2019B Question 08

Briefly explain the cardiovascular effects of central neural blockade.

Examiner Report

62.6% of candidates achieved a pass in this question.

The major domains assessed in this question were:

  • Definition of central neuraxial blockade, including understanding that spinal and epidural routes may have different effects.
  • The role of the sympathetic nervous system as the cause of CVS changes.
  • The primary CVS effects of neuraxial blockade at differing levels
  • The baroreceptor mediated reflex responses that occur as a result of these primary effects.

Credit was given for other correct relevant material.

Common problems included:

  • A misconception that neuraxial blockade only describes the spinal route.
  • Confusion as to the relative importance of venodilation and arteriolar vasodilation.
  • Poor descriptions of the baroreceptor mediated responses leading to tachycardia and vasoconstriction confined to levels above the block. Better answers were able to describe all of this and include mention of higher risk patients and reflexes such as the Bezold- Jarisch reflex, but very few recognized that blocking thoracolumbar sympathetic output will also block adrenal catecholamine release. A concise description of all this can be found in Miller 8th Edition, Chapter 56.

Model Answer

Structure:

  • Summary
  • Cardiovascular innervation
  • Direct effects
  • Compensatory effects
  • Special responses

Summary

Factor Details
Mechanism of Action

- Antagonist at voltage-dependent Na+ channel

- Epidural: Spinal nerve roots (dorsal > ventral), dorsal root ganglia, paravertebral SNS chain

 - 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

 - ∝ Block height

 - ∝ Drug dose

- ↔PSNS activity

Compensation

- ↓ Hormonal response

- ↓ Neural response if high block

Problem

- Bilateral sympatholysis is very dangerous if

 - Hypovolaemic (e.g. Dehydration in prolonged labour)

 - Fixed cardiac output (e.g. Aortic stenosis)

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

Cardiovascular Innervation: Sympathetic Nervous System

Factor Details
Pathway

- 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

Factor Details
Vascular

- Vasodilation → ↓ SVR → ↓ MAP
(less important – intrinsic tone well maintained)

- Venodilation → ↓ Venous return, ↓ cardiac output, ↓ MAP
(more important – intrinsic tone not well maintained)

Cardiac

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

Compensation

Factor Details

Neural

(seconds)

- Baroreceptors: Stretch-sensitive mechanoceptors in carotid and aortic sinuses

- ↓ MAP → ↓ Stretch → ↓ Afferent → ↓ SNS inhibition

 - ↑ HR, ↑ contractility

 - ↑ Venoconstriction → ↑ Preload

 - ↑ Vasoconstriction → ↑ SVR

Hormonal

(minutes)

- ↑ Renin-angiotensin-aldosterone system activation

 - Vasoconstriction

 - ↑ Na+/H2O reabsorption → ↑ Blood volume → ↑ Venous return

- ↑ ADH release

 - Vasoconstriction

 - ↑ H2O reabsorption → ↑ Blood volume → ↑ Venous return

- ↓ ANP release

 - ↓ Natriuresis → ↑ Blood volume → ↑ Venous return

Special Responses

Factor Details
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


Last updated 2021-08-23

results matching ""

    No results matching ""