Should beta-blockers be used for rate control in cocaine-associated sinus tachycardia without chest pain?
Date First Published:
July 17, 2026
Last Updated:
July 17, 2026
Report by:
Khunassanan Nunthakunatip, Foundation Year 2 Doctor (Manchester University NHS Foundation Trust)
Search checked by:
Dr Hazel Key, Foundation Year 2 Doctor
Three-Part Question:
In [adult patients presenting to the emergency department with cocaine toxicity and persistent sinus tachycardia without chest pain], does the use of [beta-blocker] [improve heart rate control without increasing adverse cardiovascular outcomes]?
Clinical Scenario:
A 34-year-old man presents to the emergency department with acute cocaine-associated toxicity, manifesting as agitation, hypertension, and persistent sinus tachycardia with a heart rate of 142 beats per minute. Despite appropriate first-line management with intravenous benzodiazepines, tachycardia persists. The treating clinician considers adding a beta-blocker to improve heart rate control but is concerned about the risk of adverse cardiovascular outcomes, including coronary vasospasm or hypertension due to unopposed alpha stimulation.
Search Strategy:
Ovid MEDLINE (1946 to 16 February 2026) and Embase (1974 to 16 February 2026) were searched using a combination of MeSH terms and free-text keywords: (exp Cocaine-Related Disorders/ OR Cocaine/ OR cocaine toxic*.mp. OR cocaine poison*.mp. OR cocaine intoxication.mp. OR cocaine-associated.mp. OR acute cocaine.mp.) AND (Tachycardia/ OR Tachycardia, Sinus/ OR tachycard*.mp. OR persistent tachycardia.mp. OR sinus tachycardia.mp. OR elevated heart rate.mp.) AND (Adrenergic beta-Antagonists/ OR beta-blocker*.mp. OR beta blocker*.mp. OR propranolol.mp. OR metoprolol.mp. OR labetalol.mp. OR esmolol.mp. OR carvedilol.mp. OR atenolol.mp. OR bisoprolol.mp.).
Search Details:
Searches were limited to English-language articles in human subjects. Duplicates were removed using Ovid's deduplication tool, and reference lists and Google Scholar were screened for additional studies.
Outcome:
Database searching and deduplication yielded 280 papers. Two reviewers independently screened titles, abstracts, and full texts against predefined inclusion and exclusion criteria. Papers were excluded if they focused exclusively on cocaine-induced chest pain or acute coronary syndrome, comprised non-empirical work, or reported fewer than three patients. Following title and abstract screening, 262 papers were excluded. Eighteen full texts were retrieved for detailed assessment, of which three met the inclusion criteria and were included in the final analysis.
Relevant Paper(s):
| Study Title | Patient Group | Study type (level of evidence) | Outcomes | Key results | Study Weaknesses |
|---|---|---|---|---|---|
| ADRENERGIC CRISIS FROM CRACK COCAINE INGESTION: REPORT OF FIVE CASES Kevin S. Merigian, MD,* Lynda J. Park, MD, Kenneth V. Leeper, MD, Randall G. Browning, MD, and Renee Giometi, MD 1994 United States | N = 5 Male= 80% Average age= 21 | Case series (Level 5) | Heart rate control: All five patients were reported narratively to respond clinically, but no quantitative pre- or post-treatment heart rate data were given. Adverse effects: No adverse effect observed. | Heart rate control: All five patients were reported narratively to respond clinically, but no quantitative pre- or post-treatment heart rate data were given. Adverse effects: No adverse effect observed. | Small case series with no control group. The clinical phenotype was severe adrenergic crisis following oral crack ingestion, which has limited applicability to milder ED presentations. Multiple agents were administered alongside beta-blockade, including lorazepam, haloperidol, phenytoin, diphenhydramine and morphine, making it impossible to attribute haemodynamic improvement or the absence of adverse events to beta-blockade alone. Outcome reporting was narrative only. The authors focused on unopposed alpha effects and extreme hypotension, while other clinically relevant outcomes were not systematically reported. Published in the early 1990s; cocaine purity, co-ingestants, and management standards have changed substantially since. |
| Experience With Esmolol for the Treatment of Cocaine-Associated Cardiovascular Complications I. CHARLES SAND, MD, STEVEN L. BRODY, MD, KEITH D. WRENN, MD, COREY M. SLOVIS, MD 1991 United States | N = 7 Male= 72% Average age= 31 years | Case Series (Level 5) | Heart rate control: 5/7 (71%) achieved heart rate reduction. However, only 3/7 (43%) had a good outcome,* as the remaining two experienced adverse effects alongside rate reduction. Adverse Effects: 3/7 (43%) experienced adverse effects. | Heart rate control: 5/7 (71%) achieved heart rate reduction. However, only 3/7 (43%) had a good outcome,* as the remaining two experienced adverse effects alongside rate reduction. Adverse Effects: 3/7 (43%) experienced adverse effects. | Small case series with no control group. Significant variability in esmolol dosing and infusion duration across patients. Single-centre study from 1989–1990; cocaine purity, co-ingestants, and patient demographics have changed substantially since. |
| Anaesthesia for laryngoscopy: A comparison of the cardiovascular effects of cocaine and lignocaine D. Orr I. Jones 1968 Jamaica | N = 5** No data is available for their sex and age. | Prospective non-randomised comparative clinical study (Level 3) | Heart rate control: 5/5 (100%) responded. In 2 patients with sinus tachycardia, heart rate fell from ~150 to <100 bpm within 90 seconds. In 3 patients with arrhythmias, sinus rhythm was restored within 30–60 seconds. Adverse effects: No adverse effects reported. | Heart rate control: 5/5 (100%) responded. In 2 patients with sinus tachycardia, heart rate fell from ~150 to <100 bpm within 90 seconds. In 3 patients with arrhythmias, sinus rhythm was restored within 30–60 seconds. Adverse effects: No adverse effects reported. | Small non-randomised study with no matched comparator. No demographic data reported. Cardiovascular monitoring was inconsistent. Post-operative hypotension in group A cannot be attributed to rescue propranolol as unclear whether they overlapped with the five who received it. Patients were anaesthetised and exposed to controlled topical cocaine, which does not approximate conscious recreational cocaine users. Conducted in 1968; anaesthetic and emergency practice have changed substantially since. |
Author Commentary:
Cardiovascular toxicity is among the most frequent reasons for emergency presentation after cocaine use, yet its management remains contentious. TOXBASE⁴ recommends benzodiazepines as first-line treatment and advises against beta-blockers where chest pain is present, owing to the theoretical risk of unopposed alpha-adrenergic activity. It does not address persistent sinus tachycardia without chest pain in a patient who has already received adequate benzodiazepine therapy, which is the population considered here.
All three studies reported reductions in heart rate following beta-blockade, giving a consistent direction of effect. Merigian and colleagues¹ described outcomes narratively, without pre- and post-treatment values. Sand and colleagues² recorded a mean reduction of 23% with esmolol, although the response varied considerably. Orr and Jones³ found that intravenous propranolol lowered the heart rate in two patients with sinus tachycardia and restored sinus rhythm in three with arrhythmias. All patients in Merigian and colleagues¹ and five of seven in Sand and colleagues² had received benzodiazepines before beta-blockade, mirroring the pathway in which beta-blockade follows insufficient first-line treatment and supporting the relevance of these data to a second-line role. Interpretation of Merigian and colleagues¹ is further limited by concurrent polypharmacy, as patients received several active agents alongside beta-blockade, so any change in heart rate cannot be attributed to it alone. The magnitude and reliability of the effect therefore remain uncertain, particularly as cocaine's short serum half-life means observed improvements may partly reflect spontaneous resolution rather than drug effect.
Only Sand and colleagues² reported adverse effects, which occurred in three of their seven patients. Two of these were cardiovascular: one patient developed worsening hypertension after esmolol, an example of the unopposed alpha effect that motivates caution about beta-blockade, and another became hypotensive without any improvement in heart rate. The third event, vomiting and lethargy requiring intubation, was not cardiovascular. Importantly, the patient who developed worsening hypertension had presented with a hypertensive emergency, so this is a markedly more severe phenotype this review concerns. Merigian and colleagues¹ and Orr and Jones³ reported no adverse effects attributable to beta-blockade, although their small patient numbers mean little can be concluded about safety. In one case reported by Merigian and colleagues,¹ tonic-clonic seizures developed after labetalol administration. The authors attributed this to the adrenergic crisis of crack cocaine ingestion rather than to the drug, a judgement consistent with the prominence of seizures elsewhere in the series, though the temporal association cannot be entirely discounted.
The applicability of the evidence is also constrained by the populations studied. The exclusion of chest pain and acute coronary syndrome was applied at study level rather than to individual patients, and several included patients fell outside the target phenotype. In Sand and colleagues,² two presented with chest pain and several showed electrocardiographic ischaemia. In Merigian and colleagues,¹ the dominant presentation was severe adrenergic crisis after oral crack ingestion, frequently with ischaemic changes, rather than isolated sinus tachycardia. In Orr and Jones,³ only two of the five patients given rescue propranolol had sinus tachycardia, the remainder having ventricular arrhythmias, and all were anaesthetised and exposed to controlled topical cocaine rather than presenting as conscious recreational users. The number of patients matching the target phenotype is therefore considerably smaller than the combined total of seventeen suggests, and the evidence should be read as indirectly applicable.
Taken together, the three studies are too small and methodologically limited to support any conclusion about efficacy or safety, and the cardiovascular adverse event reported by Sand and colleagues² warrants caution. Although labetalol was used within the multi-drug regimen of Merigian and colleagues,¹ no study evaluated it as a distinct intervention, and it remains the only beta-blocker endorsed by TOXBASE⁴ for cocaine-associated cardiovascular complications. Its combined alpha and beta antagonism is of particular interest, as it directly addresses the unopposed alpha activity underlying current caution. A prospective controlled trial of labetalol as an adjunct to benzodiazepines, restricted to patients with cocaine-associated sinus tachycardia without chest pain and using quantitative heart rate endpoints with systematic reporting of adverse cardiovascular events, is therefore needed to answer this specific question.
All three studies reported reductions in heart rate following beta-blockade, giving a consistent direction of effect. Merigian and colleagues¹ described outcomes narratively, without pre- and post-treatment values. Sand and colleagues² recorded a mean reduction of 23% with esmolol, although the response varied considerably. Orr and Jones³ found that intravenous propranolol lowered the heart rate in two patients with sinus tachycardia and restored sinus rhythm in three with arrhythmias. All patients in Merigian and colleagues¹ and five of seven in Sand and colleagues² had received benzodiazepines before beta-blockade, mirroring the pathway in which beta-blockade follows insufficient first-line treatment and supporting the relevance of these data to a second-line role. Interpretation of Merigian and colleagues¹ is further limited by concurrent polypharmacy, as patients received several active agents alongside beta-blockade, so any change in heart rate cannot be attributed to it alone. The magnitude and reliability of the effect therefore remain uncertain, particularly as cocaine's short serum half-life means observed improvements may partly reflect spontaneous resolution rather than drug effect.
Only Sand and colleagues² reported adverse effects, which occurred in three of their seven patients. Two of these were cardiovascular: one patient developed worsening hypertension after esmolol, an example of the unopposed alpha effect that motivates caution about beta-blockade, and another became hypotensive without any improvement in heart rate. The third event, vomiting and lethargy requiring intubation, was not cardiovascular. Importantly, the patient who developed worsening hypertension had presented with a hypertensive emergency, so this is a markedly more severe phenotype this review concerns. Merigian and colleagues¹ and Orr and Jones³ reported no adverse effects attributable to beta-blockade, although their small patient numbers mean little can be concluded about safety. In one case reported by Merigian and colleagues,¹ tonic-clonic seizures developed after labetalol administration. The authors attributed this to the adrenergic crisis of crack cocaine ingestion rather than to the drug, a judgement consistent with the prominence of seizures elsewhere in the series, though the temporal association cannot be entirely discounted.
The applicability of the evidence is also constrained by the populations studied. The exclusion of chest pain and acute coronary syndrome was applied at study level rather than to individual patients, and several included patients fell outside the target phenotype. In Sand and colleagues,² two presented with chest pain and several showed electrocardiographic ischaemia. In Merigian and colleagues,¹ the dominant presentation was severe adrenergic crisis after oral crack ingestion, frequently with ischaemic changes, rather than isolated sinus tachycardia. In Orr and Jones,³ only two of the five patients given rescue propranolol had sinus tachycardia, the remainder having ventricular arrhythmias, and all were anaesthetised and exposed to controlled topical cocaine rather than presenting as conscious recreational users. The number of patients matching the target phenotype is therefore considerably smaller than the combined total of seventeen suggests, and the evidence should be read as indirectly applicable.
Taken together, the three studies are too small and methodologically limited to support any conclusion about efficacy or safety, and the cardiovascular adverse event reported by Sand and colleagues² warrants caution. Although labetalol was used within the multi-drug regimen of Merigian and colleagues,¹ no study evaluated it as a distinct intervention, and it remains the only beta-blocker endorsed by TOXBASE⁴ for cocaine-associated cardiovascular complications. Its combined alpha and beta antagonism is of particular interest, as it directly addresses the unopposed alpha activity underlying current caution. A prospective controlled trial of labetalol as an adjunct to benzodiazepines, restricted to patients with cocaine-associated sinus tachycardia without chest pain and using quantitative heart rate endpoints with systematic reporting of adverse cardiovascular events, is therefore needed to answer this specific question.
Bottom Line:
Beta-blockers should not be used routinely for rate control in adults with cocaine-associated sinus tachycardia without chest pain. The evidence is too limited to establish efficacy or safety, and benzodiazepines with supportive care remain first-line.
Level of Evidence:
Level 3: Small numbers of small studies or great heterogeneity or very different population
References:
- Kevin S. Merigian, MD,* Lynda J. Park, MD, Kenneth V. Leeper, MD, Randall G. Browning, MD, and Renee Giometi, MD. ADRENERGIC CRISIS FROM CRACK COCAINE INGESTION: REPORT OF FIVE CASES
- I. CHARLES SAND, MD, STEVEN L. BRODY, MD, KEITH D. WRENN, MD, COREY M. SLOVIS, MD. Experience With Esmolol for the Treatment of Cocaine-Associated Cardiovascular Complications
- D. Orr I. Jones. Anaesthesia for laryngoscopy: A comparison of the cardiovascular effects of cocaine and lignocaine