Physiological Changes in Pregnancy: An Anesthesia Perspective

Summary Table of Key Changes at Term

1. Airway and Pulmonary Changes

Airway

• Capillary engorgement of nasal, oropharyngeal, and laryngeal mucosa occurs throughout pregnancy, worsening at birth due to extracellular fluid shifts and hormonal changes
• Airway edema is particularly pronounced in preeclampsia, after pushing in the second stage of labor, and with tocolytic therapy
• Mallampati scores increase throughout pregnancy and labor - failed intubation is 8x more common in obstetric patients than in the general surgical population
• Nasal instrumentation (nasopharyngeal airways, nasogastric tubes, nasal ETT) carries a bleeding risk
• Breast engorgement can impede laryngoscopy; a short-handled laryngoscope is recommended

Pulmonary Mechanics

• Progesterone stimulates the respiratory center, causing bronchodilation and increased respiratory drive
• Tidal volume (TV): ↑ 45%
• Respiratory rate: slight increase
• Minute ventilation: ↑ 50% at term
• FRC: ↓ 20-30% at term (due to ERV ↓ ~20% + RV ↓ ~25%)
• Total lung capacity: minimal decrease - cephalad diaphragm displacement is compensated by increased AP and transverse chest diameters
• FEV1, FVC, FEV1/FVC, dead space: relatively unchanged
• Closing capacity does NOT change, but the fall in FRC causes airway closure during normal tidal breathing - especially dangerous in obese patients, supine position, or on induction of anesthesia

Gas Exchange

• Chronic respiratory alkalosis: PaCO₂ ~28-32 mmHg (compensated by renal HCO₃⁻ excretion, pH ~7.44)
• PaO₂ slightly elevated (~100-110 mmHg) in the first trimester, then decreases near term due to increased O₂ consumption
• O₂ consumption increases by 20% at term (60% during labor)
• Decreased FRC + increased O₂ consumption = rapid desaturation during apnea - preoxygenation is mandatory before any intubation

Anesthetic Implications

• Faster induction and emergence with inhalational agents (increased alveolar ventilation + decreased FRC)
• MAC for volatile agents reduced by 25-40% (progesterone-mediated CNS effects)
• Preoxygenation for at least 3 minutes (or 8 vital capacity breaths) before RSI is critical
• Difficult/failed intubation rate is significantly elevated - have video laryngoscopy and surgical airway backup available

2. Cardiovascular Changes

• Cardiac output (CO): ↑ 40-50% by end of first trimester, peaks by 28-32 weeks
  • CO = Heart rate × Stroke volume; both increase
  • Heart rate: ↑ 15-25 bpm
  • Stroke volume: ↑ ~25-30%
• Systemic vascular resistance (SVR): ↓ ~20% (progesterone and placental vasodilators)
• Pulmonary vascular resistance: ↓
• Blood pressure: falls in early pregnancy (lowest ~mid-second trimester), normalizes toward term
• Central venous pressure and PCWP: unchanged despite expanded blood volume

Aortocaval Compression

• IVC compression reduces venous return by up to 30%, dropping CO and causing supine hypotensive syndrome in ~10-15% of patients
• Left lateral tilt of 15° or uterine displacement is mandatory from 20 weeks onward - during labor, recovery, or surgery
• Aortic compression reduces uteroplacental perfusion even without maternal hypotension

Electrocardiographic Changes

• Axis shifts left, ST-segment changes, and ectopic beats are common
• Sinus tachycardia is normal

Anesthetic Implications

• Induction of neuraxial or general anesthesia causes vasodilation and can exacerbate aortocaval compression
• Treat hypotension aggressively (IV fluids, vasopressors - phenylephrine preferred over ephedrine for spinal hypotension as it better preserves uteroplacental blood flow and fetal acid-base status)
• CO increases further during active labor (~15% with each contraction, up to 50% total) and peaks immediately postpartum

3. Hematology and Coagulation

• Plasma volume: ↑ 40-50%; red cell mass: ↑ ~20% → dilutional anemia (Hb ~11-12 g/dL is normal)
• Physiologic hypercoagulability (protects against hemorrhage at delivery):
  • Fibrinogen: ↑ ~100% (from ~300 to 400-600 mg/dL)
  • Factors VII, VIII, X, von Willebrand factor: ↑
  • Protein S: ↓ (anticoagulant); fibrinolysis impaired
  • D-dimer levels are elevated even in normal pregnancy
• Serum pseudocholinesterase: ↓ ~20-30% but prolonged succinylcholine effect is rarely clinically significant
• Platelets: mild decrease (gestational thrombocytopenia); levels <100,000 preclude neuraxial blockade

Anesthetic Implications

• Thrombocytopenia: platelet count must be checked before neuraxial anesthesia
  • Generally safe above 70,000-80,000/μL (some recommend 100,000); clinical judgment applies
• Hypercoagulability increases DVT/PE risk - neuraxial timing around anticoagulant dosing is critical (SOAP consensus guidelines)
• Dilutional anemia is normal; transfusion thresholds are the same as non-pregnant patients
• Pseudocholinesterase reduction: theoretically prolongs succinylcholine, but clinically rarely significant at standard doses

4. Gastrointestinal Changes

• Gastric emptying is delayed (progesterone reduces GI motility; the gravid uterus displaces the stomach and pylorus)
• Lower esophageal sphincter (LES) tone is reduced by progesterone and the upward displacement of the stomach
• Intragastric pressure increases due to the gravid uterus
• Combined: high risk of aspiration of acidic gastric contents (Mendelson's syndrome)
• Gastric acid secretion changes: gastrin is produced by the placenta → increased acid production

Anesthetic Implications

• Full stomach precautions apply from 20 weeks (some argue from the time of symptoms / diagnosis of pregnancy):
  • Rapid-sequence induction (RSI) with cricoid pressure and cuffed ETT is standard for GA after 20 weeks
  • NPO guidelines are important but insufficient protection alone
  • Sodium citrate (30 mL PO) + H₂-blocker (ranitidine) or PPI + metoclopramide are used as aspiration prophylaxis
• Neuraxial anesthesia is strongly preferred over GA for cesarean delivery to reduce aspiration risk

5. Renal Changes

• GFR increases ~50% by the second trimester (increased renal plasma flow)
• Serum creatinine and BUN fall; normal creatinine in pregnancy is ~0.4-0.5 mg/dL (a "normal" adult value of 0.9 mg/dL may indicate renal impairment)
• Glycosuria and mild proteinuria can be normal (reduced tubular reabsorption thresholds)
• Renal pelvis and ureters dilate (right > left) due to uterine compression

Anesthetic Implications

• Renal drug clearance is accelerated; dose adjustments may be needed for renally-excreted drugs
• Apparent "normal" creatinine may mask impaired renal function

6. Hepatic and Metabolic Changes

• Liver function tests can show modest changes: serum albumin decreases (~20%) due to hemodilution
• Alkaline phosphatase rises (placental isoform)
• Plasma cholinesterase (pseudocholinesterase) activity ↓ ~20-30%
• Protein binding is reduced (lower albumin + altered α₁-acid glycoprotein) → higher free fraction of protein-bound drugs (e.g., local anesthetics, opioids)

Anesthetic Implications

• Lower doses of local anesthetics may be needed - both due to reduced protein binding (more free drug) and the anatomical effect of engorged epidural veins reducing epidural space volume
• Epidural venous engorgement (from IVC compression) → reduces the volume of the epidural space → spinal and epidural doses need to be reduced by ~30% compared to non-pregnant patients
• Inhalational anesthetic metabolism: halogenated agents remain the same; hepatic blood flow changes minimally

7. Neurological and CNS Changes

• MAC is reduced by 25-40% for all volatile anesthetic agents (progesterone + endorphins raise the pain threshold)
• Spread of neuraxial blockade is increased (epidural + intrathecal) due to:
  • Reduced volume of CSF in lumbar cistern
  • Engorged epidural venous plexus
  • Progesterone-mediated enhanced sensitivity of nerve fibers
  • Reduced protein binding of local anesthetics
• Pain perception is altered by endorphins and progesterone

Anesthetic Implications

• Spinal and epidural doses are reduced by approximately 25-30% compared to non-pregnant patients
• High spinal block risk is greater than in non-pregnant patients

8. Endocrine Changes

• Progesterone and estrogen dominate, produced initially by the corpus luteum, then by the placenta
• Plasma cortisol rises (two- to fourfold) but is partly placental ACTH-mediated
• Insulin resistance increases in the third trimester (placental somatomammotropin, cortisol, and GH variant); gestational diabetes can develop
• Pituitary gland enlarges up to 120% immediately postpartum - risk of Sheehan syndrome (pituitary infarction) in severe hemorrhage

Key Anesthetic Summary Points

1. Airway: Expect edema and difficult laryngoscopy - always plan for difficult airway; short-handle laryngoscope; video laryngoscopy preferred
2. Aspiration: RSI with cricoid pressure + aspiration prophylaxis for GA after 20 weeks
3. Desaturation: Preoxygenate thoroughly; FRC is low and O₂ consumption is high - no time for apnea
4. Neuraxial dose reduction: Reduce spinal/epidural doses ~25-30%
5. Vasopressors: Phenylephrine is first-line for spinal hypotension (preserves uteroplacental blood flow)
6. Left lateral tilt: Mandatory from 20 weeks to prevent aortocaval compression
7. MAC reduction: ~25-40% less volatile agent required
8. Succinylcholine: Safe to use (pseudocholinesterase reduction is rarely clinically significant at standard doses)
9. Coagulation: Check platelets before neuraxial; fibrinogen doubled (DIC burns through it fast)
10. Creatinine and labs: Interpret differently - lower reference ranges apply

Physiological Changes in Pregnancy - Brief (Miller's Anesthesia, 10e)

Cardiovascular

• Diaphragm displaced cephalad → heart shifts left → left-axis deviation on ECG
• S1 accentuated; S3 common in 3rd trimester; benign systolic ejection murmur (tricuspid regurgitation) is normal
• CO peaks at ~28-32 weeks; rises further with each uterine contraction during labor; peaks 50% above prelabor values immediately postpartum
• Supine hypotension: IVC compression by gravid uterus from ~20 weeks → ↓ venous return → ↓ CO → hypotension; treat with left lateral tilt

Respiratory

• Progesterone stimulates respiratory center → chronic respiratory alkalosis (compensated, pH ~7.44)
• Closing capacity unchanged; but reduced FRC causes airway closure during normal tidal breathing, especially supine or obese
• Airway edema: capillary engorgement of nasal/laryngeal mucosa throughout pregnancy; worsened in preeclampsia, after pushing, with tocolytics
• Mallampati score increases as pregnancy progresses

Hematology & Coagulation

• Dilutional anemia: plasma volume ↑ > RBC mass ↑ → Hb ~11-12 g/dL is normal
• Hypercoagulable state: fibrinogen ↑ ~100%, Factors VII/VIII/X/vWF all ↑; Protein S ↓
• Serum pseudocholinesterase ↓ ~20-30% (rarely clinically significant)
• Platelets: mild decrease (gestational thrombocytopenia)

Gastrointestinal

• LES tone ↓ (progesterone)
• Gastric emptying delayed; intragastric pressure ↑
• Gastrin produced by placenta → ↑ gastric acid

Renal

• GFR ↑ ~50% → serum creatinine and BUN fall
• Normal creatinine in pregnancy: ~0.4-0.5 mg/dL (a "normal" adult Cr of 0.9 mg/dL may signal impairment)
• Glycosuria and mild proteinuria can be physiological

Neurological / CNS

• MAC reduced 25-40% (progesterone + endorphins)
• Neuraxial spread increased: engorged epidural veins compress epidural space; reduced CSF volume in lumbar cistern; progesterone sensitizes nerve fibers
• Spinal/epidural doses reduced ~25-30% vs non-pregnant

Hepatic / Metabolic

• Albumin ↓ → reduced protein binding of drugs → more free drug available
• Alkaline phosphatase ↑ (placental isoform - not pathological)
• Pseudocholinesterase ↓ (see above)

Note: Chestnut's Obstetric Anesthesia (6e) is not in the library. The above is from Miller's Anesthesia, 10e, Chapter 58 - which covers the same physiological framework. If you can upload Chestnut's PDF, I can extract directly from it.