2019B08 Briefly explain the cardiovascular effects of central neural blockade.



·         Summary

·         Cardiovascular innervation

·         Direct effects

·         Compensatory effects

·         Special responses



Mechanism of action

·   Antagonist at voltage-dependent Na+ channel

·   Epidural: spinal nerve roots (dorsal > ventral), dorsal root ganglia, paravertebral SNS chain

o Causes more hypotension for a given height and depth of block

·   Subarachnoid: spinal nerve roots, dorsal root ganglia, spinal cord

Direct effects

·   ↓SNS activity -> hypotension

o Block height

o Drug dose

·   PSNS activity


·   ↓Hormonal response

·   ↓Neural response if high block


·   Bilateral sympatholysis is very dangerous if

o Hypovolaemic (e.g. dehydration in prolonged labour)

o Fixed cardiac output (e.g. aortic stenosis)

o Susceptible to LVOT obstruction (e.g. HOCM)


Cardiovascular innervation: sympathetic nervous system


·   Premotor cell: RVM medulla (releases ACh)

·   Pre-ganglionic cell: intermediolateral column (releases ACh)

·   Post-ganglionic cell: paravertebral chain (releases NAd)

Spinal cord level

·   Upper thoracic: head, upper limb, thorax

·   Lower thoracic: abdomen, kidneys, adrenal medulla (secretes adrenaline)

·   Upper lumbar: pelvis, lower limb

Receptor effects

·   α1: vasoconstriction, venoconstriction

·   β1: ↑heart rate, ↑contractility; ↑renin release


Direct effects:


·   Vasodilation -> ↓SVR -> ↓mAP
(less important – intrinsic tone well maintained)

·   Venodilation -> ↓venous return, ↓cardiac output, ↓mAP
(more important – intrinsic tone not well maintained)


·   ↓Heart rate, ↓contractility
(only if upper thoracic)





·   Baroreceptors: stretch-sensitive mechanoceptors in carotid and aortic sinuses

·   ↓mAP -> ↓stretch -> ↓afferent -> ↓SNS inhibition

o ↑HR, ↑contractility

o ↑Venoconstriction -> ↑preload

o ↑Vasoconstriction -> ↑SVR



·   ↑Renin-angiotensin-aldosterone system activation

o Vasoconstriction

o ↑Na+/H2O reabsorption -> ↑blood volume -> ↑venous return

·   ↑ADH release

o Vasoconstriction

o ↑H2O reabsorption -> ↑blood volume -> ↑venous return

·   ↓ANP release

o ↓Natriuresis -> ↑blood volume -> ↑venous return


Special responses:

Bezold-Jarisch reflex

·   Caused by ↓venous return and ↓afterload

·   Contraction of underfilled LV -> stimulation of unmyelinated PSNS C fibres -> ↑↑PSNS output -> ↓↓HR, ↓BP, coronary vasodilatation

Reverse Bainbridge reflex

·   Caused by ↓venous return

·   ↓RA distension -> ↓activation of venoatrial stretch receptors -> ↑PSNS output and direct effect on AV node -> ↓↓HR



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