Physiologic Changes in Pregnancy
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Physiologic Changes in Pregnancy
Cindy C. Bitter
Shortly after fertilization, the ovaries and the fetal-placental complex initiate the biochemical, anatomic, and physiologic adaptive changes necessary to sustain pregnancy. These physiologic changes affect nearly every organ system and start in the first trimester and persist throughout the postpartum period. The stress of pregnancy may expose previously asymptomatic underlying disease states. Conversely, normal parameters in pregnancy may be mistaken for pathology. A meta-analysis of vital signs in normal pregnancy found significant overlap with thresholds that meet criteria for systemic inflammatory response syndrome.1
Understanding normal physiology in pregnant patients is crucial to recognizing early signs of disease and avoiding unnecessary investigations.
Upper Respiratory Tract
Mucosal edema and capillary congestion lead to engorgement of the upper airway, beginning in the first trimester and progressing throughout pregnancy. Epistaxis and nasal congestion are common throughout pregnancy and are thought to be mediated by the effects of estrogen and human placental growth hormone (GH) on the vasculature.2,3
Near term, the diaphragm elevates up to 4 cm but is partially compensated by an increase in chest diameter of up to 2 cm and an increase in the subcostal angle. Functional residual capacity (FRC) is decreased by 10% to 25% (300-500 mL) after 24 weeks’ gestation and is further reduced when term patients are placed in the supine position.4
Progesterone directly stimulates the respiratory centers in the medulla to increase respiratory drive. Minute ventilation increases by 30% to 50% at term from an increase in tidal volume without significant change in the respiratory rate. A respiratory rate greater than 20 is considered abnormal in the pregnant patient.4
Total lung capacity and residual volume are decreased, whereas forced vital capacity (FVC) is unchanged in pregnancy. These changes are summarized in Table 1.1
Increased minute ventilation results in lower arterial partial pressure of carbon dioxide (PaCO2
), which averages 26 to 32 mm Hg at term. Arterial pH is maintained in the normal range
by a decrease in serum bicarbonate to compensate for respiratory alkalosis.5
Lower bicarbonate levels shift the maternal hemoglobin oxygen dissociation curve to the right, facilitating oxygen transfer to the fetus. Lower maternal PaCO2
increases fetal off-loading of CO2
to maternal circulation for excretion.6
TABLE 1.1 Lung Volume Changes During Pregnancy
Tidal volume (TV)
Functional residual capacity (FRC)
Total lung capacity (TLC)
No change to decreased 5%
Forced vital capacity (FVC)
Vital capacity (VC)
Forced expiratory volume in 1 s (FEV1)
Peak expiratory flow rate (PEFR)
Diffusion capacity (DLCO)
Respiratory rate (RR)
Data apply to singleton and twin gestations. Abbreviations as used in pulmonary function testing are in parenthesis.
Reprinted with permission from Bobrowski RA. Pulmonary physiology in pregnancy. Clin Obstet Gynecol. 2010;53(2):285-300.
Maternal oxygen consumption increases by 20% to 40% over prepregnancy levels due to increased oxygen requirements of the fetus, placenta, and maternal organs. This results in a significant decrease in maternal oxygen reserve, which can lead to rapid development of hypoxia in the setting of respiratory compromise.
Changes to the shape of the rib cage and elevation of the diaphragm result in rotation and displacement of the heart to the left within the thorax, leading to displacement of the point of maximum impulse (PMI). Cardiac mass increases due to hypertrophy of the smooth muscle and cardiac volume increases.7
Pericardial effusions are common in pregnancy, found in 15% to 20% of first- and second-trimester patients and up to 40% of women in the third trimester. Effusions are rarely of clinical significance and typically resolve after delivery.8
Auscultation of the heart may reveal an exaggerated S1 split, a third heart sound, or a systolic ejection murmur, typically best heard at the left sternal border. These changes are found in up to 90% of pregnant women and are attributed to increased cardiac output (CO).9
The stress of pregnancy may also unmask previously silent valvular disease, and the clinician should maintain a low threshold for echocardiogram and referral if patients are symptomatic.
Arrhythmias are common in pregnancy, occurring in 68 per 100,000 pregnancies overall, and the risk increases with increasing maternal age.10
Mild sinus tachycardia is common in pregnancy, particularly in the third trimester. Pregnant patients have a mean heart rate of 75 ± 20 in the first trimester, rising to 82 ± 22 by the third trimester.1
Atrial fibrillation or atrial flutter affects 59.3 per 100,000 pregnancies, and risk increases with advanced maternal age.10
Supraventricular tachycardia, premature atrial contractions (PACs), and premature ventricular contractions (PVCs) may be seen. Women with more than 5% PVCs on Holter monitoring were found to have increased cardiac complications, including heart failure and ventricular tachycardia.11
Arterial Blood Pressure and Systemic Vascular Resistance
Arterial blood pressure decreases in pregnancy, including the systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP). Decreases in blood pressure start by 6 to 8 weeks’ gestation, reach a nadir of 5 to 10 mm Hg below preconception values by the middle of the second trimester, and approach prepregnancy values by the end of the third trimester. Systemic vascular resistance decreases approximately 20%, which decreases the DBP greater than SBP, resulting in an increased pulse pressure. Pulmonary capillary wedge pressure is unchanged during normal pregnancy.
CO increases in the first trimester and peaks at 30% to 40% above prepregnancy values near the end of the second trimester, up to 4 to 6 L/min. CO is the product of stroke volume and heart rate. Early in pregnancy, CO primarily increases due to increased stroke volume; whereas later in pregnancy, CO increases due to a combination of increased stroke volume and heart rate. The stroke volume is highly dependent on venous return, and compression of the inferior vena cava by the gravid uterus in the supine position may reduce CO in the second and third trimesters. CO increases an additional 15% in twin gestations.12
See Table 1.2
for a summary of changes in cardiac physiology by trimester.
Due to increased CO, blood flow to the brain, lungs, kidneys, and skin. The uterus receives nearly 20% of the CO at term. Increased blood flow to the lower extremities leads to elevated venous pressure, contributing to pedal edema, varicose veins, and deep venous thrombosis. Pedal edema is further exacerbated by decreased osmotic pressure due to hemodilution and compression on the vena cava by the gravid uterus.13
TABLE 1.2 Interrelationship of Changes in the Major Variables that Contribute to the Cardiovascular Changes in Pregnancy Compared with Preconception Values
↑ Sympathetic activity
LV wall mass
4 Chamber enlargement
↑ and ↓ reflect relative changes in parameters from preconception values.
* Greater increase in plasma volume relative to the increase in RBC mass results in the physiologic anemia of pregnancy.
BP, blood pressure; CO, cardiac output; HR, heart rate; LV, left ventricular; RBC, red blood cell; SVR, systemic vascular resistance.
Reprinted with permission from Sanghavi M, Rutherford JD. Cardiovascular physiology of pregnancy. Circ. 2012;130:1003-1008.
Evaluation of Cardiac Disease
Evaluation of cardiac disease is complicated by the pregnant state. Troponin values are not affected by pregnancy but creatine kinase-muscle/brain (CK-MB) is unreliable if the patient is having uterine contractions. Brain natriuretric peptide (BNP) increases in the third trimester of normal pregnancies, with higher mean values in patients with preeclampsia.14
Due to changes in thoracic anatomy, an increased cardiac silhouette is common on chest x-rays during pregnancy, which does not imply pathologic cardiomegaly. Increased vascular markings may also be seen due to increased pulmonary blood volume.
Heartburn and gastroesophageal reflux disease (GERD) occur in 40% to 85% of pregnant women, with increased incidence throughout gestation. The basal tone of the lower esophageal sphincter (LES) is unchanged in the first trimester, but the LES is less responsive to stimuli that should increase tone, such as a high-protein meal.15
As pregnancy progresses, increases in progesterone cause relaxation of the LES as well as decreases in esophageal and gastric peristalsis, resulting in worsening GERD.
Progesterone causes decreased bowel motility, contributing to an increase in constipation affecting 25% to 40% of pregnancies. Progesterone also increases aldosterone concentration, enhancing colonic absorption of water, leading to harder stools. Pregnancy-mediated effects on the hormones motilin and relaxin may also contribute. Constipation tends to be most problematic in the first and second trimesters, but mechanical effects of the gravid uterus may contribute later in pregnancy.16
Hemorrhoids are common in pregnancy and the peripartum period due to estrogen-mediated dilation of blood vessels as well as mechanical effects of the gravid uterus. Constipation further predisposes to symptomatic hemorrhoids. Iron supplementation may also cause constipation. Hypothyroidism, diabetes, pelvic floor dysfunction, neurologic disease, and colorectal disease should be considered if symptoms are severe.
There are no significant changes to liver size or morphology during normal pregnancy but hepatic blood flow increases and the portal vein diameter may increase. Alkaline phosphatase levels increase due to placental isozymes. Serum albumin concentrations decrease in pregnancy, primarily due to the increase in plasma volume. Bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT) levels decrease in pregnancy.17
Pregnancy results in decreased gallbladder contractility, possibly due to effects of progesterone. Biliary stasis and higher concentrations of cholesterol in bile fluid predispose to gallstone formation, particularly in multiparas. Gallstones occur in 5% to 12% of pregnancies, resulting in 5 hospitalizations per 1000 pregnancies, and the rate is increasing.18
Pregnancy also results in increases in serum bile acid concentrations, which contributes to intrahepatic cholestasis and pruritus gravidarum, although the mechanism is unclear.
Renal size increases by up to 30% in normal pregnancy. Dilation of the renal calyces and pelvis begins in the second trimester and occurs in up to 36% of patients in the third trimester. These changes return to normal by approximately week 20 after delivery. Compression of the ureters by the gravid uterus at the level of the pelvic brim can result in ureteral dilation, although progesterone effects on smooth muscle of the ureter may contribute. Ureteral dilation is much more common
on the right in up to 45% of patients compared to 9% on the left. Ureteral dilation may not signify obstruction, complicating the diagnosis of ureteral calculi and other renal pathology.19
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