Acute intracranial pressure elevation is a reversible cause of clinically significant bradyarrhythmia that can be resolved with cerebrospinal fluid drainage, avoiding unnecessary permanent pacemaker implantation.
Bradyarrhythmias are commonly attributed to intrinsic conduction disease, ischemia, or medication effects; however, not all etiologies are cardiac in origin. Acute elevation in intracranial pressure (ICP) can provoke clinically significant bradycardia, sometimes without the complete Cushing triad. We describe a 50-year-old nonverbal man with marginal zone lymphoma on rituximab, prior cerebrovascular accident, seizure disorder, and chronic hydrocephalus managed with a ventriculoperitoneal (VP) shunt who presented with lethargy and hypotension during rituximab infusion and was found to have pneumonia with acute hypoxemic respiratory failure (AHRF). During hospitalization, he developed recurrent profound bradycardia with sinus pauses on telemetry. Standard reversible cardiac causes were addressed and ruled out; however, given his history of hydrocephalus and concern for intermittent ICP elevation, a lumbar puncture was performed, which demonstrated an opening pressure of 22 cm H₂O. Therapeutic drainage of 28 cc of cerebrospinal fluid (CSF) resulted in immediate and durable resolution of bradycardia with stable telemetry thereafter. This case highlights acute ICP elevation as a reversible and underrecognized cause of clinically significant bradyarrhythmia and underscores the importance of considering central drivers of bradycardia in patients with neurologic comorbidity to avoid unnecessary permanent device implantation.
Naofal et al. (2026) studied this question.