Let's have a talk about A fib and sepsis.

Have you seen severe sepsis patients in new-onset A-fib?

  • Yup.

    Votes: 2 22.2%

  • Nope.

    Votes: 1 11.1%

  • Not sure if it was new onset, but they were in a-fib.

    Votes: 6 66.7%
  • Total voters
    9
D

Doczilla

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Hey guys, I normally lurk on here and chime in when I can, but I'm really interested in seeing what you guys have seen in your septic patients.

A good chunk of severe sepsis patients I have are in new-onset a-fib. More often than not, emergency rooms seem to be baffled at this information, and spend a good amount of time in denial that their shiny new arrhythmia is truly new-onset.

I would like to open this up in a two-fold manner: let me know what you've personally seen in your septic patients, and secondly, let's discuss the relationship between sepsis and new-onset a-fib. Before I give my two cents on it, I'd like to see what the prevailing mentality is on it.
 
We are all used to seeing it primarily in volume overloaded non-compliant heart failure patients, new onset from MI or post cardiac surgery etc.

Depending how septic the patient and what their other comorbidities are, it does makes sense! You have systemic inflammatory processes, electrolyte abnormalities, hypoperfusion (including cardiac), low preload (yes usually it is too much preload). In fact, the more severe the sepsis, the more likely they are to have afib! I think I have see it in over 1/4 of the septic shock patients I've treated. It is more likely if they have CAD or some other issue in their history.

Other thoughts for you to ponder:
Sepsis patients are prone to coagulopathy all the way up to DIC. Adding afib to the mix is a concern!

How important is the "atrial kick" to the CO of these patients?

How do you manage afib in a hypotensive tachycardic septic patient?

How can you reliably determine adequate preload in an new-onset afib sepsis patient?
 
For any tachycardia I ask myself whether the symptoms are the result of the tachycardia or whether the tachycardia is the result of an underlying problem (a compensatory tachycardia). For example, if you have a patient in acute pulmonary edema and the monitor shows atrial fibrillation with rapid ventricular response, it seems reasonable to me to treat the acute pulmonary edema and then re-assess the tachycardia. Often the rate will slow down on its own once the breathing problem is under control so there's no need to lead off with diltiazem or a beta blocker. I am less concerned with whether or not the atrial fibrillation is "new onset". A brief review of the literature suggests it's a marker of worse outcomes, and someone is going to have to manage the atrial fibrillation, including consideration of anticoagulation and whatever underlying cardiac disease predisposes the patient to atrial fibrillation, but it seems to me a distraction from what's going to kill the patient right now, which is sepsis. I would not jump to rate control or cardioversion.
 
I'll play.

Summit said:
How important is the "atrial kick" to the CO of these patients?
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Being that they're ready behind the eight ball due to the third spacing, vasoactive substance release, and toxins worsening both of these, not to mention the acid/base disturbances and electrolyte derangement, I'd say they need all the atrial kick they can get.

Summit said:
How do you manage afib in a hypotensive tachycardic septic patient?
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New onset? You manage the A fib by treating the sepsis. Just like you manage the DIC by treating the sepsis. Mind you, this isn't all encompassing, and there may be exceptions--- but generally speaking, you really wanna avoid any drugs that will worsen their cardiac output just to make the monitor look pretty.

Hit them with repeated 20-30ml/kg isotonic fluid challenges. I don't care if they have wet lungs, as this is probably ARDS or a primary/secondary pneumonia. Most of these patients need upwards of 8 liters of fluids within the first day.

Summit said:
How can you reliably determine adequate preload in an new-onset afib sepsis patient?
Click to expand...

I'm not sure about targeting preload, but the most important rescuscitative endpoints that are related to preload would be:

-Maintain a MAP of >65, even if you have to add pressors after a few liters of fluid
- Maintain a urine output of 40ml/hr.

The others are guided by labs, and the specific cause of the sepsis.
 
Doczilla said:
Hit them with repeated 20-30ml/kg isotonic fluid challenges. I don't care if they have wet lungs, as this is probably ARDS or a primary/secondary pneumonia. Most of these patients need upwards of 8 liters of fluids within the first day.
Click to expand...

By current trends, that might be a bit too wet.
 
Doczilla said:
I suppose it would all depend on how they meet their endpoints, primarily urine output.
Click to expand...

Right, but nowadays we tend to go to pressors earlier. Fluid isn't benign.
 
Brandon O said:
Right, but nowadays we tend to go to pressors earlier. Fluid isn't benign.
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Yeah, I gotcha, but you're addressing two pathologies here, a) the leaky bucket, and b) the uncontrolled, sustained release of nitric oxide (for one), which they have found is specifically addressed with vasopressin (probably in conjunction with norepi).

So yeah, I don't think anyone was all about fluids in lieu of other therapies; it's just that they're literally not going to stop leaking fluids into the interstitium until the underlying cause is addressed. So yeah, people have required TONS of fluids while admitted as they try to fight that uphill battle.
 
Brandon O said:
Right, but nowadays we tend to go to pressors earlier. Fluid isn't benign.
Click to expand...

When I left the SICU a few years ago, they were managing septic patients with WAAAY less fluid than was previously the trend. Patients who would have gotten 3-4 liters off the bat and then at least 250/hr for hours were getting less than half that and pressors right away rather than waiting to "see how they do" with the IVF. And they were doing as well or better, as far as I could tell.

Sepsis management isn't something I've kept up with the literature on, but my understanding is that the old "goal-directed therapy" approach has been shown no more effective than essentially basic supportive care.

As far as managing new AF in a septic patient, I would think that the hemodynamics at the time would have to guide management. An esmolol infusion may be ideal for rate control?
 
Remi said:
When I left the SICU a few years ago, they were managing septic patients with WAAAY less fluid than was previously the trend. Patients who would have gotten 3-4 liters off the bat and then at least 250/hr for hours were getting less than half that and pressors right away rather than waiting to "see how they do" with the IVF. And they were doing as well or better, as far as I could tell.

Sepsis management isn't something I've kept up with the literature on, but my understanding is that the old "goal-directed therapy" approach has been shown no more effective than essentially basic supportive care.

As far as managing new AF in a septic patient, I would think that the hemodynamics at the time would have to guide management. An esmolol infusion may be ideal for rate control?
Click to expand...

I wonder if they've become better at treating sepsis in general, and they haven't needed the amount of fluids that they used to as a result?
 
Doczilla said:
I wonder if they've become better at treating sepsis in general, and they haven't needed the amount of fluids that they used to as a result?
Click to expand...

To my recollection, the only thing we were doing differently was giving less fluid and starting pressors earlier.
 
Interesting. I suppose it makes sense, since they're using the right drugs now. It's amazing how things change.
 
I would be very hesitant to cardiovert a-fib unless I see them go into the rythem, I usually treat it with fluids.

As far as fluid in sepsis goes, where I work we try to start low dose levo early, this is because they are venous dilatated so much that the first 2L are more just getting the CVP up, making the veins more rigid makes every liter count more
 
Brandon O said:
Right, but nowadays we tend to go to pressors earlier. Fluid isn't benign.
Click to expand...

The evidenced-based sepsis guidelines call for fluid at 30ml/kg. If the patient is still hypotensive then a vasopressor is indicated with first line being Levophed. I transfer these patient pretty frequently and just had one two days ago with pressure of 75/42, lactic acid of 7.1, bands 21% and WBC was 2. After 1900ml of NSS and Levophed (5mcg/min) pressure improved to 93-106/50s.

I have not seen a lot of atrial fibrillation in sepsis patients. If the patient does present with atrial fib there is usually a history of it.
 
18G said:
The evidenced-based sepsis guidelines call for fluid at 30ml/kg. If the patient is still hypotensive then a vasopressor is indicated with first line being Levophed.
Click to expand...

This is worth a bit of clarification. 30ml/kg describes the size of each bolus during fluid resuscitation, not the total volume. The concept would be to give repeated boluses of 30ml/kg (a couple liters in most adults) until you reach your endpoints of urine output, MAP, etc. If you fail to do so, you eventually transition to pressors instead.

When to make that transition... remains controversial. Theoretically you'd do it once you've fully replenished the venous volume (i.e. optimized preload) and more volume won't increase cardiac output any further. Used to be we used a lot of things like CVP (or even wedge pressures, going further back) to determine this, which most people are now unimpressed by. Many still like ultrasound of the IVC. There are some cardiac output monitors that use the arterial line or pulse ox pleth with varying degrees of success. All rather controversial.

So a lot of people just pick a number as their threshold. Maybe when you hit 4-6 liters, you start thinking about pressors. Or sooner. Or later.

It's easy to think of fluid as being pretty benign, but as I said, that's not the current trend. It clearly causes delayed problems such as pulmonary edema, abdominal compartment syndromes, etc, and there's a concept that it worsens injury to the vascular glycocalyx, increasing permeability.
 
We administer 30ml/kg boluses to make sure the patient has a minimum of 3 liters infused. We may infuse more but this is the starting point for fluid.
 
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