Episode 14: Unstable Atrial Fibrillation Patient and Cardiac Ablation Complications

Welcome to the emDOCs.net podcast with Brit Long, MD (@long_brit) and Manpreet Singh, MD (@MprizzleER)! Join us as we review our high-yield posts from our website emDOCs.net.

  Today on the emDocs cast with Brit Long, MD (@long_brit) and Manpreet Singh, MD (@MprizzleER) we cover two posts: unstable atrial fibrillation patient and cardiac ablation complications. 

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Transcript

Brit: Welcome to the emDocs.net podcast. I’m Brit Long, and I’m joined by Manny Singh. We look at two great pieces today on managing the unstable patient with atrial fibrillation and complications of cardiac ablation.

AF is really common, but af w/ rvr can cause some issues. 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.

 So manny, let’s talk about some pearls

Manny:

• 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 when you re-evaluate the patient. If they are still just as tachycardic and hypotensive after the primary intervention, the arrhythmia may be playing a role after all. If so, cautiously proceed with the steps we will discuss later.
• 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. In these cases, it’s easier to electrically cardiovert

Brit: Great points, let’s move on to management when you think the AF w/ RVR is the issue

• 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?

 Manny:

• Start 1st w/ controlling 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
  • Norepinephris is easily available and nurses are comfortable with it.

• Control Their Rate
  • Now that we have their blood pressure looking a bit better, it’s time to 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 two 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 a loading dose of 500 mcg/kg over 1 minute, and then start an infusion of 50 mcg/kg/min 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 is reached.
  • 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

 Brit:

• 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.

 Manny:

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





Brit:

-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.

Manny: Our next post is on complications of cardiac ablation.

Cardiac ablation has been a common procedure for complicated arrhythmia since the 1990s. For tachyarrhythmias such as supra ventricular tachycardias (SVT), atrial fibrillation, atrial flutter, and Wolff-Parkinson-White, ablation is often the next line treatment after failed medical management.1 During ablation, multiple catheters are passed through a vein or artery into the heart. The catheters include a mapping catheter to identify abnormal electrical activity and an ablation catheter to heat the abnormal pathway via radio frequency energy. The heated tissue, most often near the pulmonary veins, is then scarred in order to prevent the transmission of abnormal signals.

Ablation procedures have increased 138% over the past ten years (from 1,953 in 2006 to 4,648 in 2015) with the majority being for atrial fibrillation.2The overall complication rate of cardiac ablation has been shown to be 6.29%.4 Most common complications of procedure were cardiac (2.65%), vascular (1.33%), and neurological (1.05%). 5 According one study, cardiac tamponade was the most common complication with a rate of 1.31%.3 The independent risk factors for complications included older age, complex procedures, female gender, and lower hospital volumes.6  Complication rates increased from 2.79% in the 18-44 year old age group to 6.58% in the > 75 year age group.7 Ablation for ventricular tachycardia had the highest complication rate at 9.9%, possibly due to majority of cases being nonelective (62%.)7The patient population with ventricular tachycardias also had the highest rate of comorbidities.7 White males were the highest population undergoing catheter ablation, however SVT ablation was highest in women.8

Brit:

Let’s focus on complications that we can’t miss in the Emergency Department…

Atrio-esophageal Fistula

Atrio-esophageal fistula (AEF) is a rare, yet deadly complication of cardiac ablation. In a study of 191,215 performed ablations, an esophageal perforation or fistula was reported in 31 patients.9 The average time to presentation is 19 days however can present up to 60 days later.9,10,45 One study showed an overall 1% risk where a total of four patients developed atrio-esophageal fistula.9 Three of the four had air emboli and neurologic deficits and were treated with esophageal resection. The other died from massive air embolism.11 Among the possible complications following an ablation, atrio-esophageal fistula has the second highest mortality rate after tamponade.5

As the esophagus descends into the mediastinum, it runs posteriorly to the left atrium and pulmonary veins. At some points, the esophagus is within millimeters of these structures leading to potential thermal damage.12

Although the specific cause of esophageal injury and subsequent fistula formation is unknown, direct thermal injury, ischemic injury through thermal occlusion of end- arterioles, acid reflux, and infection from the lumen are through to be mechanisms.13 Esophageal ulcers are a fairly common complication of ablations with one study showing a rate of 17%.14 Ulcers are thought to be the precipitating event to fistulization. Deneke et al assessed over 800 patients undergoing cardiac ablation with endoscopy four days after the procedure; 82% of patients had no esophageal abnormalities.15 Of the patients with esophageal findings, two thirds had only erythema and no ulcer. The five documented esophageal perforations occurred in patients with documents ulcerations.15 The progression to fistula likely initiates from the esophagus to the left atria and forms a one-way valve with the left atria. The isolated opening into the atria allows for spillage from the esophagus. Proximity of left atria and esophagus shown below in Figure 1.

With contamination of the left atria, the clinical presentation may resemble endocarditis with septic emboli.38  Patients may present with a sepsis-like picture or with neurologic sequelae. Presentation may be less obvious at the beginning stages of formation and include chest discomfort, nausea, vomiting, dysphagia, hematemesis, and melena. In a review of 53 cases of atrio-esophageal fistula after ablation, the most common presenting symptoms were fever (n=44), neurological deficits (n=27), and hematemesis (n= 19.)16 The bacteria allowed in through the one-way valve leads to bacteremia and air allowed in leads to stroke.

If atrio-esophageal fistula is on your differential, prompt diagnosis is needed as patient’s can quickly decompensate. White blood cell count should be obtained as it is an early and sensitive marker of fistula being present in all patients at presentation.17 Order blood cultures, lactic acid, as well as complete blood count, complete metabolic panel, and lactic acid. Blood cultures from  CT chest with IV contrast has shown to be most diagnostic with up to 98% (n = 95 of 98) of scans being abnormal.45 The most common findings are pneumomediastinum and pneumopericardium.18  In a study of five patients with fistula, CT detected free air in all five: in mediastinum in 3, the pericardium in 1, and left atrium in 1.39  Avoid EGD, as insufflation of balloon could lead to air emboli and thus stroke and death. Contrast will aid in observing the fistula tract. Out of 53 documented cases in a review, 27 of the fistulas were found using CT of the chest.16 When looking at the scan, keep an eye out for air or contrast extravasation from the esophagus as seen in image below (Figure 2).

Without emergent surgical treatment, mortality is 100%.19 Patients will need two large bore IVs and will be best served in a critical room. AEF often show Gram positive organisms; broad spectrum antibiotics including vancomycinshould be promptly started in these patients. Avoid esophageal manipulation including Nasogastric tube. Once diagnosis is made or suspected, emergent cardiothoracic surgery consult is needed. The surgical management options include esophageal stents and primary esophageal repair. In a retrospective cohort analysis of 29 patients, 100% of esophageal stent patients died versus 41% of primary repair patients.20

Manny:

Delayed Cardiac Tamponade

Delayed cardiac tamponade is a rare, yet deadly complication. Cardiac tamponade is a known complication of cardiac ablation, however emergency medicine physicians must keep delayed presentation on the differential for post ablation patients. In one meta-analysis, 45 out of 27,921 ablation cases resulted in delayed cardiac tamponade.22 The average number of days to presentation post procedure was 12.

During ablation procedures, tamponade is caused by mechanical trauma to the myocardium via heat, most often during linear atrial ablation and higher frequency power.23 Most common presenting symptoms were chest pain, edema, shortness of breath, feelings of doom.24  Surprisingly, only 13% of the forty-five presented with hypotension and shock. 85% presented to Emergency Department for initial care.22  Patients may also present with the classic “Beck Triad” of hypotension, jugular venous distension, and distant heart sounds, however lack of these findings does not rule out tamponade. The hallmark of cardiac tamponade is pulsus paradoxus where systolic arterial pressure drops greater than 10 mmHg during inspiration.40  Obtaining an EKG may show decreased QRS voltage globally or electrical alternans, where there is an alternating QRS amplitude or axis.42

Cardiac tamponade can be quickly assessed at bedside with point of care ultrasonography. There is a great link to a prior emDocs ultrasound post on pericardial tamponade on common findings you can look for.

Isotonic fluids should be started in order to increase cardiac output.41 If needed, dobutamine is the inotrope of choice for hypotension.43 Pericardiocentesis must be performed emergently in setting of cardiac tamponade physiology. Cardiology should be consulted as patients may need further intervention such as pericardial window in the cath lab.

 Brit:

Stroke

Thrombo-embolic event leading to cerebral ischemia is a common side effect of ablation for atrial fibrillation. The overall risk of cerebrovascular event ranges from 0.2% and 0.94%.28 Post cardiac ablation patients are at risk for cerebrovascular event up to two weeks post procedure. 29

Thrombi can form secondary to direct trauma, increased turbulence from sheath introduction, or heat from the catheter tip.13  Conversely, the introduction of air from the catheter tip is the most common cause of air embolism.30 A left atrial size >4.5 cm is also associated with higher risk of thrombus formation.28

According to the 2017 Consensus Statement on Atrial Fibrillation Ablation, anticoagulation with warfarin or other NOAC should continue for at least two months after procedure.31

Patients with cerebral thrombo-embolic events will present with neurological deficits. Recent cardiac ablation is not a definitive contraindication to TPA.28  Air embolism can present as altered mental status, seizure, or focal neurological deficits. As previously discussed, air atrio-esophageal fistula can present with air embolism and will need to be ruled out. Treatment is supportive with supplemental oxygen, fluids, and placing patient in head down position.32Treatment with hyperbaric oxygen therapy may also prevent further endothelial damage in initiated within a few hours.33

 Manny:

Atypical Migraines 

For unknown reasons, transseptal catheterization during ablation may lead to new onset migraines.  In one study, out of 2,069 patients undergoing ablation, 1.1% had new onset migraines.34 Interestingly, patients that had therapeutic levels of warfarin anticoagulation during peri-procedure period had less migraines.35 There is also an association with isolated visual auras described as a scintillating scotoma.  These symptoms usually resolve after one month post procedure.36

The most important task in these patients for emergency medicine physicians is to rule out stroke. Once CVA has been ruled out, the patient will need outpatient referral to neuro ophthalmologist.

Brit:

• The overall complication rate for cardiac ablation is 6.29%.
• Atrio-esophageal fistula has up to a 100% mortality without surgery. If considered, emergently consult cardiothoracic surgery.
• EGD may cause fatal massive air embolism in the setting of atrio-esophageal fistula. Avoid even in the case of gross hematemesis.
• Delayed cardiac tamponade may occur even up to several weeks out from the ablation.
• Stroke due to thromboembolic event 
• Atypical migraine is a rare post ablation complication and should be considered a diagnosis of exclusion.

Manny: That rounds out our summary of this great post on AFib w/ RVR and post-ablation procedures. Thanks for joining us on the podcast, and stay tuned for our next episode. Feel free to comment on our site and let us know if you have any feedback. Stay safe and healthy everyone!