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 - Venodilation → ↓ Venous return, ↓ cardiac output, ↓ MAP |
| Cardiac | - ↓ Heart rate, ↓ contractility |
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 |