The New, Improved, ACEP Clinical Policy for tPA in Stroke

Released with minimal fanfare, approved by the ACEP Board of Directors on June 24th, the revised ACEP Clinical Policy regarding the use of TPA for acute ischemic stroke has gone final.

It is, of course, a vast improvement over the 2012 version – but has, unfortunately, changed for the worse since the draft was posted.

The highlights:

  • The Level A suggestion to consider the risk of ICH with tPA administration has been eliminated.  It has been moved, nonsensically into the Level B recommendations for offering tPA – when, frankly, it’s the only consistent finding across all the evidence.
  • The Level B recommendation in which tPA “may be given” within 3 hours has been strengthened to “should be offered and may be given”.  Obviously, a profound difference.
  • The Level B recommendation for 3-4.5 hours remains unchanged, based on only one flawed piece of Class II evidence (ECASS III), and conflicting Class III evidence (ATLANTIS, IST-3, meta-analyses).
  • The Level C recommendation to engage in shared decision-making now states “when feasible”, which is obviously open to interpretation.
  • No further clarification of “carefully selected patients” or “systems … in place to safely administer the medication” is provided.

Some wins, some losses.  Obviously, the shared decision-making supporting any “offer” of tPA can be very different, depending on an individual clinicians’ interpretation of the evidence – and it is nice to see the prior COI-infested husk of rotten guidelines finally, officially, tossed on the compost heap.  Let us hope (irrationally, of course) the efforts underway in the United Kingdom spur further, independent, investigation with which to better understand and individualize the risks and benefits of treatment with tPA.

“Clinical Policy: Use of Intravenous Tissue Plasminogen Activator for the Management of Acute Ischemic Stroke in the Emergency Department”
http://www.acep.org/workarea/DownloadAsset.aspx?id=102373

A Male in his 40’s with Decreasing Chest pain – what do you think?

A male in his 40s presented with decreasing chest pain.  Here was his first ECG:
There is sinus rhythm.
The QTc is 379 ms.
There is ST elevation in V2-V4 that does not meet STEMI "criteria" of at least 1 mm in 2 or more leads (except V2 and V3, which require 2.0 mm of more for men over age 40).

So it looks like early repolarization. 





The clinicians used the subtleSTEMI formula (sidebar excel applet).  I am not sure exactly what numbers they used, but they told me the value they arrived at was 21.2.

Let's examine that:
The computerized QTc was 379 ms.
The R-wave amplitude in lead V4 is from 11-14 mm, depending on the complex used.
Here is a magnification of V3 in order to measure ST elevation at 60 ms after the J-point in lead V3:
The black arrow shows the J-point.  The red arrow is at 60 ms (1.5 small boxes) after the J-point.  The lower edge of the upper green line is where one should measure from.  The upper edge of the lower green line is at the PQ junction.  The distance between these two is 4 mm.  Some might say 3.5 mm


If we put these values into the formula, we get 6 different values depending on the measurements:

                                   RAV4 = 11 (min)                     RAV4 = 12.5 (avg)                  RAV4 = 14 (max)
_________________________________________________________________________________
STE = 3.5 mm                   22.96                                       22.5                                             22.0

STE = 4.0 mm                   23.56                                       23.1                                             22.6


Only one value is very specific for LAD occlusion (23.56, greater than 23.4)

All the rest are greater than 22.0, above which one should definitely be worried and get serial ECGs.

So a second ECG was recorded 12 minutes later:
QTc is now 383 ms.  STE 60 V3 = 3.5 mm.  RAV4 = 11-12 mm.

Formula value is now slightly lower.

These two ECGS are significantly different, but it was not noticed the treating physicians.

Look at the ECGs side by side.  And remember the pain is waning.
The first is on the left, the follow up is on the right.
The T-wave amplitude in V3 is 10 mm on the earlier and only 7 mm on the later one.

This makes it almost certain that the ST elevation on the first one is due to ischemia.

Although the clinicians were uncertain and obtained a very low formula value for both, they were worried about the patients symptoms and appropriately activated the cath lab.

The angiogram showed a 99% thrombotic occlusion with TIMI-II flow (enough coronary flow to prevent outright ST elevation).

It is probable that the artery was fully occluded at the time of maximal chest pain.

Learning Points:
1. Hyperacute T-waves diminish in size as the artery reperfuses
2. The formula is more likely to be falsely negative when there is a reperfusing artery.
3. A value less than 23.4 but still greater than 22.0 may still be due to LAD occlusion or near-occlusion.
4.  Serial ECGs are critical but they must be scrutinized for changes, which may be very subtle (see below).


Here is another case in which the T-wave subtly diminishes as the LAD spontaneously opens and pain diminishes (the first 4 are prehospital ECGs):



A Male in his 40’s with Decreasing Chest pain – what do you think?

A male in his 40s presented with decreasing chest pain.  Here was his first ECG:
There is sinus rhythm.
The QTc is 379 ms.
There is ST elevation in V2-V4 that does not meet STEMI "criteria" of at least 1 mm in 2 or more leads (except V2 and V3, which require 2.0 mm of more for men over age 40).

So it looks like early repolarization. 





The clinicians used the subtleSTEMI formula (sidebar excel applet).  I am not sure exactly what numbers they used, but they told me the value they arrived at was 21.2.

Let's examine that:
The computerized QTc was 379 ms.
The R-wave amplitude in lead V4 is from 11-14 mm, depending on the complex used.
Here is a magnification of V3 in order to measure ST elevation at 60 ms after the J-point in lead V3:
The black arrow shows the J-point.  The red arrow is at 60 ms (1.5 small boxes) after the J-point.  The lower edge of the upper green line is where one should measure from.  The upper edge of the lower green line is at the PQ junction.  The distance between these two is 4 mm.  Some might say 3.5 mm


If we put these values into the formula, we get 6 different values depending on the measurements:

                                   RAV4 = 11 (min)                     RAV4 = 12.5 (avg)                  RAV4 = 14 (max)
_________________________________________________________________________________
STE = 3.5 mm                   22.96                                       22.5                                             22.0

STE = 4.0 mm                   23.56                                       23.1                                             22.6


Only one value is very specific for LAD occlusion (23.56, greater than 23.4)

All the rest are greater than 22.0, above which one should definitely be worried and get serial ECGs.

So a second ECG was recorded 12 minutes later:
QTc is now 383 ms.  STE 60 V3 = 3.5 mm.  RAV4 = 11-12 mm.

Formula value is now slightly lower.

These two ECGS are significantly different, but it was not noticed the treating physicians.

Look at the ECGs side by side.  And remember the pain is waning.
The first is on the left, the follow up is on the right.
The T-wave amplitude in V3 is 10 mm on the earlier and only 7 mm on the later one.

This makes it almost certain that the ST elevation on the first one is due to ischemia.

Although the clinicians were uncertain and obtained a very low formula value for both, they were worried about the patients symptoms and appropriately activated the cath lab.

The angiogram showed a 99% thrombotic occlusion with TIMI-II flow (enough coronary flow to prevent outright ST elevation).

It is probable that the artery was fully occluded at the time of maximal chest pain.

Learning Points:
1. Hyperacute T-waves diminish in size as the artery reperfuses
2. The formula is more likely to be falsely negative when there is a reperfusing artery.
3. A value less than 23.4 but still greater than 22.0 may still be due to LAD occlusion or near-occlusion.
4.  Serial ECGs are critical but they must be scrutinized for changes, which may be very subtle (see below).


Here is another case in which the T-wave subtly diminishes as the LAD spontaneously opens and pain diminishes (the first 4 are prehospital ECGs):



Effects of prehospital epinephrine administration on neurological outcomes in patients with out-of-hospital cardiac arrest

20130801-060427.jpg

Just released online a retrospective study of prehospital epinephrine/adrenaline on neurologic outcomes in OHCA! Showing benefit in sub group with CPR 15-19 min duration

Read and decide for yourself!

Effects of prehospital epinephrine administration on neurological outcomes in patients with out-of-hospital cardiac arrest

Editor’s opinion: I have always believed epinephrine has a role in cardiac arrest. This study indicates that for short cardiac arrest times it adds little to outcomes which makes sense considering the other resuscitation evidence. It also indicates the longer the arrest time the worse outcomes. Once again totally logical. What it adds is more evidence refuting past studies that neurologic outcomes improve if shorter arrest times and improved ROSC. This is very logical to me.


Filed under: cardiac arrest, Prehospital medicine Tagged: adrenaline, cardiac-arrest, epinephrine, prehospital

59 Year Old Male: Unwell

It’s the middle of the afternoon when you are dispatched to the residence of a 59 year old male with a chief complaint of general illness.

When you arrive on scene you encounter a middle-aged man in obvious distressed lying on a couch. He is pale, gray, diaphoretic, and drowsy. He states that he has felt drained for the past 8 hrs; unable to catch his breath or get up off the couch with a heavy sensation in his chest. 30 minutes prior to your arrival he vomited and felt like he was going to pass-out so he decided to call 911.

His radial pulse is faint, rapid, and irregular while his skin cold and moist.

  • HR – 150 bpm, irregular
  • SpO2 – Unable to get a clear waveform
  • BP – 72/42 mmHg
  • RR – 26. labored
  • Temp – 36.6 C (97.9 F)

Breath sounds reveal crackles bilaterally.

Multiple 12-lead ECG’s are performed but suboptimal due to the patient’s increased work of breathing and inability to stay still. This is the best of the bunch:

Initial 12-Lead

BGL is 156 mg/dL.

He is a bit lethargic but properly oriented and answers questions appropriately, albeit slowly.

  • S – As above
  • A – No known drug allergies
  • M – None
  • P – Appendectomy @ 24yo
  • L – Soup 45 min prior, which he vomited soon after
  • E – Can’t recall—states he has felt terrible “all day.”

Regarding the chest heaviness…

  • O – Gradually through the morning
  • P – Nothing makes it better or worse
  • Q – Heaviness
  • R – None
  • S – Unable to quantify
  • T – Worsening x 8 hrs

What are your management priorities for this patient?

What is your interpretation of the ECG?

 

 ***UPDATE (2015/6/29/ 14:00 EDT)***

After carefully transferring the patient to the ambulance and finding him a position of comfort (head-of-bed at 60 degrees—he doesn’t like to lie flat), you succeed in obtaining a cleaner EKG. Does this change your approach to the case?

02 - 12-Lead 02