Search on website
Filters
Show more

Key Points

  • During pregnancy, parturients undergo physiologic changes that affect all organ systems, including the endocrine, cardiovascular, pulmonary, renal, hematologic, and gastrointestinal systems.
  • Hormones, gestational age, and fetal size precipitate these physiologic changes.
  • The clinical implications for anesthesia are outlined below.

Introduction

  • Table 1 summarizes the physiological changes in pregnancy.

Table 1. Physiological changes in pregnancy
Abbreviations: beta-hCG, beta human chorionic gonadotropin; TSH, thyroid-stimulating hormone; CO, cardiac output; SVR, systemic vascular resistance; SV, stroke volume; LV, left ventricle; BP, blood pressure; HR, heart rate; TV, tidal volume; MV, minute ventilation; pO2, partial pressure of oxygen; pCO2, partial pressure of carbon dioxide; O2, oxygen; ERV, expiratory reserve volume; FRC, functional reserve capacity; RV, residual volume; TLC, total lung capacity; IRV, inspiratory reserve volume; IC, inspiratory capacity; VC, vital capacity; CC, closing capacity; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity; GFR, glomerular filtration rate; UTI, urinary tract infection; RAAS, renin-angiotensin-aldosterone-system; ULN, upper limit of normal; BUN, blood urea nitrogen; RBC, red blood cell; L, liter; vWF, von Willebrand factor; VTE, venous thromboembolism; MAC, monitored anesthesia care; CSF, cerebrospinal fluid; SI, sacroiliac

Endocrine Changes

  • Hormones produced during pregnancy result in endocrine changes (Table 1).
  • The placenta produces beta human chorionic gonadotropin (beta-hCG), which increases progesterone and estrogen levels. Beta-hCG stimulates the corpus luteum to produce progesterone, which helps maintain the pregnancy.1,2
  • Initially, thyroid-stimulating hormone (TSH) decreases in the 1st trimester but rises thereafter as the placenta releases thyrotropin-releasing hormone, which increases the release of TSH and prolactin.2,3
  • Insulin resistance occurs later in pregnancy to ensure glucose is preferentially directed to the fetus for development.2,3

Clinical Implications for Anesthesia

  • Thyroid hormones have been linked to nausea during pregnancy.2
  • To counter the diabetogenic state, pregnant women will increase insulin production. When production is insufficient, gestational diabetes mellitus develops. Fetal macrosomia and neonatal hypoglycemia can occur.2,3

Cardiovascular Changes

  • Overall, vasodilation and increased cardiac output occur, peaking at 20-24 weeks and 20-28 weeks, respectively.1-3
  • Normal electrocardiography changes include atrial and ventricular ectopics, inverted or changes in T wave morphology in the inferior and lateral leads, ST segment depression, and leftward QRS axis shift.2,3

Clinical Implications for Anesthesia

  • Supine hypotension syndrome occurs when there is aortocaval compression leading to decreased preload, hypotension, and decreased placental perfusion.2-4
  • Increased sympathetic activity decreases the risk of supine hypotension by increasing systemic vascular resistance to maintain blood pressure. Neuraxial and general anesthesia can impair sympathetic tone, leading to maternal hypotension and decreased placental perfusion.3,4
  • Immediately after delivery, autotransfusion from the contracting uterus occurs, leading to increased cardiac output (80-100%).1-4
  • Patients with cardiovascular disease, including stenotic valvular lesions, pulmonary hypertension, and heart failure, are at an increased risk.4

Pulmonary Changes

  • Respiratory changes in pregnancy are due to hormonal, physiologic, metabolic, and physical changes (Table 1).1-3
  • Progesterone leads to an increased tidal volume.
  • Respiratory alkalosis compensated by renal bicarbonate excretion occurs in pregnancy (Table 2).
  • Diaphragm elevation from a gravid uterus alters lung volumes and capacities.

Clinical Implications for Anesthesia4

  • Decreased functional residual capacity (FRC) and increased oxygen consumption will increase the risk of rapid desaturation.
  • Decreased FRC and closing capacity increases the risk of atelectasis in the supine position.
  • Due to vascular engorgement of the airway, there is an increased risk of edema and bleeding with manipulation.

Table 2. Arterial blood gas values in pregnancy2,3
Abbreviations: mmHg, millimeters of mercury; mEq/L, milliequivalents per liter

Oxygen Dissociation Curve1,3

  • To promote oxygen transfer from maternal to fetal blood across the placenta, the maternal oxyhemoglobin dissociation curve shifts to the right, favoring oxygen dissociation. P50 is the oxygen tension when hemoglobin is 50% saturated with oxygen.
  • The maternal dissociation curve shifts right while the fetal curve shifts left (Figure 1).
    • P50 of maternal hemoglobin rises at term: 30 vs 26 mmHg3
    • P50 of fetal hemoglobin: 18 mmHg (higher affinity for oxygen)3

 

Figure 1. Oxyhemoglobin dissociation curves1,3
Blue line, Fetal hemoglobin. Green line, Nonpregnant adult hemoglobin. Orange line, Maternal hemoglobin. mmHg, millimeters of mercury

Renal Changes

  • The main factors affecting renal changes during pregnancy include: (Table 1)1-3,5
    • Increased CO increases renal perfusion
    • Increased progesterone and relaxin cause urinary tract dilation
    • The renin–angiotensin–aldosterone system is activated, resulting in sodium and water retention.

Clinical Implications for Anesthesia1,4

  • Increased urinary stasis and urinary tract dilation can increase the risk of urinary tract infections and pyelonephritis.
  • Typically, serum creatinine and BUN decrease during pregnancy due to increased clearance. Therefore, “normal values” for serum creatinine and BUN levels are considered abnormal.

Hematologic Changes

  • Hematologic adaptations during pregnancy are essential for preparation for delivery (Table 1).1-4,6
  • Dilutional physiologic anemia is characterized by increased plasma volume compared to red blood cell mass expansion (Figure 2).
  • A progressive hypercoagulable state persists throughout pregnancy in preparation for blood loss at delivery.

Clinical Implications for Anesthesia

  • Despite an increased plasma volume, postpartum hemorrhage can cause profound anemia.4
  • Pregnancy is a hypercoagulable state, increasing the risk of venous thrombosis.1
  • Thrombocytopenia occurs in about 6-10% of pregnancies, the major cause being gestational thrombocytopenia. It is essential to check a platelet count in patients at risk of thrombocytopenia.4

Figure 2. Physiologic anemia in pregnancy3,6
Purple line, plasma volume; Red line, red blood cell mass

Gastrointestinal Changes

  • Physiologic gastrointestinal adaptations in pregnancy are influenced by hormonal effects (progesterone) and mechanical pressure from the enlarging uterus.
  • These changes contribute to common symptoms such as nausea, vomiting, reflux, and constipation, and predispose to complications such as hyperemesis gravidarum and hemorrhoids (Table 1).1-3,7

Clinical Implications for Anesthesia

  • Decreased esophageal sphincter tone, delayed gastric emptying, and increased gastric pressure from the uterus can increase the risk of aspiration. The administration of aspiration prophylaxis should be considered for surgical procedures.4

Neurologic Changes

  • Physiologic neurologic adaptations in pregnancy are influenced by hormonal effects (progesterone) and anatomic changes in the neuraxis.
  • These changes include decreased minimum alveolar concentration for inhalational anesthetics, increased sensitivity to local anesthetics requiring lower neuraxial doses, and greater spread of neuraxial blockade due to epidural venous engorgement and reduced cerebrospinal fluid (CSF) volume (Table 1).3,4
  • Increased intraoperative awareness is also reported in cesarean delivery with general anesthesia compared with other general anesthesia cases.4

Clinical Implications for Anesthesia

  • Anatomically, the epidural veins are engorged, and the size of the epidural space decreases, resulting in a decreased volume of CSF. A lower CSF volume may lead to greater spread of local anesthetic, especially in the third trimester.3,4

Musculoskeletal Changes

  • Musculoskeletal changes in pregnancy are influenced by hormonal effects (relaxin, estrogen), weight gain, and mechanical shifts from the enlarging uterus.
  • These changes include abdominal muscle stretching with diastasis recti, ligamentous laxity with widening of the symphysis pubis, increased joint stress from weight gain, edema-related joint/nerve compression, hyperlordosis from altered center of gravity, and pelvic floor descent with pudendal nerve compression (Table 1).2,8

Clinical Implications for Anesthesia

  • Lumbar lordosis and altered spinal anatomy could make neuraxial block placement challenging and may require the use of ultrasound guidance.9
  • Joint laxity and edema increase the susceptibility to pressure injuries, requiring frequent repositioning.8

Skin Changes

  • Hormonal (estrogen and progesterone) and vascular changes influence dermatologic adaptations during pregnancy.1,10
  • Estrogen and progesterone can stimulate excess melanin production, resulting in melasma (hyperpigmentation of the face) and darkening of the areola, axilla, and genitals.1 Additionally, a hypoestrogenic state can result in the formation of spider angiomas, which often resolve following childbirth.10

Clinical Implications for Anesthesia

• Maternal thermoregulation occurs through increased cutaneous blood supply, which raises maternal skin temperature.1

References

  1. Kepley JM, Bates K, Mohiuddin SS. Physiology, Maternal Changes. In: StatPearls (Internet). Treasure Island (FL): StatPearls Publishing; March 12, 2023. Accessed August 24, 2025. PubMed
  2. Soma-Pillay P, Nelson-Piercy C, Tolppanen H, Mebazaa A. Physiological changes in pregnancy. Cardiovasc J Afr. 2016;27(2):89-94. PubMed
  3. Melaku L. Physiological changes in the pregnancy and anesthetic implication during labor, delivery, and postpartum. Open Anesthesia J. 2022;16: e258964582207130. Link
  4. Page SM, Rollins MD. Physiology and pharmacology of obstetric anesthesia. In Pharmacology and Physiology for Anesthesia (Second Edition). 2019; 732-751. Elsevier. Link
  5. Odutayo A, Hladunewich M. Obstetric nephrology: renal hemodynamic and metabolic physiology in normal pregnancy. Clin J Am Soc Nephrol. 2012;7(12):2073-80. PubMed
  6. Patel PB, Patel N, Hedges MA, et al. Hematologic Complications of Pregnancy. European Journal of Haematology. 2025;114(4):596-614. PubMed
  7. Hill CC, Pickinpaugh J. Physiologic changes in pregnancy. Surgical Clinics of North America. 2008;88(2):391-401. PubMed
  8. Thabah M, Ravindran V, Thabah M, Ravindran V. Musculoskeletal problems in pregnancy. Rheumatology International. 2014-09-25;35(4). PubMed
  9. Bhatia P, Chhabra S. Physiological and anatomical changes of pregnancy: Implications for anaesthesia. Indian J Anaesth. 2018;62(9):651-7. PubMed
  10. Muallem MM, Rubeiz NG. Physiological and biological skin changes in pregnancy. Clinics in Dermatology. 2006;24(2):80-3. PubMed

Other References

  1. Hofer J. Maternal comorbidities combined with physiologic changes in pregnancy requiring ICU admission. OA-SOAP Fellows Webinar. 2018. Link