2017B03 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.

 

List:

·         Intro

·         Status awake

·         Status with sevoflurane anaesthesia

·         Other responses

 

Intro:

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

·         If awake: immediate neural response, subsequent hormonal and rheologic responses

·         If anaesthetized: all responses attenuated; high risk decompensation and death

 

Effects of 30% blood loss:

Graph summary

VR = (MSFP – RAP) / RVR

      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

à ↑CO, ↑SVR, ↑mAP

·   Afferent limb:

o Stretch-activated mechanoreceptors on C fibre visceral afferents

o ↓Stretch -> ↑output to medulla and hypothalamus

o Arterial pressure: carotid and aortic sinuses

o Blood volume: receptors in atria and great veins

·   Efferent limb:

o ↑SNS output from rostral ventrolateral medulla

o ↓PSNS output from vagal centres

o ↑ADH release

o ↓ANP release

Mobilisation of blood reservoirs

à ↑Blood volume ~500mL -> ↑MSFP

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

·   Mechanism: ↑SNS output -> α1 -> vasoconstriction

Reabsorption of interstitial fluid

à ↑Blood volume -> ↑MSFP

·   Mechanism: ↑SNS output -> constriction of pre-capillary sphincters -> ↓capillary hydrostatic pressure -> net fluid reabsorption

Restlessness

à ↑MSFP, ↑venous return

·   ↑SNS -> ↑skeletal muscle pump activity

Central ischaemic response

à ↑CO, ↑SVR, ↑mAP

·   CNS hypoperfusion -> ↑↑SNS output

·   For redirection of flow to vital organs in extremis

 

If anaesthetized with sevoflurane:

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:

o Direct effects exacerbated

o All compensatory responses attenuated

o Effects are dose-dependent

·   Protective:

o Relative preservation of baroreceptor reflex

o ↑SNS output in Guedel’s stage 2

 

Other responses:

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)

 

 

 

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