What is the mechanism of the Bezold-Jarisch reflex in patients undergoing neuroaxial anesthesia?

Mechanism of Bezold-Jarisch Reflex in Neuroaxial Anesthesia

The Bezold-Jarisch reflex during neuroaxial anesthesia occurs when sympathetic blockade causes decreased venous return and reduced ventricular filling, triggering mechanoreceptors in the inferoposterior left ventricular wall that send signals via unmyelinated vagal C-fibers to produce paradoxical bradycardia, hypotension, and potentially apnea. 1, 2

Pathophysiological Mechanism

The reflex operates through a specific anatomical and physiological pathway:

• Mechanoreceptor activation: Sensory receptors located specifically in the inferoposterior wall of the left ventricle detect vigorous ventricular contraction against a relatively empty chamber 1, 3

• Afferent pathway: These cardiac receptors transmit signals to the brainstem via unmyelinated vagal C-fibers, which are slow-conducting nerve fibers 1, 3

• Central processing: The vagal afferents project to cranial medullary centers that control respiration, heart rate, and vasomotor tone 3

• Efferent response: The reflex produces a triad of inhibitory effects—bradycardia (via increased vagal efferent activity to the heart), hypotension (via vasodepression), and bradypnea or apnea (via respiratory center inhibition) 1, 2, 3

Trigger During Neuroaxial Anesthesia

The specific mechanism by which spinal or epidural anesthesia precipitates this reflex involves:

• Sympathetic blockade: Neuroaxial anesthesia blocks sympathetic outflow, causing venous pooling in the lower extremities and splanchnic circulation 2, 4

• Reduced preload: This venous pooling dramatically decreases venous return to the heart, resulting in a relatively empty left ventricle 2, 5

• Hypercontractile state: The ventricle continues to contract vigorously despite reduced filling, creating the mechanical stimulus that activates the ventricular mechanoreceptors 5, 6

• Paradoxical response: Rather than compensatory tachycardia (which would be expected with hypotension), the reflex produces bradycardia—a counterintuitive response that can rapidly progress to severe hemodynamic compromise 2, 5

Clinical Presentation Specifics

The reflex manifests with a characteristic temporal pattern during neuroaxial anesthesia:

• Insidious hypotension first: Blood pressure decreases without initial changes in heart rate, central venous pressure, or other hemodynamic parameters 5

• Delayed bradycardia: Heart rate reduction follows the blood pressure drop, which distinguishes this from typical vasovagal responses 5

• Rapid deterioration: The reflex can progress within minutes to profound bradycardia (heart rates as low as 17 bpm), severe hypotension (systolic pressures in the 30s mmHg), and bradypnea (respiratory rates of 6/min or less) 2

• Risk of cardiac arrest: Without prompt recognition and treatment, the reflex can progress to asystole or ventricular arrhythmias 2, 4

Critical Distinction from Vasovagal Response

The Bezold-Jarisch reflex differs mechanistically from vasovagal reactions:

• Origin: The Bezold-Jarisch reflex originates from cardiac ventricular mechanoreceptors, while vasovagal reactions typically involve emotional or pain triggers with different receptor activation 1

• Clinical features: While both can cause hypotension and bradycardia, vasovagal reactions classically include pallor, weakness, nausea, and diaphoresis as prominent features 1

High-Risk Clinical Contexts

Certain situations during neuroaxial anesthesia increase susceptibility:

• Sitting position: Upper extremity blocks performed with the patient sitting dramatically increase risk due to enhanced venous pooling 4

• Rapid onset blocks: Combined spinal-epidural techniques with rapid sympathetic blockade create sudden preload reduction 2

• Obstetric patients: Pregnant patients undergoing cesarean section with neuraxial anesthesia face particular risk, with potential for both maternal and fetal compromise 2

Immediate Management Priorities

Recognition and treatment must be rapid:

• Stop anesthetic administration immediately upon recognition of the reflex pattern 2

• Atropine administration: Give 0.01 mg/kg as bolus, with consideration for continuous infusion at 0.01 mg·kg⁻¹·h⁻¹ to prevent recurrence 5

• Epinephrine: In severe cases with profound bradycardia and hypotension, epinephrine may be required for immediate resuscitation 2

• Positioning: Place patient in left-lateral position (especially in obstetric cases) to improve venous return 2

• Aggressive fluid resuscitation: Intravenous fluids help restore preload and ventricular filling 2, 5

Prevention Strategies

Minimize risk through specific precautions:

• Continuous cardiac monitoring: All patients receiving neuroaxial anesthesia require continuous ECG and blood pressure monitoring throughout the procedure and recovery period 7, 4

• Avoid sitting position: When feasible, perform blocks in supine or lateral positions to reduce venous pooling 4

• Gradual dosing: Titrate local anesthetic doses carefully rather than using large boluses that cause rapid sympathetic blockade 2

• Maintain preload: Ensure adequate intravenous fluid administration before and during block placement 2