Maternal Cardiovascular and Hemodynamic Adaptations to Pregnancy

6/23/15, 4:52 AMMaternal cardiovascular and hemodynamic adaptations to pregnancy

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Official reprint from UpToDate www.uptodate.com 2015 UpToDate

AuthorMichael R Foley, MD

Section EditorsCharles J Lockwood, MD, MHCMBernard J Gersh, MB, ChB, DPhil,FRCP, MACC

Deputy EditorKristen Eckler, MD, FACOG

Maternal cardiovascular and hemodynamic adaptations to pregnancy

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: May 2015. | This topic last updated: Sep 09, 2014.

INTRODUCTION The major hemodynamic changes induced by pregnancy include an increase in cardiac output,sodium and water retention leading to blood volume expansion, and reductions in systemic vascular resistance andsystemic blood pressure. These changes begin early in pregnancy [1], reach their peak during the second trimester, andthen remain relatively constant until delivery (figure 1). They contribute to optimal growth and development of the fetusand help to protect the mother from the risks of delivery, such as hemorrhage. Knowledge of these cardiovascularadaptations is required to correctly interpret hemodynamic and cardiovascular tests in the gravida, to predict the effectsof pregnancy on the woman with underlying cardiac disease, and to understand how the fetus will be affected bymaternal cardiac disorders.

The cardiovascular changes associated with normal pregnancy will be reviewed here. The management of specificcardiac disorders, such as acquired and congenital heart disease, heart failure, and arrhythmias, are discussedseparately. (See "Acquired heart disease and pregnancy" and "Pregnancy in women with congenital heart disease:General principles" and "Management of heart failure during pregnancy".)

CHANGES IN BLOOD VOLUME Expansion of the plasma volume and an increase in red blood cell mass begin asearly as the fourth week of pregnancy, peak at 28 to 34 weeks of gestation, and then plateau until parturition [2-4].Plasma volume expansion is accompanied by a lesser increase in red cell volume (figure 2) [5]. As a result, there is amodest reduction in hematocrit, with peak hemodilution occurring at 24 to 26 weeks. The blood volume in pregnantwomen at term is about 100 mL/kg [6].

Plasma volume Total body volume expansion is accompanied by retention of 900 to 1000 meq of sodium and 6 to 8liters of water, distributed among the fetus, amniotic fluid, and extracellular and intracellular spaces [7,8]. Plasma volumeincreases by 10 to 15 percent at 6 to 12 weeks of gestation [9-11], expands rapidly until 30 to 34 weeks, after whichthere is only a modest rise. The total gain at term averages 1100 to 1600 mL and results in a plasma volume of 4700 to5200 mL, 30 to 50 percent above that found in nonpregnant women [4,9]. Mild edema is commonly seen.

Plasma renin activity tends to be increased and atrial natriuretic peptide levels are slightly reduced, suggesting that theincrease in plasma volume represents underfilling due to systemic vasodilatation and the ensuing rise in vascularcapacitance, rather than true blood volume expansion which would produce the opposite hormonal profile (low plasmarenin activity, elevated atrial natriuretic peptide) [12,13]. Furthermore, the degree of sodium retention is physiologicallyregulated, as increasing sodium intake does not produce further volume expansion [7]. Humoral factors that contribute tovolume regulation during pregnancy are discussed separately. (See "Maternal endocrine and metabolic adaptation topregnancy", section on 'Adrenal gland'.)

There are no specific measures that can be taken to expand the plasma volume in pregnant women and there is noevidence that the expansion of plasma volume would reverse or prevent associated poor pregnancy outcomes. Inprinciple, increasing dietary protein may improve colloid oncotic pressure (COP) which would shift extravascular fluid tothe intravascular space. Increasing maternal hydration may also act synergistically with a higher COP to improve



intravascular volume. There is also at least one anecdotal case of a patient given serial colloid infusions and furosemidewho had a successful pregnancy outcome, but we do not recommend this in the absence of data from well-designedstudies.

Red blood cell mass Red blood cell mass begins to increase at 8 to 10 weeks of gestation and steadily rises, inwomen taking iron supplements, by 20 to 30 percent (250 to 450 mL) above nonpregnant levels by the end of pregnancy[4,14-17]. Among women not on iron supplements, the red cell mass may only increase by 15 to 20 percent [18].Increased plasma erythropoietin induces the rise in red cell mass, which partially supports the higher metabolicrequirement for oxygen during pregnancy [19].

Physiologic anemia A greater increase in intravascular volume compared to red cell mass results in the dilutionalor physiologic anemia of pregnancy. This becomes most apparent at 30 to 34 weeks of gestation when plasma volumepeaks in relation to red cell volume.

The physiologic effects of hypervolemia and anemia during pregnancy has several benefits:

The absence of physiologic anemia appears to be harmful [21,22]. A population-based, case-control study using datafrom the Swedish Medical Birth Register found that women with a hemoglobin concentration of 14.6 g/dL or higher at thefirst prenatal visit were at increased risk of stillbirth (odds ratio (OR) 1.8), antepartum stillbirth without malformations (OR2.0), and preterm and small for gestational age nonmalformed stillbirth (OR 2.7 and 4.2, respectively) [21]. The elevatedrisk persisted despite a subsequent fall in hemoglobin concentration and after excluding women with preeclampsia. It ishypothesized that high blood viscosity increases the risk of thrombosis in the uteroplacental circulation.

Assuming normal renal function, blood volume and constituents return to nonpregnant values by eight weekspostpartum, a result of diuresis. Hemoglobin begins to increase from the third postpartum day [6].

CHANGES IN SYSTEMIC HEMODYNAMICS Maternal and fetal metabolic requirements increase as pregnancyprogresses. A change in the volume and distribution of cardiac output (the product of stroke volume and heart rate)occurs during pregnancy to meet these demands (figure 3).

Cardiac output The cardiac output rises 30 to 50 percent (1.8 L/min) above baseline during normal pregnancy; one-half of this increase occurs by 8 weeks of gestation [23-27]. The degree of change is acutely influenced by posture, asthe cardiac output is higher when the pregnant woman is in the left lateral decubitus position, particularly in the latter partof pregnancy [5,28,29]. By comparison, assumption of the supine position can lower the cardiac output by as much as25 to 30 percent due to compression of the inferior cava by the gravid uterus, leading to a substantial reduction invenous return to the heart.

Decreased blood viscosity (from greater increases in plasma volume than red cell volume) results in reducedresistance to flow, facilitating placental perfusion and lowering cardiac work.

Total blood volume increases to approximately 50 percent above nonpregnant values near term to provide somereserve against the normal blood loss during parturition (about 300 to 500 mL for vaginal delivery, 600 to 1000 mLfor cesarean delivery) and peripartum hemorrhage [3,4]. Following delivery, as much as 500 mL of bloodsequestered in the uteroplacental unit is autotransfused to the maternal circulation, thereby minimizing adversecirculatory 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 thefetus, excrete maternal and fetal waste products, and assist maternal temperature control, respectively. Theincreases in renal blood flow and glomerular filtration rate during pregnancy are largely mediated by the ovarianhormone relaxin, the release of which is increased by human chorionic gonadotropin [20]. (See "Renal and urinarytract physiology in normal pregnancy".)



The elevation in cardiac performance results in part from changes in three important factors that determine cardiacoutput:

In early pregnancy, increased cardiac output is primarily related to the rise in stroke volume; in late pregnancy, heart rateis the major factor. The ejection fraction is unchanged from normal nonpregnant values, making it a reliable indicator ofleft ventricular function during pregnancy, although the direct effect of pregnancy on left ventricular contractility remainscontroversial [30]. Regardless of the mechanism, the stress induced by the increase in cardiac output can cause womenwith underlying and, in some cases, asymptomatic heart disease to decompensate during the latter half of pregnancy.(See "Management of heart failure during pregnancy".) Changes in maternal heart rate, stroke volume, and cardiacoutput during pregnancy measured in the lateral and supine positions are demonstrated in the figure (figure 3).

Twin pregnancy The cardiovascular changes in women carrying twins are greater than those described above forsingleton pregnancies. Two-dimensional and M-mode echocardiography of 119 women (in the left lateral position) withtwins showed that cardiac output was 20 percent higher than in women carrying singletons, and peaked at 30 weeks ofgestation [31]. This increase was due to a 15 percent increase in stroke volume and 3.5 percent increase in heart rate.

Vascular resistance and blood pressure Systolic and diastolic blood pressure (BP) typically fall early in gestationand are about 5 to 10 mmHg below baseline in the second trimester, declining to a mean of about 105/60 mmHg [24,32-37]. 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, which in pregnancy appears to parallel changesin afterload [38]. Both creation of a high flow, low-resistance circuit in the uteroplacental circulation and vasodilatationcontribute to the decline in vascular resistance [24]. The factors responsible for the vasodilatation are incompletelyunderstood, but one of the major findings is decreased vascular responsiveness to the pressor effects of angiotensin IIand norepinephrine [39-41]. Several additional mechanisms for the fall in vascular resistance have been proposed:

The possible role of humoral agents, such as estrogens, progesterone, and prolactin, in mediating the vasodilationremains to be established [12]. In animals, as an example, estrogen and prolactin can both lower vascular resistanceand raise cardiac output [5].

Central hemodynamic changes As noted, cardiac function in the structurally normal heart is determined by preload,afterload, heart rate, and contractility. Although changes in blood volume during pregnancy affect right ventricularpreload, central venous pressure remains in the normal nonpregnant range throughout pregnancy due to the reduction incardiac afterload induced by the substantial decrease in both systemic vascular resistance and pulmonary vascularresistance (ie, afterload to the left and right heart, respectively) [45].

The inherent contractility of the myocardium is stable to slightly improved in pregnancy [46,47]. Pulmonary capillarywedge pressure and pulmonary artery systolic and diastolic pressures remain in the normal nonpregnant range since thehypervolemia of pregnancy is balanced by the fall in pulmonary vascular resistance.

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 [48-51].

Supine hypotensive syndrome Uterine enlargement beyond about 20 weeks' size can compress the inferior vena

Preload is increased due to the associated rise in blood volumeAfterload is reduced due to the decline in systemic vascular resistance (see below) [24]Maternal heart rate rises by 15 to 20 beats/min [24].

Increased endothelial prostacyclin [42]Enhanced nitric oxide production [43]Reduced aortic stiffness [44].



cava (IVC), markedly reducing cardiac preload. This occurs primarily in the supine position and is relieved by displacingthe uterus to the left and off the IVC by placing a wedge under the woman's right side, having the woman lie on her leftside, or adjusting the operating table to a 30 left lateral tilt [52]. Other, less common, causes of supine hypotensioninclude aortic compression and neurogenic etiologies.

The reduction in preload can result in maternal hypotension, usually within 3 to 10 minutes, associated with one or moresigns and symptoms of reflex autonomic activation and/or reduced cardiac output (table 1) [52,53]. The earliest sign ofdeveloping supine hypotension is an increase in maternal heart rate and a decrease in pulse pressure indicatingsignificantly reduced venous return [52]. Although these alterations are the best indicators of an impending attack, manywomen remain asymptomatic.

In addition, a reduction in placental perfusion may result in nonreassuring changes in the fetal heart rate with no orminimal decrease in upper extremity maternal blood pressure [54]. Therefore, it is important to position the parturient inthe left lateral tilt position for procedures (eg, labor and delivery, surgery, nonstress test, ultrasound) and to avoid thesupine position, even in symptom-free women.

VASCULAR CHANGES The vascular system is more compliant during pregnancy. Although not consistently found,specific changes have been reported in the aortic media of pregnant women. [55]. These include: fragmentation ofreticular fibers; a decrease in acid mucopolysaccharides, loss of normal corrugation of elastic fibers; and hypertrophyand hyperplasia of smooth muscle cells [56]. In addition, a small increase in the aortic diameter occurs, which increasesits compliance [57].

Aortic dissection is rare in normal young women, but when dissection occurs it usually does so during pregnancy [58-60]. Dissecting aneurysm may result, in part, from the alterations described above and the occasional coincidence ofpregnancy and clinically isolated annuloaortic ectasia, even though this occurs with a 2:1 to 8:1 male predominance [61].

UTERINE BLOOD FLOW Uterine artery blood flow has been reported to increase from 50 to 60 mL/minute in the latefirst trimester, to 185 mL/minute at 28 weeks, and to 450 to 750 mL/minute at term [62,63]. Cardiac output and uterineartery diameter also increase with advancing gestation. In early pregnancy, the uterus receives 3 to 6 percent of cardiacoutput; at term, the proportion is about 12 percent [62,64].

CHANGES IN SYSTEMIC COAGULATION Pregnancy is associated with changes in several coagulation factors thatresult in a 20 percent reduction of prothrombin and the partial thromboplastin times [65-67]:

The net effect of these pregnancy-induced changes is to produce a hypercoagulable state, which is a double-edgedsword of protection (eg, hemostasis contributing to reduced blood loss at delivery) and risk (eg, thromboembolicphenomenon) [68]. Venous thrombosis in pregnancy occurs in approximately 0.7 per 1000 women, and is three to fourfold higher in the puerperium than during pregnancy [69,73]. The risk is increased in women with underlying inheritedthrombophilia (eg, factor V Leiden or the prothrombin gene mutation) [74-76]. (See "Deep vein thrombosis in pregnancy:Epidemiology, pathogenesis, and diagnosis" and "Deep vein thrombosis and pulmonary embolism in pregnancy:Prevention" and "Deep vein thrombosis and pulmonary embolism in pregnancy: Treatment" and "Inheritedthrombophilias in pregnancy".)

ARRHYTHMIAS AND PALPITATIONS The exact mechanism of increased arrhythmia burden during pregnancy isunclear, but has been attributed to hemodynamic, hormonal, and autonomic changes related to pregnancy. (See

Resistance to activated protein C increases in the second and third trimesters [67]Protein S decreases [68]Factors I, II, V, VII, VIII, X, and Xll increase [68-70]Activity of the fibrinolytic inhibitors PAI-1 and PAI-2 increases, although total fibrinolytic activity may not be impaired[71,72]



"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 palpitationsdoes not differ from nonpregnant women. (See "Overview of palpitations in adults".)

HEMODYNAMIC CHANGES RELATED TO LABOR AND DELIVERY Normal labor and delivery is associated withsignificant 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 oranalgesia.

Cardiac output Blood from the uterine sinusoids is forced into the systemic circulation with each uterine contraction,thereby increasing preload during labor (figure 4).

The cardiac output and systemic vascular resistance gradually return to nonpregnant levels over a period of threemonths or more [77].

Blood pressure Systolic and diastolic blood pressure increase 15 to 25 and 10 to 15 percent, respectively, duringeach uterine contraction. The rise in systemic blood pressure is dependent upon the duration and intensity of uterinecontractions, position of the parturient, and the amount of pain and anxiety she is feeling. The increases in arterialpressure associated with each uterine contraction are mirrored by a rise in pressure in the amniotic fluid, intrathoracicvenous, cerebrospinal fluid, and extradural compartments (figure 5).

Bearing down or pushing during the second stage of labor alters the blood pressure and heart rate in a similar way to theValsalva maneuver; these changes are less pronounced if the gravida is positioned in the left lateral versus supineposition. The hemodynamic changes resulting from a Valsalva maneuver vary with the different phases.

Changes in baroreceptor sensitivity during pregnancy and associated with maternal position may also play a role. As anexample, one study of normotensive pregnant women noted a marked decrease in baroreflex sensitivity for heart rate inthe supine position, but not while standing [78].

POSTPARTUM HEMODYNAMIC RESOLUTION The postpartum period is marked by significant hemodynamicalterations. Fluctuations in cardiac output, stroke volume, and heart rate occur after delivery. Within the first ten minutesfollowing a term vaginal delivery, the cardiac output and stroke volume increase by 59 and 71 percent, respectively [79].At one hour postpartum, both the cardiac output and stroke volume remain increased (by 49 and 67 percent,

Cardiac output increases by 15 percent above prelabor levels in early labor and by approximately 25 percentduring the active phase.

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 significantautotransfusion associated with uterine involution that is more pronounced than the normal blood loss of delivery.

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, strokevolumes, 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 leftventricular volume.

Phase 4 is characterized by increases in stroke volume and arterial pressure and reflex slowing of heart rate (theovershoot).



respectively) while the heart rate decreases by 15 percent; blood pressure remained unchanged [80].

The increases in stroke volume and cardiac output most likely result from improved cardiac preload from autotransfusion of utero placental blood to the intravascular space. As the uterus decompresses following delivery, areduction 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 strokevolume in 15 healthy nonlaboring patients at 38 weeks of gestation, and again at 2, 6, 12, and 24 weeks postpartumdemonstrated a gradual diminution in cardiac output from 7.42 L/min at 38 weeks gestation to 4.96 L/min at 24 weekspostpartum [81]. As early as two weeks post partum there were substantial reductions in left ventricular size andcontractibility as compared to term pregnancies.

EVALUATION OF THE CARDIOVASCULAR SYSTEM IN PREGNANCY The physiologic and anatomic adaptationsto pregnancy influence the interpretation and evaluation of the gravida's cardiovascular status.

Physical examination The circulatory and respiratory changes during normal pregnancy are sometimes erroneouslyattributed to heart disease. The clinician caring for the gravida should be aware of these normal maternal cardiovascularadaptations to pregnancy.

Echocardiogram Physiologic multivalvular regurgitation, predominantly right-sided, is a frequent normal findingduring late gestation and may persist throughout the early post partum period [83]. In addition, chamber enlargement,valvular annular dilatation, and a small asymptomatic pericardial effusion are frequent normal incidental findings duringlate gestation [25,83,84].These findings appear to be caused by pregnancy-related hypervolemia and are important

Breathlessness (innocent hyperpnea), easy fatiguability, decreased exercise tolerance, basal rales that disappearwith cough or deep breathing, and peripheral edema commonly occur during pregnancy in normal women.

The systemic arterial pulse is characterized by a rapid rise and a brisk collapse (small water hammer) beginning inthe first trimester.

The jugular venous pulse is more conspicuous after the 20th week because brisk X and Y descents make the Aand V waves more obvious. Mean jugular venous pressure, as estimated from the superficial jugular vein, remainsnormal.

The pregnant woman's heart is shifted to the left, anterior, and rotated toward a transverse position as the uterusenlarges. As a result, the apical impulse is shifted cephalad to the fourth intercostal space and laterally to themidclavicular line. The left ventricular impulse is relatively hyperdynamic but not sustained; the right ventricle maybe palpable because, like the left ventricle, it handles a larger volume of blood that is ejected against relatively lowresistance. As pregnancy progresses, enlargement of the breasts and abdomen makes accurate palpation of theheart difficult, if not impossible.

Auscultatory changes accompanying normal gestation begin in the late first trimester and generally disappearwithin a week after delivery. A higher basal heart rate, louder heart sounds, wide splitting of S1, splitting of S2 inthe third trimester, and a systolic ejection murmur (up to grade 2/4) over the pulmonary and tricuspid areas areregularly detected upon cardiac auscultation. A third heart sound is present in most pregnant women; the fourthheart sound is rarely heard. The venous hum is almost universal in normal women during gestation. The mammarysouffle (systolic or continuous) is heard over the breasts in late gestation and is peculiar to pregnancy; it isespecially common postpartum in lactating women.

Diastolic murmurs are uncommon in normal pregnant women. When they occur, they may reflect increased flowthrough the tricuspid or mitral valve or physiologic dilatation of the pulmonary artery. However, these murmursmore likely represent a pathologic condition necessitating further study [82].



considerations when interpreting an echocardiogram in a pregnant patient.

Electrocardiogram Normal anatomic and physiologic changes of the heart and chest wall during pregnancy causechanges in the electrocardiogram that are unrelated to disease. The heart is rotated toward the left, resulting in a 15 to20 left axis deviation. Marked variation in chamber volumes, especially left atrial enlargement, leads to stretching of thecardiac conduction pathways and predisposes to alterations in cardiac rhythm. Periods of supraventricular tachycardiaand ventricular extrasystoles are a common finding. Other findings, which can be normal, include transient ST segmentand T wave changes, the presence of a Q wave and inverted T waves in lead III, an attenuated Q wave in lead AVF, andinverted T waves in leads V1, V2 and, occasionally, V3 [46,85,86]. (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 ventricularhypertrophy 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 heartborder. The majority of these changes are temporary and return to normal by eight weeks postpartum.

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Topic 443 Version 10.0

Expansion of the plasma volume and an increase in red blood cell mass begin as early as the fourth week ofpregnancy, peak at 28 to 34 weeks of gestation, and then plateau. Plasma volume expansion exceeds the increasein 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 insystemic 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 systemic coagulation'above.)

Labor and delivery is associated with significant hemodynamic changes due to anxiety, exertion, pain, uterinecontractions, uterine involution, and bleeding. Infection, hemorrhage, and the administration of anesthesia oranalgesia also play a role. (See 'Hemodynamic changes related to labor and delivery' above.)

The physiologic and anatomic adaptations to pregnancy influence the interpretation and evaluation of the pregnantwoman's cardiac evaluation. (See 'Evaluation of the cardiovascular system in pregnancy' above.)



GRAPHICS

Hemodynamic changes in normal pregnancy

Normal pregnancy is characterized by an increase in cardiac output, areduction in systemic vascular resistance, and minimal change in meanblood pressure. These changes are associated with a 10 to 15 beat/minincrease in heart rate.

Graphic 54685 Version 3.0



Total blood volume, plasma volume and red cellvolume in normal pregnancy

Data from Shnider SM, Levinson G. Anesthesia for Obstetrics, 3rd ed,Williams & Wilkins, Baltimore, p. 8.



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Systemic hemodynamics during normal pregnancy

Data from: Bonica JJ, McDonald JS. Principles and Practice of Obstetric Analgesiaand Anesthesia, 2nd ed, Williams & Wilkins, Baltimore, 1994. p.60.




Signs and symptoms attributed to supine hypotensive syndrome inpregnancy

Faintness

Dyspnea

Dizziness

Restlessness

Nausea

Vomiting

Chest pain

Abdominal pain

Visual disturbances

Numbness

Paresthesias

Headache

Cold, clammy skin

Pallor

Cyanosis

Hypotension




Cardiac output during normal labor, delivery, andpostpartum

Data from Bonica, JJ, McDonald, JS. Principles and Practice of ObstetricAnalgesia and Anesthesia, 2nd ed, Williams &Wilkins, Baltimore, 1994. p. 62.




Hemodynamics with contractions

Data from: Bonica JJ, McDonald JS. Principles and Practice of Obstetric Analgesiaand Anesthesia, 2nd ed, Williams & Wilkins, Baltimore, 1994. p.66.


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Maternal Cardiovascular and Hemodynamic Adaptations to Pregnancy