FRCA Notes

Neuraxial-Induced Hypotension During Caesarean Section

Hypotension following spinal anaesthesia is the most common physiological disturbance an obstetric anaesthetist will manage.

The most relevant curriculum item is perhaps: "Describes the effects of aortocaval compression and how to avoid it" (Core curriculum)

Resources


Mechanism

  • Spinal anaesthesia blocks preganglionic sympathetic fibres, causing:
    • Arterial vasodilation → ↓ SVR
    • Venodilation and peripheral pooling of blood → ↓ venous return
  • This is compounded by aortocaval compression in the supine position: the gravid uterus compresses the IVC, further reducing venous return and cardiac output
  • The primary derangement is a fall in SVR; this is why vasopressors, rather than fluid, are the mainstay of treatment

Definition

  • There is no single agreed definition; one review found 15 different definitions in use, which makes comparing studies difficult
  • The international consensus statement recommends:
    • Maintain SBP ≥90% of baseline (measured before the spinal)
    • Avoid SBP <80% of baseline

Consequences of untreated hypotension

  • Maternal:
    • Nausea, vomiting and dizziness
    • Loss of consciousness and, in extremis, cardiac arrest
  • Foetal:
    • Uteroplacental blood flow is pressure-dependent with no autoregulation; maternal arterial pressure is the prime determinant of foetal perfusion
    • Hypotension → ↓ uteroplacental flow → foetal acidaemia

  • Identifying higher-risk patients allows more aggressive prophylaxis e.g. additional fluid, higher starting vasopressor dose
  • Most individual predictors are only weakly or inconsistently associated with hypotension
Patients at higher risk of hypotension
↑ BMI and ↑ weight gain during pregnancy
↑ maternal age
Gravidity >3
Previous history of hypotension
↑ baseline HR and ↓ baseline SBP
↑ caval compression e.g. polyhydramnios, multiple gestation

Predictive monitoring

  • Non-invasive continuous cardiac output monitors:
    • Stroke volume variation (SVV) >7% predicts hypotension with sensitivity and specificity of roughly 84%
    • Change in SV with passive leg raise is less accurate

  • Perfusion index (PI) from the pulse oximeter plethysmograph:
    • Ratio of pulsatile to non-pulsatile signal; a high PI reflects low peripheral vascular tone
    • A high resting PI predicts a greater vasopressor requirement

  • Point-of-care ultrasound:
    • IVC or IJV collapsibility index: sensitivity and specificity >80%
    • Change in subaortic VTI with passive leg raise

  • These remain largely research tools; costs and lack of prospective validation currently limit routine use

Fluids

  • Withholding fluid worsens hypotension, but fluid alone does not correct the underlying fall in SVR
  • Timing:
    • Preload: given before the spinal
    • Coload: given rapidly at the time of the spinal
  • Effectiveness
    • Colloid preloading or coloading is most effective
    • Crystalloid coloading is next most effective
    • Crystalloid preload is largely ineffective as it rapidly redistributes
    • However, the evidence is insufficient to declare one strategy clearly superior
  • When a prophylactic vasopressor infusion is used, the choice of fluid appears to matter little; practice is therefore often dictated by local availability and cost
  • Excessive fluid loading risks iatrogenic overload

Positioning

  • During insertion: evidence comparing sitting and lateral positions is conflicting, with no clear winner
  • After insertion: the supine position reduces cardiac output by ~16% and aortic flow at the bifurcation by ~32% compared with the left lateral position
  • Left uterine displacement:
    • 15° left lateral tilt is the practical maximum; it reduces but does not abolish IVC compression
    • In elective cases with a coload and phenylephrine infusion, tilt does not appear to alter neonatal acid-base status
    • It should be continued routinely, and particularly in non-elective cases where the foetus may already be compromised

  • Vasopressors are the mainstay of prevention and treatment
  • Prophylactic infusions are preferred over reactive boluses; the lag between NIBP readings and bolus treatment leads to under- or over-treatment
  • The infusion should be started immediately after intrathecal injection and titrated to BP and HR
  • Tighter control (SBP close to 100% baseline) is associated with less nausea and a higher umbilical arterial pH
Drug Receptors Action Onset; duration (min) Effect on HR Bolus Infusion
Phenylephrine α1 Direct 1; 5-10 ↓ 100μg 25-50μg/min
Noradrenaline α1, α2, β1 Direct 1; 5-10 ↔ 6μg 0.02-0.08μg/kg/min
Ephedrine α1, α2, β1, β2 Indirect 2-5; 60 ↑ 5-10mg Not recommended
Adrenaline α1, α2, β1, β2 Direct 1; 5-10 ↑ Not recommended 0.01-0.03μg/kg/min

Phenylephrine

  • Pure α1 agonist: arteriolar vasoconstriction → ↑ SVR, directly treating the underlying problem
  • Rapid onset and short duration make it easily titratable by infusion; most anaesthetists are familiar with it
  • Minimal placental transfer and minimal effect on foetal acid-base status
  • Main drawback: baroreceptor-mediated reflex bradycardia → ↓ cardiac output
    • Despite this, even large doses have not been shown to worsen neonatal outcome in low-risk cases
  • Phenylephrine remains the first-line vasopressor

Noradrenaline

  • Potent α agonist with weak β1 activity, which offsets reflex bradycardia; net effect on HR is roughly neutral
  • Approximately 6 times as potent as phenylephrine
  • Compared with phenylephrine it maintains BP equally well, with a higher HR and cardiac output and less bradycardia
  • A large RCT found noradrenaline non-inferior to phenylephrine for umbilical arterial pH (confirmed for elective, but inconclusive for non-elective cases)
  • A network meta-analysis ranked noradrenaline as the vasopressor least likely to cause foetal acidosis, followed by mephentermine, metaraminol, phenylephrine and lastly ephedrine
  • Concerns about extravasation via peripheral cannulae are not well supported by evidence; local tissue complications occur in <2% when dilute solutions are used

Advantages of noradrenaline Disadvantages of noradrenaline
Less bradycardia than phenylephrine Requires careful preparation and dilution; risk of drug error
Better maintenance of cardiac output Close monitoring of the cannula site is needed
Possibly better placental perfusion and foetal acid-base status Less familiar to many anaesthetists in this setting
Safe peripherally at dilute concentrations Clinical outcome benefit over phenylephrine remains unproven

Ephedrine

  • Indirect sympathomimetic (presynaptic noradrenaline release) with predominantly β effect: ↑ cardiac output with less effect on SVR, so it does not address the main derangement
  • Slow onset, long duration and tachyphylaxis make it poorly titratable
  • Lipophilic; crosses the placenta and ↑ foetal metabolism → foetal acidosis (worse cord pH than phenylephrine)
  • Still useful after delivery for hypotension accompanied by bradycardia

Others

  • Metaraminol: mixed direct and indirect α agonist; commonly used in the UK as an alternative to phenylephrine with similar effect
  • Adrenaline: little evidence; small studies suggest an infusion of 0.03μg/kg/min is effective without excessive tachycardia

  • Colloid preload or crystalloid coload
  • 15° left lateral tilt after insertion of the spinal
  • Start a prophylactic vasopressor infusion at the time of intrathecal injection
  • Use more cautious starting rates for patients with pre-eclampsia
  • Consider using glycopyrrolate (pre-delivery) or ephedrine (post-delivery) if there is maternal bradycardia <60npm
  • If infusion requirements are unexpectedly high, check the infusion tubing, cannula site and BP cuff before escalating further

  • Multifactorial:
    • Block of cardioaccelerator fibres (T1-T4) with a high block
    • Reflex bradycardia from excessive phenylephrine
    • Paradoxical bradycardia from severely reduced venous return: the Bezold-Jarisch reflex
    • Surgical stimulation e.g. peritoneal traction, uterine exteriorisation → ↑ vagal tone
    • Any other cause of bradycardia, including cardiac disease
  • Bradycardia with hypotension implies ↓ cardiac output and is more concerning than an isolated low HR with a normal BP
  • Management:
    • Reduce the phenylephrine infusion if BP allows, or switch to noradrenaline
    • Anticholinergic e.g. glycopyrrolate 200μg
    • Ephedrine after delivery
    • Treat severe bradycardia or cardiovascular collapse as per ALS guidelines, with appropriate modifications for pregnancy

Pre-eclampsia

  • Spinal hypotension is less common (~15% compared with >30% in normotensive women) because of:
    • Higher circulating endogenous vasoconstrictors e.g. endothelin, thromboxane
    • Earlier delivery of smaller babies, so less aortocaval compression
  • These patients are more sensitive to exogenous vasopressors; the effective phenylephrine bolus dose is around a third lower
  • Uteroplacental blood flow is often already compromised, so hypotension is less well tolerated by the foetus
  • Start lower and titrate carefully; phenylephrine and noradrenaline appear equally effective

General anaesthesia

  • Hypotension is less pronounced than with spinal anaesthesia, but can follow induction and is worsened by aortocaval compression; left lateral tilt is still required
  • The opposite problem may arise: an exaggerated pressor response to laryngoscopy, particularly in hypertensive disorders of pregnancy
  • See GA for LSCS

Other causes of hypotension to consider

  • Haemorrhage
  • Oxytocin: vasodilation and tachycardia, particularly with rapid bolus; give slowly
  • High or total spinal block
  • Anaphylaxis
  • Amniotic fluid embolism