Category Archives: EBM

Dexmedetomidine in the ED

Is a viable alternative sedative/hypnotic agent for procedural sedation in the ED?

Mark Estrellado MD, PGY3

Given the regularity of noninvasive and minimally invasive procedures that emergency physicians must perform on a daily basis, proficiency in the art of procedural sedation remains an indispensable component of their already broad repertoire of skills. And while every discussion on the topic of procedural sedation most often begins with the description of the “ideal sedative” as an inexpensive agent that is easily administered, has a rapid and predictable onset and dissipation of effect without prolonged accumulation despite repeated dosing, and is free of adverse side effects and drug interactions, no such agent exists. Instead, the ED physician’s current armamentarium consists of a handful of agents–namely benzodiazepines, opioids, propofol, ketamine, and etomidate–each of which have proven useful when taking into account each individual patient’s comorbidities and when utilized in the appropriate setting.3 Nevertheless, the issue of respiratory depression remains a constant concern, and this is where dexmedetomidine has garnered increasing attention over the last two decades as a potential addition to the current set of sedation agents.


Unlike its other sedative counterparts, dexmedetomidine exerts its effects primarily via presynaptic α-2 agonism resulting in lower levels of norepinephrine, and consequently, decreased sympathetic drive.1-2 This manifests in profound analgesia and sedation with decreased heart rate and blood pressure. Associated respiratory depression is virtually nonexistent, with maintenance of both rate and depth of ventilation.4 Given its respiratory profile, dexmedetomidine  was originally used as a short-term sedative for mechanically vented critically ill patients.5 More recently, however, there seems to be a growing trend towards expanding its use for sedation and analgesia in adult and pediatric patients undergoing small, minimally invasive surgical and diagnostic procedures.


While evidence in the current literature is still modest at best, several experimental and observational studies suggest that dexmedetomidine may be just as efficacious, if not superior when compared to other sedative agents. Several case reports highlight the successful use of dexmedetomidine during airway surgical procedures (e.g. microlaryngeal surgery, bronchoscopy, laryngoscopy), where dexmedetomidine was either the sole anesthetic agent or supplemented with small doses of fentanyl and topical lidocaine. Recovery times in these reports were not prolonged compared to conventional anesthetics.6-7

A randomized, double-blind study compared dexmedetomidine with midazolam for intravenous sedation during dental surgery under local anesthesia. The study concluded that sedation with dexmedetomidine was comparable to midazolam, but also provided more “predictability” as it was associated with less “restlessness” and “disinhibition among patients.” While the majority of patients in the study did rate dexmedetomidine’s analgesic effect as satisfactory, however, researchers found its amnestic effects to be unreliable.8-10

In 56 patients undergoing endarterectomy with regional anesthesia, dexmedetomidine proved an acceptable alternative to sedation using midazolam and fentanyl, without showing superiority to conventional sedation techniques used during awake carotid endarterectomy.11

In another study by Kaygusus et al., the combination of dexmedetomidine with a small dose of fentanyl was used safely and effectively when compared to the standard propofol regimen used during extracorporeal shockwave lithotripsy.12

In the pediatric setting, dexmedetomidine has been garnering popularity as an alternative to propofol among nonanesthesiologists for sedation of children during diagnostic CT and MRI imaging. Comparative studies have seen an association between using higher doses of dexmedetomidine and higher rates of completion of imaging without the need to administer another sedative. One study found that utilizing higher doses of dexmedetomidine even resulted in shorter recovery times, which the authors attributed to the lower use of barbiturates for rescue sedation.13-14


Nevertheless, several controversies surrounding dexmedetomidine’s efficacy and safety profile have hindered its universal acceptance. Despite a growing number of positive studies, dexmedetomidine’s effectiveness as a sedative agent has not been uniformly successful, particularly for invasive procedures. For instance, in a prospective study where dexmedetomidine was used as the sole agent during cardiac catheterization in pediatric patients, investigators found that, not only did dexmedetomidine have a longer time of onset, but also more than half of the subjects required additional propofol boluses in order to facilitate successful cannulae placement.15 Concerns have also arisen regarding dexmedetomidine’s hemodynamic effects, especially when used in higher doses. As a case in point, in a randomized, single-blind study comparing the use of dexmedetomidine and fentanyl versus midazolam and meperidine for outpatient colonoscopies, Jalowiecki et al. reported a higher incidence of hypotension and bradycardia in the dexmedetomidine group, prompting the investigators to terminate the study prematurely.16 Given these issues, the addition of a second agent–ketamine–in conjunction with dexmedetomidine has been proposed by some as a more preferable alternative. An NMDA receptor antagonist, ketamine causes dose dependent direct stimulation of the CNS that leads to increased sympathetic nervous system outflow, manifesting as increases in systemic and pulmonary blood pressure, heart rate, and cardiac output without producing any significant respiratory depression.17 As such, ketamine may complement the limitations of dexmedetomidine as a sole anesthetic agent.


Current literature regarding the use of a dexmedetomidine-ketamine combination is severely limited at present, but the preliminary findings show some promise. A prospective randomized trial by Tosun et al. compared dexmedetomidine-ketamine to propofol-ketamine for pediatric patients with acyanotic congenital heart disease undergoing cardiac catheterization found that sedation was effective in both regimens without any clinically significant differences in hemodynamic stability or respiratory status between the two.18 However, the dexmedetomidine-ketamine group required more supplemental boluses of ketamine. Koruk et al. conducted a similar prospective investigation comparing dexmedetomidine-ketamine versus midazolam-ketamine during extracorporeal shockwave lithotripsy for pediatric patients, again showing that sedation was equally effective in both groups, with the incidence of nausea and vomiting significantly lower in the dexmedetomidine-ketamine group.19 Additional evidence regarding the potential utility of the dexmedetomidine-ketamine combination comes by way of small retrospective case series and anecdotal case reports, several of which attest to the achievement of a satisfactory level of sedation even in patients with significant comorbid conditions–e.g. obstructive sleep apnea, pulmonary hypertension–with minimal adverse effects observed.20-27


Overall, while the existing data is still insufficient to make any definitive conclusions at this time, the potential for the dexmedetomidine-ketamine combination to be a viable sedative/hypnotic alternative for procedural sedation is undeniable. From a theoretical standpoint, the two agents have the capacity to complement each other’s limitations. When used in tandem, dexmedetomidine may limit the tachycardia, hypertension, and “emergence phenomenon” commonly associated with ketamine. Conversely, ketamine may counteract the bradycardia and hypotension seen with dexmedetomidine and may help achieve a more rapid time of onset of sedation compared to dexmedetomidine alone. Ultimately, more large randomized-control trials must be conducted with direct comparisons to other commonly used regimens in order to gain a better sense of the impact, if any, that dexmedetomidine-ketamine will have in the practice of procedural sedation in the ED.



1) Scholz J, Tonner PH. α2-Adrenoceptor anesthesia: a new paradigm. Curr Opin Anaesthesiol 2000;13:437-42.

2) Chiu TH, Chen MJ, Yang YR, Yang JJ, Tang FL. Action of dexmedetomidine on rat locus coerleus neurons: intracellular recording in vitro. Eur J Pharmacol 1995;285:261-8.

3) Jacobi J, Fraser GL, Coursin DB, et al. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult. Crit Care Med. 2002;30:119–141

4) Bhana N, Goa KL, McClellan K. Dexmedetomidine. Drugs 2000;59: 263-8.

5) Dyck JB, Shafer SL. Dexmedetomidine pharmacokinetics and pharmacodynamics. Anaesthetic Pharmacology Review. 1993;1:238–245.

6) Jense RJ, Souter K, Davis J, Romig C, Panneerselvam A, Maronian N. Dexmedetomidine sedation for laryngeal framework surgery. Ann Otol Thinol Laryngol. 2008;117:659–664.

7) Ohata H, Tanemura E, Dohi S. Use of high-dose dexmedetomidine infusion for anesthesia and sedation in a patient for microlaryngeal surgery maintained with spontaneous breathing. Masui. 2008;57:428–432.

8) Ogawa S, Seino H, Ito H, Yamazaki S, Ganzberg S, Kawaai H. Intravenous sedation with low-dose dexmedetomidine: its potential for use in dentistry. Anesth Prog. 2008;55:82–88.

9) Cheung CW, Ying CLA, Chiu WK, Wong GTC, Ng KFJ, Irwin MG. A comparison of dexmedetomidine and midazolam for sedation in third molar surgery. Anaesthesia. 2007;62:1132–1138.

10) Ustun Y, Gunduz M, Erdogan O, Benlidayi ME. Dexmedetomidine versus midazolam in outpatient third molar surgery. J Oral Maxillofac Surg. 2006;64:1353–1358.

11) McCutcheon CA, Orme RM, Scott DA, Davies MJ, McGlade DP. A comparison of dexmedetomidine versus conventional therapy for sedation and hemodynamic control during carotid endarterectomy performed under regional anesthesia. Anesth Analg. 2006;102:668–675.

12) Kaygusuz K, Gokce G, Gursoy S, Ayan S, Mimaroglu C, Gultekin Y. A comparison of sedation with dexmedetomidine or propofol during shockwave lithotripsy: a randomized controlled trial. Anesth Analg. 2008;106:114–119.

13) Mason KP, Zurakowski D, Zgleszewski SE, et al. High dose dexmedetomidine as the sole sedative for pediatric MRI. Pediatr Anesth. 2008;18:403–411.

14) Koroglu A, Demirbilek S, Teksan H, Sagir O, But AK, Ersoy OM. Sedative, haemodynamic and respiratory effects of dexmedetomidine in children undergoing magnetic resonance imaging examination: preliminary results. Br J Anaesth. 2005;94:821–824.

15) Munro HM, Tirotta CF, Felix DE, et al. Initial experience with dexmedetomidine for diagnostic and interventional cardiac catheterization in children. Pediatr Anesth. 2007;17:109–112.

16) Jalowiecki P, Rudner R, Gonciarz M, Kawecki P, Petelenz M, Dziurdzik P. Sole use of dexmedetomidine has limited utility for conscious sedation during outpatient colonoscopy. Anesthesiology 2005;103:269-75.

17) J Albanèse, S Arnaud, M Rey, L Thomachot, B Alliez, C Martin Ketamine decreases intracranial pressure and electroencephalographic activity in traumatic brain injury patients during propofol sedation. Anesthesiology: 1997, 87(6);1328-34

18) Tosun Z, Akin A, Guler G, et al: Dexmedetomidine-ketamine and propofol-ketamine combinations for anesthesia in spontaneously breathing pediatric patients undergoing cardiac catheterization. J Cardiothor Vasc Anesth 2006; 20:515–519

19) Koruk S, Mizrak A, Gul R, et al: Dexmedetomidine-ketamine and midazolam-ketamine combinations for sedation in pediatric patients undergoing extracorporeal shock wave lithotripsy: A randomized prospective study. J Anesth2010; 24:858–863

20) Bozdogan N, Sener M, Caliskan E, et al: A combination of ketamine and dexmedetomidine sedation with caudal anesthesia during incarcerated inguinal hernia repair in three high-risk infants. Pediatr Anesth 2008; 18:1009–1011

21) Barton KP, Munoz R, Morell VO, et al: Dexmedetomidine as the primary sedative during invasive procedures in infants and toddlers with congenital heart disease. Pediatr Crit Care Med 2008; 9:612–615

22) Luscri N, Tobias JD: Monitored anesthesia care with a combination of ketamine and dexmedetomidine during magnetic resonance imaging in three children with trisomy 21 and obstructive sleep apnea. Pediatr Anesth 2006; 16:782–786

23) Iravani M, Wald SH: Dexmedetomidine and ketamine for fiberoptic intubation in a child with severe mandibular hypoplasia. J Clin Anesth 2008; 20:455–457

24) Mahmoud M, Tyler T, Sadhasivam S: Dexmedetomidine and ketamine for large anterior mediastinal mass biopsy.Pediatr Anesth 2008; 18:1011–1013

25) Munro HM, Felix DE, Nykanen DG: Dexmedetomidine/ketamine for diagnostic cardiac catheterization in a child with idiopathic pulmonary hypertension. J Clin Anesth 2009; 21:435–438

26) Rozmiarek A, Corridore M, Tobias JD: Dexmedetomidine-ketamine sedation during bone marrow aspirate and biopsy in a patient with duchenne muscular dystrophy. Saudi J Anaesth 2011; 5:219–222

27) Corridore M, Phillips A, Rabe A, et al: Dexmedetomidine-ketamine sedation in a child with a mediastinal mass.World J Pediatr Cong Heart Surg (in press)28)

28) Shukry M, Miller J: Update on dexmedetomidine: use in nonintubated patients requiring sedation for surgical procedures. Therapeutics and Clinical Risk Management 2010; 6:111-121

29) Gerlach A, Dasta J: Dexmedetomidine: An Updated Review. Annals of Pharmacotherapy 2007;  41:245-253

30) Tobias J: Dexmedetomidine and Ketamine: An Effective Alternative for Procedural Sedation? Pediatric Crit Care Med 2012; 13(4):423-27

Cancel the Cath Lab Activation; Its only an NSTEMI

By Andrew Barbera, PGY3

Who Needs a Cath?


63 year old male with history of HTN, OA s/p R hip replacement, PTSD was BIBEMS after syncopal event. Pt states that evening he felt acute general weakness when he was on the subway. The weakness worsened when he got off the subway and was walking in the street. He then developed acute severe SOB and he stopped and rested himself on the trunk of a car. Pt then lost consciousness and awoke in the ambulance. Pt stated upon awakening he was alert and oriented. Pt denied CP, palpitations, diaphoresis or dizziness before passing out or during initial ED evaluation. Pt also denied any recent exercise intolerance, recent chest pain, orthopnea or additional symptoms. Pt reported normal stress test done 6 months ago at VA for unknown reason. Initial EMS ekg showed sinus rhythm, slight left axis deviation, LBBB with 0.5 mm ST depression II, III, avF, I, aVL. Repeat EKG on ED presentation showed NSR, slight left axis deviation, with no ST-T depression/elevations or rhythm issues. Pt had received 162mg of asa by ems prior to ED arrival. During ED evaluation pt developed an episode of acute, moderate, left sided, pressure like CP. Pt was given sublingual nitro and morphine with full resolution within 45 min. Repeat EKG during this episode showed NSR, comparing the previous one, new TWI in III and aVF. Pt’s initial troponin was negative at 0.021, but repeat troponin was positive at 3.37. Cardiology was consulted. Pt diagnosed with NSTEMI. Cardiology at the time declined emergent transfer for coronary cath, and wanted to optimize the patient on medical management. Pt was loaded with 600mg of Plavix and heparin bolus and drip was started. Pt was transferred to CCU for additional medical management and cardiac monitoring.


CCU course pt remained chest pain free, serial EKG’s remained unchanged and pt had serial troponins that were down trending. Pt was additionally risk stratified with ECHO for wall motion abnormalities (hypokinesis) and LVEF and found to be normal. Pt was optimized on medical management with metoprolol, atorvastatin, Plavix and asa. Pt was discharged home with close cardiology follow up.


This made me think what are the indications for cardiac revascularization (aggressive) vs. medical management (conservative) in pts with NSTEMI. According to the 2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction, Pt’s with NSTEMI who have signs of persistent angina or electrical and or hemodynamic instability should receive early cardiac revascularization.[1] Pt’s with acute decreased LVEF (40% or less) or signs of heart failure should also be considered for early cardiac revascularization. Additionally pts with any signs of continued or repeat ischemia, or new serious arrhythmia.[2]

Additionally there are several randomized trials including FRISC II, TACTICS-TIMI 18, both of which showed a significant lower rate of primary end point of death or repeat MI, especially in high risk individuals. [3]


In summary it seems that high-risk patients with NSTEMI/Unstable angina should undergo early cardiac revascularization. Patients with signs and symptoms of ongoing or repeat ischemia have better outcomes after reperfusion vs. conservative therapy, along with patients who have failed medical therapy. Pts that are lower risk for repeat or continued ischemia may have greater risk/benefit from the conservative medical management.



[1] Wright RS, Anderson JL, Adams CD, et al. 2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/ Non-ST-Elevation Myocardial Infarction (Updating the 2007 Guideline): A Report of the American College of Cardiology Foundation/American Heart Association . Circulation 2011:2022–2060.

[2] Unstable Angina Treatment & Management. Unstable Angina Treatment & Management: Approach Considerations, Initial Medical Management, Further Medical Management. Available at: Accessed September 2016.

[3] Kumar A, Cannon CP. Acute coronary syndromes: diagnosis and management, part I. Mayo Clin Proc. 2009;84(10):917-38.

Why Not Dobutamine?

Why Not Dobutamine?

PGY3 Neil McCormack


A patient rolls into the emergency room. You don’t need this. You’ve got a lot of other patients. This patient however is in shock. They are hypotensive and with a decreased mental status. You need to give them something and the attending asks what vasopressors you would like. “Why not dobutamine” the intern asks. With a sigh and a heavy eye roll you turn away. But… Why not dobutamine?



Dobutamine            Dobutamine is a synthetic catecholamine used primarily for cardiac stress testing outside of the hypotensive patient (8). This is due to the positive inotropic effects it plays on the heart. Dobutamine acts via a 3:1 selective agonist effect on β1 and β2 receptors respectively. This causes increased contractility of the heart (9). There is, however, a side effect of reflexive decrease in systemic vascular resistance (SVR) causing potential for worsening of hypotension. This is not seen in higher doses of dobutamine and the reason for this is because of dobutamine’s partial α1 agonist effect (9). Given this information, we can intuitively think that giving dobutamine would be a good option for use in a hypotensive patient. But what does the literature say?

There have been a few studies that look at the use and effectiveness of dobutamine in the setting of hypotension (1, 2, 9, 10, 12, 13). Partially due to the α1 partial agonist effect, dobutamine is not a first line recommended treatment option alone in patients with septic or hypovolemic shock (3, 4, 9). It has been proposed as a first line treatment for sepsis patients if used in conjunction with another vasopressor (example: norepinephrine) to prevent the reflexive SVR decrease and hypotension. In the absence of using multiple vasopressors, dopamine and norepinephrine have been listed as the first line drugs of choice for septic shock patients. According to the “Surviving Sepsis” guidelines (3, 4), norepinephrine is the first line vasopressor of choice for sepsis patients. However, dobutamine is the recommended inotropic agent to be used in combination to improve cardiac output (without going to supranormal levels of cardiac output) (3).



But what if this patient has a bad heart? The evidence for use of dobutamine in patients with cardiogenic shock is more favorable (7, 12, 14). Patients who need inotropic support primarily are recommended to undergo dobutamine therapy as their vasopressor of choice in the beginning. This is due to the positive effect that dobutamine has on the contractility of the heart muscle itself. It has been shown as well that dobutamine appears to have a more favorable effect on right ventricular (RV) contractility than on left ventricular (LV) though it is effective in both settings (14). The downside of dobutamine alone is, as mentioned, it is only a partial α1 agonist and thus, if the blood pressure does not respond to the increased inotropic effects, a second line agent will need to be added. In a trial looking at epinephrine vs dobutamine/norepinephrine, there was no difference in the overall outcomes of patients but the epinephrine patients had more side effects (including arrhythmias).

What does all this mean? Well what this means is that the intern may have, in fact, been correct to suggest that we use dobutamine for our now hypotensive patient. It all depends on the suspected cause (IE: cardiogenic vs septic vs other causes of hypotension). It is important to keep in mind, though, that unless this patient has a purely cardiogenic cause (such as severe heart failure), they may also require a second pressure support in order to maintain a healthy blood pressure.



1) Bangash, Mansoor N, Ming-Li Kong, and Rupert M Pearse. “Use of Inotropes and Vasopressor Agents in Critically Ill Patients.” British Journal of Pharmacology 165, no. 7 (April 2012): 2015–33. doi:10.1111/j.1476-5381.2011.01588.x.

2) Beale, Richard J., Steven M. Hollenberg, Jean-Louis Vincent, and Joseph E. Parrillo. “Vasopressor and Inotropic Support in Septic Shock: An Evidence-Based Review.” Critical Care Medicine 32, no. 11 Suppl (November 2004): S455–65.

3) Campaign, Surviving Sepsis. “Leitlinienempfehlungen Zur Sepsistherapie.” Sepsis Und MODS, 2015, 377.

4) Dellinger, R. Phillip, Mitchell M. Levy, Jean M. Carlet, Julian Bion, Margaret M. Parker, Roman Jaeschke, Konrad Reinhart, et al. “Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008.” Critical Care Medicine 36, no. 1 (January 2008): 296–327. doi:10.1097/01.CCM.0000298158.12101.41.

5) Huang, Xuan, Shu Lei, Mei-fei Zhu, Rong-lin Jiang, Li-quan Huang, Guo-lian Xia, and Yi-hui Zhi. “Levosimendan versus Dobutamine in Critically Ill Patients: A Meta-Analysis of Randomized Controlled Trials.” Journal of Zhejiang University. Science. B 14, no. 5 (May 2013): 400–415. doi:10.1631/jzus.B1200290.

6) Levy, Bruno, Pierre Perez, Jessica Perny, Carine Thivilier, and Alain Gerard. “Comparison of Norepinephrine-Dobutamine to Epinephrine for Hemodynamics, Lactate Metabolism, and Organ Function Variables in Cardiogenic Shock. A Prospective, Randomized Pilot Study.” Critical Care Medicine 39, no. 3 (March 2011): 450–55. doi:10.1097/CCM.0b013e3181ffe0eb.

7) Lewis, Tyler, Caitlin Aberle, Diana Esaian, and John Papadopoulos. “EFFICACY AND SAFETY OF MILRINONE VERSUS DOBUTAMINE IN CARDIOGENIC SHOCK.” Critical Care Medicine 43, no. 12 Suppl 1 (December 2015): 34. doi:10.1097/01.ccm.0000473960.43621.41.

8) Miller, Todd D., J. Wells Askew, and Nandan S. Anavekar. “Noninvasive Stress Testing for Coronary Artery Disease.” Heart Failure Clinics 12, no. 1 (January 2016): 65–82. doi:10.1016/j.hfc.2015.08.006.

9) Müllner, M., B. Urbanek, C. Havel, H. Losert, F. Waechter, and G. Gamper. “Vasopressors for Shock.” The Cochrane Database of Systematic Reviews, no. 3 (2004): CD003709. doi:10.1002/14651858.CD003709.pub2.

10) Rudis, M. I., M. A. Basha, and B. J. Zarowitz. “Is It Time to Reposition Vasopressors and Inotropes in Sepsis?” Critical Care Medicine 24, no. 3 (March 1996): 525–37.

11) Smith, Maria A. “Use of Vasopressors in the Treatment of Cardiac Arrest.” Critical Care Nursing Clinics of North America 17, no. 1 (March 2005): 71–75, xi. doi:10.1016/j.ccell.2004.09.010.

12) Steltzer, H., P. Simon, A. N. Owen, M. Thalmann, and A. F. Hammerle. “The Effects of Dobutamine Therapy in Critically Ill Patients Measured by Transoesophageal Echocardiography and Intracardiac Monitoring.” Anaesthesia 49, no. 5 (May 1994): 432–37.

13) “Vasopressors and Inotropes in Shock.pdf,” n.d.

14) Vincent, J. L., C. Reuse, and R. J. Kahn. “Effects on Right Ventricular Function of a Change from Dopamine to Dobutamine in Critically Ill Patients.” Critical Care Medicine 16, no. 7 (July 1988): 659–62.


Dilt v. Metoprolol in Afib/RVR

by Najm Haque, PGY2


Atrial fibrillation with rapid ventricular response is a common emergency room problem. Patient with stable blood pressure who present in Afib with RVR need medications to control their heart rate (unstable patients require more cardioversion). Traditionally, these patients receive beta blockers or calcium channel blockers in IV form for rate control. The most common medications used in the US are metoprolol and diltiazem, but it is unclear which is superior.


Fromm et al Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department

This study was published in the Journal of Emergency Medicine in April 2015 and compared how fast rate control was achieved in diltiazem vs metoprolol. This was a prospective, double-blind study which compared the effects of both medications at 30 minutes, as well as looking at mean decrease in heart rate, and adverse effects. Patients were randomized and either received Diltiazem 0.25 mg/kg IVP (maximum dose of 30mg) or Metoprolol 0.15mg/kg IVP (maximum dose of 10mg). A second escalation dose of 0.35mg/kg of diltiazem (max of 30mg) or 0.15mg/kg of metoprolol (max of 10mg) was given at 15 minutes if target HR was not achieved. The results of the study showed that diltiazem reached the target HR of <100 much more frequently at 5 minutes (50% vs 10.7%) and at 30 minutes (95.8% vs 46.4%) when compared to metoprolol. There was no difference in adverse effects.



Demircan C, Cikriklar HI, Engindeniz Z, et al. Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation.

This study was published in the Journal of Emergency Medicine in 2005. Similar to the study by Fromm et al, this study compared diltiazem (0.25mg/kg, max of 25mg) and metoprolol (0.15mg/kg, max of 10mg), was prospective and randomized, and used a target heart rate < 100. They compared the two medications at intervals of 2, 5, 10, 15, and 20 minutes. In each interval, the success rate of diltiazem was higher than metoprolol, and at 30 minutes 90% of patients receiving diltiazem reached the target heart rate while 80% of patients receiving metoprolol reached the target heart rate. In addition, the decrease in heart rate was higher in the group receiving diltiazem than the group receiving metoprolol.


Scheuermyer FX, Grafstein E, Stenstrom R, et al. Safety and efficiency of calcium channel blockers versus beta-blockers for rate control in patients with atrial fibrillation and no acute underlying medical illness.

This study was published in 2013 and compared the effect of calcium channel blockers and beta blockers in ER patients with known Afib who present with Afib with RVR. The primary outcome of this retrospective cohort study was hospital admissions and patients with underlying medical conditions requiring hospitalization were excluded (which means this study looked for patients who were admitted to the hospital for Afib with RVR and no other medical problem). The study enrolled 259 patients over a 4 year period and noted patients receiving CCBs were more likely to be admitted (31% vs 27%) although this was statistically insignificant. Secondary outcomes were ED length of stay, adverse effects, return visits in 7 or 30 days, and the incidence of stroke or death in 30 days. In all categories, both CCBs and beta blockers were essentially equal.


What do these studies tell us?

The studies by Fromm et al and by Demircan et all are essentially the only two studies published which compare diltiazem and metoprolol directly in an emergency room population. The first of these studies (Demircan) noted that diltiazem was slightly better than metoprolol in achieving a target heart rate while the most recent study by Fromm noted that diltiazem was significantly better than metoprolol. Of note, Fromm did use a higher maximum dose of diltiazem (30mg vs 25mg). Both studies did an adequate job of excluding patients with other conditions which caused the afib with RVR. The third study compared the broad group of CCBs vs beta blockers and concluded there was no difference, but it does not specify which medications were used and it’s primary end point was not heart rate but whether or not a patient was admitted to the hospital. So what should you do in the emergency room? In patients who present with Afib with RVR with no other underlying condition like infection, ingestion, STEMI, it appears diltiazem is more effective than metoprolol in achieving rate control. However, if there is an underlying condition like sepsis, there is currently no published data about what agent should be given.



What about using both?

If a patient is given 2 doses of metoprolol without resolution of rapid ventricular response, the instinct is to give diltiazem to try and achieve better rate control. However, there is a theoretical risk of causing the patient to go into complete heart block if this is done. There are no published case reports of this happening, so the risk is purely theoretical, but the administration of both medications should be avoided.

Demircan C, Cikriklar HI, Engindeniz Z, et al. Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation. Emerg Med J 2005;22(6):411-4. Erratum in: Emerg Med J 2005;22(10):758.  PubMed PMID: 15911947.


Scheuermeyer FX, Grafstein E, Stenstrom R, et al. Safety and efficiency of calcium channel blockers versus beta-blockers for rate control in patients with atrial fibrillation and no acute  underlying medical illness. Acad Emerg Med 2013;20(3):222-30. PubMed PMID: 23517253.


Fromm C, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med. 2015 Apr 22. [Epub ahead of print]