Initial Dose of Intravenous Atropine for Patients With Symptomatic Bradycardia　― A Scoping Review ―

Abstract

Intravenous atropine is widely recommended as the first-line treatment for symptomatic bradycardia, but because the optimal initial dose remains uncertain, the aim of this scoping review was to examine the existing literature on the efficacy and safety of intravenous atropine at specific doses in adult patients with symptomatic bradycardia and to identify gaps in evidence. A systematic search of 4 databases (PubMed, CENTRAL, Web of Science, and Ichushi-Web) was conducted from inception to December 16, 2024. Studies were included if they reported administration of a specified dose of atropine in adult patients, regardless of study design. No randomized controlled trials directly comparing 0.5 mg vs. 1.0 mg were found. A total of 19 studies were included and categorized into groups based on initial atropine dose: low (<0.5 mg), moderate (0.5 mg ≤ dose <1.0 mg), high (≥1.0 mg), and those spanning multiple categories. No consistent relationship was found between atropine dose and clinical outcomes, such as heart rate response or adverse effects. None of the moderate-dose studies reported worsening bradycardia. Moderate-dose atropine could be safe, and the current practice of using 0.5 mg as an initial dose in Japan, where 0.5 mg/mL prefilled syringes are commercially available, appears clinically reasonable. However, in the absence of high-quality comparative data, future research should apply rigorous study designs to determine the optimal atropine dose in emergency care settings.

Central Figure

Medical professionals frequently encounter patients with arrhythmias across a wide range of clinical settings.^1,2 Among these, symptomatic bradycardia, defined as bradycardia accompanied by acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock,³ is a medical emergency requiring immediate treatment. Although atropine is commonly used in electrophysiological studies to assess atrioventricular block,⁴ it is also a first-line treatment to stabilize hemodynamics in patients with symptomatic bradycardia.^3,5–7

The 2023 European Society of Cardiology guidelines for the management of acute coronary syndromes recommend intravenous administration of positive chronotropic agents (e.g., adrenaline, vasopressin, and/or atropine) as a Class I treatment for sinus bradycardia with hemodynamic intolerance or for high-grade atrioventricular block without a stable escape rhythm.⁵ When atropine is ineffective, temporary pacing is recommended as Class I therapy. Nonetheless, the initial intravenous dose of atropine recommended for symptomatic bradycardia varies across clinical guidelines. For instance, the 2020 Japanese Circulation Society (JCS)/Japanese Society of Electrocardiography Joint Guidelines and the Japan Resuscitation Council (JRC) Guidelines 2015⁸ recommends an initial dose of 0.5 mg,⁷ while the 2018 American College of Cardiology/American Heart Association (ACC/AHA)/Heart Rhythm Society (HRS) Guideline⁶ suggests a range of 0.5–1.0 mg. More recently, after the release of the 2020 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care,³ the AHA has recommended 1.0 mg as the initial dose in their advanced cardiac life support (ACLS) algorithm for adult bradycardia.⁹ Notably, none of these recommendations are supported by a Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) framework or by high-quality comparative evidence.

In response to this gap, the JRC Cardiac Arrhythmia Task Force for the JRC Resuscitation Guidelines 2025, comprising members from the JCS and the Japanese Society of Internal Medicine, conducted this scoping review to map the existing evidence and identify key knowledge gaps regarding the optimal initial dose of intravenous atropine for symptomatic bradycardia. Through discussion with the Guideline Editorial Committee, we established the following clinical questions (CQ) and the Population, Intervention, Comparator, Outcome, Study design, and Time frame (PICOST) framework:

CQ: Is intravenous atropine 1.0 mg reasonable as the initial treatment for patients with symptomatic bradycardia to improve hemodynamic instability?

P (Population): Adult patients (aged ≥18 years) with symptomatic bradycardia

I (Intervention): Intravenous administration of atropine 1.0 mg

C (Comparator): Intravenous administration of atropine 0.5 mg

O (Outcome):

Critical outcomes: All-cause death, cardiac death

Important outcomes: Fatal arrhythmia, ischemic symptoms associated with increased heart rate, worsening bradycardia

S (Study design): Eligible study designs included randomized controlled trials, nonrandomized comparative trials, interrupted time series with a comparison group, controlled before–after studies, cohort studies, and case series with ≥5 cases. Conference abstracts and unpublished sources were excluded.

T (Time frame): From database inception to December 16, 2024

Methods

This scoping review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement,¹⁰ and the PRISMA extension for scoping reviews (PRISMA-ScR).¹¹ It did not require institutional review board approval, as it involved only publicly available data.

Systematic Search and Study Selection

We included studies consistent with the prespecified PICOST framework published by December 16, 2024, without language restrictions. Articles with eligible study designs were extracted. Conference abstracts and unpublished sources were excluded. We searched PubMed (MEDLINE and PMC), Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science, and Ichushi-Web according to the time frame. The search strategy was initially drafted by 2 librarians (S.S. and T.N.) and finalized by the task force members (Supplementary Appendix). The search results were imported into Rayyan,¹² and duplicates were removed by 1 reviewer (M.S.). Next, 2 reviewers (M.S. and M.Y.) independently screened the titles and abstracts and subsequently assessed the full texts of potentially relevant studies. Disagreements were resolved through discussion with a third reviewer (T.F.).

After full-text screening, we found no studies that fulfilled the prespecified PICOST criteria. Consequently, in a post hoc decision, 4 reviewers (H.N., M.S., M.Y., and T.F.) agreed to broaden the inclusion criteria to encompass studies that reported intravenous administration of atropine at a specified dose in patients with symptomatic bradycardia, even if the study design was non-comparative.

Data Extraction and Synthesis of Results

A data-charting form was initially drafted by 1 reviewer (M.Y.) and subsequently finalized through consensus among task force members. Data extraction was performed by M.Y. and independently reviewed and updated by the 3 other reviewers (M.S., T.F., and H.N.). We extracted data on study characteristics, including the name of the first author, year of publication, study design, number of patients, clinical setting (i.e., the location where the intervention was performed and the patient population), administered atropine dose, and weight-based dose (if applicable). Key outcome data were also collected, such as changes in heart rate and the occurrence of adverse effects. To facilitate synthesis, we categorized the studies into 3 groups based on the initial atropine dose: low dose (<0.5 mg), moderate dose (0.5 mg ≤ dose <1.0 mg), high dose (≥1.0 mg). Studies that included multiple initial doses spanning ≥2 of these categories were classified as low–moderate dose, moderate–high dose, or variable dose, respectively. Within each category, we summarized the reported effects on heart rate and adverse outcomes.

Results

The systematic literature search identified 5,393 records (Figure). After removing 850 duplicates, 4,543 titles and abstracts were screened, of which 4,509 were excluded. We assessed the full text of 34 articles for eligibility. As none met the prespecified PICOST criteria, a meta-analysis was not feasible. Following further discussion, we included 19 articles^13–31 that reported the efficacy and safety of intravenous atropine at a specified dose in adult patients with symptomatic bradycardia for data charting.

Figure.

Flow diagram of this study.

Study Characteristics

Based on the initial dose of atropine, the included studies were categorized as follows: low dose (<0.5 mg; 2 articles^13,14), moderate dose (0.5 mg ≤ dose <1.0 mg; 2 articles^16,17), and high dose (≥1.0 mg; 4 articles^25–28) (Table). The remaining studies, which reported multiple initial doses, were classified into 3 groups: low–moderate dose (1 article¹⁵), moderate–high dose (7 articles^18–24), variable dose (3 articles^29–31). Three studies^13,14,30 reported weight-based atropine dosing. None of the studies provided explicit justification for the selected atropine dose. No clear difference in heart rate increase was observed between studies using a moderate dose,^16,17 and those using a high dose.^24–27 Two low-dose studies,^13,14 both involving patients under spinal or general anesthesia, reported worsening bradycardia as an adverse effect, whereas no such events were reported in moderate-dose studies.^16,17 Overall, we did not observe a consistent association between the initial atropine dose and heart rate changes or adverse effects.

Table.

Summary of the Included Articles

Study	Article type	No. of patients	Clinical setting	Atropine dose	Weight-based dose	Heart rate change	Adverse effects
Nishikawa et al. (1990)13	Case series	74	Operating room; patients under spinal anesthesia	Low dose (2 μg/kg (n=18), 4 μg/kg (n=21), 6 μg/kg (n=35))	2 μg/kg (n=18), 4 μg/kg (n=21), 6 μg/kg (n=35)	Significant increase in 4 μg/kg (17±16%) and 6 μg/kg (20±12%) groups (mean±SD, changes from baseline); no significant change in 2 μg/kg group	Decreased heart rate (56% of 2 μ/kg , 9% of 4 μg/kg, 3% of 6 μg/kg)
Smith et al. (1994)14	Case series	15	Operating room; patients undergoing radical prostatectomy with general anesthesia	Low dose (5 μg/kg (n=15))	5 μg/kg (n=15)	HR to ≥70 beats/min in median 270 s (range 30–490 s); 10 required second dose	Recurrent bradycardia (n=5)
Adgey et al. (1968)15	Observational study	126	Mobile intensive-care unit; patients with AMI	Low-moderate dose (aliquots of 0.6 mg (minimum 0.3 mg))	N/A	Atropine was administered until a satisfactory ventricular rate and 64% of patients showed prompt systolic BP increase Atropine effect on AV conduction was influenced by the time of onset of AVB. Within 8 h: 10/20 (50%) improved AVB, 5/20 (25%) improved to normal AV conduction. >8 h: 1/11 (9%) showed favorable response	Ventricular extrasystoles in a few patients
Choi et al. (2021)16	Observational study	46	Operating room; patients undergoing open shoulder arthrotomy with general anesthesia	Moderate dose (0.5 mg)	N/A	Unspecified	Unspecified
Fujii et al. (2018)17	Observational study	108	Operating room; patients with transurethral, perineal, and lower limb surgery with spinal anesthesia	Moderate dose (0.5 mg)	N/A	Shown in the figure; however, exact value unspecified	Unspecified
Carp et al. (1979)18	Case series	23	Unspecified setting; patients with AMI	Moderate-high dose (0.8 or 1.0 mg)	N/A	HR increased in 14/15 (93%) sinus bradycardia (≥20%: 12/15 (80%), 5–20%: 2/15 (13%) AVB improved in 9/16 (56%) patients	Atrial flutter (n=1), ventricular escapes (n=1), ventricular paroxysmal tachycardia (n=1), ventricular flutter (n=1), cardiac arrest (n=3)
Chadda et al. (1975)19	Observational study	68	Emergency room or coronary care unit; patients with AMI	Moderate-high dose (0.6–1.0 mg)	N/A	From 46±14 to 79±12 beats/min in 61/68 patients	Anginal chest pain (n=2), urinary retention (n=1)
Feigl et al. (1984)20	Case series	27	Coronary care unit: patients with AMI	Moderate-high dose (0.5–1.0 mg)	N/A	Complete restoration in normal conduction (n=5), elevated by 21–45/min (mean 28) (n=12), elevated by 10–35/min (mean 16) (n=8)	Unspecified
Okuyan et al. (2010)21	Case series	40	Coronary care unit; patients with mad honey intoxication	Moderate-high dose (0.5–1.0 mg)	N/A	Responded well (33/40, 82.5%); however, exact value unspecified	Unspecified
Scheinman et al. (1975)22	Observational study	56	Coronary care unit; patients with acute AMI	Moderate-high dose (0.5–1.0 mg (0.6 mg (n=34), 1.0 mg (n=15), unspecified (n=5))	N/A	Absolute or mean increase in HR were +32/min (0.5 or 0.6 mg), +27/min (0.8 mg), and +35/min (1.0 mg)	VT or VF (3/56, 5.3%), sustained sinus tachycardia (3/56, 5.3%), PVCs (3/56, 5.3%), psychosis (1/56, 1.8%)
Swart et al. (1999)23	Observational study	131	Prehospital and emergency department; patients with AMI	Moderate-high dose (0.97±0.55 mg (n=131, total amount during prehospital interval), 1.2±0.96 mg (n=56, total amount during ED interval), 1.5±1.0 mg (n=131, total amount during total course of care))	N/A	NSR during hospital care (34/131, 26%), during ED care (17/131, 13%), and over course of care (41/131, 31.3%)	Frequent PVC (n=3), acute myocardial infarction (n=1), myocardial ischemia (n=1), VT (n=1), others (n=2)
Thomas et al. (1966)24	Case series	6	Intensive care unit: patients with AMI	Moderate-high dose (0.6 mg (n=4), 1.2 mg (n=2))	N/A	HR increased to normal range (n=6) (0.6 mg (n=3): +44±24/min, 0.6 mg (n=1): to normal HR, 1.2 mg (n=2): +55±21/min)	Excessive increase in blood pressure (n=2), dry mouth (n=1), visual hallucination (n=1)
Altun et al. (1998)25	Observational study	8	Unspecified setting; patients with AMI	High dose (1.0 mg)	N/A	No change in atrial rate, AV conduction, or ventricular rate in 15 min after atropine administration	Unspecified
Morrison et al. (2008)26	Randomized controlled trial	Unspecified	Prehospital; patients with symptomatic bradycardia	High dose (1.0 mg)	N/A	Unspecified	Unspecified
Onodera et al. (1992)27	Case series	19	Unspecified setting; patients with AMI	High dose (1.0 mg)	N/A	Shown in the figure; however, exact value unspecified	Unspecified
Varriale et al. (1992)28	Observational study	6	Coronary care unit; patients with AMI	High dose (1.0 mg)	N/A	HR restoration to normal range (n=6)	Unspecified
Chadda et al. (1977)29	Observational study	100	Unspecified setting; patients with AMI	Variable dose (0.4–0.6 mg (n=72), 0.8–1.5 mg (n=28))	N/A	Mean increase in HR was 50±23 in the group receiving ≥0.8 mg, 31±18 in the group receiving 0.4–0.6 mg Higher number of patients in the group given ≥0.8 mg (16/28, 56.9%) had an inappropriate response (HR ≥100/min) when compared with those given the 0.4 to 0.6 mg dose (7/72, 9.6%)	Angina with increased HR after atropine 0.8 mg (n=2), increased frequency in PVC (n=2)
Klein et al. (1975)30	Observational study	17	Coronary care unit; patients with AMI	Variable dose (0.3 mg (n=2), 0.4 mg (n=1), 0.5 mg (n=3), 0.6 mg (n=6), 0.8 mg (n=1), 1.0 mg (n=4))	0.0053–0.0088 mg/kg (n=11), 0.0120–0.0148 mg/kg (n=3), 0.0089–0.0119 mg/kg (n=3)	Increase 20–72/min from baseline in 0.0053–0.0088 mg/ kg (n=11), 51–92/min in 0.0120–0.0148 mg/kg (n=3), unspecified in 0.0089–0.0119 mg/kg (n=3)	HR >120/min (n=4), AV dissociation (n=4)
Wei et al. (1983)31	Observational study	9	Unspecified setting; patients with AMI	Variable dose (0.4–1.0 mg)	N/A	Responded after atropine administration (n=9)	Unspecified

AMI, acute myocardial infarction; AV, atrioventricular; AVB, atrioventricular block; ED, emergency department; HR, heart rate; N/A, not applicable; NSR, normal sinus rhythm; PVC, premature ventricular contraction; SB, sinus bradycardia; VF, ventricular tachycardia; VT, ventricular fibrillation.

Discussion

In this scoping review, we identified 19 articles describing the efficacy and safety of intravenous atropine administered at specific doses in adult patients with symptomatic bradycardia. However, none of the included studies directly compared 0.5 mg and 1.0 mg intravenous doses, precluding any definitive conclusions regarding their relative effectiveness or safety. Across the included studies, initial atropine dosing varied, and no clear rationale for dose selection was reported. Furthermore, we found no consistent association between atropine dose and clinical outcomes such as heart rate response or adverse effects.

Our findings highlight a critical gap in the evidence base for an intervention frequently used in emergency cardiovascular care. Unlike long-term treatments for bradycardia, including leadless pacemakers, which have seen rapid technological and evidence-based advancement,^32–34 the initial pharmacologic management with atropine has not been reviewed in rigorous comparative trials. Several barriers likely contribute to this paucity of data, including the acute and emergency nature of symptomatic bradycardia, which complicates prospective trial enrollment, and ethical challenges in randomizing doses in time-sensitive, potentially life-threatening conditions.

Despite these challenges, the lack of standardized, evidence-based recommendation on atropine dosing may lead to practice variability and uncertainty in clinical decision-making. For example, some guidelines recommend an initial dose of 0.5 mg,⁷ while others have shifted toward 1.0 mg⁹ without any high-quality comparative evidence. This heterogeneity underscores the need for harmonization of clinical practice guidelines, which could be supported by robust observational studies or pragmatic trials designed to account for the realities of emergency care settings.

Two studies using a low dose of atropine^13,14 reported worsening bradycardia as an adverse effect, whereas no such events were observed in the moderate-dose studies.^16,17 Paradoxical bradycardia following low-dose atropine administration has been previously described in case reports.^35,36 However, most of these reports involved anesthetized patients undergoing elective surgery, and the relationship between low-dose atropine and worsening bradycardia in patients with symptomatic bradycardia in emergency settings remains unclear. The findings of this review suggest that moderate-dose atropine is generally safe, supporting the use of 0.5 mg as an initial dose in Japan, where 0.5 mg/mL prefilled syringes are commonly used. Nevertheless, given the absence of high-quality comparative data, clinical judgment should remain paramount, and institutional protocols should be periodically reviewed in accordance with evolving guideline recommendations and local resource availability. In addition, future studies should consider defining weight-based dose recommendations similar to those outlined in the Pediatric Advanced Life Support guidelines.³⁷

Study Limitations

No randomized controlled trials were included, which limits the strength of the available evidence and precludes formal assessment using the GRADE framework. Additionally, following full-text screening, we made a post hoc decision to include non-comparative studies reporting specific atropine doses. Although this allowed for broader data mapping, it represented a deviation from the original protocol and may have introduced selection bias.

Conclusions

This scoping review highlights a critical lack of evidence supporting the use of a specific initial dose of intravenous atropine for the treatment of symptomatic bradycardia. We found no comparative studies of 0.5 mg and 1 mg, so the optimal dose could not be determined; however, no differences were found in efficacy or worsening of bradycardia in the studies of each dose. The initial dose of 0.5 mg used in Japan, where 0.5 mg/mL prefilled syringes are commercially available, is considered valid. Future comparative studies to determine the optimal dose of atropine are needed.

Acknowledgments

The authors thank Mr. Shunya Suzuki and Ms. Tomoko Nagaoka, librarians at Dokkyo Medical University, Tochigi, Japan, for their support in the literature search.

During the preparation of this manuscript, the author(s) used ChatGPT-4o for idea generation and English refinement.

This work was supported by the Japan Resuscitation Council, Japan Circulation Society, and JSPS KAKENHI Grant Number JP23K08454.

Disclosures

T.M. is a member of Circulation Reports’ Editorial Team and reports research grants from Amgen. The other authors declare no conflicts of interest with regard to this article.

IRB Information

Not applicable.

Data Availability

All data used in this analysis are available from PubMed (MEDLINE and PMC), Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science, and Ichushi-Web databases.

Supplementary Files

Please find supplementary file(s);

https://doi.org/10.1253/circrep.CR-25-0169

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