Does Citalopram Cause Bradycardia?
Yes, citalopram can cause bradycardia, though it occurs infrequently (0.1-1% of patients at therapeutic doses), and clinicians should monitor heart rate particularly during the first week of therapy and in high-risk populations. 1
Mechanism and Incidence
Citalopram-induced bradycardia appears to be a distinct phenomenon from its more widely recognized QT prolongation effects:
The FDA drug label classifies bradycardia as an "infrequent" adverse effect (0.1-1%) occurring at therapeutic doses, separate from the dose-dependent QT prolongation that prompted maximum dose restrictions. 1
Bradycardic outliers (heart rate <50 bpm with ≥25% decrease from baseline) occurred in 0.9% of citalopram-treated patients versus 0.4% of placebo patients in premarketing trials. 1
The sinus bradycardia seen at therapeutic doses appears mechanistically distinct from the QTc abnormalities observed in overdose situations. 2
Clinical Presentation and Risk Factors
Symptomatic bradycardia can manifest with presyncope, hypotension, and heart rates as low as 39 beats/min, even at standard doses of 20 mg daily. 2
Key risk factors requiring heightened vigilance include:
Elderly patients (age >60 years) are at increased risk and warrant closer monitoring. 2
Patients with pre-existing cardiac disease or conduction abnormalities should be monitored carefully, as citalopram can exacerbate underlying sinus node dysfunction. 3
Concurrent use of other negative chronotropic agents (beta-blockers, calcium channel blockers, digoxin, antiarrhythmics) creates additive bradycardic effects. 3
Metabolic disturbances (hypokalemia, severe acidosis) may potentiate cardiac effects. 3
Time Course and Reversibility
The bradycardia associated with therapeutic citalopram use is reversible upon discontinuation:
In documented cases, bradycardia and hypotension resolved within 48 hours after stopping citalopram. 2
This contrasts with overdose scenarios where cardiac toxicity may be delayed up to 32 hours post-ingestion and persist for 24+ hours after presentation, likely due to active metabolites. 4
Critical Management Algorithm
Initial Assessment
Obtain baseline ECG before initiating citalopram to document heart rate, QRS duration, and QTc interval. 1, 2
Identify contraindications: baseline bradycardia, second- or third-degree AV block without pacemaker, sick sinus syndrome, or concurrent use of multiple negative chronotropic drugs. 3
Monitoring Protocol
Check heart rate and blood pressure within the first week of therapy and after any dose adjustments. 2
For high-risk patients (elderly, cardiac disease, multiple medications), consider more frequent monitoring or ambulatory ECG during the first 2-4 weeks. 2
When Bradycardia Develops
If symptomatic bradycardia occurs (heart rate <50 bpm with symptoms or <40 bpm regardless of symptoms), immediately discontinue citalopram and manage the reversible cause per ACC/AHA/HRS guidelines. 3
Permanent pacing is not indicated for medication-induced bradycardia; withdrawal of the offending drug is first-line management. 3
Switch to an alternative antidepressant with lower cardiac risk, such as sertraline or an SNRI (duloxetine, venlafaxine), which have minimal cardiac conduction effects. 5
Common Pitfalls to Avoid
Do not overlook drug-drug interactions: The combination of citalopram with other QT-prolonging or bradycardic agents (e.g., sotalol, beta-blockers, digoxin) creates compounded risk. 6, 7
Do not assume bradycardia only occurs in overdose: Therapeutic doses of 20 mg can cause clinically significant bradycardia requiring hospitalization. 2
Do not continue citalopram in patients developing new bradycardia without ruling out the drug as causative: The Naranjo Algorithm supports citalopram as a highly probable cause when temporal correlation exists. 7
Do not use citalopram as first-line in patients already on digoxin or other sinoatrial node inhibitors: Case reports document severe bradycardia (93.7% of beats <60 bpm) when escitalopram (citalopram's active enantiomer) was combined with digoxin. 7
Alternative Antidepressant Selection
When cardiac risk factors are present, SNRIs (particularly duloxetine) are preferable to citalopram because they cause minimal cardiac conduction effects and no clinically important ECG changes at therapeutic doses. 5
If an SSRI is required, sertraline or fluoxetine carry lower QTc and bradycardic risk than citalopram or escitalopram. 5