Saturday, September 13, 2014

POCUS-FOCUS #1: Recognizing Hypertrophic Cardiomyopathy

Welcome to the first of what I hope will be a continuing series of concise monthly videos or e- learning material FOCUSed on POCUS (Point-Of-Care-UltraSound). The intention of the series is to draw attention to supplemental or more advanced uses for POCUS, interesting cases, important EM Ultrasound literature, online resouces (FOAM), and other fun EM Ultrasound tidbits.

The first POCUS-FOCUS topic will be:
Differentiating Hypertrophic Cardiomyopathy (HCM) from both hypertensive heart disease (HHD) AND Athletic heart.

I will keep this simple and focused on scanning techniques that most EM-trained docs should be able to perform, while avoiding much the more difficult and advanced methods.
HCM: A genetic protein mutation leading to inappropriate LV muscular thickness (anywhere) but more often septal leading to obstruction of the LVOT (left ventricular outflow tract) and often malignant dysrhythmia.

Our job in the ED: Risk stratifying and screening appropriate patients with concerning clinical and/or family history for HCM. Our job is NOT TO DIAGNOSE HCM. We should simply search for evidence that this may be the underlying etiology of the presenting complaint which could alter our disposition or management.

What you should do?: Perform focused cardiac ultrasound (FoCUS). Most importantly the Parasternal Long Axis and the Parasternal Short Axis ; if desired use M-mode which will ensure more accurate phase (end-diastole). Measure the LV thickness at end diastole at various different locations.

PSSA: Measure Base, Mid, and Apical LV Thickness _________________________________________________________________

PSLA (with M-mode): Measure LV thickness @ the trough (end diastole) -Septal wall AND posterior wall (yellow) measurements (then calculate ratio)

What measurements should worry you?

Guidelines differ however it appears widely accepted that LV thickness in ANY myocardial segment >15mm is concerning for HCM. Also, septal to posterior (s/p) wall thickness ratio > 1.3 (in normotensive) and > 1.5 (in hypertensive patients) is considered highly suspicious for HCM
Hypertensive hearts MAY also have larger septal thickness compared to posterior. They are not always concentrically hypertrophic as is classically taught. Athlete hearts are often much less thick than both HHD and HCM.
Here are some tables with important measurements, these are the some of the values from which the guidelines have been derived:

Bonus (more advanced US technique/interpretation): There are no pathognomonic findings on echo for HCM, given that hypertension can give profound LV thickness, even asymmetric septal thickness. However, there is a finding called SAM (systolic anterior motion) which is anterior motion of the anterior leaflet of the mitral valve toward the septum just after systole begins (which is why HCM becomes obstructive – particularly in hypovolemia/Valsalva/etc). See the table above which reveals that no normal or hypertensive patients demonstrated SAM and 36/47 HCM patients did. This finding is very specific, but not so sensitive, for HCM.
You can see this as an EM doc at the bedside ... I PROMISE. Just watch the LVOT (left ventricular outflow tract) –particularly the anterior mitral leaflet- in these parasternal long axis (PSLA) clips of NORMAL patients and HCM patients.

Sheikh N. The electrocardiographic phenotype in athletes with hypertrophic cardiomyopathy: implications for pre-participation cardiovascular evaluation using electrocardiography. Heart. 2014 Jun;100 Suppl 3:A51
Bart et al. Measurement of Left Ventricular Wall Thickness and Mass by Echocardiography. Circulation. 1972;45:602-611
Williams, et al. Echocardiography in hypertrophic cardiomyopathy diagnosis, prognosis, and role in management. Eur J Echocardiogr (2009) 10 (8):iii9-iii14. (
Doi, et al. Echocardiographic differentiation of hypertensive heart disease and hypertrophic cardiomyopathy. Br Heart J 1980;44:395-400 doi: 10.1136/hrt.44.4.395
Lang, R. M., et al. (2005). "Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology." J Am Soc Echocardiogr 18(12): 1440-1463. 

Saturday, January 4, 2014

Sux in Head Injury

The confirmation Ive been looking for!

US Diagnosis of Intraperitoneal Air

Very cool, from this study. Id be curious if this reverb artifact exists without significant free fluid?

This demonstrated free intraperitoneal fluid in Morison’s pouch (Video Clip S1). Upon attempting views of the pelvis, distinct hyperechoic foci with reverberation artifacts were visualized within the free fluid, suggesting associated free intraperitoneal air (Video Clip S2). 

A new syncope rule? The Anatolian Syncope Rule (Turkey)

Check out this Turkish paper which has developed a syncope rule VERY sensitive for adverse events. Makes me rethink butting heads with medicine when they ask for orthostatics (as this syncope rule finds orthostasis highly correlating with adverse events). It is yet to be validated by anyone outside of Turkey.

Of important note the rule is, as they state: 
The newly proposed ASR performed with higher sensitivity but lower specificity when predicting mortality

Read the paper here.

Below are the 6 parameters with high predictive value for adverse events:
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Im not sure how to interpret the "precipitating cause" (maybe someone -Melville or Amisha?), from their results section they state:

 Precipitating factors were drugs, diabetes and neurologic disorders in patients with orthostatic syncope (40% of the known precipitating group). Fever, dehydratation, fasting and long standing were the precipitating factors in vasovagal syncope (45% of the known precipitating group). The other 15% were due to arrhythmia and cardiogenic causes.

Wednesday, January 1, 2014

Why do we discharge, and can we predict bounce back?

Fascinating paper on discharge decision making. They analyzed why the physician discharged.

Most physicians (even these Canadians who we often perceive as being more algorithmic) stated they used clinical judgement (nearly70%) compared to evidence-based reasoning.

Also, the adverse event rate in 366 discharges was low. 10. With only one death. HOWEVER, upon review by 3 trained ED physicians almost all of these were deemed to be PREVENTABLE.

Its a provocative paper and offers and interesting discussion on discharge decision making which is one of the heaviest tasks we have.

Here is the Paper.

Tuesday, December 17, 2013

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.

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

     -makes no mention of analyzing ventricular paced ECGs
     -V-Paced not included in definition of LBBB

Monday, October 28, 2013

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):


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 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.

Inline image 3

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.
  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.

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:
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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).

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