G5i: The cardiovascular response to central neural blockade
Definitions
- CNB achieved by subarachnoid or epidural anaesthesia
- Injection of local anaesthetic (Ropi, Bupi) +/- opioid (fentanyl, morphine)
- pre-ganglionic fibres lie in thoraco-lumbar spinal cord → ∴blocking output will alter vasomotor tone & CV function normally strictly regulated by SNS
CVS Response = ↓MAP
- Anaesthetics block β-preganglionic sympathetic fibres
- Inhibition:
- α1 ( vaso & venoconstriction)
- β1 (vaso/veno-constriction)
- β2 (VD liver, skeletal m.)
- Resulting:
- Vasodilation → ↓afterL
- Venodilation → venous pooling → ↓preL → F-S = ↓CO
Level of Block & CVS Effect
- Symp. block
→ From RVLM (medulla)
→ Preganglionic symp fibres run in columns in SC from T1 – L3
- T1 – T4
- Vasomotor to aorta
- Symp. outflow to H
- Unable to ↑HR/FoC with SNS stimulation
- Profound ↓MAP
- T5 – L3
- Vasomotor to abdominal organs, peripheral muscles, renal plexus, LL
- Sacral: no symp. chain blockade → minimal effect on tone/BP
- Lower thoracic/renal: ↓SVR → RAS still able to activate → BP preserved
- Mid thoracic: ↓SVR → no compensatory RAS activation. But preserved BaroR → mild ↓MAP
- Brain stem/High thoracic: blocks vasomotor tone
- Inhibits cardiac symp. compensation → profound ↓MAP
- Unopposed vagal tone → may cause cardiac arrest
Compensatory Mechanisms
High Pressure Afferents
- High P BaroR detects ↓ stretch
- Remove inhibition of symp. outflow from vasomotor centre (RVLM)
- ↑symp & ↓ parasymp. outflow
- H → ↑HR, ↑FoC
- Resistance Vessels → VC → ↑SVR
- Capacitance Vessels → VC → ↑VR
→ Unable to compensate for large blood vol. pooling in capacitance system
2. β1 activation of RAAS
- ↑renin → ↑AII → vaso & veno constriction
3. ↑ADH from PPG → ↑H2O absorption & direct CV
Low Pressure Afferents
- BaroR in atria, Great Veins → ↓stretch → ↓ANP → ↓inhibition of ADH → ↓natriuresis & diuresis
Juxtaglomerular Reflex
- ↓GFR → ↓flow through DCT → activation JG cells → ↑renin → ↑AII → vaso & veno constriction