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• Maternal physiology changes occur in pregnancy due to hormonal changes (progesterone, estrogen, HPL, hCG), mechanical effects of the enlarging uterus, increased metabolic demands (MRO2 increases by 20% at term), and placental circulation acting as a low-pressure AV shunt.

Cardiovascular System Changes

• Heart rate increases by 15% by the end of the first trimester, then by 25% by the mid-third trimester.
• Stroke volume increases by 20-30% from 8/40 to 32/40, due to increased blood volume (40%).
• Cardiac output increases by 30% from 8/40 to 32/40, due to increased heart rate and stroke volume (associated with increased blood volume), decreased total peripheral resistance (TPR) (associated with increased venous return), and increased MRO2.
• Systemic vascular resistance decreases by 20-30% by the end of the first trimester due to placental circulation (10% of cardiac output) acting as a low resistance AV shunt, and progesterone and PG-mediated peripheral vasodilation (especially in renal, splanchnic, heart, breasts, and skin circulation).
• Pulmonary vascular resistance decreases by 35% by the end of the first trimester due to progesterone/prostaglandins.
• Tissue blood flow increases, particularly to the uterus/placenta, heart, kidneys, GIT, breasts, and skin, due to increased cardiac output and hormone-mediated regional vasodilation; cerebral blood flow is not affected.
• Blood pressure decreases (MAP, DBP > SBP) by 10% (especially at 20/40) due to decreased SVR, but normalizes towards term.
• Central venous pressure and pulmonary capillary wedge pressure remain unchanged.

Aortocaval Compression

• The abdominal aorta and IVC may be occluded by the effects of the gravid uterus as early as the second trimester (maximum effect at 36-38/40), especially when supine.
• Complete compression of the IVC is characterized by compensatory vasoconstriction, tachycardia, maintaining venous return, cardiac output, and MAP in 85%
• "Supine hypotension syndrome" occurs in 15% as compensatory mechanisms are insufficient, leading to decreased venous return, cardiac output, and MAP causing hypotension, bradycardia, pallor, syncope, N/V, and sweating.
• Partial compression of the abdominal aorta decreases uteroplacental blood flow by 20% (causing fetal distress) and renal blood flow.
• Positioning the mother on her left side can prevent this.

During Labor

• Cardiac output increases by 15% in early labor, 30% in the first stage, 45% in the second stage, and 65% postpartum, normalizing 2/52 postpartum.
• Uterine contractions and involution postpartum squeeze 300 mL of blood out of the uterus into circulation ("Autotransfusion"), increasing venous return, stroke volume, and cardiac output.
• Blood pressure increases by 10-20 mmHg with uterine contractions, normalizing 2/52 postpartum.
• Central venous pressure increases (4-6 cmH2O) due to increased venous return associated with autotransfusion.

Respiratory System

• Diaphragm is displaced upwards by 4 cm due to gravid uterus, but contractility is not markedly restricted.
• Anterior-posterior and transverse diameters increase by 2-3 cm, increasing circumference by 5-7 cm, due to "Relaxin" that relaxes ligaments of ribs.
• Upper respiratory tract (vocal cords, nasal mucosa) becomes swollen due to capillary engorgement.

Changes in Lung Volumes

• Occur early and continue to change progressively during pregnancy (especially from 20/40), normalizing 2-5 days postpartum.
• Expiratory reserve volume and residual volume (including functional residual capacity and total lung capacity) decrease due to the elevated diaphragm (secondary to gravid uterus) and increased pulmonary blood volume.

Minute and Alveolar Ventilation

• Increases early (especially after 10/40) and gradually during pregnancy (by 50-70% at term) due to increased tidal volume (by 40% at term) and increased respiratory rate (by 15% at term).
• Progesterone stimulates medullary respiratory centers, increasing sensitivity to PaCO2 (left shift in CO2 response curve).

During Labor

• Minute ventilation/alveolar ventilation increases further (by 160%) due to pain and increased MRO2 associated with uterine contractions, potentially causing transient decreases in PaCO2 (to 20 mmHg).

Arterial Blood Gas Changes

• Increased minute ventilation causes decreased PCO2 and increased PO2 which creates favorable gradients for O2/CO2 across the placenta.
• Decreased PCO2 causes respiratory alkalosis, but pH is compensated renally by increasing HCO3- excretion and decreasing base excess.

Lung Mechanics

• Work of breathing remains unchanged due to balance between decreased airway resistance and decreased total compliance of the respiratory system.
• Airway resistance decreases by 35%, and anatomical dead space increases by 45% due to progesterone-mediated large airway dilation.
• Total compliance of the respiratory system decreases due to decreased chest wall compliance secondary to elevation of the diaphragm by the gravid uterus (lung compliance is unchanged).
• Flow-volume curves remain unchanged while sitting.
• Airway closure (and atelectasis) occurs when supine only, with up to 50% of women having FRC < CC when supine.

Tissue O₂ Delivery to Tissues

• Oxygen flux increases (by 10% at term) due to increased cardiac output, increased PO2, and increased tissue blood flow, despite limitations in CaCO2 by anemia of pregnancy, right shift in Hb ODC, and Hb being maximally saturated.
• Tissue MRO2 increases during pregnancy (by 20% at term).

Hematological Changes

• Physiological anemia of pregnancy occurs from 6-8/40 to 28-32/40, with increased blood volume by 40% (1.2-1.5 L) due to increased plasma volume by 50% (due to Na+/H2O retention by estrogen activation of RAAS) and increased red cell volume by 30% (due to renal EPO synthesis).
• Plasma volume increases more than red cell volume, and plasma volume increases faster than red cell volume leading to decreased RBC count, Hb, and Hcrit (4.6 to 3.6 x 10º/mm², 140 to 120 g/L and 41 to 35% by 28-32/40 respectively).
• Platelets decrease (5-20%) due to hemodilution.
• White blood cell count increases (9000/mm³) due to increased PMNL and monocytes.
• Acquired hypercoagulable state prepares for blood loss at delivery, increasing coagulation factors and fibrinolysis
• Total amount of proteins increases, but concentrations vary (total protein, y-globulins, albumin decrease due to hemodilution, total, a-globulins, beta-globulins, fibrinogen, and CRP increase)
• Plasma oncotic pressure declines (14%) due to decreased albumin.

Endocrine Changes

• The placenta produces 4 hormones: human chorionic gonadotropin, human placental lactogen, estrogen, and progesterone.
• hCG is a peptide hormone synthesized by syncytiotrophoblast cells increases until it peaks at 10-12 weeks, then decreases until term which maintains corpus luteal function (estrogen and progesterone production) that maintains pregnancy until the placenta takes over.
• hPL is a peptide hormone increases throughout pregnancy and peaks near term that promotes fetal growth by regulating maternal metabolism, its secretion increasing with decreased maternal BGL and exerts "insulin antagonist" effect.
• Estrogen and progesterone are steroid hormones produced by the corpus luteum in the 1st trimester and then the placenta (using precursors from fetal adrenal cortex) increases gradually until term, responsible for several maternal physiological changes.
• Pituitary gland: PRL and ACTH and MSH increase while GH and FSH/LH decrease.
• Others: cortisol, renin/AII, aldosterone, T3/T4, prostaglandins and PTH all increase.

Metabolic System

• BMR and MRO2 increase by 20% at 36/40, then decrease to 15% above baseline at term due to demands of fetus, hypertrophy of maternal tissues, and increased cardiorespiratory work a/w pregnancy.
• Blood glucose levels are elevated from increased HPL, cortisol and estrogen, which also increase placental glucose for fetal use and gestational diabetes Insulin levels increase from the end of 1st TM to 32/40, then decrease to baseline at term due to increased BGL.
• Fat is stored in the first half of pregnancy, and mobilized in the second half of pregnancy.
• Maternal plasma amino acids decrease due to increased hepatic gluconeogenesis, placental transfer for fetal use, and urinary losses.

Additional Physiological Changes

• Maternal weight increases due due to increased uterine/breast tissue mass, ECFV, and fat stores.

Gastrointestinal System

• Gastro-oesophageal reflux increases due to incompetent lower esophageal sphincter (LES) function (decreased LES tone, changes in angle of gastro-oesophageal junction) and elevated intra-gastric pressure (IGP; gravid uterus effect).
• GI motility reduces causing decreased gastric motility/emptying, intestinal motility, and gallbladder contraction while gastric acidity increases.
• Cephalad displacement of stomach/intestines increases intra-gastric pressure.
• Hepatic changes: unchanged hepatic blood flow, fatty changes, glycogen depletion, lymphocytic infiltration, and SER proliferation all can also happen with increased CYP430 and ALP levels.
• Renal changes lead to: increased GFR and RBF, glycosuria, proteinuria, increased HCO3 excretion, increased RAAS effects, and dilation of the renal pelvis, calyces, and ureters.
• CNS changes: analgesia, increased sedation, and increased epidural venous engorgement.
• Musculoskeletal changes: Relaxin from placenta causes ligament relaxation and increased lumbar lordosis.

Anaesthetic Implications

• Increased risk of hypoxemia and desaturation (decreased maternal oxygen reserve, difficult intubation).
• Changes in anaesthetic requirements: rapid induction/recovery, decreased dose of anaesthetic agents, and decreased LA during neural block.
• Risk of aorto-caval compression due to Abdominal aorta and IVC.
• Increased risk of aspiration during GA relates to gastro-oesophageal reflux, decreased GI motility/emptying, increased gastric acid volume, and difficult intubation.

Placenta

• The endocrine section produces hCG, HPL, oestrogen, and progesterone
• Immunological function protects fetus from rejection and infection It transports substances between maternal and fetal plasma (gas exchange, nutrient transfer, wastes removal)
• Metabolic functions synthesize glycogen FAT, cholesterol and other enzymes.

Blood Supply

• Blood supply comes from the uterine and ovarian Arteries ( Arcuate arteries, Radial arteries that penetrate myometrium )
• Maternal bood with the intervillous space bathes the chorionic villi which is how fetal blood with chorionic villi can work with capillaries and into the umbilical vein

Placental Transfer Influences

• Mechanism of placental membrane exchange follows simple and passive diffusion If small/lipid or soluble respiratory gasses, steroids & fat soluble vitamins use no energy/gradients passively diffused

Ueteroplacental Blood Flow

• Blood flow is affected by the Uterine Blood flow
• If arterial blood flow increased or contractions in the tone decreased the umbilical bloodfloow will be more ideal

Gas Exchange

• Gas exchange across the placenta occurs by what’s known as “flow-limited passive diffusion”
• Amount of O2 exchanged is determined by the number of foetal and arterial blood flows so to maintain the exchange: both flows in the foetal blood must be maternal between the intervillious
• Double the amount of Bohr effect
• HbF helps in carrying O2 in the mother's blood and helps o2 from maternal ood to assist the fetal blood also The placenta has limited O@ it can make itself depending on if it’s transferred or not Factorers: Rates of factor of blood between both flows which influence uetrerin / foetel blood levels