levels in early labor and by approximately 25 percent
during the active phase. Fluctuations in cardiac output may be minimized with adequate pain control during
labor. With epidural anesthesia, the baseline increase in cardiac output is reduced; however, the increases
associated with uterine contractions persist. (See "Pharmacologic management of pain during labor and
delivery".)
● The additional exertion associated with pushing in the second stage results in a 50 percent rise in cardiac
output.
● Immediately postpartum, cardiac output increases to 80 percent above prelabor values due to significant
"autotransfusion" associated with uterine involution that is more pronounced than the normal blood loss of
delivery.
The cardiac output and systemic vascular resistance gradually return to nonpregnant levels over a period of three
months or more [82].
Increased blood pressure — Systolic and diastolic blood pressure increase 15 to 25 and 10 to 15 percent,
respectively, during each uterine contraction. The rise in systemic blood pressure is dependent upon the duration
and intensity of uterine contractions, position of the parturient, and the amount of pain and anxiety she is feeling.
The increases in arterial pressure associated with each uterine contraction are mirrored by a rise in pressure in the
amniotic fluid, intrathoracic venous, cerebrospinal fluid, and extradural compartments (figure 6).
Bearing down or pushing during the second stage of labor alters the blood pressure and heart rate in a similar way
to the Valsalva maneuver; these changes are less pronounced if the gravida is positioned in the left lateral versus
supine position. The hemodynamic changes resulting from a Valsalva maneuver vary with the different phases.
● During phase 1, with the onset of the maneuver, there is a transient increase in left ventricular output.
● During the straining phase, phase 2, there is a decrease in venous return, right and left ventricular volumes,
stroke volumes, mean arterial pressure, and pulse pressure; this is associated with a reflex increase in heart
rate.
● During phase 3 (release of Valsalva), which only lasts for a few cardiac cycles, there is a further reduction in
left ventricular volume.
● Phase 4 is characterized by increases in stroke volume and arterial pressure and reflex slowing of heart rate
(the overshoot).
Changes in baroreceptor sensitivity during pregnancy and associated with maternal position may also play a role.
As an example, one study of normotensive pregnant women noted a marked decrease in baroreflex sensitivity for
heart rate in the supine position, but not while standing [83].
POSTPARTUM HEMODYNAMIC RESOLUTION — The postpartum period is marked by significant hemodynamic

alterations. Fluctuations in cardiac output, stroke volume, and heart rate occur after delivery. Within the first 10
minutes following a term vaginal delivery, the cardiac output and stroke volume increase by 59 and 71 percent,
respectively [84]. At one hour postpartum, both the cardiac output and stroke volume remain increased (by 49 and
67 percent, respectively) while the heart rate decreases by 15 percent; blood pressure remained unchanged [85].
The increases in stroke volume and cardiac output most likely result from improved cardiac preload from auto
transfusion of utero placental blood to the intravascular space. As the uterus decompresses following delivery, a
reduction in the mechanical compression of the vena cava allows for further increases in cardiac preload.
These cardiovascular physiologic changes resolve slowly after delivery. A study that evaluated cardiac output and
stroke volume in 15 healthy nonlaboring patients at 38 weeks of gestation, and again at 2, 6, 12, and 24 weeks
postpartum demonstrated a gradual diminution in cardiac output from 7.42 L/min at 38 weeks of gestation to 4.96
L/min at 24 weeks postpartum [86]. As early as two weeks postpartum, there were substantial reductions in left
ventricular size and contractibility as compared with term pregnancies.
EVALUATION OF THE CARDIOVASCULAR SYSTEM IN PREGNANCY — The physiologic and anatomic

adaptations to pregnancy influence the interpretation and evaluation of the gravida's cardiovascular status.
Physical examination — The circulatory and respiratory changes during normal pregnancy are sometimes
erroneously attributed to heart disease. The clinician caring for the gravida should be aware of these normal
maternal cardiovascular adaptations to pregnancy.
● Breathlessness (innocent hyperpnea), easy fatiguing, decreased exercise tolerance, basal rales that disappear
with cough or deep breathing, and peripheral edema commonly occur during pregnancy in normal women.
(See "Maternal adaptations to pregnancy: Physiologic respiratory changes and dyspnea".)
● The systemic arterial pulse is characterized by a rapid rise and a brisk collapse (small water hammer)
beginning in the first trimester.
● The jugular venous pulse is more conspicuous after the 20th week because brisk X and Y descents make the
A and V waves more obvious. Mean jugular venous pressure, as estimated from the superficial jugular vein,
remains normal.
● The pregnant woman's heart is shifted to the left, anterior, and rotated toward a transverse position as the
uterus enlarges. As a result, the apical impulse is shifted cephalad to the fourth intercostal space and laterally
to the midclavicular line. The left ventricular impulse is relatively hyperdynamic but not sustained; the right
ventricle may be palpable because, like the left ventricle, it handles a larger volume of blood that is ejected
against relatively low resistance. As pregnancy progresses, enlargement of the breasts and abdomen makes
accurate palpation of the heart difficult, if not impossible.
● Auscultatory changes accompanying normal gestation begin in the late first trimester and generally disappear
within a week after delivery. A higher basal heart rate, louder heart sounds, wide splitting of S1, splitting of S2
in the third trimester, and a systolic ejection murmur (up to grade 2/6) over the pulmonary and tricuspid areas
are regularly detected upon cardiac auscultation. A third heart sound is present in most pregnant women; the
fourth heart sound is rarely heard. The venous hum is almost universal in normal women during gestation. The
mammary souffle (systolic or continuous) is heard over the breasts in late gestation and is peculiar to
pregnancy; it is especially common postpartum in lactating women.
● Diastolic murmurs are uncommon in normal pregnant women. When they occur, they may reflect increased
flow through the tricuspid or mitral valve or physiologic dilatation of the pulmonary artery. However, these
murmurs more likely represent a pathologic condition necessitating further study [87].
Echocardiogram — Physiologic multivalvular regurgitation, predominantly right-sided, is a frequent normal finding

during late gestation and may persist throughout the early postpartum period [88]. In addition, chamber
enlargement, valvular annular dilatation, and a small asymptomatic pericardial effusion are frequent normal
incidental findings during late gestation [28,88,89]. These findings appear to be caused by pregnancy-related
hypervolemia and are important considerations when interpreting an echocardiogram in a pregnant patient.
Electrocardiogram — Normal anatomic and physiologic changes of the heart and chest wall during pregnancy
cause changes in the electrocardiogram that are unrelated to disease. The heart is rotated toward the left, resulting
in a 15- to 20-degree left axis deviation. Marked variation in chamber volumes, especially left atrial enlargement,
leads to stretching of the cardiac conduction pathways and predisposes to alterations in cardiac rhythm. Periods of
supraventricular tachycardia and ventricular extrasystoles are a common finding. Other findings, which can be
normal, include transient ST segment and T-wave changes, the presence of a Q wave and inverted T waves in
lead III, an attenuated Q wave in lead AVF, and inverted T waves in leads V1, V2 and, occasionally, V3 [25,90,91].
(See "Ventricular arrhythmias during pregnancy" and "Supraventricular arrhythmias during pregnancy".)
Chest radiograph — The left, anterior, superior rotation of the heart and hypervolemia give the illusion of
ventricular hypertrophy and cardiomegaly on chest radiographs; increased pulmonary vascular markings are also
common. Rotation of the heart may also cause an indentation of the esophagus by the left atrium and straightening
of the left heart border. The majority of these changes are temporary and return to normal by eight weeks
postpartum.
SUMMARY AND RECOMMENDATIONS
● Expansion of the plasma volume and an increase in red blood cell mass begin as early as the fourth week of
pregnancy, peak at 28 to 34 weeks of gestation, and then plateau. Plasma volume expansion exceeds the
increase in red cell volume, leading to "physiologic anemia." (See 'Changes in blood volume' above.)
● The major hemodynamic changes induced by pregnancy include an increase in cardiac output and reductions
in systemic vascular resistance and systemic blood pressure. Cardiac output peaks a few minutes after
delivery, before gradually returning to prepregnancy levels. (See 'Changes in systemic hemodynamics' above
and 'Postpartum hemodynamic resolution' above.)
● Changes in several coagulation factors produce a hypercoagulable state. (See 'Changes in coagulation'
above.)
● Labor and delivery is associated with significant hemodynamic changes due to anxiety, exertion, pain, uterine
contractions, uterine involution, and bleeding. Infection, hemorrhage, and the administration of anesthesia or
analgesia also play a role. (See 'Changes related to labor and delivery' above.)
● The physiologic and anatomic adaptations to pregnancy influence the interpretation and evaluation of the
pregnant woman's cardiac evaluation. (See 'Evaluation of the cardiovascular system in pregnancy' above.)
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Topic 443 Version 16.0
GRAPHICS
Hemodynamic changes in normal pregnancy
Normal pregnancy is characterized by an increase in cardiac output, a reduction

in systemic vascular resistance, and minimal change in mean blood pressure.
These changes are associated with a 10- to 15-beat/minute increase in heart
rate.
BP: blood pressure; SVR: systemic vascular resistance.
Graphic 54685 Version 6.0
Maternal cardiovascular changes during pregnancy by trimester
SVR: systemic vascular resistance; LV: left ventricular; LVEDD: left ventricular end diastolic diameter.
Adapted from: Ashrafi R, Curtis SL. Heart disease in pregnancy. Cardiol Ther 2017.
Cardiac output during normal labor, delivery, and

postpartum
Data from: Bonica JJ, McDonald JS. Principles and Practice of Obstetric Analgesia and
Anesthesia, 2 nd ed, Williams & Wilkins, Baltimore 1994. p.62.
Total blood volume, plasma volume, and red cell volume

in normal pregnancy
Data from: Shnider SM, Levinson G. Anesthesia for Obstetrics, 3 rd ed, Williams &
Wilkins, Baltimore 1993. p.8.
Systemic hemodynamics during normal pregnancy
Signs and symptoms attributed to supine hypotensive syndrome in pregnancy
Faintness
Dyspnea
Dizziness
Restlessness
Nausea
Vomiting
Chest pain
Abdominal pain
Visual disturbances
Numbness
Paresthesias
Headache
Cold, clammy skin
Pallor
Cyanosis
Hypotension
Hemodynamics with contractions

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7/10/2018 Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes - UpToDate

Official reprint from UpToDate®

Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes

Author: Michael R Foley, MD

● (See "Acquired heart disease and pregnancy".)

● (See "Pregnancy in women with congenital heart disease: General principles".)

● (See "Pregnancy in women with congenital heart disease: Specific lesions".)

● (See "Management of heart failure during pregnancy".)

CHANGES RELATED TO PREGNANCY

Changes in blood volume

• Preload is increased due to the associated rise in blood volume

• Afterload is reduced due to the decline in systemic vascular resistance

• Maternal heart rate rises (see 'Heart rate' above)

● Increased endothelial prostacyclin [43]

● Enhanced nitric oxide production [44]

● Reduced aortic stiffness [45]

● Free protein S decreases [73]

● Factors I, II, V, VII, VIII, X, and XII increase [73-75]

● (See "Deep vein thrombosis in pregnancy: Epidemiology, pathogenesis, and diagnosis".)

● (See "Deep vein thrombosis and pulmonary embolism in pregnancy: Prevention".)

● (See "Deep vein thrombosis and pulmonary embolism in pregnancy: Treatment".)

● (See "Inherited thrombophilias in pregnancy".)

POSTPARTUM HEMODYNAMIC RESOLUTION — The postpartum period is marked by significant hemodynamic

EVALUATION OF THE CARDIOVASCULAR SYSTEM IN PREGNANCY — The physiologic and anatomic

Echocardiogram — Physiologic multivalvular regurgitation, predominantly right-sided, is a frequent normal finding

SUMMARY AND RECOMMENDATIONS

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 443 Version 16.0

Hemodynamic changes in normal pregnancy

Normal pregnancy is characterized by an increase in cardiac output, a reduction

BP: blood pressure; SVR: systemic vascular resistance.

Graphic 54685 Version 6.0

Maternal cardiovascular changes during pregnancy by trimester

Graphic 114204 Version 1.0

Cardiac output during normal labor, delivery, and

Graphic 79834 Version 3.0

Total blood volume, plasma volume, and red cell volume

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Systemic hemodynamics during normal pregnancy

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Signs and symptoms attributed to supine hypotensive syndrome in pregnancy

Cold, clammy skin

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Hemodynamics with contractions

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