Next week I’ll be re-certifying in Basic Life Support and in Advanced Cardiac Life Support. In addition to reviewing all the course materials before the courses, I like to review additional resources.
Dr. Justin Morganstern has written this outstanding post from First10EM:
Management of unstable atrial fibrillation in the emergency department: An approach to the initial management of the severely hypotensive atrial fibrillation patients December 7, 2015
Here is Dr. Morganstern’s post [I place it in my blog because it makes it easier for me to find the post and it helps me remember the subject matter].
You are finishing up your charts and getting ready to head home for the night, having already handed over to the night doc who is currently wrapped up with a moderately unwell trauma patient. The charge nurse asks you to just look at one patient who she thinks has SVT before you head home. You walk into the room and see a grey, diaphoretic man, who you later find out is 67 years old. The chart in your hand says that he has a history of hypertension and hyperlipidemia, but is otherwise healthy. The monitor reveals a heart rate of approximately 205, but it jumps around a lot from beat to beat, and a blood pressure of 86/43. He is satting 100%, but is on a nonrebreather. The ECG is narrow complex and irregularly irregular. His wife tells you this all started about 1 hour ago with complaints of dizziness and palpitations but no chest pain….
First question: Is the atrial fibrillation the cause of the problem, or just a symptom?
If the patient’s hypotension and tachycardia are due to sepsis or hemorrhage, controlling the rapid heart rate is not going to help. In fact, the rapid heart rate is probably necessary to maintain an adequate cardiac output. In these situations, the goal should be treating the underlying cause. However, it can be very difficult to determine whether rapid atrial fibrillation is the cause of, or the result of hypotension. The rule of thumb I have used is that if the rate is less than 150, hypotension is unlikely to be the result of atrial fibrillation, whereas if the rate is greater than 150, the arrhythmia is probably at least a component of the patient’s shock.
According to the ACLS guidelines, management is very straight-forward. The patient is unstable, so electrically cardiovert him. Unfortunately, cardioversion never seems to work in these really sick patients. However, I will always give cardioversion a shot first.
- Dose: Use full dose electricity on the first attempt (200 joules on my biphasic machine)
- Positioning: An anterior-posterior pad positioning is probably better than anterior-lateral
- Sedation: Sure, a little pain is better than death – but although your patients may not appreciate how sick they really are, they will certainly remember any pain you inflict. Some sedation and analgesia will be greatly appreciated. The choice of agent is difficult. Essentially all sedatives will drop your blood pressure, which could be catastrophic. Ketamine, my go to in many other scenarios, can increase heart rate and has a prolonged sedative effect, which is problematic when I am trying to assess ongoing shock and mental status. Therefore, etomidate is my first line agent for this patient, at a dose of 0.1mg/kg or approximately 7-10mg. A subdissociative dose of ketamine or a small dose of fentanyl may also be reasonable
- I will usually try 2 or 3 shocks in rapid sequence, but if the first is not successful, I have rarely seen success on a second or third
- Anticoagulation: If the onset of atrial fibrillation is unknown, or the patient is in permanent atrial fibrillation, the risk of stroke after cardioversion is increased. In the unstable patient, a rapid attempt at cardioversion is still warranted, but starting heparin as soon as possible afterwards is a good idea
Unfortunately, cardioversion rarely works in truly unstable atrial fibrillation. At this point, the key question is: Is this WPW* (Wolff-Parkinson-White syndrome)?
The main feature I watch for is bizarre appearing QRS complexes that change in width from beat to beat. Also, atrial fibrillation with a rate greater than 220-250 is not compatible with AV node conduction, but rather an accessory pathway.
For all other patients, the next step is to manage the hypotension:
Definitive therapy of hypotension requires correction of the arrhythmia. However, the patient is in shock and the rate control agents we need to use will worsen hypotension.
Management of hypotension almost always start with some fluids. With rapid atrial fibrillation resulting in cardiogenic shock, you have to be very careful of causing pulmonary edema. Also, there little reason to believe that this patient is significantly fluid depleted. However, the rate control agents are all vasodilatory, and therefore some fluid resuscitation may be helpful. I generally hang a small (500ml) normal saline bolus and reassess frequently.
The primary temporizing treatment of this patient’s hypotension will be a vasopressor. In general, I prefer controlled drips of pressors when I have the option. In this scenario, I want vasoconstriction with limited impact on heart rate (chronotropy). My go to agent would be norepinephrine, started at 5mcg/min and titrated to a diastolic blood pressure of 60.
However, we all know that starting drips in emergent situations can take much too long. In practice, my go to vasopressor is often going to be push dose phenylephrine:
Draw up 1ml of phenylephrine (10mg/ml) into a syringe
Inject the entire 1ml (or 10mg) into a 100ml bag of normal saline
You now have 10mg in a total of 100ml, or 100mcg/ml
Inject 0.5-2ml (50-200mcg) every 1-5minutes, as needed
Goal of diastolic blood pressure of ≥ 60
Don’t just read about it, watch Dr. Scott (Hollywood) Weingart show you how to mix push dose phenylephrine:
Once the blood pressure is temporized, it’s time to start the real treatment of this patient’s shock: getting control of the heart rate. The two options I would consider are diltiazem and amiodarone. (Some people would consider beta-blockers here, but I think there is ample evidence that calcium channel blockers are more effective at rapidly achieving rate control, which is exactly what I want here.) I actually don’t think there is much of a difference between amiodarone and diltiazem, but the cardiologists I work with always seem to prefer amiodarone. Personally, I think diltiazem does a better job of rapidly achieving rate control.
150mg IV bolus (slow IV push, or infused over 10 minutes), then 1mg/min IV infusion (for the first 6 hours – so hopefully someone has taken over by then)
I give this is one of two ways:
Diltiazem 25 mg in a minibag and slowly dripped in over about 10-15 minutes
Diltiazem 5-10mg (small doses) pushed by me every 1-2 minutes
After an appropriate heart rate is reached (for these very sick patients I am generally happy to get them to less than 130), I switch to either the conventional diltiazem drip at 5-15mg/hr or 30-60mg of PO diltiazem
There may be some value to giving IV calcium (1 or 2 grams of calcium gluconate) before starting the diltiazem to reduce the hypotensive effects of the medication
The atrial fibrillation still isn’t controlled – what now?
The good news is that unlike electrical cardioversion, rate control with diltiazem is almost always effective. If the patient remains unstable and you have not been able to control the heart rate, it is time to rapidly involve the expertise of a cardiologist. . . .Despite unstable atrial fibrillation being a relatively common problem, information on its management seems (at least based on my review) to be very sparse. Almost every textbook and guideline that I found just states that you should follow the ACLS protocol and electrically cardiovert patients that are unstable. I could not find a single textbook that explored what to do when cardioversion does not work, which seems to be the majority of the time. Understandably, there are also no clinical trials that cover these very sick patients. Therefore, most of the above it based on collated expert opinion and common sense. I cannot support this approach with evidence, but I don’t think that there is any evidence based approach to the dying rapid atrial fibrillation patient.
The most common alternate management strategy I have encountered focuses on just using fluid boluses to support the pressure while loading amiodarone. There is no evidence that vasopressors help patients, so I can’t argue, but I have a hard time not temporarily making the numbers better while I wait for rate control to occur. Maybe I am treating my own anxiety more than the patient?
Author Justin Morgenstern
Posted on December 7, 2015
Categories Cardiology, Front Page