Champagne Lit Review: Sgarbossa in Ventricular Pacing

Sgarbossa in Ventricular Pacing

Slightly off conference topic, we had a case in the department where a patient with active chest pain had Sgarbossa criteria in the presence of ventricular pacing. Cardiology did not consider it  STEMI. There was delayed PCI, which later showed 100% LAD occlusion. I decided to pursue the literature:

Mattu seems convinced. The literature however is not very robust. Theoretically, right sided endocardial paced rhythms should have similar electrical patterns to LBBB and thus reflect the same obscuration during ischemia. The high specificities in the studies below gives confidence that we are looking at STEMI equivalents, but there aren't huge numbers (like the tens of thousands in the LBBB Gusto group) enough to change protocols or to convince lazy cardiologists to treat these as STEMIs.

Still seems like the right thing to do, with good but limited evidence in its support. I'd call these STEMI codes and let the cardiologists decide. Especially if the patient looks sick and vomits on your pants.

 

Mattu Lecture on Sgarbossa in Pacemaker

Original Sgarbossa GUSTO V-Paced Subset data (n=17)

94%/88%/82% specificity for the three criteria

Sgarbossa Sensitivity in V-Paced: validation study of Sgarbossa GUSTO Ventricular paced date (n=57)

high SPECIFICITY for concordant depression V1-3 and Excessive discordance

The original NEJM Sgarbossa GUSTO-1 paper

     -makes no mention of analyzing ventricular paced ECGs

     -V-Paced not included in definition of LBBB

Paper excluding 5mm excessive discordance as STEMI criteria

Conference Follow Up: 10/23/13

As usual, here is a brief supplementary email for this week's conference:

Each week I send a post conference email I'm gonna add 2 new musicians I think you should check out (lemme know what you think of the idea):

MUSIC

#1 Canadian indie rock band based out of montreal

#2 Cool Icelandic composer/mixes w/ electronic

Now to the Medicine:

Chest Tube Placement:

Video on procedure (skip to the 4 minute mark!)

Some people were asking about Clamshell Thoracotomy, here is a fantastic overview with graphic images from the trauma.org atlas.

Troponin (nice grand rounds Joe):

Here is a great overview and simplification of the very complicated discussion regarding HIGH SENSITIVITY TROPONIN, from Academic Life in EM.

Some of the most interesting bullet points from this review were these:

• High sensitivity Tn requires only 2 to 3 hours between time of initial lab and repeat Tn to see a conclusive increase to rule in AMI [1]
• A normal hsTn at 3 hours has a NPV of 99% in excluding AMI [2] 

Here are the references for those bullets:

1.  V.S. Mahajan, and P. Jarolim, "How to interpret elevated cardiac troponin levels.", Circulation, 2011. http://www.ncbi.nlm.nih.gov/pubmed/22105197
2.  A.S.V. Shah, D.E. Newby, and N.L. Mills, "High sensitivity cardiac troponin in patients with chest pain.", BMJ (Clinical research ed.), 2013. http://www.ncbi.nlm.nih.gov/pubmed/2387815

The Overtesting/Overscreening Phenomenon (as discussed by Dr. Jahnes):

Here is a link to the pubmed search results for ALL of Dr. V Prasad's papers. (Dr. Jahnes' new hero)

This one was my favorite, it was a literature review on contradictory data regarding medical therapies. 

This is a BMJ article on the evidence for over diagnosis of PE:

Submassive Pulmonary Embolism Journal Club

Here is a great summary of the management of submassive PE

Perhaps this discussion will clarify some of the words that were incapable of leaving my mouth this morning (hah), it is a podcast summarizing the submassive PE thrombolysis trials. Keep in mind the bias as the two physicians talking are prominent authors and Stavros is the MAPPET lead investigator. (grain of salt required).

ACEP Clinical Policy on PE Management:

Journal Club Articles

Here is a nice general overview of the topic if you're interested in reading before you get to the individual studies. 

http://circ.ahajournals.org/content/123/16/1788.full

Articles:

http://www.nejm.org/doi/pdf/10.1056/NEJMoa021274

http://journal.publications.chestnet.org/article.aspx?articleid=1090134

Abstract: (article to come in full form from the library) http://www.ncbi.nlm.nih.gov/pubmed/23102885

9/11/13 Post Conference Summary

This is the second post-conference email. Hope it helps.

Vasopressors in Shock (Lecture by Dr. Keshava)

This is a GREAT SUMMARY of the updates in the surviving sepsis guidelines of 2012.

-30cc/kg bolus (1A)

-albumin if using high volumes (2B)

-NOT providing steroids if fluids work

• Authors strongly recommend norepinephrine (Levophed) as the first choice for vasopressor therapy (Grade 1B). Vasopressin 0.03 units / minute is an alternative to norepinephrine, or may be added to it (Grade 2A).
• When a second agent is needed, epinephrine is their weakly-recommended vasopressor choice (Grade 2B).

Pediatric LP/Septic Workups (Lecture by Kirsten Malone):

Good Video of infant LP

-attached to this email is the uptodate.com summary of the three major infant fever protocols

-there is a lot of controversy regarding continuing to follow these protocols, this is because the protocols were developed in the 90's before true herd effect of H.flu, '88 pneumococcal vaccine, and the updated 2000 pneumococcal vaccine. 

-Some people believe prevalance has dramatically decreased, which significantly decreases pre-test (pre-septic workup) probability

CPC: Cases: 

Aortic Dissection: Attached to this email is the IRAD study which is retrospective analysis of clinical features of  confirmed Ao Dissection.

Also, this study is a validation study of a prediction tool developed by AHA used IRAD data. 

Asthmatic: 

Continuous Bladder Irrigation:

-funny how the resident was making recommendations for us to NOT perform this in the ED. Thanks to Melville for pointing out that the Uro attendings more often than not are the ones who ask us to perform this.

-not sure if anyone heard me belly laugh when he commented that "if the pt needs CBI, it probably needs a Urologist to urgently evaluate the patient". HAHA. I can count on one hand the times ive seen a uro attending in the ED. We manage their patients, including procedural complications, bleeding, obstruction, etc. I find it funny that the thought is that we should be waiting for them to evaluate these pts.

- Ok enough ranting. Here is some info:

-CBI Procedure Video

-Foley Irrigation Video (skip to minute 3, this is an old school vid)

-Cool lecture on Obstruction

FAST

-Check out Sonospot.com and go to the Sono Studies or Sono Tutorial on the right side menu and find E-FAST

Attached is a lecture I gave on the EVIDENCE FOR FAST EXAM

Studies:  in blunt trauma

Pediatric Sepsis Management:

-as Dr. Melville pointed out, rule #1 is DO NOT SIT AND INTELLECTUALIZE while the kid is dying.

-aside from that , here are some guidelines.

Ultrasound Competition WINNER for AUGUST

Dr. Laura Melville  AND Dr. Mike McMahon

Youngish F hx thombophilia, DVT, PE s/p IVC placement presenting to the ID for suprapubic pain sudden, back pain for a week and arrived hypotensive, diaphoretic and tachycardic.

Vitals 70systolic, HR 120s. sat 99%.

In ED bedside echo showed massively dilated >1:1 RV:LV and PSS showed D sign. This essentially diagnosed PE.

Arrival to ED. pt got intubated, pressors, recieved tPA in ED. She was admitted to the ICU and found to have bilateral PE's with RLL infarction.

Update:

4 days later:  Discharged. Placed on Xarelto. Pt extubated, off pressors, ECHO shows normal LV EF 62%, RV pressure = 50

Conference Follow Up: September 4th 2013

Dr. Gatton's Trauma lecture:

1 - Hypothermia in trauma? We discussed how although we always learn that hypothermia is bad for trauma ... it is part of the deadly triad. However, there are some theories that it could improve outcomes, particularly in head trauma. See this cochrane review on hypothermia in head trauma. Although limited in study quality, and finding no statistically significant improved outcome, there was a trend toward mortality benefit. Take a look at it yourself.

"The review authors found that fewer people died or became severely disabled if they were treated with hypothermia, but this finding may be due to chance. It was also found that patients given hypothermia were more likely to develop pneumonia, and some patients died from pneumonia, but the increased risk of pneumonia could also be due to chance. "

2- Hyperventilation in ICH. We discussed the role of hyperventilation to decrease ICP and improv CPP in intracranial hemorrhage/trauma. Below are some resources on this debated topic.

Here is a great review article in CHEST. 

AHA Intracranial Hemorrhage GUIDELINES:

"Hyperventilation
Hyperventilation is one of the most effective methods available for the rapid reduction of ICP. The CO₂ reactivity of intracerebral vessels is one of the normal mechanisms involved in the regulation of CBF. Experimental studies using a pial window technique have clearly demonstrated that the action of CO₂ on cerebral vessels is exerted via changes in extracellular fluid pH.⁷⁴ Molecular CO₂ and bicarbonate ions do not have independent vasoactivity on these vessels. As a result, hyperventilation consistently lowers ICP. Despite the effectiveness of hyperventilation in lowering ICP, broad and aggressive use of this treatment modality to substantially lower PCO₂ levels has fallen out of favor, primarily because of the simultaneous effect on lowering CBF. Another characteristic of hyperventilation that limits its usefulness as a treatment modality for intracranial hypertension is the transient nature of its effect. Because the extracellular space of the brain rapidly accommodates to the pH change induced by hyperventilation, the effects on CBF and on ICP are short-lived. In fact, after a patient has been hyperventilated for >6 hours, rapid normalization of arterial PCO₂ can cause a significant rebound increase in ICP. The target levels of CO₂ for hyperventilation are 30 to 35 mm Hg. Lower levels of CO₂ are not recommended.^75"

Bites:

1- Study on primary vs secondary closure of dog bite wounds: Great discussion of dog bites. Study showed significant cosmetic improvement with early closure with no statistically significant change in infection rate.

2- Link on how and when to report animal bites to the NYC.gov health department.

Oncologic Emergencies

1- Attached are two awesome Evidence Based Medicine articles from 2010 on Oncologic Emergencies. 

2- We discussed the early ultrasonographic signs of pericardial tamponade. We can all easily see effusions, but which ones are resulting in tamponade physiology require some advanced echo techniques that we can all learn. This will make us rock stars when presenting the patient with greater urgency to our Cardiothoracic colleagues. See the below links for studies and tips.

 Probably the best ARTICLE on US Findings in Tamponade

Here is a fantastic review from Stanford's ICU with great diagrams, images and figures to explain the physiology. 

NEJM Review Article on Tamponade: 

n the absence of my- ocardial disease or injury, echocardiography dem- onstrates the usually circumferential fluid layer and compressed chambers with high ventricular ejection fractions.24 Doppler study discloses marked respiratory variations in transvalvular flows. One mechanism of pulsus paradoxus is visible: on inspi- ration, both the ventricular and atrial septa move sharply leftward, reversing on expiration1; in other words, each side of the heart fills at the expense of the other, owing to the fixed intrapericardial volume. The inferior vena cava is dilated, with little or no change on respiration.Among echocardiographic signs, the most char- acteristic, although they are not entirely specific, are chamber collapses, which are nearly always of the right atrium and ventricle. During early diastole, the right ventricular free wall invaginates, and at end di- astole, the right atrial wall invaginates.25 Right ven- tricular collapse is a less sensitive but more specific finding for tamponade, whereas right atrial col- lapse is more specific if inward movement lasts for at least 30 percent of the cardiac cycle. Right atrial collapse may be seen in patients with hypo- volemia who do not have tamponade. In about 25 percent of patients, the left atrium also collapses, and this finding is highly specific for tamponade. Left ventricular collapse usually occurs under spe- cial conditions such as localized postsurgical tam- ponade. These wall changes occur when respective chamber pressures temporarily fall below the peri- cardial pressure.24,25 

Should we be ok letting the GI specialist sleep?

Variceal bleeding is a frightening condition seen infrequently in the ED, but when it shows its face it sparks high anxiety. It is one of the most rapid type of not compressible bleeding (unless you consider the blakemore), in my eyes it is comparable to intraperitoneal traumatic bleeding.  Can we as EP's simply rely on medical management and stabilization or is our gut right when we say, "where is G.I. , they've got to come in for this?" This is a debate, seemingly more one-sided as most of the literature on it is from gastroenterology journals and may be skewed toward our colleagues' opinion (our 'Annals' does not have a single paper with "esophageal varices" or "variceal" in the abstract or title). What is the right thing to do for our patients?

You can imagine, a "cushy" subspecialty like gastroenterology having private conversations amongst
each other at national conferences, discussing how they could convince the world that they need not speed over to the hospital at 4am for an emergent endoscopy.  Their desire to never be awoken from their slumber however has given birth to a hubris of new extremes.  With a massive review paper published in the Canadian Journal of Gastroenterology titled, "Emergency management of bleeding esophageal varices: Drugs, bands or sleep?"  they have comfortably convinced themselves that because the jury is still out, they will continue to sleep. 

In conclusion of this extensive study they authors state:

"Timing of definitive endoscopic treatment has not been clearly defined. Delaying endoscopic treatment may make it easier to perform in a clear, bloodless field, especially for band ligation. Current data suggest no difference in control of hemorrhage or mortality in the setting of pharmacological therapy if endoscopic treatment is delayed up to 48 h. Therefore, to the probable delight of gastroenterologists on call, we recommend that emergency endoscopic treatment (less than 6 h from presentation) be reserved for continuing bleeding resistant to initial pharmacological treatment."

The interesting thing is that they confidently make a very serious, consequence-heavy "recommendation" to delay emergent endoscopy several paragraphs after this one (within their limitations section) :

"Excellent meta-analyses are available for octreotide, terlipressin and comparisons with sclerotherapy; however, pharmacological treatment and band ligation have not been directly compared. Therefore, while band ligation may appear to be superior to other methods of treatment, this conclusion is still premature."

As well as, and perhaps more strikingly after this one:

"The only study to directly address timing was by Shemesh et al (35), who analyzed whether emergency sclerotherapy was more effective than stabilization and elective sclerotherapy ... Emergency therapy stopped all acute bleeding and resulted in decreased rebleeding in hospital (4.7% versus 17.1%, P=0.027) and by one year (7.0% versus 17.1%, P=0.027). There was an insignificant trend showing improved mortality in hospital and at one, three and five years after follow-up in the emergency sclerotherapy group."

The above was within their "can or should we wait" section. Aside from the casual mention of the ONLY study that EVER addressed emergency endoscopic intervention (scleropathy in the study) vs. stabilization and waiting, they also appear to believe that "band ligation may appear to be superior to other methods." This was clearly pointed out in their mention of a meta-analysis by Gross et al (Endoscopy. 2001 Sep; 33(9):737-46) showing banding more successful than pharmacologic treatment (without timing directly compared). 

Shockingly (phh), they have a small section of the review boasting combined pharmacologic and endoscopic therapy as improving mortality and "initial control of bleeding" (once again without specified timing). This was from a meta-analysis in Hepatology. (Hepatology. 2002 Mar; 35(3):609-15)

It appears their main reasoning for recommending delayed endoscopic therapy is the lack of evidence to the contrary at the moment. They point to various end-point, inclusion criterion, timing, and dosing differences amongst the studies they used. One study they use to demonstrate "no difference in bleeding or mortality" between emergent and delayed endoscopy firstly used scleropathy (which they deem inferior to ligation) and secondly although it had no statistically significant differences in end points it does have some trends that are notable. (Lancet. 1993 Sep 11; 342(8872):637-41)
Of note, scleropathy now has been almost entirely abandoned as "standard of care" as Villanueva et al demonstrate in this study from 2008.


What's new:

New literature appears to support our "gut" that waiting and watching these variceal bleeders decompensate in our ED is not ideal management:

(2012 Paper:) A prospective cohort study published in 2012 revealed statistically significantly differences in bleeding and mortality.  "In hematemesis patients, 6-week re-bleeding rate (18.9% vs. 38.9%, p=0.028) and mortality (27% vs. 52.8%, p=0.031) were lower in those with early (≤ 12 h) than delayed (>12h) endoscopy."

(2005 and 2010 Papers):  Consensus papers from the international expert "Baveno" consensus group which has standardized the methodology of studying variceal hemorrhage recommends performing endoscopy "as soon as possible."

Likely adding to the G.I. chatter in support of staying in bed:

(2009 Paper): Cheung et al conclude no clinical difference in bleeding or mortality in 4 vs. 8 vs 12 hour endoscopy. However, these were all hemodynamically stable bleeders. No patient with unstable hemodynamics was included.
Of note, this study is listed as being cited in 24 other peer reviewed articles. We always have to keep in mind the inclusion criteria. I think this study can essentially be written off, as the debate we are having is whether the sickest, most unstable (requiring crystalloid and blood resuscitation, and medications) should be getting emergent endoscopy.


Also interesting: 

The NNT review for Octreotide is pretty sobering as well. No mortality benefit from their perspective.


I believe that yes, this is still a controversy. Until a well done, multi-centered RCT is performed comparing apples and apples, with timing being the only variant, we may not ever have a solid answer. Until then, I think that there is plenty of good science as well as expert consensus recommending emergent, "as soon as possible" endoscopic therapy of acute variceal bleeders. I will continue to fight for this, for my patient in the ED exanguinating from above and below while awaiting midnight consultation.