Supine Hypotension Syndrome (Aortocaval Compression Syndrome)

Definition

Supine hypotension syndrome is defined as a decrease in mean arterial pressure of >15 mm Hg 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 abdominal aorta by the gravid uterus.

Also called: aortocaval compression syndrome or inferior vena caval syndrome — Miller's Anesthesia, 10e

Incidence

Finding	Incidence
IVC compression in supine position (term)	Nearly all term parturients
Symptomatic supine hypotension syndrome	8–10% (Miller's) / ~5% (Morgan & Mikhail)
Aortoiliac artery compression	15–20% of pregnant patients

The discrepancy between universal IVC compression and low symptomatic incidence is explained by compensatory mechanisms (see below).

Pathophysiology

Aortocaval compression diagram showing cross-sectional views supine vs lateral, and graphs of HR, SV, and CO vs gestation

Fig. 58.1 from Miller's Anesthesia, 10e — Aortocaval compression: (A) cross-sectional anatomy supine vs lateral; (B) effect on HR, stroke volume, and cardiac output throughout gestation

Step-by-step mechanism:

Gravid uterus (significant from ~20 weeks, maximal at term) compresses the IVC against the lumbar vertebrae (L3–L5) in the supine position
→ Reduced venous return to the right heart → ↓ preload
→ ↓ Stroke volume → ↓ Cardiac output by 10–20% compared to lateral position
Collateral return via epidural venous plexus, azygos, and vertebral veins (these become engorged)
Simultaneous aortoiliac compression → ↓ uterine and placental perfusion

Clinical Features

Symptom	Notes
Hypotension	MAP falls >15 mmHg
Tachycardia	HR rises >20 bpm (compensatory)
Diaphoresis / pallor	Sympathetic activation
Nausea and vomiting	Common
Dizziness / changes in mentation	Cerebral hypoperfusion

— Morgan & Mikhail's Clinical Anesthesiology, 7e; Miller's Anesthesia, 10e

Why Most Women Remain Asymptomatic

The key compensatory mechanism is a reflexive increase in peripheral sympathetic nervous system activity → ↑ systemic vascular resistance → maintains arterial blood pressure despite ↓ cardiac output.

This is critically important for anaesthesia:

"The reduced sympathetic tone from neuraxial or general anesthetic techniques impairs the compensatory increase in vascular resistance and exacerbates the impact of hypotension from supine positioning." — Miller's Anesthesia, 10e

This is why spinal/epidural anaesthesia (especially for caesarean section) dramatically increases the risk and severity of hypotension in the supine parturient.

Consequences for the Fetus

↓ Uterine blood flow → fetal hypoxia, acidosis
Aortoiliac compression reduces uterine artery flow even if maternal BP appears maintained (because collaterals may maintain maternal BP while uterine flow is still reduced)
Can lead to fetal bradycardia and non-reassuring fetal heart rate patterns

Prevention and Management

Positioning (First-line)

Left uterine displacement (LUD) — the cornerstone of prevention
Options: lateral decubitus, right hip elevation 10–15 cm (wedge/blanket/table tilt)
Historical standard: 15-degree left tilt

Controversy — Does 15° Tilt Work?

In an MRI study, IVC volume did not differ significantly between supine and 15° left-tilt. Only at 30° tilt did IVC volume increase. Additionally, in a RCT of spinal anaesthesia for caesarean section with phenylephrine infusion, there was no difference in neonatal acid-base status between supine and 15° left-tilt positions. — Miller's Anesthesia, 10e

Practical implication: With adequate vasopressor support, the 15° tilt may be less critical than previously thought, but LUD remains standard practice.

Vasopressors (when positioning alone is insufficient)

Drug	Notes
Phenylephrine (α-agonist)	Currently preferred — more effective, associated with less fetal acidosis than ephedrine
Ephedrine (α + β agonist)	Traditional "vasopressor of choice" historically — associated with more fetal acidosis (crosses placenta, stimulates fetal metabolism)

"Clinical studies suggest that the α-adrenergic agonist phenylephrine is more effective in treating hypotension in pregnant patients and is associated with less fetal acidosis than ephedrine." — Morgan & Mikhail's Clinical Anesthesiology, 7e (Key Concept 6)

Timing — When Is the Risk Highest?

Timing	Reason
≥20 weeks gestation	Uterus large enough to compress IVC
Term (≥36 weeks)	Maximum compression
During spinal/epidural anaesthesia	Loss of compensatory sympathetic tone
Immediately after delivery	Sudden relief of IVC compression → massive ↑ venous return → CO surges up to 80% above late third-trimester values — greatest cardiac strain

Additional Sequelae of Chronic IVC Compression

Ankle oedema
Varicose veins
Increased risk of lower extremity DVT (venous stasis)

High-Yield Exam Points

IVC compressed in nearly ALL term patients; only 5–10% symptomatic
Definition: MAP ↓ >15 mmHg + HR ↑ >20 bpm
Mechanism: IVC compression → ↓ venous return → ↓ CO; collaterals via azygos/epidural veins
Neuraxial and general anaesthesia abolish the sympathetic compensatory response → exacerbate hypotension
Prevention: left uterine displacement (10–15 cm wedge under right hip)
Vasopressor of choice: phenylephrine > ephedrine (less fetal acidosis)
Post-delivery: sudden relief → CO surges 80% → greatest haemodynamic stress
Aortic compression (not just IVC) can reduce uterine perfusion even when maternal BP is "normal"

Sources: Miller's Anesthesia (10e), Morgan & Mikhail's Clinical Anesthesiology (7e)

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Supine Hypotension Syndrome

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It includes all sections — definition, incidence, pathophysiology, clinical features, management (positioning + vasopressors controversy), fetal consequences, timing table, and the high-yield exam points — formatted with colour-coded headings and clean tables.

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