Unstable Atrial Fibrillation: A Guide to Management

Authors: Melodie Blackmon, DO (EM Resident, UT Health San Antonio) and Nurani Kester, MD (EM Attending, UT Health San Antonio) // Reviewed by: Skyler Lentz, MD (@skylerlentz); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case:

Your shift is almost over when you get a call from EMS: “We are coming at you with a 62-year-old female who is having palpitations and weakness. She’s pretty tachycardic in the 160’s, but our 12 lead isn’t working. I think it looks like sinus tach on the monitor. Her blood pressure is 90/62 mm Hg. We’ve got some fluids going and will be there in 5 minutes”.

In rolls your 62-year-old female with PMHx of HTN and DM. She is breathing rapidly and isn’t really answering your questions with more than a “yes/no”. She is pointing to her chest, and manages to get out that she feels dizzy. Her initial vitals are as follows: HR 173 bpm, BP 86/43 mm Hg, RR 18 bpm, O2 96% RA, T 98.4 F. You hook her up for a quick 12 lead EKG that shows the following.

Introduction

This article will focus on the management of atrial fibrillation in the hemodynamically unstable patient. Hemodynamic instability, as defined by the American Heart Association, includes systolic blood pressure < 90 mm Hg, altered mental status, cardiac ischemia, or severely decompensated heart failure due to the underlying rhythm.1 While these are good guidelines to keep in mind, remember that stability exists along a clinical spectrum. For example, you may have a young otherwise healthy patient with a systolic pressure of 85 mg Hg who is alert and texting on her phone, and next door a 65 year old female with a systolic pressure of 85 mm Hg who is diaphoretic, dizzy, and unable to communicate with you. One of these needs cardioversion, while the other likely does not.

 

Let’s Start With Some Pitfalls

  • It is easy to fall into the trap of seeing a hypotensive patient in a-fib with RVR and assume that the arrhythmia is the reason for the hemodynamic instability. While this may be the case, don’t forget that another underlying process may be causing the hypotension—the arrhythmia may be an innocent bystander. This can be particularly true if the patient has a known history of atrial fibrillation. Make sure to evaluate for other causes of shock. If another cause of shock is identified (ex: hypovolemia, hemorrhage, sepsis, PE, etc.), treat the underlying cause; treating the compensatory tachycardia may worsen the situation.2,3,4  One helpful tip is that if the HR is <150, the hypotension is likely caused by something other than the arrhythmia. If the HR is >150, the arrhythmia is more likely to be the culprit.2,5  Once the underlying cause is treated, their heart rate should decrease appropriately; don’t forget to re-evaluate. If they are still just as tachycardic and hypotensive after the primary intervention, they the arrhythmia may be playing a role after all. If so, cautiously proceed with the steps below.
  • Another very important point is to beware of Wolff Parkinson White! If your patient is in a-fib with a rate >250 and a wide QRS, think WPW. Don’t block the AV node, or you could send them in to V-fib.6

 

Back to our case: After a thorough history you have no reason to suspect any other reasons for the patient to be hypotensive, and based on the EKG you don’t think this is WPW.

 

Management

  • Cardioversion: Bring on the Lightning!

    • Synchronized cardioversion: this is the step that most of us probably reflexively think of when we hear “unstable A-fib”. Let’s start by talking about pad placement. There are studies comparing the anterior-lateral vs. anterior-posterior pad placement for cardioversion, and the results are conflicting. Some studies suggest there is no difference, while others show a higher chance of success when using the anterior-posterior placement.7,8,9 For this reason, many experts advocate for the anterior-posterior pad placement.
    • If you have time to sedate before delivering the shock, it’s a good idea to do so; your patient will thank you! Etomidate is a good option, as it is short acting, and won’t tank their blood pressure. Ketamine is another great drug to consider that won’t drop their blood pressure. One downside to Ketamine is that it is longer acting than Etomidate. Assessing mental status is very important in hemodynamically unstable patients, and with Ketamine, they will be sedated longer than they will with Etomidate.
      • Dose (Etomidate): Start with 0.1mg/kg IV; repeat if needed
      • Dose (Ketamine): Start with 0.5mg/kg IV; repeat if needed
    • Once the pads are on, charge up to 200J, synchronize and get ready to deliver a shock.1,10 It is often taught to start out low, and step the energy up as needed, but a recent study showed a higher first-time success rate when you start out high.10 Another thing to consider is placing some pressure on the pads using an old disconnected paddle. The goal of cardioversion is to deliver as much current to the myocardium as possible to cause depolarization. Transthoracic impedance (TTI) is the body’s resistance to the flow of current, and several studies have demonstrated that applying pressure to the pads decreases the TTI by improving electrical contact at the electrode skin interface, and reducing thoracic volume.11,12,13 This can be especially helpful in obese patients, as increased BMI has been associated with an increased TTI. It is thought that by decreasing TTI, you may have improved success with the cardioversion. The optimal amount of pressure for an adult is 8 kg.11,12  You can try cardioversion a few times, but unfortunately, a-fib can be refractory to electrical cardioversion.
    • At this point you may be wondering about anticoagulation. We are taught to anti-coagulate our patients before cardioverting them if their arrhythmia has been present for >48 hours, or the duration of the arrhythmia is unknown. While it is true that anticoagulation should happen before cardioverting stable patients, if your patient is unstable do not wait. Cardiovert first, but heparin should be started immediately after the patient is stabilized.1,2

 

Most of us know the textbook answer to “cardiovert” with our unstable patients in a-fib… but what about when that fails?

 

  • Control Their Blood Pressure

    • Ultimately, to control the BP you have to fix the heart rate, but your patient is already tanking. The drugs to control the rate will drop the blood pressure even more. For this reason, we need to temporarily stabilize the blood pressure. Phenylephrine is a good choice, because it will give you alpha-1 vasoconstriction, without stimulating the beta-receptors and raising the rate. In addition to giving their blood pressure a boost before giving them an AV-nodal blocker, raising their BP will allow the coronary arteries to fill better, which means better cardiac perfusion. A well-perfused heart will be more likely to be responsive to the medications given in the next steps.
      • Dose (push): 50-200 mcg q1-2 mins PRN (goal diastolic >60)
      • Dose (drip): 40-180 mcg/min, titrated to goal

 

  • Control Their Rate

    • Now that we have their blood pressure looking a bit better, it’s time to try and control that rate. In stable patients, we like to use a beta-blocker or calcium channel blocker. In the crashing patient, Amiodarone is a better choice because it doesn’t negatively affect the blood pressure as much as the previously mentioned medications.3,14
      • Dose: Give a 150 mg bolus (slow push or over 10 mins) -> 1 mg/min IV infusion.
      • Can re-dose 150 mg 2 additional times if the rate does not respond after 30-40 minutes.
    • Esmolol, a cardioselective beta-blocker, is another good option because of its quick “on/off properties”. It quickly takes effect, can be titrated to effect, and has a short half-life, which means we can turn it off and quickly have it out of their system if their blood pressure drops.15 One study recently done in ED patients showed that Esmolol had better rate control than Amiodarone, with similar effects on blood pressure.15
      • Dose: Bolus loading dose of 500 mcg/kg over 1 minute, -> 50 mcg/kg/min infusion for 4 minutes.
      • If the desired effect is not reached, may increase in 50 mcg/kg per minute increments until the max dose of 200 mcg/kg per minute.
    • If you do choose to use Diltiazem, don’t give a big push dose like we do for stable patients; instead, use a slow drip, or small frequent doses. Once you achieve the rate you want, you’ll need to either start a drip, or give an oral dose of Diltiazem to maintain lasting rate control.2,6 It is currently recommend to avoid the use of the non-dihydropyridine calcium channel blockers in patients with heart failure with reduced ejection fraction due to the negative inotropic effects (this is true for both the crashing and stable patient!).16,17
      • Dose (initial): 2.5 mg/min over 10-15 minutes 2 OR 5 mg doses every 1 minute.
      • Dose (once desired rate achieved): Drip at 5-15 mg/hr OR 30-60 mg PO. 2

 

  • Don’t Forget the ‘Lytes

    • If the patient is still not responding to your treatment, another tool in the box is Magnesium. Magnesium works synergistically with other AV nodal blockers to help slow the rate.18,19
      • Dose: 2-4 g over 10-15 minutes
    • A recent study suggests that maintaining serum potassium >3.8 is associated with increased rate of first-time success with cardioversion.20 Grab a VBG with electrolytes early, and if their K is low, replete.

 

  • Shock Them Again

    • If none of the above has worked, try cardioverting again. If they are not responsive by this point, there is a high likelihood something else is going on. Re-evaluate for other causes of their shock as discussed above, or underlying causes that may make their A-fib refractory to treatment. Consult cardiology if you still think this shock is due to the underlying arrhythmia.

 

Back to the Drawing Board: Broaden the Differential

As discussed, if you’ve gone through the entire management algorithm and are still unable to rate control your patient, there is a high likelihood that this is not “just a-fib”. Recall the “PIRATES” mnemonic for the etiology of a-fib and run through these causes to try and determine what else is going on. There are certain things, such as thyrotoxicosis, and severe electrolyte derangements that make a-fib refractory to treatment, and in these cases, you will need to treat the underlying cause first in order to get the arrhythmia under control.

 

Causes of Atrial Fibrillation: PIRATES

Take Home Points

-Don’t prematurely assume that the hypotension in your patient with a-fib is due to the arrhythmia. Do a thorough evaluation for other causes of shock before lowering the rate.

-When cardioverting your unstable patient with a-fib, do it right the first time; start out at 200J and consider adding external pressure to the anterior pad.

-Use push dose phenylephrine or a drip to stabilize the BP before trying to control the rate.

-Consider Amiodarone or Esmolol as the drug of choice for rate control in the crashing patient with a-fib.

 

References/Further Reading:

  1. Fuster V, Ryden L, Asinger R, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology. Circulation. 2001; 104(17): 2118-2150.
  2. Long B, Robertson J, Koyfman A, et al. Emergency medicine considerations in atrial fibrillation. The American Journal of Emergency Medicine. 2018; 36 (6): 1070-1078.
  3. Atzema C, Barrett T. Managing Atrial Fibrillation. Ann Emerg Med. 2015l 65(5): 532-539.
  4. Scheuermeyer F, Pourvali R, Rowe B, et al. Emergency department patients with atrial fibrillation or flutter and an acute underlying medical illness may not benefit from attempts to control rate or rhythm. Ann Emerg Med. 2015; 65(5): 511-522.
  5. Morgenstern J. Unstable Atrial Fibrillation: ED Management. First 10EM. https://first10em.com/atrial-fibrillation/. Accessed October 2019.
  6. Weingart S. The Crashing Atrial Fibrillation Patient. EMCrit RACC. https://emcrit.org/emcrit/crashing-a-fib/. Accessed October 2019.
  7. Kirkland S, Stiell I, AlShawabkeh T. The efficacy of pad placement for electrical cardioversion of atrial fibrillation/flutter: a systematic review. Acad Emerg Med. 2014; 21(7):717-726.
  8. Botto G, Politi A, Bonni W, et al. External cardioversion of atrial fibrillation: role of paddle position on technical efficacy and energy requirements. Heart. 1999; 82(6): 726-730.
  9. Kirchhof P, Eckardt L, Loh P, et al. Anterior-posterior versus anterior-lateral electrode positions for external cardioversion of atrial fibrillation: a randomized trial. The Lancet. 2002;360(9342): 1275-1279.
  10. Glover BM, Walsh SJ, McCann CJ, et al. Biphasic energy selection for transthoracic cardioversion of atrial fibrillation. The BEST AF Trial. Heart. 2008; 94(7):884-887.
  11. Deakin C, Sado D, Petley G, et al. Differential contribution of skin impedance and thoracic volume to transthoracic impedance during external defibrillation. Resuscitation. 2003; 60(2004): 171-174.
  12. Ramirez D, Fiset S, Cleland M, et al. Effect of Applying Force to Self Adhesive Electrodes on transthoracic Impedance: Implications for Electrical Cardioversion. Pacing and Clinical Electrophysiology. 2016; 39(10):1141-1147.
  13. Cohen J, Ibrahim B, Denier D, et al. Active Compression Cardioversion for Refractory Atrial Fibrillation. American Journal of Cardiology. 1997; 80 (3): 354-355.
  14. Bosch NA, Cimini BS, Walkey AJ. Atrial Fibrillation in the ICU. CHEST. 2018; 154(6):1424-1434.
  15. Kolia M, Beltramini A, Nagash M, et al. Esmolol Compared with Amiodarone in the Treatment of Recent-Onset Atrial Fibrillation (RAF): An Emergency Medicine External Validity Study. Journal of Emer Med. 2018; 56(3): 308-318.
  16. Kotecha D, Piccini J. Atrial fibrillation in heart failure: what should we do? Eur Heart J. 2015; 36(46):3250-3257.
  17. Kahn M, Ahmed F, Ludwig N, et al. Atrial fibrillation in heart failure: The sword of Damocles revisited. World J Cardiol. 2013; 5(7): 215-227.
  18. Bouida W, Beltajef K, Msolli MA, et al. Low-dose Magnesium Sulfate Versus High Dose in the Early Management of Rapid Atrial Fibrillation: Randomized Controlled Double-blind Study (LOMAGHI Study). Acad Emerg Med. 2019; 26(2): 183-191.
  19. Onalan O, Crystal E, Daoulah A, et al. Meta-analysis of magnesium therapy for the acute management of rapid atrial fibrillation. Am J Cardiolo. 2007; 15:99 (12): 1726-1732.
  20. Kyo M, Hosokawa K, Ohshimo S, et al. High serum potassium level is associated with successful electrical cardioversion for new-onset atrial fibrillation in the intensive care unit: A retrospective observational study. Anaesth Intensive Care. 2019; 47(1):52-59.

3 thoughts on “Unstable Atrial Fibrillation: A Guide to Management”

  1. Hi. Great review. My only disagreement is with using ketamine at 0.5mg/kg. This right in the middle of the sub dissociative dose range. Go with 1mg/kg IV. Yes, the duration of action is longer, but they will wake up with no memory of the event vs. waking up thinking they journeyed through hell.

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