What is the Bezold‑Jarisch reflex, its triggers, clinical presentation, and recommended management?

Bezold-Jarisch Reflex: Definition, Triggers, and Management

What It Is

The Bezold-Jarisch reflex is a cardioinhibitory reflex originating from mechanoreceptors in the inferoposterior wall of the left ventricle that produces a triad of bradycardia, hypotension, and sometimes apnea, transmitted through unmyelinated vagal C-fibers. 1, 2, 3

• The reflex represents an inappropriate activation of inhibitory cardiac sensory receptors that increases parasympathetic activity while simultaneously suppressing sympathetic tone 3
• Unlike vasovagal syncope, the Bezold-Jarisch reflex originates specifically from ventricular mechanoreceptors rather than from emotional or orthostatic triggers 1, 4

Clinical Triggers

The most important clinical contexts where this reflex occurs are:

• Acute myocardial infarction, particularly inferior wall MI, where ischemia directly stimulates ventricular mechanoreceptors 1, 3
• Neuraxial (spinal/epidural) anesthesia, where sympathetic blockade causes decreased venous return and reduced ventricular filling, paradoxically activating mechanoreceptors in an "empty" ventricle 1, 4
• Coronary arteriography, where contrast injection or catheter manipulation can trigger the reflex 3
• Severe hypovolemia or relative hypovolemia, resulting in uncoupled cardioinhibition 5
• Chemical stimulation by veratrum alkaloids, serotonin, nicotine, capsaicin, or certain anesthetic agents 2

Clinical Presentation

The classic triad consists of:

• Profound bradycardia (heart rate can drop to <20 bpm in severe cases) 4
• Severe hypotension (systolic blood pressure can fall to 30s mmHg) 4
• Bradypnea or apnea (respiratory rate <6/min) 2, 4

Key distinguishing features from vasovagal syncope: 1

• Absence of prodromal symptoms (no pallor, sweating, nausea beforehand)
• More severe hemodynamic compromise requiring immediate intervention
• Occurs in specific high-risk contexts (MI, neuraxial anesthesia) rather than emotional/orthostatic triggers
• Can progress to ventricular arrhythmias in severe cases 4

Immediate Management Algorithm

When Bezold-Jarisch reflex is suspected, follow this sequence:

1. Stop the precipitating factor immediately (halt anesthetic administration, stop contrast injection) 1

2. Restore preload aggressively:

   • Rapid intravenous fluid bolus 1, 4
   • Position patient supine or in left-lateral decubitus (if pregnant) 4

3. Administer atropine as first-line anticholinergic to block vagal efferent pathway 1

4. Escalate to epinephrine in severe cases with profound bradycardia/hypotension unresponsive to atropine 1, 4

5. In obstetric patients: Initiate continuous fetal monitoring and prepare for emergent cesarean delivery if fetal bradycardia develops 4

6. Monitor for secondary arrhythmias (ventricular tachycardia can follow the initial bradycardia) 4

Critical Pitfalls to Avoid

• Do not mistake this for simple vasovagal syncope – the Bezold-Jarisch reflex requires more aggressive intervention and occurs in distinctly different clinical contexts 1
• Do not delay epinephrine in severe cases – atropine alone may be insufficient when profound bradycardia and hypotension coexist 1, 4
• Do not overlook the respiratory component – bradypnea/apnea may require ventilatory support 2, 4
• In anaphylaxis, bradycardia from Bezold-Jarisch reflex can mask the typical tachycardia, potentially delaying recognition of anaphylaxis in patients with heightened vagal tone or on beta-blockers 1

Pathophysiological Context

The reflex serves as a defense mechanism but becomes pathological when inappropriately activated 2, 6. The arterial baroreflex normally provides negative feedback to stabilize blood pressure, but during Bezold-Jarisch reflex activation, the ventricular mechanoreceptor input overrides normal baroreflex control, creating paradoxical hypotension despite already low blood pressure 6, 3. This explains why the hemodynamic collapse can be so profound and why aggressive intervention is necessary rather than allowing "natural" compensatory mechanisms to restore homeostasis.