Can haloperidol (antipsychotic medication) cause bradycardia (abnormally slow heart rate)?

Can Haloperidol Cause Bradycardia?

Haloperidol is not typically associated with bradycardia as a primary adverse effect; its predominant cardiac risk is QTc prolongation (7 ms mean prolongation) leading to ventricular arrhythmias, not bradycardia. 1

Primary Cardiac Risk Profile

Haloperidol's well-established cardiovascular toxicity centers on QTc prolongation and ventricular arrhythmias, not bradycardia:

• QTc prolongation: 7 ms mean prolongation, with significantly higher risk via IV administration 1
• Ventricular arrhythmias: 46% increased risk of ventricular arrhythmia and/or sudden cardiac death (adjusted OR 1.46,95% CI 1.17-1.83) 1
• Torsades de pointes: Multiple doses, especially IV, are associated with this potentially fatal polymorphic ventricular tachyarrhythmia 1

Evidence Regarding Bradycardia

The evidence for haloperidol-induced bradycardia is extremely limited and contradictory:

Animal Study Findings

• In a 2020 porcine AMI model, high-dose haloperidol (1.0 mg/kg) significantly reduced heart rate during acute myocardial infarction 2
• This bradycardic effect occurred alongside QT prolongation and reduced blood pressure 2

Human Clinical Evidence

• A 2025 meta-analysis of 84 RCTs (n=12,180 patients) found no increased risk of major adverse cardiac events with haloperidol versus placebo (RR 0.93,95% CI: 0.80-1.08), with 97.8% of events being deaths rather than arrhythmias 3
• Bradycardia is not mentioned in major cardiology guidelines addressing haloperidol's cardiac effects 4, 1
• Guidelines discussing drug-induced bradyarrhythmias list digoxin, verapamil, diltiazem, beta blockers, and clonidine—but not haloperidol 4

Case Report Context

• One case report describes torsades de pointes (not bradycardia) in a patient with pre-existing complete heart block receiving IV haloperidol, highlighting that bradycardia was a pre-existing condition, not caused by haloperidol 5

Clinical Implications

The absence of bradycardia from established guidelines and the focus on QTc prolongation/ventricular arrhythmias indicates bradycardia is not a clinically significant concern with haloperidol. 4, 1

High-Risk Situations for Haloperidol (QTc-Related, Not Bradycardia)

• Female gender and age >65 years 1
• Baseline QTc >500 ms 1
• Electrolyte abnormalities (hypokalemia, hypomagnesemia) 1
• Concomitant QTc-prolonging medications 1
• IV administration (higher risk than oral/IM) 1
• Pre-existing bradycardia or complete heart block 5

Monitoring Recommendations

• Baseline ECG before initiating haloperidol 1
• Follow-up ECG after dose titration 1
• Discontinue if QTc exceeds 500 ms or increases >60 ms from baseline 1
• For IV doses >5 mg, obtain baseline ECG and continuous monitoring 1

Common Pitfalls

• Confusing bradycardia with QTc prolongation: Haloperidol's cardiac toxicity manifests as QTc prolongation and ventricular arrhythmias, not bradycardia 1
• Route matters: IV haloperidol carries substantially higher cardiac risk than oral or IM formulations 1
• Pre-existing conduction disease: Patients with complete heart block or severe bradycardia may be at higher risk for any cardiac complications 5