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Supine Hypotension Syndrome (Aortocaval Compression Syndrome)

Definition

Supine hypotension syndrome is defined as a decrease in mean arterial pressure of >15 mmHg with a compensatory increase in heart rate of >20 beats/min when a term parturient lies supine, caused by compression of the inferior vena cava (IVC) and aorta by the gravid uterus.
Miller's Anesthesia 10e

Incidence

  • IVC compression occurs in nearly all term parturients in the supine position
  • Symptomatic supine hypotension syndrome occurs in only 8–10% of women (Miller's) — also quoted as ~5% (Morgan & Mikhail's)
  • Significant aortoiliac artery compression occurs in 15–20% of pregnant patients

Mechanism / Pathophysiology

Aortocaval compression: cross-sectional views supine vs lateral, with graphs of heart rate, stroke volume, and cardiac output by gestational week
FIG. 58.1 — Miller's Anesthesia 10e. (A) Supine position compresses both IVC and aorta against L5; lateral position decompresses both. (B) Cardiac output (supine vs lateral) at increasing gestational age — note the lateral position allows ~50% CO increase vs ~40% supine at term.
  1. IVC compression by the gravid uterus at L5 → ↓ venous return → ↓ preload → ↓ stroke volume → ↓ cardiac output (10–20% reduction vs upright position)
  2. Aortic compression → ↓ uteroplacental blood flow (independent of the BP at the brachial artery — femoral and uterine artery pressures may be critically low even when arm BP appears maintained)
  3. Collateral venous return: Blood from the lower extremities is diverted via the epidural venous plexus, azygos, and vertebral veins, which become engorged → contributes to distension of epidural veins (relevant to neuraxial blocks)
  4. Uterine contraction: Reduces caval compression but exacerbates aortic compression
Onset from approximately 20 weeks' gestation, worst at term.

Compensatory Responses

Most women do not become symptomatic because of intact compensatory mechanisms:
  • Reflex sympathetic activation → ↑ systemic vascular resistance → maintains arterial blood pressure despite reduced cardiac output
  • Therefore brachial artery BP may be falsely reassuring — uteroplacental flow can still be compromised
Key anaesthetic implication: Neuraxial and general anaesthesia abolish sympathetic compensation, unmasking the full haemodynamic effect of aortocaval compression. This is the principal reason supine positioning under anaesthesia is dangerous.

Clinical Features

  • Hypotension
  • Pallor
  • Diaphoresis
  • Nausea and vomiting
  • Changes in mentation / dizziness
  • Fetal bradycardia and acidosis (uteroplacental insufficiency)

Sequelae of Chronic Partial IVC Obstruction (Third Trimester)

  • Venous stasis in lower limbs → oedema, varicosities, deep vein thrombosis
  • Engorgement of epidural venous plexus → increased risk of intravascular injection during epidural placement; reduced epidural space volume → lower dose requirements for neuraxial blockade (30% reduction in local anaesthetic dose)

Prevention & Management

Positioning

  • Avoid supine position whenever neuraxial blockade is used
  • Left uterine displacement (LUD): Place a wedge or tilt table >15° under the right hip, displacing the uterus to the left
    • Classic teaching: 15° tilt. This has been challenged — MRI studies show IVC volume is not significantly different between supine and 15° tilt; 30° tilt significantly increases IVC volume
    • A randomised trial of spinal anaesthesia + phenylephrine infusion: no difference in neonatal acid-base status between supine and 15° tilt, but supine patients had lower cardiac output and required more phenylephrine
    • Current recommendation (Miller's): Continue to use LUD during induction of neuraxial anaesthesia and during any episode of maternal hypotension or fetal compromise; further studies are needed to define optimal tilt angle

Vasopressors

  • Phenylephrine (α-agonist): now preferred first-line vasopressor for neuraxial hypotension in obstetrics — more effective and associated with less fetal acidosis than ephedrine
  • Ephedrine (mixed α/β): traditionally first-line but clinical evidence shows greater fetal acidosis (β-adrenergic effect increases fetal metabolism)
Morgan & Mikhail's Clinical Anesthesiology 7e, Key Concept 6

Immediate treatment of acute episode

  1. Turn patient to left lateral decubitus or full lateral position
  2. IV fluid bolus (co-load with spinal anaesthesia)
  3. Vasopressor (phenylephrine infusion preferred)
  4. Supplemental oxygen
  5. Assess fetal heart rate

Special Considerations Under Anaesthesia

Anaesthetic typeRisk
Spinal (e.g., for LSCS)Highest risk — sudden sympathectomy + aortocaval compression → precipitous hypotension
EpiduralSlower onset allows partial compensation; still significant
General anaesthesiaVolatile agents ↓ SVR; loss of sympathetic tone unmasks compression

Exam Summary Points

  1. Mechanism = IVC + aorta compressed by gravid uterus at L5 after 20 weeks
  2. Incidence of symptomatic syndrome = ~5–10%; IVC compression = nearly all term patients
  3. Most women are asymptomatic because of intact sympathetic compensation — anaesthesia abolishes this
  4. CO drops 10–20% supine vs upright; aortic compression causes uteroplacental ischaemia even when arm BP is maintained
  5. Epidural vein engorgement (from IVC compression) = reduced epidural volume → lower LA doses needed + ↑ intravascular injection risk
  6. Treatment = LUD (>15–30°), lateral positioning, phenylephrine, IV fluid
  7. Left uterine displacement: 15° tilt is contested; 30° tilt is more effective; current practice maintains its use

Sources: Miller's Anesthesia 10e (Ch. 58 — Aortocaval Compression, pp. 8805–8809) | Morgan & Mikhail's Clinical Anesthesiology 7e (Ch. 40 — Maternal & Fetal Physiology, pp. 1571–1576)
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