The ICU Bounce Back

We’ve all experienced it. A seriously injured trauma patient is admitted to the ICU and begins the process of recovery. Everything looks well, and after a few days they’re transferred to a ward bed. But then they languish, never really doing what we expect. Finally (and usually in the middle of the night), they begin to look bad enough where we have to transfer them back to the ICU. Before or after the call to the Rapid Response Team. Yes, it’s the feared “unexpected readmission to ICU.”

What’s the problem here? A failure of the ICU team? Did they send the patient out too soon? Did we all miss something about the patient? And is there any way we can avoid this problem? The major issue is that these “bounce backs” tend to do poorly compared to patients who successfully stay in their ward bed. Estimates are that mortality for patients successfully and finally discharged from the ICU range from 4-8%, whereas the mortality in bounce back patients is 20-40%!

Researchers at the Medical University of South Carolina in Charleston looked at the characteristics that defined the bounce back patient. They reviewed nearly 2000 patients discharged from their trauma ICU and analyzed the variables that predicted an unplanned bounce back. They noted the following interesting factoids:

  • More than two thirds of bounce backs occurred within 3 days
  • Males, patients with an initial GCS < 9, transfer during the day shift  were the major risk factors
  • More comorbidities was associated with a higher chance of bounce back
  • Mortality in the bounce back group was 20%
  • The most common immediate factors causing bounce back were respiratory failure or bleeding

Bottom line: This is an intriguing single-institution study that supports my own personal observations. Fewer bounce backs occur at night because staffing tends to be lower and there is more resistance to transfers out of the ICU then. Both the ICU team and the ward team need to scrutinize every transfer carefully. Significant head injury or the presence of medical comorbidities should trigger a careful assessment to make sure that the transfer is appropriate. Otherwise, your patient may be placed in unnecessary jeopardy.

Next, I’ll discuss when an unexpected return to ICU is not an unexpected return!

Reference: Intensive care unit bounce back in trauma patients: An analysis of unplanned returns to the intensive care unit. J Trauma 74(6):1528-1533, 2013.


What is this rhythm?

Unfortunately, I remember who sent this EKG to me, or the clinical information, but it is a very interesting tracing.

What is it?

Below is an annotated version:

There is isorhythmic dissociation (see below), with escape beats in complexes 1-4 and 9-14.  In beat 4, you can see a bit of a P-wave, and then 5 thru 8 have sinus rhythm.

Aside: "Isorhythmic dissociation:" the P-wave just happens to arrive at the same time as the escape beat, so that the P-wave and QRS are dissociated even though they are happening about the same time ("isorhythmic").   ........AV Dissociation does not always mean AV Block!! There can be dissociation without block, as here.  See more posts below.

Whenever the beat is fully sinus, the QRS is normal.

Whenever it is an escape beat, the QRS has a tall R-wave, along with an inferior and right axis, similar to a left posterior fascicular block (LPFB).  

But since there is no LPFB in sinus rhythm, the escape cannot be coming from the AV node; if it were, the QRS would not be different.  [The QRS in sinus rhythm and junctional rhythm are the same, because sinus rhythm goes through the AV node.]

The escape must be originating from a more inferior location that activates the left anterior fascicle preferentially, thus mimicking an LPFB.  

1. This confused me, because any beat that initiates in the left anterior fascicle should also have a RBBB morphology, which is not present here.

2. Also: why does the sinus rhythm come and go?

I asked my very smart friends Ken Grauer and Christopher Watford for their opinions.

Ken gave this great explanation, also referring to insights by Christopher:

"It’s a beautiful example of AV dissociation beginning with beat #4 where the P wave comes right at the onset of the QRS. There is underlying marked sinus arrhythmia with accelerated idioventricular rhythm (AIVR) at a rate of ~80/minute (arising from a septal focus) — such that when the sinus rate is faster (beats #5-thru-8), we have sinus rhythm — and when we have slight slowing of the sinus arrhythmia rate to below ~80/minute — then the accelerated septal focus takes over (beginning with beat #9). Note the sinus P wave peaking back again at the end of the tracing (at the onset of beat #14). So, the mechanism for AV dissociation here is a combination of “default” (when the sinus rate slows to below 80/minute) + “usurpation” (due to the slightly accelerated ventricular septal focus.

"The QRS morphology as Steve and Christopher have described is fairly narrow with left posterior hemiblock (LPHB) morphology, but lacking the RBBB characteristic that is usually seen in V1 with the more typical fascicular ventricular tachycardias...... I imagine, depending on where in the septal the focus is, that you might get a hemiblock pattern with narrow QRS and no RBBB (as we see here)."

Here are more posts on AV dissociation and AV block

AV Dissociation Lecture by K. Wang (28 minutes)

A Mystery Rhythm, Explained by K. Wang's Ladder Diagram.

Atrial Flutter. What else?? (AV dissociation with block)