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 | - ↓ Cardiac output - ↓ MAP - ↓ Tissue perfusion |
| Baroreceptor response | 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 | - 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) |