From Scott Weingart EMCrit Interview: Who needs the Cath Lab now??

Who Needs the Cath Lab/Cards Consult?

Thanks to Scott Weingart of EMCrit for amassing all the indications in one place and interviewing me on the topic!!

Here is the post on EMCrit, with podcast of the interview.

Left Bundle Branch Block with Subacute STEMI

An elderly woman with no prior known cardiac history presented with approxiately 9 hours of chest pain, much improved by arrival and essentially resolved after a single sublingual Nitroglycerine.  She was  hemodynamically stable.

Here is her ECG:

There is sinus bradycardia and Left Bundle Branch Block. 

The ST segments are appropriately discordant, except that in lead II there is some ST elevation; the QRS in lead II is a bit more positive than negative, so the ST segment should be negative or isoelectric, but it is elevated.  This is a sign of STEMI.

More importantly,  though lead III has a discordant ST segment, it is out of proportion.  The STE is 3 mm in the presence of a 12 mm S-wave, for a ratio of 0.25, thus highly likely to be STEMI.

What is unusual is that the T-wave is concordant.  This is likely due to prolonged (subacute) STEMI, or to some reperfusion (the patient is pain free after NTG), or both.

There are also two signs of a fragmented QRS, which are equivalent to Q-waves in LBBB: "Cabrera's sign" (notch greater than 50 ms on the ascending limb of the S-wave in one of V3-V5), seen here in lead V3; also "Chapman's sign," (notch on the ascending limb of the R-wave in I, aVL, or V6), seen here in I, aVL, and V6.

Case continued

The physician only activated the cath lab after having a previously normal ECG faxed, and after the first troponin I returned at 41 ng/mL.  This very elevated troponin shows that the infarct has been going on for quite a while and is consistent with the ECG.



He did record another ECG:

No significant change

Outcome:

The RCA was 100% acutely occluded and was opened and stented.

Second troponin I was 70 ng/mL, Third was too high to measure.

An echocardiogram showed a new inferoposterior wall motion abnormality


Ischemic T-waves in LBBB

We showed that Concordant T-waves are weakly sensitive and specific indicators of MI [combination of STEMI and NonSTEMI] (1).

With reperfusion, even in LBBB, T-waves often invert with reperfusion.  Here is a great case of STEMI in LBBB, with Reperfusion T-waves after PCI.
       



1.  Dodd KW. Elm KD. Smith SW. Terminal T-Wave Concordance Increases the Sensitivity of Electrocardiographic Diagnosis of Acute MyocardialInfarction in Left Bundle Branch Block (full text link).  (Abstract 15666) Circulation. 2014;130:A15666; November 2014.

Is this Type 2 Brugada syndrome/ECG pattern?

Introduction

Types 2 and 3 Brugada have been merged into Type 2.  The diagnoses have been perplexing for years because they have been based on a "saddleback" morphology.  However, saddleback morphology is a very common normal variant: "saddleback" morphology is rarely Brugada pattern and even more rarely Brugada syndrome.

For an important update on this post, go here:

Non-Vagal Syncope and Saddleback Morphology in V2

This is a post showing the difficulty of the decision to place an implanted defibrillator.

Case 1

A young athlete presented with syncope.  Here was his ECG:

There is an rSr' with ST elevation and postive T-wave, creating a "Saddleback" in both V1 and V2

Is this Type 2, or Type 3, Brugada pattern?

Brugada syndrome is a condition which can lead to polymorphic ventricular tachycardia, ventricular fibrillation, and sudden death.  Identifying it before death is important.

Brugada syndrome requires BOTH 1) Brugada ECG pattern and 2) clinical criteria.

Here is an example of type I Brugada pattern during fever that disappeared after antipyresis.  It can be transitory and uncovered in a variety of situations (see below).

The recognition and management of Type 1 Brugada pattern ECG is not entirely straightforward, but, in my opinion, it is far easier than the recognition and management of patients with possible Type 2/3 Brugada (Type 3 has morphology has now been incorporated into type 2).   Here one of the Brugada brothers outlines the management of possible Brugada syndrome, but does not discuss type 2 in enough detail for me to understand it.

Many articles and web sites simply state that a Type 2 Brugada pattern has a "saddleback" in V2.   They discuss it no further.  This is not helpful, because a saddleback is a very common pattern in V2 (up to 7% in of patients with no apparent heart disease) and is a normal variant in the vast majority of cases, especially in athletes.

Saddleback is called saddleback because of an r'-wave (rSr') with an upright T-wave, forming a saddle.  This is also known as right ventricular conduction delay, and, if the QRS is wide enough (but not greater than 120 ms), it is incomplete right bundle branch block (I-RBBB).

How does a non-electrophysiologist go about suspecting Type 2 Brugada?

Again, one must distinguish between the syndrome and the ECG morphology.  The morphology alone is not enough for the diagnosis.  There must also be the right clinical context (see below) or positive electrophysiologic testing.

How do we recognize type 2 Brugada morphology on the ECG?  Fortunately, there was a consensus paper on this topic written by Bayes de Luna and the Brugada brothers.  Here is the full text of it.

There is also a very nice paper (full text html link): Differential diagnosis of rSr' pattern in Leads V1-V2: Comprehensive Review and Proposed Algorithm.  This is by the same authors of the new criteria for type 2 Brugada, so it is fairly authoritative.  (Here is a link to the full text pfd).

Here is a differential diagnosis of rSr', modified from the rSr' paper:

A. Benign Patterns:  -r' is of fast inscription, unlike in RBBB or Brugada, both of which have a wider R'.  Caused by:
   1. Higher placement of leads V1, V2
   2. Normal variant, with late activation of the posterobasal LV
   3. Incomplete RBBB, with delayed conduction through right bundle.  No associated adverse outcomes.  However, there is a higher incidence of subsequent development of complete RBBB.
   4. Athletes: 35-50% due to physiologic RV enlargement
   5. Pectus Excavatum, due to change of heart location in chest

B. Pathological Patterns: -r' often taller then -r, with slower ascent/descent
   1. Type 2 Brugada pattern
   2. RV enlargement, hypertrophy from a variety of pathologies
   3. Arrhythmogenic RV dysplasia (ARVD)
   4. WPW
   5. Hyperkalemia
   6. Na channel blockers (anti-dysrhythmics, TCAs)



Let's go back to our case, with more detail:

A young athlete had a painful condition for which he was seen in the ED.  After an episode of pain, he had a syncopal spell with complete loss of consciousness and postural tone, with spontaneous awakening.  There was a prodrome which seemed vasovagal in character.  He had started having lower abdominal discomfort and pressure, associated with some diaphoresis, then started feeling dizzy and passed out.  He spontaneously regained consciousness.  He had no prior history of syncopal spells.   There was no family history of premature sudden cardiac arrest in first degree relatives. There was no history of exertional syncope or post-exertional syncope.  He had a normal exam in the ED.

Here is the ECG again:

Is it type 2 Brugada pattern?
Is it type 2 Brugada syndrome?

The short answer is NO.

1. It is not type 1 Brugada.
2. The takeoff/downstroke of the ST segment in V1 and V2 is not flat enough ("beta" angle not wide enough) for it to be type 2 Brugada.  A pronounced r'-wave is common in athletes.

Here is the long answer

Below I summarize the paper I mentioned above, entitled (with full text link): Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report

Diagnosis of Brugada Syndrome requires both:

1. Brugada pattern ECG (either Brugada Type 1, or the newly defined Brugada Type 2)
Findings may be dynamic and are sometimes concealed; findings may be observed only in certain circumstances such as fever, intoxication, electrolyte imbalance, presence of sodium channel medications/drugs, or vagal stimulation.
2. At least one of the following:
(a) survivor of cardiac arrest,
(b) witnessed/recorded polymorphic ventricular tachycardia (VT),
(c) history of nonvagal syncope,
(d) familial antecedents of sudden death in patients younger than 45 years without acute coronary
syndrome
(e) Type 1 Brugada pattern in relatives.

Type 1 Morphology

Here is Type 1 pattern in V1 and/or V2, which is quite recognizable:

R' wave must have amplitude of at least 2 mm
Corrado index (see below) = 1.5/0.5 = 3.0. Thus it is greater than 1.0.

Criteria for Type 1 Morphology:
1. R'-wave at least 2 mm in V1 or V2
2. But no distinct R'-wave because the ST segment takes off at an angle from the peak
3. The ST segment is convex upward ("coved"). [They use terminology of "concave downward"]
4. The peak at the high takeoff does not correspond with the J-point.  It is BEFORE the J-point, as measured in other leads (such as lead II across the bottom).
5. Gradual downsloping of ST segment such that at 40 ms after the takeoff, the decrease in amplitude is less than 4 mm (in this example, it is less than 1 mm).  In normal RBBB, the decrease in amplitude is much greater (see this example).
6. ST is followed by a symmetrically negative T-wave
7. "The duration of QRS is longer than in RBBB," and "there is a mismatch between V1 and V6." This criterion is perplexing and not well explained.
8. The downsloping should be such that the Corrado index is greater than 1.0 (see example above).
Corrado index is the ratio:
[ST elevation at the J-point]
divided by
[ST elevation at 80 ms after the J-point].

In athletes, the index is less than 1.0 due to a horizontal or upsloping elevated ST segment, as here:

Corrado index less than 1 in an athlete, as ST segment slopes up

Criteria for Type 2 Brugada:

In the consensus paper we are discussing here, types 2 and 3 Brugada have been merged into one type called type 2. They specify the criteria to be used (below).

Here is an example from the article:

First, there must be:
a) An RSr' with a typical saddleback pattern in V1 and/or V2.
b) V1 may have either an upright, flat, or inverted T-wave (in our case above it is inverted).
c) T-wave in V2 is usually but not always positive.
d) Minimum ST segment ascent of 0.5 mm.  There could be no saddle without an ascent.

Once these are fulfilled, there should be, in lead V2:

1.  High take-off of the descending limb of the r' at least 2 mm above the isoelectric line (in our case, it is greater than 2 mm).   The r'-wave is thus not distinct, as it is in benign causes of rSr'

2.  Mismatch between QRS duration in leads V1 and V6 (longer in lead V1).  This helps to distinguish from RBBB, in which the QRS duration is equal in V1 and V6.

3. As with Type 1, the peak of the r'-wave does not correspond to the J-point in other leads.

4. The base of the triangle outlined should be longer than 3.5 mm.  This confirms that the slope of the ST segment is flat enough for the diagnosis.  I explain this in an annotated version here:

Explanation
1. Draw a horizontal line from top of r' wave (black line 1)
2. Draw a horizontal line 5 mm below this (green line 2)
3. Extend the downsloping r'-ST segment (black line 3) until it intersects the green line
4. Measure the base.  
If greater than 3.5 mm, then meets criteria (this is equivalent to a 35 degree beta angle)

I have done this with lead V1 of our ECG:

The distance from the S-wave to the almost vertical line is less than 3.5 mm, so does not meet criteria.  

How about in lead V2?

This drawing is incorrect, and only to show how it should NOT be done.
Both lines must be drawn from where the downsloping begins at the top of the r' wave.

The data for this comes from this study comparing patients with known high risk type 2 Brugada syndrome to athletes with rSr'.  The full text can be found here.

The criteria as studied in these comparison populations were approximately 90% sensitive and 90% specific in this study.


Case Progress:

This was recorded later:

All the suspicious findings are gone. There is only normal variant ST elevation (early repol)

In patients with Brugada, the Brugada morphology can be unmasked by recording V1 and V2 at higher interspaces (see this paper).

In another paper, it is shown that healthy patients may have false positive Type 2 morphology if the leads are placed too high, but NOT type 1 (full text link)!  (Chung EH.  Brugada-type patterns are easily observed in high precordial lead ECGs in collegiate athletes. Journal of Electrocardiology 47 (2014) 1–6.)

This was done here:

V1, V2 recorded one interspace higher, does not uncover type 1 Brugada pattern.  It does show a pronounced rSr'
Recording V1 and V2 one or two interspaces higher, over the area of the heart that is most likely to produce the Brugada pattern, should make the pattern more apparent.  If it did so, that would be very suggestive of Brugada.
Notice that there is T-wave inversion in V2 (but not Brugada pattern!).  
High lead placement is one of the causes of "abnormal" T-wave inversion in V2 and beyond. 

This recording also suggests that the initial ECG was recorded too high, as it is very similar to that first ECG

Additional etiologies were considered for his syncope given he is a collegiate athlete including HOCM, catecholaminergic polymorphic VT, and arrhythmogenic right ventricular dysplasia. Transthoracic echo did not show any evidence of HOCM or right ventricular dysplasia.  EF was normal. He had no known family history of sudden cardiac death at a young age.

The electrophysiologist was confident that this was not Brugada, that a procainamide challenge test could be done but that this would normally be done only for "unexplained" syncope, not for typical vasovagal syncope.  The patient was discharged with no exercise limitations.  He left open the possibility of an exercise test to rule out catecholaminergic polymorphic VT (CPVT), which occurs during stress and exercise.  However, without an exertional component, the probability of CPVT was very low.

Case Conclusion

In fact, this ECG is either:
1) a typical athlete's mimic of type 2 Brugada, or 
2) a too-high recording, or 
3) BOTH.  


Case 2

Here is a patient who presented with recurrent pre-syncope and palpitations.

Here is lead V2 blown up:

The base of the triangle is about 3.5 mm, and it meets the other criteria.

The electrophysiologist was worried enough about type 2 Brugada that he placed an implantable loop recorder.


Case 3

This 40-something patient presented with dizziness and chest pain.  The dizziness seemed to be vertigo more than pre-syncope.

Here the lines are drawn:

The base is greater than 3.5 mm, and other criteria for type 2 Brugada Pattern are present.

In this case, the patient underwent a stress test for his chest pain, but the diagnosis of type 2 Brugada was dismissed because of the absence of clinical criteria.  Dizziness due to vertigo was not enough.

There is Brugada Pattern, but not Brugada syndrome




Here is a comprehensive article inherited dysrhythmias: Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes

A Male in his 50's with epigastric pain

This was sent by a recent residency graduate who works at a hospital without a cath lab.  As you might imagine, our graduates have learned to scrutinize ECGs for subtle findings:

This middle-aged male with a history of smoking and alcohol use who had not had medical contact in many years presented with sharp, severe, "indigestion" in his epigastrium.  Medics gave him nitro and aspirin without improvement.  He received more nitro and also a "GI cocktail" in the ED without improvement.

Here is his initial ECG:

There is subtle scooped ST depression in III and aVF, and subtle ST elevation in aVL  (and also I).  The T-wave in aVL is very large compared to the QRS.  There is also a "down-up" (reverse biphasic) T-wave in V2.  This finding is very suspicious for posterior MI.
Since lateral and posterior MI are in one vascular territory (the circumflex), these findings are highly suspicious for circumflex occlusion.

Remember that circumflex occlusion results in diagnostic ST elevation (1 mm in two consecutive leads) in only about 50% of cases.  The lateral wall is often referred to as being "electrocardiographicaly silent".

Part of the reason for this is that the QRS axis is often perpendicular to lead aVL, so there is often very little QRS voltage in aVL: when there is low QRS voltage, there is also low T-wave voltage.  So one must rely an subtle findings that do not reach 1 mm if one is to make the diagnosis.

Often the findings of ST elevation in aVL are best seen in the reciprocal ST depression in inferior leads.

Here is another case for contrast, in which ST elevation in aVL with reciprocal ST depression in lead III is a false positive:

 

http://hqmeded-ecg.blogspot.com/2011/12/subtle-lateral-st-elevation-false.html

This was a false positive cath lab activation.
Here there is a lot of voltage in aVL, so you can't blame subtle ST elevation on lack of QRS voltage. 

Case continued:

The physician was worried about all these findings but was reluctant to activate.  The first troponin I returned at 0.031 ng/mL (less than 99% cutoff of 0.32).

At one hour, with the patient still in pain, he repeated the ECG:

There are some subtle changes: mostly a more upright T-wave in III and V2

The physician started a nitro drip and heparin and consulted a cardiologist at a referral institution.

The patient's pain increased while waiting for transport and another ECG was recorded:

No significant change

Just after leaving, the second troponin I returned at 0.90 ng/mL (positive).  The physician called the referral hospital to recommend immediate cath given a now objective diagnosis of NonSTEMI and with pain refractory to medical therapy.

On arrival, he did not go immediately to the cath lab.

Later that night he did go.  The circumstances surrounding that delayed decision are uncertain.

He had a 100% mid circumflex occlusion with otherwise clean coronaries.  It was stented.

I do not have the peak troponin or echo results.

Learning points:

1. Many occlusions do not reach 1 mm of ST Elevation.  These NonSTEMIs with occlusion can be recognized and need immediate cath lab activation.

2. The ACC/AHA recommends immediate cath for patients with ACS who have uncontrolled symptoms.

Chest Pain, LVH with Incomplete LBBB, and ST Elevation

A middle aged male with history of bicuspid aortic valve and aortic stenosis complained of 30 minutes of chest pain and dyspnea.  He described it as tightness and pressure.  Vital signs were normal and he appeared well.

Here is the initial ECG:

There is profound LVH with incomplete LBBB, with a QRS of 118 ms.  There is marked ST elevation in precordial leads. Although this can be seen with this degree of LVH and incomplete LBBB, one must entertain the possibility of anterior STEMI.
The ST/S ratio is 5/28 in lead V2, for a ratio of 0.18.   
Though 0.18 is less than 0.25, and of course also less than 0.20, it is still quite a high ratio.   A mean maximal ST/S ratio for a cohort of patients with complete LBBB is 0.10 (95% CI: 0.9-0.11).  

Worried about STEMI, a bedside echo was immediately recorded. Here is the parasternal long axis:

There is profound LVH and good wall motion

Here is a still image:

The arrows highlight the wide aortic root

A parasternal short axis was done:

This shows profound LVH with overall good wall motion.  In particular, the anterior wall and septum have good wall motion.  This makes anterior STEMI very unlikely.

The aortic root was not initially noticed, but the physicians were confident there was no STEMI.

Suddenly the pain resolved spontaneously after 45 minutes.

The initial troponin I returned elevated at 0.128 ng/mL, at which point another ECG was recorded:

No change, consistent with the interpretation that this is the baseline ECG

The on-call cardiologist was consulted for management of this patient with a positive troponin and worrisome ST segments.  Because of the history of bicuspid aortic valve, the cardiologist was concerned about possible Aortic Dissection and suggested a chest CT.

After a second look at the echo, there was more suspicion of dissection, and a CT was ordered.  Here is one image:

This shows a large aortic root aneurysm that also has a subtle dissection (low density thin lines in the midst of the contrast is a dissection flap)

A repeat ECG was essentially unchanged.

Consistent with massive LVH

The patient went to the Operating Room.

(I am not completely certain that there was no involvement of the coronary cusps, with resulting partial occlusion of the left main and resulting NonSTEMI, but the serial ECGs do not support this).

A later transesophageal echo showed that the initial dissection flap obstructed the right coronary cusp and resulted in occlusion of the RCA, but then a hole in the flap developed which restored flow to the RCA.  This is probably why the pain was relieved after 45 minutes.

Learning points:

1) Massive LVH can evolve over time to incomplete, or complete, LBBB, and it can have ST elevation that mimics STEMI.
2) Use ED echo to confirm good wall motion when there is anterior ST elevation due to LVH
3) Don't forget aortic dissection!

Paced rhythm. Is there Ischemic ST elevation?

An elderly male with a dual chamber pacemaker and severe dilated non-ischemic cardiomyopathy presented with dyspnea.  He had not had an angiogram in 10 years.  Although he had severe heart failure, the etiology of acute dyspnea was not readily apparent.  The differential was pneumonia/sepsis, heart failure exacerbation, pulmonary embolism, or possibly ACS.

He had an ECG recorded:

There are P-waves but a ventricular paced rhythm.  The heart rate is 118.
Is there excessive discordant ST elevation in anterior leads? ST/S ratios have not been studied for paced rhythm, but we have studied them for LBBB, and perhaps this knowledge can be applied to paced rhythm (?)  This is uncertain, but I do it frequently and I think it works. 
If we do apply these rules, the ST/S ratio is highest in V2 and V3.  In these leads, the STE at the J-point is 4 mm in V2 and 4-5 mm in V3, with a 27-28 mm S-wave, for a max ratio somewhere between 0.145 - 0.185.

These ratios are a bit higher than normal for a maximal ST/S ratio, but they are not higher than cutoffs of 0.20 (more sensitive, less specific) or 0.25 (very specific).  

So this is unlikely to represent acute anterior STEMI, but let's compare to a previous ECG:

There is much less STE here.  The ratio is closer to 0.06.

Should you worry that there is an increase in the ST elevation and ST/S ratio?  Normally, yes.

But look at the heart rate: the bottom ECG has a heart rate of 79.  The top one has a rate of 118.

Tachycardia results in increased discordant ST elevation in paced rhythm and in LBBB.  All of this ST segment shift can be attributed to tachycardia.

Outcome:

 Troponins were mildly elevated (up to 0.176 ng/mL).  The patient was diagnosed with acute decompensated heart failure.   As the heart failure was managed, and the heart rate decreased, the ST segments shifted down.  There was no wall motion abnormality.

Exacerbation of heart failure can also exaggerate ST elevation in Paced rhythm and LBBB, as demonstrated in this case.



Learning Points:

1.  Tachycardia can exaggerate the appropriately discordant ST elevation in paced rhythm (and in LBBB)

2. Heart Failure can also exaggerate this ST elevation. 

Chest Pain: What do you see on the ECG?

I saw this ECG, knowing only that there was a chief complaint of chest pain:

What do you see?

I thought: "This looks like it could be an acute inferior MI."   This is because of the extremely subtle ST elevation in lead III, Q-wave in lead III, biphasic T-wave in aVF, and reciprocal subtle ST depression in aVL.

I went to find the providers because I thought this ECG is so subtle that it could easily be missed by anyone.

Here was the history:

A male in his 40s was eating a heavy meal when he developed "sharp" midsternal non-radiating chest pain of 10/10 severity.  Then he vomited and his pain decreased to 1/10.   About 20 hours later, his pain remained 1/10 and he presented to the ED because a friend suggested he should.  Exam was normal.

His pain resolved with both a nitro and an antacid.

Indeed, the ECG had been read as "no evidence of ischemia" by several providers.

After pain resolution, another ECG was recorded:

ST elevation and Depression is almost completely resolved. The probability of MI is increased.

The interpretation remained "no evidence of ischemia."

His initial troponin returned elevated at 0.746 ng/mL (99% cutoff, 0.030).  

He was appropriately treated for NonSTEMI.  He remained pain free, so no emergent cath was necessary.  10 hours later, this ECG was recorded:

Significant evolution of deeper T-wave inversion is present in inferior leads, diagnostic of inferior NonSTEMI.

The angiogram showed a 95% mid-RCA lesion that was stented.

Commentary

There are many NonSTEMIs that truly have normal or non-diagnostic ECGs, but there are also many that are read as negative when they are at least highly suggestive of ischemia.

In this case, the initial troponin was positive and the diagnosis therefore should not be in doubt.  

Which begs the question: Would more accurate interpretation of the ECG add any value?

I believe the answer is yes.

1. If recognized, it can heighten your suspicion of NonSTEMI and help prevent a missed MI.  The troponin might be negative (not in this case) and you might send such a patient home.  It has happened!  And unstable angina still exists, despite rumors of its demise.

2. If immediately recognized, it can speed the evaluation and disposition.  This patient, even if he had had a negative initial troponin, should not be admitted to "observation," but rather should be an inpatient.  You can order that inpatient bed right away.

3. Immediate recognition facilitates more rapid use of nitro, a P2Y12 inhibitor, and use of anti-thrombotics such as heparin.

4. In a patient with ongoing, refractory chest pain, such an ECG tells you that it is most likely ACS and puts you on notice that more rapid angiography may be necessary if symptoms cannot be resolved medically.

ResQCPR System Approved by FDA. First and only CPR adjunct ever approved.

Keith Lurie and his colleagues have spent over 25 years trying to improve outcomes in cardiac arrest.  I know him personally.  He is very smart and very hard working, and has impeccable integrity.   He is more committed to saving lives than anyone I know.

I asked Dr. Lurie to tell us about this device he has worked on for so long and which has finally been FDA approved.

I do not promote any commercial products on my site, nor have any advertisements.

I am promoting this because it saves lives, neuro intact.

We have been using the inspiratory threshold device for years in our ED and all over Minnesota, where we have the highest cardiac arrest survival rates in the country, according to the CARES Registry.

Keith developed the system and founded Advanced Circulatory Systems, the manufacturer and marketer.  Advanced Circulatory Systems was recently bought by Zoll.

He has no more personal interest in this, so there is no longer a conflict of interest.  He only wants to save lives.

Full text of ResQTrial, funded by NIH.  One of the great emergency medicine NIH studies.


ResQCPR System

The ResQCPR System was approved by the FDA on Friday March 7, 2015. The ResQCPR System is a combination of the ResQPUMP, a manual active compression decompression (ACD) CPR device, and the ResQPOD, an impedance threshold device  (ITD). It is the first and only CPR adjunct the FDA has ever approved to increase the likelihood of survival after non-traumatic cardiac arrest. ZOLL Medical is the manufacturer of this new device (http://www.advancedcirculatory.com/resqcpr-system/). 

The ResQCPR System was approved based upon clinical data from a clinical trial called the ResQTRIAL, published in Lancet showing this system increases 1-year neurologically intact survival after cardiac arrest by 49% relative to conventional CPR in patients in cardiac arrest of a primary cardiac etiology,¹ (full text link) and by 34% for all patients in non-traumatic cardiac arrest, regardless of the etiology.² This is an important milestone in the history of CPR. Widely used, the ResQCPR System will save many lives.

The combination of the ResQPUMP and ResQPOD works by lowering pressures inside the chest with each decompression. This negative intrathoracic pressure pulls more venous blood back to the heart from the brain and the rest of the body, which in turn increases the refilling of the heart. With the next compression, circulation to the heart and brain is nearly three times higher with the ResQCPR System compared with conventional CPR. In addition, the ResQPUMP has a gauge and metronome to help guide compression depth, active decompression height, and the correct compression rate. The ResQPOD has a timing light to help guide the correct ventilation rate. More details related to the ResQCPR System can be found on the ZOLL website (www.zoll.com). Research supporting the new ResQCPR System indication for use includes: Aufderheide  - Lancet 2011 (http://www.ncbi.nlm.nih.gov/pubmed/21251705) and Frascone – Resuscitation 2013 (http://www.ncbi.nlm.nih.gov/pubmed/23669489).

To reduce any misconceptions, the ResQCPR System is not just a manual version of the LUCAS device (with or without an ITD). The LUCAS device does not perform active decompression to any significant degree (it pulls up only 3 lbs), although it does help assure full chest wall recoil. The ResQCPR System is the only FDA-approved device that allows the user to perform full active chest wall decompression (~15 lbs of upward force on average), thereby helping to lower pressures inside the chest, and lower ICP, with each decompression. This generates increased circulation to the heart and brain. At present, no automated CPR devices have an approved indication for survival like the ResQCPR System. Now that the ResQCPR System has been approved, efforts are underway to develop a better automated system that provides similar benefits to the ResQCPR System.

Another misconception is that the ResQCPR System was evaluated in the Resuscitation Outcomes Consortium (ROC) PRIMED Study. That was not the case. In the ROC RPIMED study, patients were only treated with conventional manual CPR. They were then randomized to either a sham (or placebo) ITD or an active (functional) ITD, and either 30 seconds or 3 minutes of CPR before analysis and shock. The first ROC PRIMED paper reported no difference between the active and sham device,³ or 30 seconds and 3 minutes of CPR.⁴ As we know it was a complicated study. More recently the ROC investigators published three more papers showing there was a wide range in compression rate and compression depth in the ROC PRIMED study.^5,6 When the rate and depth were outside the AHA-recommended range, survival rates decreased. When the compression rate and depth were within the AHA-recommended range, use of the active ITD increased the number of patients who lived with good brain function by more than 25% compared with the sham ITD.⁷ The ROC PRIMED study and its reanalysis demonstrated how critical it is to perform high quality CPR, at the correct rate and depth, and to guide rescuers so they can perform high quality CPR. (Yannopoulos Circulation 2014: http://circ.ahajournals.org/content/130/Suppl_2/A9.abstract?sid=aefe5b91-bc4b-4ac4-9415-b0bbc86a2284). It is reasonable to conclude that the ITD should be recommended for use if caregivers are able to monitor their CPR quality and use feedback tools to assure that compressions are delivered at the right rate and depth. We do that here in Minnesota, and often use the LUCAS device to provide CPR after ALS arrives. Based upon the Cardiac Arrest Registry to Enhance Survival (CARES)(www.mycares.net), Minnesota leads the nation in the highest survival rates with good neurological function (13%) of any state in the CARES database. The average survival rate with good neurological function nationwide for those who participate in CARES is 8%.

¹Aufderheide TP, Frascone RJ, Wayne MA, et al. Standard cardiopulmonary resuscitation versus active compression-decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomized trial. Lancet 2011;377(9762):301-311.

²Frascone RJ, Wayne MA, Swor RA, et al. Treatment of non-traumatic out-of-hospital cardiac arrest with active compression decompression cardiopulmonary resuscitation plus an impedance threshold device. Resuscitation 2013;84:1214-1222.

³Aufderheide TP, Nichol G, Rea TD, et al. A trial of an impedance threshold device in out-of-hospital cardiac arrest. N Engl J Med 2011;365(9):798-806.

⁴Stiell IG, Nichol G, Leroux BG, et al. Early versus later rhythm analysis in patients with out-of-hospital cardiac arrest. N Engl J Med 2011;365(9):787-797.

⁵Idris AH, Guffey D, Aufderheide TP, et al. Relationship between chest compression rates and outcomes from cardiac arrest. Circulation 2012;125:3004-3012.

⁶Stiell IG, Brown SP, Nichol G, et al. What is the optimal chest compression depth during out-of-hospital cardiac arrest resuscitation of adult patients? Circulation 2014;130(22):1962-1970.

⁷Yannopoulos D, Abella B, Duval S, Aufderheide T. The effect of CPR quality: a potential confounder of CPR clinical trials. Circulation 2014;130:A9.

Kaplan Meier curve of neurologically intact survival:

ResQCPR System Information Sheet

ResQCPR^™ System: A System for Survival

The Problem

Every day, sudden cardiac arrest, the number one killer in the US, takes the lives of 1500 Americans. Current survival rates are generally poor, with fewer than 10% of patients surviving out-of-hospital cardiac arrest. There is now new hope for the people who experience cardiac arrest.

The Solution

The newly-approved ResQCPR™ System delivers Intrathoracic Pressure Regulation (IPR) Therapy during cardiac arrest resuscitation. IPR Therapy regulates pressure in the chest to enhance perfusion in states of low blood flow, such as cardiac arrest and shock. In a pivotal clinical trial, use of the ResQCPR System increased one-year survival by 49% compared to patients receiving conventional CPR.^1,2 The ResQCPR System is the only CPR device with an approved indication to increase the likelihood of survival.³ If implemented widely, this could mean that thousands more people would survive cardiac arrest every year.

Product Description

The ResQCPR^™ System is a device combination that includes both the ResQPUMP^â
ACD-CPR Device and the ResQPOD^â ITD 16.

The ResQPUMP ACD-CPR Device is a re-usable, hand-held device comprised of a suction cup that is placed on the chest, and a handle that contains a force gauge and metronome. It is the only device approved in the US that allows the caregiver to perform active compression decompression CPR (ACD-CPR), which compresses the chest like manual CPR, but allows the user to actively re-expand the chest to generate the negative pressure (or vacuum) that helps to refill the heart (i.e. create preload).

The ResQPOD ITD 16 is an impedance threshold device (ITD) that helps to further enhance negative intrathoracic pressure by preventing the influx of unnecessary air through the open airway during active chest wall recoil. It is disposable and fits into the airway circuit between the airway adjunct (e.g. facemask, endotracheal tube) and the ventilation source (e.g. ventilation bag).  

ResQCPR System Impact

When used together, the ResQPUMP and ResQPOD work synergistically to enhance the vacuum in the chest during CPR more effectively than either device individually:

   Airway Pressures During Conventional CPR:

  and  CPR with the ResQCPR System:

                         

Research Summary

The ResQCPR System has been extensively researched. Pre-clinical studies⁴ have been conducted and have shown that use of an ITD during ACD-CPR:

·       Lowered intracranial pressure (ICP), resulting in improved cerebral perfusion pressure⁵

·       Increased blood flow during resuscitation to near-normal levels⁶

·       Improved neurologically-intact survival⁵

Clinical studies have shown that use of an ITD during ACD-CPR:

·       Increased survival at one year by 34% in patients who arrested from non-traumatic etiologies²

·       Increased survival at one year by 49% in patients who arrested from cardiac etiologies²

·       Provided near-normal systolic and diastolic blood pressures⁷

·       Significantly enhanced the intrathoracic vacuum with both a facemask and ET tube⁸

Features and Benefits

·       Only device with an approved indication to increase the likelihood of survival³

·       Only device that enables rescuers to provide ACD-CPR

·       Cost-effective

·       Lightweight, portable and compact

·       Latex free

·       Can be applied rapidly by basic or advanced life support caregivers

·       Designed to promote high quality resuscitation:

o  ResQPOD contains timing lights, intended to promote proper ventilation rate

o  ResQPUMP contains metronome, intended to promote proper compression rate

o  ResQPUMP contains force gauge, intended to guide compression and lifting forces

Performing ResQCPR: Abbreviated Instructions⁹

1. Assess for signs of life.

2. Send for AED.

3. Begin ACD-CPR compressions ASAP:

            A. Place ResQPUMP between nipples and above xiphoid process.

            B. Perform ACD-CPR:

    Compression: to 2” (5 cm) depth and note force required to achieve that depth.

                Decompression: Lift to -10 kgs.

                Rate: 80 per minute

4. Apply ResQPOD ITD           

            A. Attach early to facemask. Maintain tight facemask seal.

            B. Begin ventilations at appropriate compression to ventilation ratio.

            C. Move to advanced airway once tube placement is confirmed and secured.

            D. Use lights to guide ventilations. Do not hyperventilate.

5. Remove BOTH devices when pulse returns.

           

Product Numbers

Part #	Description	Description
12-0825-000	ResQCPR System	Includes one ResQPUMP ACD-CPR Device and two ResQPOD ITD 16s
12-0823-000	ResQPUMP ACD-CPR Device	Replacement component
12-0822-000	ResQPOD ITD 16	Replacement component
12-0586-000	Suction cup for ACD-CPR Device	Replacement component
12-0935-000	ResQCPR Carrying Case	Designed to carry one ResQPUMP, two ResQPODs and other accessories needed to rapidly initiate ResQCPR
12-2116-000	ManiKIT	Allows many CPR manikins to be adapted for ResQCPR training
12-2117-000	ResQTRAINER	Training tool that helps learn psychomotor skills of ACD-CPR
12-0869-000	ResQCPR Demo Kit	ResQMAN Demonstrator with ResQPOD ITD

Availability and Customer Service

The ResQCPR System is available solely through ZOLL Medical Corporation. Customer Service is available to answer questions regarding product features and benefits, individual purchases, pricing, refunds, rebates, shipping status, or other service related information. Contact our Customer Service representatives by phone or e-mail:

ZOLL - Chelmsford (Resuscitation Products)
Monday – Friday; 8:30 am to 7:00 pm Eastern Standard Time
Direct:              978-421-9440
Toll-free:          800-348-9011
Fax:                 978-421-0015
E-mail: info@zoll.com

Email:               esales@zoll.com

Website:          www.zoll.com

References

1Patients in cardiac arrest from cardiac etiologies

²ResQCPR System Summary of Safety and Effectiveness Data approved by Food & Drug Administration 2015

³FDA-approved indication for use: The ResQCPR System is intended for use as a CPR adjunct to improve the likelihood of survival in adult patients with non-traumatic cardiac arrest.

⁴Pre-clinical study results are not necessarily representative of clinical study results.

⁵Metzger et al. Improved cerebral perfusion pressures and 24-hour neurological survival in a porcine model of cardiac arrest with ACD-CPR and augmentation of negative intrathoracic pressure. Crit Care Med 2012;40(6):1851-6.

⁶Voelckel et al. Effects of ACD-CPR with the inspiratory threshold valve in a young porcine model of cardiac arrest. Pediatr Res 2002;51(4):523-7.

⁷Plaisance et al. Inspiratory impedance during ACD-CPR: a randomized evaluation in patients in cardiac arrest.

⁸Plaisance et al. Use of an inspiratory ITD on a facemask and ET tube to reduce intrathoracic pressure during the decompression phase of ACD-CPR. Crit Care Med 2005;33(5):990-994.

⁹See product insert for complete instructions for use.

Improper use of the ResQCPR System could cause ineffective chest compressions and decompressions, leading to suboptimal circulation during CPR and possible serious injury to the patient. The ResQCPR System should only be used by personnel who have been trained in its use. The ResQPUMP should not be used in patients who have had a recent sternotomy as this may potentially cause serious injury. Improper positioning of the ResQPUMP suction cup may result in possible injury to the rib cage and/or internal organs, and may also result in suboptimal circulation during ACD-CPR.