2020B Question 01

a) Describe the immediate cardiovascular responses to the sudden loss of 30% blood volume in a healthy awake person. b) How are these responses different if the patient is undergoing anaesthesia with sevoflurane?

Examiner Report

The expected domains for this question were:

  • Context on degree of blood loss and its effect on volume status
  • A description of sympathetic nervous system responses
  • Other humoral/endocrine mediated responses.
  • Effects of sevoflurane on the cardiovascular system; application of this to a shocked state

To pass, candidates were required to consider the context, describe autonomic nervous system mediated mechanisms, and describe how sevoflurane affects these responses. The first section was generally well answered, with higher scores achieved with additional detail regarding humoral/endocrine changes, blood reservoir mobilisation and blood flow distribution. The second section had a much greater variation in the quality of answers. A significant portion of candidates provided just one or two brief notes resulting in at best a borderline pass mark overall. Better answers gave an overview of sevoflurane’s effects on the cardiovascular system, especially the baroreceptor reflex, noting how sevoflurane would interfere with homeostatic responses to haemorrhage.

Model Answer

Structure:

  • Introduction
  • Status awake
  • Status with sevoflurane anaesthesia
  • Other responses

Introduction

TRerm Detail
Quantification

- 30% blood loss (~1500mL) = Class 3 shock

- Severe, life-threatening

If awake

- Immediate neural response

- Later hormonal and rheologic responses

If anaesthetised

- All responses attenuated

- High risk of decompensation and death

Effects of 30% Blood Loss

Response Mechanism
Graph

↑ Blood loss → ↓ MSFP → ↓ CO

↑ Blood loss → SNS tone → ↑ Slope of VR and Starling Curve → ↑ CO

 - VR: Venous return

 - MSFP: Mean Systemic Filling Pressure

 - RAP: Right Atrial Pressure

 - RVR: Resistance to Venous Return

Direct effect

- ↓↓ MSFP → ↓ VR

- ↓ Cardiac output

- ↓ MAP

- ↓ Tissue perfusion

Baroreceptor response

↑ CO, ↑ SVR, ↑ MAP

Afferent limb:

- Stretch-activated mechanoreceptors on C fibre visceral afferents

- ↓ Stretch → ↑ Output to medulla and hypothalamus

- Arterial pressure: Carotid and aortic sinuses

- Blood volume: Receptors in atria and great veins

Efferent limb:

- ↑ SNS output from rostral ventrolateral medulla

- ↓ PSNS output from vagal centres

- ↑ ADH release

- ↓ ANP release

Blood reservoir mobilisation

↑ Blood volume ~500mL → ↑ MSFP

- Source: Spleen red pulp, liver sinusoids, skin arterioles / venules / A-V anastomoses

- Mechanism: ↑ SNS output → Α1 → Vasoconstriction

Interstitial fluid reabsorption

↑ Blood volume → ↑ MSFP

- Mechanism: ↑ SNS output → Constriction of pre-capillary sphincters → ↓ Capillary hydrostatic pressure → Net fluid reabsorption

Restlessness

MSFP, ↑ Renous return

- ↑ SNS → ↑ Skeletal muscle pump activity

Central ischaemic response

↑ CO, ↑ SVR, ↑ MAP

- CNS hypoperfusion → ↑↑ SNS output

- For redirection of flow to vital organs in extremis

Endocrine response

Minutes to hours

- ↑ ADH → ↑ H2O reabsorption from collecting duct → Water preservation

- ↑ RAAS → ↑ Na+/H2O reabsorption → ECF preservation

Rheologic response

Days to weeks:

- ↑ EPO → ↑ Erythropoiesis → Restoration of red cell mass

If Anaesthetized with Sevoflurane

Effects Detail
Cellular effects

- Inhibition of L-Ca2+ channels (heart and vasculature)

- ↑ Nitric oxide release (vasculature)

- GABA potentiation → ↓ Medullary SNS output (heart and vasculature)

Physiological effects

- ↓ Contractility

- Relative preservation of baroreceptor reflex → ↑ HR

- Venodilatation → ↓ Venous return, ↓ Preload

- Vasodilatation → ↓ SVR, ↓ Afterload

- ↓ Cardiac Output

- ↓ MAP

Effects on shock

Detrimental:

- Direct effects exacerbated

- All compensatory responses attenuated

- Effects are dose-dependent

Protective:

- Relative preservation of baroreceptor reflex

- ↑ SNS output in Guedel’s stage 2

Other Responses

Effects Detail
Decompensation

- ↑↑ SNS

- ↑ Metabolic rate (↑ Cardiac, respiratory, skeletal muscle work)

- ↑ Anaerobic metabolism

- ↓ PH

- ↓ Inotropy, arrhythmia, death

- Greatly increased risk under sevoflurane anaesthesia

Ischaemic pre-conditioning

- Brief ischaemic episode improves tolerance of subsequent episode

- Mechanism: Activation of sarcolemmal and mitochondrial K+-ATP channel

- Mimicked by volatile anaesthesia (anaesthetic pre-conditioning)


Last updated 2021-08-23

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