Strategies to Avoid Hypotension During Afib Rate Control


Rapid ventricular response in atrial fibrillation patients is a daily occurrence in the emergency department.

Rapid ventricular response in atrial fibrillation patients is a daily occurrence in the emergency department.

Rate control through atrioventricular node-blocking agents is a standard approach for stable patients, while good old electricity works for those who are unstable. But there is an in-between group that presents a different challenge: those with atrial fibrillation who are relatively hypotensive, meaning they have a systolic blood pressure in the 90s or low 100s.

In these patients, pharmacologic rate control may improve systolic blood pressure by slowing the ventricular rate sufficiently to allow for adequate filling, and thus improve cardiac output. However, this is almost always balanced with the risk of hypotension caused by drugs like diltiazem or metoprolol.

In order to avoid the initiation of amiodarone or digoxin—which are both notorious for their myriad of short-term adverse events, long-term toxicity, and clinically significant drug-drug interactions—there are certain strategies that seem to be overlooked. These include the use of low-dose diltiazem, extended bolus diltiazem, or esmolol. (Administration of calcium prior to the use of a calcium channel blocker is not generally regarded as effective.)

Traditional teachings of rate control with diltiazem point to doses starting at 0.25 mg/kg followed by 0.35 mg/kg if the first bolus is unsuccessful.

While these doses are certainly effective and associated with lower incidences of hypotension than verapamil, they may be less than ideal in every patient. Therefore, individualizing doses for patients in this relative hypotension range poses a potential advantage.

In one 2011 study, investigators randomized a population of patients presenting to the emergency department with atrial fibrillation with rapid ventricular response to low- (<0.2 mg/kg), standard- (>0.2 to <0.3 mg/kg), or high-dose diltiazem (>0.3 mg/kg) to achieve a positive clinical response, which was defined as a reduction in ventricular response rate to 100 bpm or at least 20% from baseline within 30 minutes.1 Safety was also assessed with regards to episodes of systolic blood pressure <90 mm Hg or reductions of at least 20% from baseline, respiratory failure requiring intubation, cardiac arrest, or onset of unstable rhythms that occurred within 30 minutes.

Patients who received low-dose diltiazem (0.14 mg/kg + 0.04) achieved a similar rate of overall clinical success (p=0.605), yet a lower incidence of overall complications (p=0.025) that was driven by a lower incidence of systolic blood pressure reductions by at least 20% between groups (low: 18.0%; standard: 33.7%; high 38.9%, p=0.047). However, these patients were normotensive at the time of administration of the study drug, which limited the ability to extrapolate to the relative hypotensive population in question.

Nevertheless, aside from scant case reports, there is virtually no evidence to go on. The authors concluded that this is a promising dosing alternative, but it is certainly not ready for widespread implementation.

A slightly different approach to diltiazem in this scenario is a bolus-from-the-bag approach that involves administering diltiazem 2.5 mg/min (maximum 50 minutes) until the desired heart rate is achieved. Although this was studied in supraventricular tachycardia, it seems to be a reasonable approach that maximizes the dose and limits hypotension by infusing the bolus much slower than what is normally done in the emergency department.2

Esmolol is on its way to become one of the new favorite drugs in emergency medicine, at least in my opinion.

Because of its relative “novelty” and association with high cost in its branded days, esmolol is often not thought of as a therapeutic option. In recent years, however, the drug has developed a following for its novel application in septic shock and refractory ventricular fibrillation.3,4

Nevertheless, esmolol is still underutilized in atrial fibrillation with rapid ventricular response, particularly in the relative hypotensive patient. Because of the drug’s rapid-on, rapid-off kinetics (onset in seconds with a half-life of about 9 minutes), it could be quickly shut off if hypotension were to occur.

Unfortunately, evidence for the use of esmolol is lacking in the relative hypotensive patient, let alone the emergency department, given that most research comes from postoperative settings with limited generalizability. However, the pharmacology/kinetics and lack of alternatives make esmolol a promising option.

Administering the bolus is critical for the effectiveness of esmolol. In my anecdotal experience, if 500 mcg/kg is recommended, it is perceived to be a high dose and avoided. Simply taking advantage of the metric system and recommending 0.5 mg/kg followed by the drip at 50 mcg/kg/min tends to be more successful.

There is no right answer when choosing a rate control strategy for the atrial fibrillation patient with rapid ventricular response and a systolic blood pressure in the 90s to low 100s who is not otherwise hemodynamically unstable. Most of the time, slowing the ventricular rate will improve the patient’s systolic blood pressure, but there may be an opportunity to use alternative dosing strategies for diltiazem or another drug altogether, such as esmolol.

Click here to read more about atrial fibrillation.


1. Lee J, et al. Low-dose diltiazem in atrial fibrillation with rapid ventricular response. Am J Emerg Med. 2011 Oct;29(8):849-854.

2. Lim SH, et al. Slow-infusion of calcium channel blockers in the emergency management of supraventricular tachycardia. Resuscitation. 2002 Feb;52(2):167-174.

3. Morelli A, et al. Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock: a randomized clinical trial. JAMA. 2013 Oct 23;310(16):1683-1691.

4. Driver BE, et al. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation. Resuscitation. 2014 Oct;85(10):1337-1341.

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