Intravenous Diltiazem Dosing for Atrial Fibrillation
For acute rate control in atrial fibrillation with rapid ventricular response, administer diltiazem 0.25 mg/kg (actual body weight) IV over 2 minutes as the initial bolus dose. 1, 2, 3
Initial Bolus Dosing
The standard initial dose is 0.25 mg/kg IV over 2 minutes (approximately 20 mg for an average 70-80 kg patient). 3, 1, 2
If inadequate response after 15 minutes, administer a second bolus of 0.35 mg/kg IV over 2 minutes (approximately 25 mg for an average patient). 3, 4
The ACC/AHA guidelines establish this as a Class I recommendation (Level of Evidence B) for hemodynamically stable patients, with diltiazem demonstrating superior efficacy compared to beta-blockers for rapid rate control. 5, 1
Response typically occurs within 4-5 minutes of bolus administration, with 93-94% of patients achieving adequate rate control (defined as >20% reduction in heart rate, conversion to sinus rhythm, or heart rate <100 bpm). 4, 6
Continuous Infusion for Sustained Control
Following successful bolus dosing, initiate continuous infusion at 10 mg/hour to maintain rate control for up to 24 hours. 3, 1, 2
The infusion rate may be titrated in 5 mg/hour increments: start at 5 mg/hour for some patients, increase to 10 mg/hour, and up to a maximum of 15 mg/hour as needed for further heart rate reduction. 3, 6
At 10 hours of infusion, 47% of patients maintain response at 5 mg/hour, 68% at 10 mg/hour, and 76% at 15 mg/hour. 6
Do not exceed 24 hours of infusion or rates >15 mg/hour, as diltiazem exhibits dose-dependent, non-linear pharmacokinetics and safety data beyond these parameters is lacking. 3
Lower Dose Strategy to Minimize Hypotension
Consider using a lower initial dose of ≤0.2 mg/kg (approximately 10-15 mg) in patients at risk for hypotension, as this achieves similar efficacy (70.5% response rate) with significantly lower rates of hypotension (18% vs 35% with standard dosing). 7
This lower-dose approach is particularly relevant given that hypotension is the most common adverse effect, occurring in 35-42% of patients receiving standard or higher doses. 7
Critical Contraindications and Precautions
Absolutely contraindicated in patients with:
Exercise caution in patients with renal or hepatic impairment, as diltiazem clearance may be reduced. 2
Despite concerns, diltiazem has been shown safe and effective even in patients with moderate to severe heart failure (NYHA Class III-IV, mean EF 36%), with a 97% response rate and no significant adverse events in this population. 8
Monitoring Requirements
Continuously monitor blood pressure, heart rate, and cardiac rhythm during IV administration. 1
Target heart rate goals are either lenient control (<110 bpm at rest) or strict control (<80 bpm at rest), depending on symptom burden. 1, 2
Assess heart rate response both at rest and during exercise to ensure adequate rate control throughout daily activities. 5, 2
Transition to Oral Therapy
Once acute rate control is achieved and the patient is stable, transition to oral diltiazem extended-release 120-360 mg once daily for long-term management. 1, 2
The extended-release formulation has a half-life of 4-9.5 hours, while immediate-release has a half-life of 3-4.5 hours. 2
Pharmacokinetic Considerations
Plasma diltiazem concentrations of 79 ng/mL, 172 ng/mL, and 294 ng/mL are required to produce 20%, 30%, and 40% reductions in heart rate, respectively. 9
The elimination half-life after infusion is approximately 6.8-6.9 hours, with a volume of distribution of 299-411 liters. 9
Diltiazem exhibits non-linear pharmacokinetics with dose-dependent decreases in systemic clearance at higher infusion rates. 9
Common Pitfalls to Avoid
Do not use diltiazem as a rhythm control agent—it is purely for rate control and does not convert atrial fibrillation to sinus rhythm (only 18% spontaneous conversion rate). 6, 2
Avoid administering subsequent boluses too quickly—wait the full 15 minutes between doses to assess response and avoid cumulative hypotensive effects. 3, 4
Do not use in patients with accessory pathways, as AV nodal blockade can lead to unopposed conduction through the bypass tract. 1