Maternal-Fetal Physiology

Maternal-Fetal Physiology

• Physiological adaptations throughout pregnancy occur to accommodate new demands.
• These adaptations support the fetus, protecting both the fetus and mother while preparing the uterus for labor.

Cardiovascular System

• Cardiac output increases by 30-50%, with half of this increase occurring by 8 weeks.
• This increase caused initially by the increased stroke volume.
• In late pregnancy, the increased heart rate is a major factor.
• Ejection fraction remains unchanged.
• Cardiac output is affected by posture.
• Cardiac output is highest in the left lateral recumbent position.
• The supine position lowers cardiac output by 30% because of inferior vena cava (IVC) compression.
• Increased preload (ventricular filling) and decreased SVR (systemic vascular resistance) elevate cardiac performance.
• Maternal heart rate increases by about 20 bpm.
• Intravascular pressure decreases early in gestation and mean blood pressure falls to 105/60 in the second trimester.
• Diastolic blood pressure decreases more than systolic.
• Reduced systemic vascular resistance (SVR) is a result of high flow, low resistance, and vasodilation, and is possibly related to increased nitric oxide, endothelial prostacyclin, and hormonal changes.
• Blood flow increases in most body areas, with the majority of cardiac output going to the placenta, kidneys, and skin.
• Uterine blood flow increases from 25mL/min to 1200mL/min, with blood flow at term being 750mL/min.
• Contractions force around 500mL blood from the uterus into systemic circulation, while cardiac output increases 15% in early labor, 25% in the active phase, and 50% in the second stage.
• Immediately postpartum, cardiac output peaks at 80% above prelabor values due to autotransfusion associated with uterine involution.

Hematologic System

• Plasma volume begins to rise by the 4th week and peaks between 28-34 weeks.
• Plasma volume increases to 40-50% above nonpregnant levels, with a gain of ~1100-1600 mL on average, and is associated with the retention of 900-1000 mEq of sodium.
• Red blood cell mass increases starting at 8-10 weeks.
• Increases of 20-30% occur in women who are taking iron (Fe), while increases of 15-20% if there is no iron supplementation.
• The increase in red blood cell mass is caused by increased plasma erythropoietin, and supports the higher metabolic oxygen requirement of pregnancy.
• Intravascular volume increases more than red blood cell mass, resulting in dilutional or physiologic anemia, with a decrease in hematocrit despite the increased total RBC count.
• Decreased viscosity facilitates placental perfusion and reduced cardiac workload.
• Physiological changes provide a reserve against blood loss at parturition and postpartum hemorrhage.
• Pregnancy leads to a hypercoagulable state with the increased risk of pulmonary embolus, spontaneous abortion, or intrauterine fetal demise.
• Resistance to activated protein C develops, protein S decreases, and Factors I, II, V, VII, VIII, X, and XII increase.
• Venous thrombosis occurs in about 0.7/1000 pregnancies.

Respiratory System

• Upper airways: mucosal edema and vascularity increase and lead to rhinitis and epistaxis.
• Thoracic circumference increases by 8%.
• Elevation of diaphragm by 5 cm occurs as pregnancy progresses.
• Dyspnea increases 15% by 10 weeks, 50% by 19 weeks, and 76% by 31 weeks.
• As pregnancy progresses, the enlarging uterus elevates the resting position of the diaphragm but diaphragmatic contractility is unaffected.
• FEV1 remains unchanged, functional reserve capacity (FRC) decreases 10-25%, total lung capacity (TLC) decreases minimally, minute ventilation increases by 20-40%, and alveolar ventilation increases by 50-75%.
• Total body oxygen consumption increases about 15-20%.
• Half of the oxygen consumption is accounted for by the uterus, and the other half is from increased maternal renal and cardiac work.
• Both cardiac output and alveolar ventilation are elevated higher than required to meet the increased oxygen consumption.
• A pregnant patient will experience compensated respiratory alkalosis.
• Carbon dioxide diffuses faster than oxygen
• PaCO2 decreases (27-34), bicarbonate increases (18-21), and pH stays between 7.40-7.45.
• PaO2 increases (101-104), the A-a gradient increases causing increased oxygen uptake.
• Airway resistance remains unchanged or even decreases and tidal volume increases causing marked decreases in pCO2 which is the cause of dyspnea in up to 70% of pregnant women.

Renal Physiology

• The urinary collecting system undergoes marked dilation, including calyces, renal pelvices, and ureters.
• Progesterone causes decreased ureteral tone and peristalsis.
• The enlarged uterus partially obstructs the ureter at the pelvic brim, and in addition enlargement of ovarian vessels also partially obstructs the ureters.
• Hydronephrosis develops from the obstruction of the ureters and is more common on the right side due to dextrorotation of the uterus.
• The dilated collecting system will hold an excess of 200-300 mL of urine, creating an ideal reservoir for bacteria and increasing the risk for UTIs, stones, and pyelonephritis.
• Renal blood flow and GFR both rise markedly in pregnancy beginning within the first month, and plateau at 40-50% above nonpregnant levels by the end of the first trimester.
• Kidneys enlarge approximately 1.5 cm.
• Elevated GFR is reflected in lower serum creatinine and urea nitrogen (BUN).
• Small amounts of glucosuria or ketonuria may be seen because of higher rates of filtration.
• Persistent hyperventilation leads to renal losses of bicarb.
• Reduced renal buffering ability due to bicarb loss predisposes pregnant women to metabolic acidosis, such as ketoacidosis or lactic acidosis.

Endocrine System

• The thyroid enlarges in many pregnancies due to iodine deficiency.
• TSH levels are modestly reduced in the first trimester in response to increasing human chorionic gonadotropin (hCG); this may be misinterpreted as hyperthyroidism.
• Total thyroid levels (total T3 and T4) increase, while active thyroid hormone (free T3 and free T4) remain at normal levels.
• There is a disparity between total thyroid hormone and free hormone levels because 85% of T3 and T4 are bound to thyroid binding globulin (TBG).
• TBG increases twofold during pregnancy in response to estrogen, the thyroid then increases its production of thyroid hormone in order to maintain active levels.
• Maternal T4 crosses the placenta throughout pregnancy, and fetal thyroid function and self-regulation begins around 20 weeks.
• Maternal hyperthyroidism may inhibit fetal thyroid development if not corrected by 20 weeks of gestation.
• Glucocorticoid production increases, as does corticosteroid binding globulin (CBG).
• Corticotropin Releasing Hormone (CRH, which is produced by the placenta) rises exponentially throughout pregnancy and stimulates maternal ACTH production.
• Cortisol levels are 3 times higher in the third trimester than during pre-pregnancy.
• Placental hormones, especially in the third trimester, affect maternal glucose and lipid metabolism to ensure an adequate supply of nutrients to the fetus.
• Carbohydrate (CHO) metabolism supplies glucose and amino acids to the fetus while providing extra free fatty acids, ketones, and glycerol for maternal fuel sources.
• Hyperplasia of pancreatic Beta cells occurs with increasing insulin secretion and progressive insulin resistance, mostly due to Human Placental Lactogen (HPL) and occurs beginning in the middle of the second trimester.
• Gestational diabetes occurs when maternal pancreatic function cannot overcome this insulin resistance.
• Lower fasting glucose levels occur despite insulin resistance due to increased storage of glycogen, increased peripheral glucose utilization, decreased hepatic glucose production, and glucose consumption by the fetus.
• Transient hyperglycemia occurs after meals due to the insulin resistant state, and then followed by transient hypoglycemia between meals due to continuous fetal draw from the circulating glucose supply.
• Normal mean fasting glucose is 56 mg/dL.
• Insulin resistance and relative hypoglycemia result in increased lipolysis
• This allows the mother to preferentially use fats for fuel (FFAs, TGs, KBs), preserve much of the available glucose and amino acids for the fetus and minimize protein catabolism.
• Triglycerides and cholesterol increase in pregnancy by 300% and 50% respectively.
• The liver increases triglyceride production and lipoprotein lipase activity is suppressed decreasing adipocyte catabolism.
• High TGs allow for maternal fuel, CHO sparing.
• High cholesterol aids placental steroidogenesis.

Gastrointestinal System

• Pregnancy has little, if any effect on GI secretion or absorption, but it does affect motility.
• Intestinal motility is slowed due to pregnancy hormones, likely progesterone and estrogen, leading to bloating and constipation.
• Mechanical factors, like compression from the uterus, impact gastric function.

Skin

• Hyperpigmentation of skin occurs in 90% of pregnancies.
• Melanocyte-stimulating hormone increases, causing the darkening of the areolae, umbilicus, vulva, and perianal skin in the first trimester, along with the linea alba becoming linea nigra.
• Striae Distensae are thin, atrophic, pink or purple linear bands that develop on abdomen, breasts and/or thighs, and usually begin to appear in the late second trimester in 80-90% of gravidas due to stretching of the skin.
• Adrenocorticosteroids and estrogen also promote the tearing of collagen matrix within the dermis.
• Striae are permanent, yet the coloration fades with time becoming white/silvery, and creams and ointments that claim to prevent or treat striae have not been proven and are unlikely to have any benefit.