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IC established!
We'll have several different sections reporting in - recent research, local topics, or highlighting areas of the Sponsor Hospital Council of Greater Bridgeport protocols.

*** Keep in mind - this website does not replace your protocols, and these posts do not reflect SHCGB or Bridgeport Hospital policies. This is a place to discuss research, controversies, or discuss possible future protocols. When in doubt, check your current protocols through the official source.

Saturday, April 6, 2013

When the STEMI disappears before you get to the ED!

So what do you do when your STEMI disappears? 

Spontaneous reperfusion (SR) is well-described in the cardiology literature. One moment you have a classic STEMI on the ECG, and the next you have nada. I wrote about just such a patient in a prior post. In that case, EMS had acquired this ECG in a patient with chest pain:

However, when her symptoms improved they ran a second ECG, and found:

This dramatic improvement suggests 2 questions. First, is this a good sign? Second, did the medics do anything (like oxygen, nitro, or aspirin) that could have caused the improvement?

Is this a good sign?
In a 2008 study (Spontaneous reperfusion in ST-elevation myocardial infarction: comparison of angiographic and electrocardiographic assessments.), finding ≥ 70% resolution of ST elevation on the ECG was a very good sign, and predicted a far lower rate of bad things - mortality and re-infarct rates were 0% as illustrated in this graph:

SR = Spontaneous reperfusion
Other studies have also shown that  resolution of the ST elevation before PCI is associated with patent vessels before PCI, after PCI, and better outcomes overall. The table below gives you the numbers. (TIMI 3 flow = normal blood flow in the coronary artery, 0 = complete occlusion)


Even if PCI was significantly delayed, the patients with SR in a 2008 study did very well. Only 8% of those patients had primary PCI (as opposed to 100% of the patients with persistent ST elevation. Again, check the graph:

A = PCI or lysis;  B = Primary PCI only
Onto the second question...
Do oxygen, aspirin, nitroglycerin, or morphine cause spontaneous reperfusion?
Hard to say. 

Although SR may occur in up to 15% of STEMIs, this isn't well-studied. One of the studies mentioned above (Relation of clinically defined spontaneous reperfusion to outcome in ST-elevation myocardial infarction) checked whether SR occured more often in patients who received aspirin or heparin from EMS or in the ED, and didn't find an association:

Dr Smith describes a STEMI case in which he felt that nitroglycerin had caused SR, and thus contributed to a delay in PCI. In his discussion he cites an abstract (copied below) from an EMS study, possibly the world's only clinical study on this topic. The brief version is that 6% of STEMI patients had partial or total SR in the period after NTG administration. Of course, it was retrospective, uncontrolled, etc. 

On top of that, it's hard to say if 6% is a high rate or not. Some researchers think the overall rate of SR in STEMI is about 15%, so 6% may actually be lower than expected.

As for oxygen, there's no evidence of any sort, good or bad.

The Bottom Line
Although a good number of patients have serial ECGs that show resolution of ST elevations, we don't exactly know why. Although these patients appear to be at lower risk of complication, it is hardly zero risk. When in doubt, get ECGs early and often.

Mahoney BD, Hildebrandt DA, Allegra P. 
Normalization of Diagnostic For STEMI Prehospital ECG with Nitroglycerin Therapy
Prehospital Emergency Care 2008;15:105, Abstract 24.
Hypothesis. The decision to take a patient for emergent reperfusion therapy is largely determined by an ECG diagnostic for ST Elevation Myocardial Infarction (STEMI). Hildebrandt et al have proven that  prehospital 12 Lead ECGs followed by an immediate call for reperfusion team mobilization reduce door to balloon times.We hypothesize that prehospital ECGs will normalize in some STEMI patients after  nitroglycerin (NTG)therapy or due to spontaneous reperfusion.  NTG therapy before an ECG, or the absence of a prehospital ECG capacity in some services may lead to missing the early diagnosis of STEMI thus delaying reperfusion therapy. 

Methods. A prospective analysis of consecutive adult patients  presenting to an urban/suburban two paramedic ambulance service fromJuly 15, 2006, to August 15, 2007, who have diagnostic ECGs for STEMI.  Paramedics managing a possible myocardial infarction patient were instructed to obtain rapidly an ECG prior to treatment with NTG. If the initial ECG was diagnostic for STEMI the paramedic called to mobilize the reperfusion team. A second ECG was done prior to arrival at the ED. The ECGs were later reviewed by emergency physicians and cardiologists who confirmed the presence of a diagnostic prehospital ECG and STEMI.  

Results. During the 13 month interval, 87 patients had an initial ECG that was diagnostic for STEMI. These patients received no NTG from the paramedics prior to obtaining the first ECG. An average of 16 minutes 42 seconds later, 3 patients had an ECG that was no longer diagnostic for STEMI and 3 had a partial normalization in their ECG that made diagnosis of STEMI more difficult. 

Conclusions. Prehospital ECGs diagnostic for STEMI can normalize or become nondiagnostic after NTG administration or due to spontaneous reperfusion or evolution. In the absence of a prehospital ECG, it is possible that 6 of 87 (7%) of STEMI patients in this study would have had reperfusion delayed due to a rapid change in their ECG. Limitations include no control group receiving NTG prior to the first ECG.

Wednesday, April 3, 2013

Hyperoxia during CPR associated with improved survival

There has been some great discussion on the web recently about the potential danger of hyperoxia. Mike McEvoy was interviewed on EMS 12-lead about the emergency and ICU evidence, and a vigorous discussion took place on EMTLIFE about the same topic. Rogue Medic weighed in as well, asking the question "How many hundreds of thousands of patient have we killed with oxygen and our refusal to require evidence of improved outcomes?" 

In the midst of this heated dialogue about reactive oxygen species, a recent study was published that may be an important addition to this discussion. 

The new paper
The study, "Increasing arterial oxygen partial pressure during cardiopulmonary resuscitation is associated with improved rates of hospital admission," was conducted in an Austrian EMS system. The ambulances are staffed with physicians, and are equipped with portable ABG analyzers as well. They retrospectively analyzed all non-trauma cardiac arrest calls over a 7-year span, and found 145 patients that had received ABG analysis of the PaO2 during the code. The ABGs were obtained after compressions, intubation, and 100% oxygen had been started. 

After dividing the patients into low, intermediate, and high levels of PaO2, they examined which patients had survived to hospital admission (HA), as well as the "cerebral performance category"(CPC) of the longer-term survivors. About half of the 145 cardiac arrest patients with an ABG had ROSC.

It turned out that patients with intermediate (61-300 mm Hg) or high (> 300 mm Hg) levels of PaO2 were incrementally more likely to survive to hospital admission. This positive association did not extend to showing a significant improvement in cerebral performance in survivors, however, despite a suggestive trend.

How does this fit with prior studies?
One retrospective study conducted in the ICU demonstrated an association between post-ROSC hyperoxia and increased mortality, while a similar trial showed no consistent association. No other trials have looked at pre-ROSC PaO2, however.

The accompanying editorial attempts to explain this seeming paradox - that hyperoxia pre-ROSC increases survial, but worsens survival post-ROSC - but I wonder if it is premature to try and reconcile these studies. Given all the known limitations of retrospectively-obtained data, and of this trial in particular, perhaps we should await controlled trials that more clearly define the role of oxygen levels and survival. As the authors note, "Reasons for the benefit of higher oxygen tensions during CPR can more easily be hypothesized than explained." Given the conflicting data, it might behoove us to proceed cautiously in modifying the targets for oxygen delivery in cardiac arrest.

Monday, April 1, 2013

Can capnography help the intubated trauma patient?

I had a conversation with a paramedic student recently, regarding a dyspneic patient who had either CHF or COPD. While I was explaining the utility of checking for JVD and other old-fashioned tests, she replied with "How about we just check the end-tidal CO2?" The dialogue about capnography continued something like this:
Paramedic: "The waveform might show some shark-fining, which would point to COPD, but if the nebs weren't working, and the patient looked shocky, you might worry that poor perfusion from CHF is producing a falsely low PetCO2, and you could start nitro."

Me: "After we intubate them, yellow means yes!"
I realized I wasn't contributing much to that discussion. 

Around the same time, I found a new study that looked at the use of end-tidal capnography to adjust ventilations for trauma patients, and the results were intriguing. So, in the interest of sounding smarter to the paramedic students, I plunged into the world of EMS capnography.

(Very) Brief review of capnography for EMS
People breath in oxygen, and breath out carbon dioxide. The level of carbon dioxide in the arterial blood is a very important number, and it's written as PaCO2, or the Partial pressure, in the artery, of CO2. Typically it runs around 35 - 45 mm Hg.

Google images - who knew?
This number is the one that counts when we're adjusting the rate or volume on a ventilator. Only problem is that we need to use a needle to draw an arterial blood gas (ABG), and then use a sizable machine to analyze the blood. It hurts too!

Of course, we breath out carbon dioxide, so we can also check the Partial pressure of CO2 as we breath out, especially the very last bit, at the end of the tide of airflow; the PetCO2. The point labeled "D" in the figure below marks the point at which PetCO2 is measured.


Usually the PaCO2 and the PetCO2 are pretty close to one another, and the arterial level is typically only 3-5 points higher than the end-tidal level. Another way to put it:
                   PaCO2 - PetCO2 ≤ 5 mm Hg
Well, usually that is ...

EMS and end-tidal capnography
EMS has been able to use capnography to do some important things. Rather than copy an extensive list, I'll turn this over to Peter Canning, over at Street Watch. He has compiled a list of the 10 Things Every Paramedic Should Know About Capnography, and it's a great focused summary. (Meaning, 90% of what I know comes from this article!). 

Of course, capnography can used to confirm intubation. It can also be used in cardiac arrest to check for ROSC, or assist in deciding on termination of efforts. Some evidence suggests that it has a role in diagnosing obstructive lung disease (asthma, COPD), as well as various other problems. 

First on his list, however, is its utility in monitoring ventilations, avoiding hypo- and hyperventilation. In the hospital, this is simple: If the PaCO2 from the ABG  is less than 35, the patient is being hyperventilated, and either the rate or the tidal volume needs to be decreased. With capnography, the numbers and waveform would look like this:

If the PaCO2 over 45, one of those parameters needs to be increased, because the patient is being hypoventilated


Because capnography is so much simpler and faster than using ABGs, it has been hoped that EMS could be able to modify ventilations just as well as in-hospital people can. So what does this recent study tell us about that potential?

"Utility of Prehospital Quantitative End Tidal CO2?"
Missouri EMS researchers wanted to test how well patients could be ventilated by EMS after intubation. They choose to focus on patients who had suffered either severe trauma or burns, and ended up with 160 patients (87% trauma, 13% burn-relate) who were transported to a level 1 trauma center. Overall, these were serious trauma cases - 75% had a GCS < 8 prior to intubation, and 1 out of 5 died in the hospital.

Paramedics had been trained in the use of end-tidal capnography to avoid hyper- or hypo-ventilation. During transport EMS recorded the PetCO2 levels, and adjusted the ventilations accordingly. Upon arrival to the ED, ventilations were maintained at the same rate and volume that EMS had used, and an ABG was obtained. The PaCO2 from this ABG was then analyzed against the end-tidal reading obtained during transport.

On average, the prehospital PetCO2 (34 mm Hg) was significantly lower than the ED PaCO2 (44 mm Hg); i.e. PaCO2 - PetCO2 = 10 mm Hg.  

This overall  difference between the PaCO2 and the PetCO2 only got larger when the sicker subsets of patients were examined. 
  • Patients who died during hospitalization: PaCO2 - PetCO2 = 17 mm Hg.
  • Patients with a pH < 7.2: PaCO2 - PetCO2 = 20 mm Hg.

So, were these results expected? What has the rest of the prehospital capnography literature showed? And how should we use capnography in the future?

FIrst, I'll review the studies that suggested that end-tidal capnography was potentially very accurate, and then I'll go over the studies that highlighted problems in applying it to the EMS patient population.

Studies that showed benefit of capnography
A 2003 helicopter study had suggested that capnography could help prevent hypoventilation in severely injured patients. Randomly assigned helicopter medics were able to use PetCO2 monitoring to adjust ventilation of intubated trauma patients, and ABGs were checked upon arrival to the trauma center. The patients were a mix of general poly-trauma, with high injury severity scores. The study suggested a big benefit - medics who had access to the ETCO2 monitor were far more likely to avoid hypoventilation and achieve normoventilation (although there was no change in hyperventilation).

Next, end-tidal CO2 was used to manage ventilations in a 2004 ground EMS study conducted in San Diego. The researchers enrolled 291 patients with severe head injury who had been intubated. Most of the patients had ventilation managed through standardized setting, but for about 1/2 of the patients the paramedics had ventilator management protocols that targeted a PetCO2 of 30-35 mm Hg, and avoided a PetCO2 < 25 mm Hg. As in the present study, the PaCO2 was confirmed by ABG after arrival at the ED. The use of the end-tidal capnography resulted in about 8% less hyperventilation.
Studies that suggested problems with it.
A 2005 study was conducted by a French EMS agency that uses specialist physicians, and uses ambulances equipped with ventilators, end-tidal capnography, and portable ABG analyzers as well. They looked at 100 patients that had been intubated over the course of 16 months, and examined how the PetCO2 levels corresponded to the PaCO2. An important note: only the PaCO2 values were used to adjust the vent. The patients were a mix of medical and trauma. They found that, even though, on average, the PaCO2 was the same as the PetCO2, there was significant variability in individual patients.
  •  For 27% of the patients: PaCO2 - PetCO2 > 10 mm Hg
  •  For 2% of the patients: PaCO2 - PetCO2 < -10 mm Hg
In other words, over a third of the patients would have been ventilated using false setting, had PetCO2 been used. In graph form:

An ED-based study from 2009, by Korean researchers, looked at 66 patients with severe head injury who had been intubated in the ED, and were mechanically ventilated. ABGs were obtained simultaneously with PetCO2 readings, and the paired values were compared. In general there was a good correlation between the two methods, and the PaCO2 exceeded the PetCO2 by less than 4 mm Hg, on average. However, this relationship broke down in the sicker patients; e.g. those with acidosis, greater injury scores, hypotension, or chest trauma.

A second 2009 trial conducted on 180 trauma patients who were intubated in the ED showed an extremely poor relationship between PaCO2 and PetCO2 obtained simultaneously. In the subset of patients with an isolated mild head injury the correlation was somewhat better. Noentheless, the authors concluded that: 
If the recommendations for ventilation to an PetCO2 of 35 mm Hg to 40 mm Hg were implemented in this population, 80% of patients would have a PaCO2 > 40 mm Hg and 30% would have a PaCO2 > 50 mm Hg.
Not good!

How to use the results of this new study.

Although these studies employed a variety of protocols (for example, different definitions of hyperventilation), 2 common threads  emerge. 

The first is that if the trauma is either mild, or limited to the head, then PetCO2 is probably an accurate surrogate for PaCO2, and can be used to modify ventilations. On the other hand, if a person has sustained trauma to multiple organ systems, or is showing any signs of shock, then the PetCO2 may (or may not) significantly underestimate the PaCO2 - there's no way to know. You're flying blind, vent-wise.

It turns out that this is sort of a common theme in using end-tidal capnography - it works best in patients with a single problem, but loses utility when the patient gets complex. Specifically, PetCO2 is no longer accurate when the patient has problems both with ventilation and perfusion.

Take asthma and CHF as another example. Both can present with hypoxia, true, but asthma usually only involves the lung, a ventilation problem. A number of studies have shown that certain qualitative aspects of the waveform - the "shark's fin" - may serve as a way to demonstrate improvement or worsening. 

On the other hand, CHF can involve both the pulmonary and the cardiac systems, at the least. There can be a complex relationship between things that drive the PetCO2 down (like poor perfusion from systolic failure) and those that drive it up (such as impaired ventilation from coexistent COPD). 

With these complexities, it isn't at all clear how to use end-tidal capnography in CHF, despite the advice offered in some EMS magazines. The best research that described using capnography to diagnose CHF versus COPD/asthma comes from a single article in the Croatian Medical Journal. Not something to hang your hat on.

By way of contrast, you can use PetCO2 to predict the degree of metabolic acidosis in pediatric DKA (studies here and here), or in pediatric gastroenteritis. These are strictly problems of metabolic acidosis (which would be reflected in the PetCO2), while only in the rare extreme cases would perfusion be affected.

The Bottom Line
The current study is consistent with prior studies, and it appears that end-tidal capnography is not yet reliable enough to use in severely traumatized or burned patients. Using capnography in this population runs the risk of underestimating the PaCO2, leading to hypoventilation.