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Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes

Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes
Literature review current through: May 2024.
This topic last updated: Feb 05, 2024.

INTRODUCTION — Many physiologic changes occur during pregnancy to accommodate maternal and fetal needs as pregnancy progresses. Most of these changes begin soon after conception and continue until late gestation. Pregnancy-related hemodynamic changes include increased cardiac output, expanded blood volume, reduced systemic vascular resistance (SVR) and blood pressure (BP), and a small increase in heart rate. Knowledge of these cardiovascular adaptations is required to correctly interpret hemodynamic and cardiovascular tests in pregnant and postpartum patients, predict the effects of pregnancy on the patient with underlying heart disease, and understand how the fetus may be affected by maternal cardiac disorders.

The cardiovascular changes associated with normal pregnancy will be discussed here. The management of specific cardiovascular disorders in pregnancy is reviewed separately. For example:

(See "Acquired heart disease and pregnancy".)

(See "Pregnancy in women with congenital heart disease: General principles" and "Pregnancy in women with congenital heart disease: Specific lesions".)

(See "Pregnancy and valve disease".)

(See "Pulmonary hypertension with congenital heart disease: Pregnancy and contraception".)

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

(See "Peripartum cardiomyopathy: Etiology, clinical manifestations, and diagnosis" and "Peripartum cardiomyopathy: Treatment and prognosis".)

(See "Chronic hypertension in pregnancy: Prenatal and postpartum care" and "Gestational hypertension" and "Preeclampsia: Antepartum management and timing of delivery".)

ANTEPARTUM ADAPTATION

Changes in plasma volume, red blood cell mass, and coagulation factors — Plasma volume expands by 10 to 15 percent at 6 to 12 weeks of gestation, increases rapidly to reach 40 to 50 percent above the prepregnancy level at 30 to 34 weeks, and then plateaus or falls slightly until delivery [1-3]. Increased red blood cell (RBC) production begins at approximately 16 weeks of gestation and progressively accelerates, reaching a 25 percent increase above the prepregnancy level by 34 weeks. Since plasma volume expansion is greater than the increase in total RBC volume, hematocrit/hemoglobin is modestly reduced, a dilutional anemia termed "physiologic anemia of pregnancy." Peak hemodilution occurs at 24 to 26 weeks [4]. (See "Maternal adaptations to pregnancy: Hematologic changes", section on 'Plasma volume' and "Maternal adaptations to pregnancy: Hematologic changes", section on 'Red blood cells'.)

Plasma volume expansion and dilutional anemia during pregnancy have physiological benefits:

Reduction in blood viscosity reduces resistance to flow, facilitating placental perfusion and lowering cardiac work.

The large increase in total intravascular volume near term provides some reserve against the normal blood loss from giving birth (approximately 300 to 500 mL for vaginal birth, 600 to 1000 mL for cesarean birth), as well as peripartum hemorrhage. As much as 500 mL of blood can be sequestered in the uteroplacental unit and autotransfused to the maternal circulation after fetal expulsion, thereby minimizing adverse circulatory effects from postpartum blood loss. However, patients with underlying cardiopulmonary disease may not tolerate such changes.

Increased cardiac output distributed to the placenta, kidneys, and skin helps to provide nutrients to the fetus, excrete maternal and fetal waste products, and assist maternal temperature control, respectively. (See "Maternal adaptations to pregnancy: Kidney and urinary tract physiology".)

Pregnancy is a prothrombotic state due to increases in the coagulation factors II, VII, VIII, IX, X, XII, von Willebrand factor, and fibrinogen. In addition, free protein S levels decrease due to increased protein S binding. Antithrombin III levels also decrease. Resistance to activated protein C increases, as do levels of type 1 plasminogen activator inhibitory (PAI-1) [5]. These changes promote hemostasis and inhibit the fibrinolytic system, which serves to prevent excessive bleeding during placental separation, but also increases the risk of pregnancy-associated venous thromboembolism. This risk is up to six to ten times that of the nonpregnant reproductive age female population, with an absolute risk up to 12.2 per 10,000, compared with 2 per 10,000 in nonpregnant individuals [6,7]. (See "Maternal adaptations to pregnancy: Hematologic changes", section on 'Coagulation and fibrinolysis' and "Deep vein thrombosis in pregnancy: Clinical presentation and diagnosis".)

Changes in systemic hemodynamics — Hemodynamic changes begin soon after conception, reach their peak during the second and early third trimesters, and then remain relatively constant until labor and delivery [1-3].

Cardiac output — Cardiac output increases substantially during pregnancy, in part, from changes in three important factors that determine cardiac output:

Increased preload, due to the rise in blood volume (see 'Changes in plasma volume, red blood cell mass, and coagulation factors' above)

Reduced afterload, due to the decline in systemic vascular resistance (SVR) (see 'Systemic vascular resistance' below)

Increased heart rate (see 'Heart rate' below)

Cardiac output begins to increase as early as six weeks of gestation and continues to increase until 20 to 24 weeks of gestation, peaking at levels 30 to 40 percent above the nonpregnant level (increasing from 5 to 7 L/min) (figure 1) [8-10]. In early pregnancy, the increase is primarily due to a rise in stroke volume. One meta-analysis reported stroke volume increased 8 percent increase (6 mL) in the first trimester [11]. In late pregnancy, the major contributing factor is the faster heart rate. The increase in cardiac output is not linear: the slope slows in the late-second trimester and drops slightly in the late-third trimester, although it remains above baseline until the postpartum period. The drop in cardiac output in the late-third trimester may be due to compression of the inferior vena cava (IVC) by the enlarged uterus and increased blood flow to the uteroplacental circulation.

The increase in cardiac output contributes to optimal fetal growth and development; the uterus receives 3 to 6 percent of cardiac output in early pregnancy and approximately 12 percent of cardiac output at term [12,13]. However, the increase in cardiac output can cause patients with underlying heart disease to decompensate during the latter half of pregnancy. (See "Management of heart failure during pregnancy".)

Heart rate — Resting heart rate begins to rise in the first trimester, with an average increase of 10 to 30 beats per minute (bpm) [14-16]. In a three-center, prospective, longitudinal cohort study, the median heart rate at 12 weeks was 82 bpm (3rd to 97th centiles: 63 to 105 bpm) and rose progressively until 34 weeks to a maximum of 91 bpm (3rd to 97th centiles: 68 to 115 bpm), as shown in the figure (figure 2) [17]. Heart rate then decreased slightly at 40 weeks to a median of 89 bpm (3rd to 97th centiles: 65 to 114 bpm). Thus, the upper limit of the resting heart rate typically is not greater than 115 bpm, and a heart rate exceeding 115 bpm warrants evaluation.

Blood pressure — Beginning in the first trimester, systolic BP, diastolic BP, and mean arterial pressure decrease (figure 3). The fall in diastolic BP is greater than the fall in systolic BP throughout pregnancy, thus widening the pulse pressure. As pregnancy progresses, BPs return to baseline and may overshoot the prepregnancy level in the late third trimester.  

Although most studies have reported the aforementioned pattern [18], emerging data suggest that the fall in BP is less than previously reported and the pattern of change is also different. The reason is unclear, but one hypothesis is that the standardized technique used for measuring BP in contemporary studies is different from techniques used in the past.

In a three-center, prospective cohort study including 1041 patients [17]:

Systolic BP decreased from 12 weeks of gestation (median 114 mmHg; 3rd to 97th centiles: 95 to 138 mmHg) to reach a nadir at 18.6 weeks (median 113 mmHg; 3rd to 97th centiles: 95 to 136 mmHg).

Systolic BP then rose progressively to 40 weeks to a maximum median of 121 mmHg (3rd to 97th centiles: 102 to 144 mmHg). The third centile for systolic BP was never less than 94 mmHg and was greater than 96 mmHg in all groups.

Diastolic BP decreased from 12 weeks of gestation (median 70 mmHg; 3rd to 97th centiles: 56 to 87 mmHg) to its nadir at 19.2 weeks (median 69 mmHg; 3rd to 97th centiles: 55 to 86 mmHg).

Diastolic BP then increased to 40 weeks to a maximum median of 78 mmHg (3rd to 97th centiles: 62 to 95 mmHg).

These changes are shown in the following figure (figure 4).

In a longitudinal cohort study in eight countries including 4321 patients [19]:

Median systolic BP was lowest at 12 weeks of gestation: 111.5 mmHg (95% CI 113-118 mmHg), rising to a maximum of 119.6 mmHg (95% CI 118.9-120 mmHg) at 40 weeks, a difference of 8.1 mmHg (95% CI 7.4-8.8 mmHg).

Median diastolic BP decreased minimally between 12 weeks (69.1 mmHg, 95% CI 68.9-69.3 mmHg) and 19 weeks (68.5 mmHg, 95% CI 68.3-68.7 mmHg), and then increased to a maximum at 40 weeks (76.3 mmHg, 95% CI 75.9-76.8 mmHg), a difference of 7.8 mmHg (95% CI 7.3-8.2 mmHg).

The applicability of these findings to individuals with a BMI >30 kg/m2 is uncertain as these patients were excluded from the studies.

Systemic vascular resistance — Systemic vasodilation begins at approximately five weeks of gestation and SVR drops progressively throughout pregnancy. In a meta-analysis of 39 studies, the lowest value (396 dyne s/cm6) was 30 percent below the nonpregnant baseline and occurred in the early third trimester [11]. The decline in SVR can be attributed to the high-flow, low-resistance circuit in the uteroplacental circulation and vasodilatation [14].

The factors responsible for vasodilatation are incompletely understood, but one of the major findings is decreased vascular responsiveness to the pressor effects of angiotensin II and norepinephrine [20-22]. Several additional mechanisms for the fall in vascular resistance have been proposed and include: increased endothelial prostacyclin [23], enhanced nitric oxide production [24], and reduced aortic stiffness [25]. The possible role of humoral agents, such as estrogens, progesterone, and prolactin, in mediating the vasodilation remains to be established [26]. In animal studies, estrogen and prolactin can both lower vascular resistance and raise cardiac output [27].

Central venous pressure — 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 SVR and pulmonary vascular resistance (ie, afterload to the left and right heart, respectively) [28].

Uteroplacental circulation — The uteroplacental circulation supports fetal growth and development. During pregnancy, uterine vascular tone is relaxed due to the varying effects of a variety of factors, including nitric oxide, renin-angiotensin, estrogen, progesterone, and prostacyclin, as well as uterine spiral artery dilation due to vascular remodeling in response to decidual natural killer (NK) cell activity and extravillous cytotrophoblast invasion [29,30].

By five weeks of gestation, the uterine arteries have increased both in length and diameter, and by 20 weeks the uterine artery diameter has doubled [29,31]. Estimating uteroplacental blood flow is difficult because no technique concurrently measures blood flow in the placenta and uterine, ovarian, and collateral vessels. 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 [12,32,33]. As discussed above, this represents 3 to 6 percent of cardiac output in early pregnancy and approximately 12 percent of cardiac output at term [12,13].

By 6 to 8 weeks after implantation, human trophoblasts have invaded maternal tissues and begun placental development, which continues until approximately 19 to 20 weeks [29]. Abnormalities of vascular remodeling likely contribute to pregnancy-related complications such as preeclampsia and fetal growth restriction. The depth of trophoblast invasion has been reported to be more shallow in patients with preeclampsia, fetal growth restriction, and spontaneous preterm birth compared with unaffected pregnant individuals [34-37]. (See "Preeclampsia: Pathogenesis", section on 'Abnormal development of the placenta'.)

Other vascular changes — The vascular system is more compliant during pregnancy. Although not consistently found, specific changes in the aortic media have been reported, such as fragmentation of reticular fibers, a decrease in acid mucopolysaccharides, loss of normal corrugation of elastic fibers, and hypertrophy and hyperplasia of smooth muscle cells [38,39]. In addition, a small increase in the aortic diameter occurs, which increases aortic compliance [40].

Systemic changes in the vascular system during pregnancy contribute to the following:

Increased cerebral blood flow – Several studies have reported a small increase in cerebral blood during normal pregnancy, accompanied by a progressive decrease in cerebral vascular resistance [41-44].

Increased risk of aortic dissection – Aortic dissection is rare, however, the incidence is increased in pregnant patients with bicuspid aortic valve or connective tissue disorders, such as Marfan syndrome and Loeys-Dietz syndrome [45]. Aortic dissection is one of the most common causes of death in pregnancy. Most cases are caused by hereditary thoracic aortopathy and many patients are unaware of their condition at the time of the event [46]. (See "Heritable thoracic aortic diseases: Pregnancy and postpartum care" and "Heritable thoracic aortic diseases: Preconception risk assessment and management" and "Bicuspid aortic valve: Preconception and pregnancy care" and "Management of Marfan syndrome and related disorders".)

Special considerations

Multiple gestation — The cardiovascular changes in individuals carrying twins are greater than those described above for singleton pregnancies. Two-dimensional and M-mode echocardiography of 119 patients (in the left lateral position) carrying twins suggested that cardiac output was 20 percent higher than in those carrying singletons, and peaked at 30 weeks of gestation [47]. This increase was due to a 15 percent increase in stroke volume and 3.5 percent increase in heart rate. A subsequent study using impedance cardiography also reported higher cardiac output in twin pregnancies related to higher mean heart rate (100 versus 85 bpm), greater stroke volume (83 versus 64 mL), and lower SVR [48]. In one study, chorionicity appeared to have an effect on maternal hemodynamics [49]. 

Impact of maternal position — As the pregnancy progresses, certain hemodynamic factors can be influenced substantially by maternal position. For example, the cardiac output is higher when the pregnant individual is in the left lateral decubitus position, particularly after 20 weeks of gestation [27,50]. By comparison, the cardiac output may decrease by as much as 25 to 30 percent in the supine position 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 shown in the figure (figure 5).

Supine hypotensive syndrome — Supine hypotensive syndrome is a phenomenon in pregnant people characterized by acute hypotension associated with increased heart rate and possibly pallor and sweating that occurs within 3 to 10 minutes of lying supine [51]. Uterine enlargement beyond approximately 20 weeks' size can compress the inferior vena cava (IVC), which markedly reduces cardiac preload. The reduction in preload can result in maternal hypotension associated with one or more signs and symptoms of reflex autonomic activation and/or reduced cardiac output [51,52]. In normal, healthy pregnant patients, supine hypotension occurs primarily in the supine position or with prolonged standing; other less common causes are aortic compression and neurogenic etiologies.

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. Although these alterations are the best indicators of an impending attack, many individuals remain asymptomatic. Theories as to why certain individuals are more symptomatic than others relate to a less developed venous collateral system and an abnormally decreased baroreflex gain [53]. If symptoms are present, they are generally relieved by changing to a left lateral decubitus position or manually displacing the uterus to the left side of the abdomen.

A reduction in placental perfusion may result in nonreassuring changes in the fetal heart rate, even with no or minimal decrease in upper extremity maternal BP [54]. Therefore, it is important to avoid the supine position even in symptom-free patients and to ensure that pregnant patients are positioned in the left lateral tilt position for procedures (eg, labor and delivery, surgery, nonstress test, ultrasound), particularly after 20 weeks of gestation.

INTRAPARTUM CHANGES — Significant hemodynamic changes can occur intrapartum due to multiple factors, such as pain, uterine contractions, exertion, uterine involution, hemorrhage, infection, and administration of medications, such as for anesthesia, analgesia, or tocolysis (eg, terbutaline, nifedipine).

Cardiac output

In patients without epidural anesthesia, basal cardiac output between contractions increases by 12 percent above prelabor levels [8]. During contractions, cardiac output increases progressively as labor advances, increasing by a mean value of 34 percent above prelabor levels at full dilation. The increase is due to blood forced into the systemic circulation from the uterine sinusoids with each uterine contraction as well as pain, thereby increasing preload [8]. While epidural anesthesia reduces the increase due to pain, the increase associated with uterine contractions persists. (See "Pharmacologic management of pain during labor and delivery".)

In the second stage, exertion associated with pushing increases cardiac output up to 50 percent above the prelabor level [55].

Blood pressure — During each uterine contraction, systolic and diastolic BP can increase 15 to 25 and 10 to 15 percent, respectively. The rise in systemic BP depends upon the duration and intensity of the contractions, the parturient's position (changes are minimized in the left lateral position), and the degree of pain and anxiety experienced. The increases in arterial pressure associated with each uterine contraction are mirrored by a rise in pressure in the amniotic fluid, intrathoracic veins, cerebrospinal fluid, and extradural compartment.

Pushing during the second stage alters the BP and heart rate in a similar way to the Valsalva maneuver. The hemodynamic changes resulting from a Valsalva maneuver vary with its different phases:

During phase 1 (onset of the maneuver), left ventricular output transiently increases.

During phase 2 (straining phase), venous return, right and left ventricular volumes, stroke volumes, mean arterial pressure, and pulse pressure decrease accompanied by a reflex increase in heart rate.

During phase 3 (release of Valsalva), which only lasts for a few cardiac cycles, left ventricular volume is further reduced.

During phase 4, stroke volume and arterial pressure increase accompanied by reflex slowing of the heart rate (the overshoot).

The effects of Valsalva can be minimized by open glottis pushing in which the patient slowly exhales through pursed lips rather than holding their breath and contracts the abdominal musculature to provide the predominant expulsive force.

POSTPARTUM CHANGES

Immediately postpartum — Within the first 10 minutes following a term vaginal birth, the cardiac output and stroke volume increase by 59 and 71 percent, respectively [56]. At one hour postpartum, both cardiac output and stroke volume remain increased (by 49 and 67 percent, respectively) while the heart rate decreases by 15 percent; BP remains unchanged [57]. These changes may be altered in the setting of uterine atony, postpartum hemorrhage, or sepsis.

The increases in stroke volume and cardiac output most likely result from improved cardiac preload from autotransfusion of uteroplacental blood to the intravascular space. Preload also increases following expulsion of the fetus, amniotic fluid, and placenta due to a reduction in the mechanical compression of the vena cava.

Resolution to prepregnancy parameters — The cardiac output and systemic vascular resistance (SVR) gradually return to nonpregnant levels over a period of three months or more [58]. 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 [59]. As early as two weeks postpartum, there were substantial reductions in left ventricular size and contractibility as compared with term pregnancies.

BP peaks three to six days postpartum and then usually returns to baseline by 14 days postpartum [60]. Heart rate also usually returns to baseline by 14 days postpartum.

Assuming normal renal function and diuresis, blood volume and blood constituents return to nonpregnant levels by eight weeks postpartum. Hemoglobin begins to increase from the third postpartum day.

EVALUATION OF THE CARDIOVASCULAR SYSTEM IN PREGNANCY — The physiologic and anatomic adaptations to pregnancy influence the interpretation and evaluation of the pregnant patient's cardiovascular status. It is important to be able to recognize the expected changes in the cardiovascular system to identify abnormal responses to pregnancy [61]. It is usually possible to distinguish normal pregnancy symptoms from pathologic changes by careful history, imaging, and physical examination. Patients with worrisome symptoms should be evaluated and never routinely dismissed as normal pregnancy findings without further investigation.

History

Palpitations occur frequently during pregnancy and are a common indication for cardiac evaluation. The differential diagnosis of palpitations is extensive and the diagnostic evaluation of pregnant individuals with palpitations does not differ from that in nonpregnant patients (see "Evaluation of palpitations in adults"). 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".).

Dyspnea is common as pregnancy progresses because progesterone directly increases minute ventilation. (See "Maternal adaptations to pregnancy: Dyspnea and other physiologic respiratory changes".)

Increased fatigue and decreased exercise tolerance commonly occur during pregnancy.

Physical examination

Beginning in the first trimester, the systemic arterial pulse is characterized by a rapid rise and a brisk collapse (small water hammer).

After the 20th week of gestation, the jugular venous pulse is more visible due to brisk X and Y descents, which result in more obvious A and V waves. Mean jugular venous pressure, as estimated from the superficial jugular vein, remains normal.

As the uterus enlarges, the patient's heart is shifted to the left, anterior, and rotated toward a transverse position. 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. However, breast and abdominal enlargement makes accurate palpation of the heart more difficult as pregnancy progresses.

Auscultatory changes regularly detected on cardiac auscultation begin in the late first trimester and include a higher basal heart rate, louder heart sounds, wide splitting of S1, and a systolic ejection murmur (up to grade 2/6) over the pulmonary and aortic areas. A third heart sound is present in many pregnant individuals [62]. The venous hum is almost universal in normal patients during gestation. The mammary souffle (systolic or continuous) is heard over the breasts in late gestation and is common postpartum in lactating individuals. Abnormal findings include holosystolic murmurs, diastolic murmurs, fourth heart sound, or an exaggerated second heart sound suggesting pulmonary hypertension.

Peripheral edema may develop during the later stages of pregnancy and is often worse with prolonged standing and immediately postpartum.

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 transient and return to normal in the early postpartum period.

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.

Sinus tachycardia is common, as the heart rate increases approximately 10 percent above baseline values.

Premature ventricular or atrial ectopic beats may be seen in 50 to 60 percent of pregnant patients presenting with palpitations and generally resolve spontaneously after delivery [63]. (See "Ventricular arrhythmias during pregnancy" and "Supraventricular arrhythmias during pregnancy".)

Other findings, which may be normal, include, shortened PR interval, increased R/S ratio in leads V1 and V2, Q waves and inverted T waves in the inferior leads, and nonspecific transient ST-T changes.

Echocardiography — The echocardiogram during pregnancy has several expected changes [64,65].

The volume of the cardiac chambers increases slightly, reflected in an increase of 0.4 to 0.5 cm in the left atrial size and 0.2 to 0.4 cm in the left ventricular diastolic dimension.

The ventricular global systolic function does not change significantly; however, global longitudinal strain declines to the lower end of the normal range in the later stages of pregnancy, after which it remains stable until term [66].

The left ventricular mass increases by 5 to 10 percent, which results in eccentric hypertrophy [67].

Each of the valves may develop trivial-to-mild regurgitation, particularly in the third trimester.

Small pericardial effusions are common, reported in up to 25 to 40 percent of normal pregnancies [68].

These findings appear to be caused by pregnancy-related hypervolemia and are important considerations when interpreting an echocardiogram in a pregnant patient. The changes resolve within three to six months after giving birth. It has been reported that approximately 10 percent of echocardiography requests for low-risk pregnant patients have abnormal findings, the most common being slight elevations of pulmonary arterial pressure. Individuals with higher parity and those with chronic hypertension were more likely to have an abnormal echocardiogram [69].

SUMMARY AND RECOMMENDATIONS

Overview – Pregnancy-related changes in the cardiovascular system begin soon after conception and continue throughout gestation. Knowledge of these changes is required to correctly interpret hemodynamic and cardiovascular tests in pregnant and postpartum patients, predict the effects of pregnancy on the patient with underlying heart disease, and understand how the fetus may be affected by maternal cardiac disorders. (See 'Introduction' above.)

Antepartum changes

Plasma volume expands by 40 to 50 percent and red cell mass expands by 25 percent above prepregnancy levels, resulting in a dilutional anemia (physiologic anemia of pregnancy). (See 'Changes in plasma volume, red blood cell mass, and coagulation factors' above.)

Cardiac output peaks at levels 30 to 40 percent above prepregnancy levels (figure 1). The increase results, in part, from (see 'Cardiac output' above):

-Increased preload, due to the rise in blood volume (see 'Changes in plasma volume, red blood cell mass, and coagulation factors' above)

-Reduced afterload, due to the decline in systemic vascular resistance (SVR) (see 'Systemic vascular resistance' above)

-Increased heart rate (figure 2) (see 'Heart rate' above)

Systolic blood pressure (BP), diastolic BP, and mean arterial pressure decrease from prepregnancy levels (figure 3). The fall in diastolic BP is greater than the fall in systolic BP throughout pregnancy, thus widening of the pulse pressure. (See 'Blood pressure' above.)

Intrapartum changes – In patients without epidural anesthesia, basal cardiac output between contractions is increased by 12 percent above prelabor levels. During contractions, cardiac output increases progressively as labor advances, with a mean increase of 34 percent above prelabor levels at full dilation. Pain and blood forced into the systemic circulation from the uterine sinusoids with each contraction account for the increase. In the second stage, pushing increases cardiac output up to 50 percent above the prelabor level. BP also increases intrapartum. (See 'Intrapartum changes' above.)

Postpartum changes – Immediately after delivery, cardiac output and stroke volume increase by 59 and 71 percent, respectively, and then gradually return to prepregnancy levels over three months or more. BP peaks three to six days postpartum and then usually returns to baseline by 14 days postpartum. Heart rate also usually returns to baseline by 14 days postpartum. (See 'Postpartum changes' above.)

Key points in cardiac evaluation of pregnant patients:

Palpitations occur frequently during pregnancy. The differential diagnosis and diagnostic evaluation do not differ from that in nonpregnant patients. (See 'History' above.)

Auscultatory changes may include louder heart sounds, wide splitting of S1, and a systolic ejection murmur (up to grade 2/6) over the pulmonary and aortic areas, a third heart sound, and venous hum. Holosystolic and diastolic murmurs are not normal. (See 'Physical examination' above.)

Modest changes in the chest radiograph, electrocardiogram, and echocardiography also occur. Leftward cardiac rotation and pregnancy-related hypervolemia account for many of these changes. (See 'Chest radiograph' above and 'Electrocardiogram' above and 'Echocardiography' above.)

Multiple gestation – The cardiovascular changes in individuals carrying a multiple gestation are greater than those described above for singleton pregnancies. (See 'Multiple gestation' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Michael R Foley, MD, who contributed to earlier versions of this topic review.

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Topic 443 Version 32.0

References

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