Monday, June 1, 2015

Guest Post: Supraglottic Airway Devices Should Be Your First Line

This is a guest post written by Jeff Poland, NRP, FAWMc, FACPMc, for the Great EMS What-If-We’re-Wrong-A-Thon. I have a lot of experience in prehospital and perioperative airway management, and on every other day of the year am a stark proponent of the use of supraglottic airway devices only as a rescue airway in emergency situations – almost (around 99.9999999999999% of the time) never as a first line. But, below outlines the best reasoning I can come up with for why:

Supraglottic Airway Devices Should Be Your First Line

While endotracheal intubation has long been touted as the gold standard for airway securement, increasingly we are seeing more and more services and geographic areas move away from endotracheal intubation (ETI) in favour of first line placement of a supraglottic airway (SGA), with the option of ETI if the SGA fails. This is a prudent and much-needed step in the right direction for the following reasons:

Several studies [1,2] have indicated that prehospital intubation has a very low success rate. Intubation is a skill which requires a great deal of practice, and has no correlation with the experience that a paramedic has [3]. In other words, if you don’t do the skill a lot, you aren’t very good at it, and I think that is something that we all can agree on. With most of fire-based EMS, and a lot of third service EMS, focusing on a 5:1 paramedic:patient ratio [4], and the already low frequency of patients requiring this delicate procedure, which, if it fails, is catastrophic for the patient, most paramedics, especially in those systems, simply do not get the required amount of practice to remain proficient.

One of the main concerns regarding airway management is that the airway needs to work. SGAs are dislodged only minimally, and rarely are placed wrong [5]. When your patient needs an airway now, you should just put in a SGA and not have to worry about it any more. An old co-worker of mine once told me “why would I use an ET tube when this (the King Airway) is easier, quicker, and I absolutely know it’s in?” High-stress situations such as cardiac arrest and unconscious/unresponsive patients often have providers anxiety levels up, and an unrecognized oesophageal intubation is almost universally lethal. On the other hand, I have had one endotracheal intubation using a King Airway, and that required 45 minutes, a low profile MAC 3, an airway manikin, and a set of long Magill forceps. (Beth Lattone, of the Community College of Aurora’s Paramedic Program, if you’re reading this, this definitely was not on one of your airway heads, so I don’t even know why I brought it up.)

Supraglottic airways have also been shown to provide some measure of protection against vomiting [6]. This has been shown to be similar to that provided by cricoid pressure, a recognized mainstay in every emergency and failed airway algorithm, although it is much easier to use an SGA than it is to use cricoid pressure. Given that they can protect the airway up to 120cmH2O of pressure, tell me again how ETI is the gold standard?

Furthermore, the King LT has been shown to be equal to ETI in cardiac arrest, and the authors also claim that because of the more rapid airway control, it could be considered superior [7]. Instead of mucking around with trying to get a good laryngoscopic view during cardiac arrest, why not just pop in the SGA and not have to worry about it later on?

ETI is an old skill. Technology is increasing, and making things both better and easier for the provider. Why are some people so focused on keeping the old technology and refusing to adapt to the changing world? So many physicians have gone on record saying that they don’t support paramedics intubating, we continue to have abysmally high failure (and worse, unrecognized oesophageal intubation) rates, and those are time and cost consuming to fix. More and more paramedic programs are getting away with 5 simulated intubations, period, in order to pass, and it sounds like we are rapidly recognizing that ETI in the prehospital setting needs to go the way of the dodo. Even anaesthesiologists are using more and more SGAs for more and more cases. Isn’t it about time we get on board with these changes, and leave ETI for the docs who want to stay outdated?

While those are some compelling arguments against endotracheal intubation, I still firmly maintain my view that SGAs are a second-line intervention when ETI fails. Want to find out why? Join myself and my esteemed colleague Benjamin Dowdy on 21 June 2015 while we debate this issue live. For any further questions or comments, I can be contacted at



Wednesday, February 20, 2013

Challenging Tradition: Better Precordial Lead Placement

This post is part of a series presenting challenges to the traditions of EMS.

Challenging Tradition: Better Precordial Lead Placement

Application of the precordial electrodes for a 12-Lead ECG is a process steeped in over 75 years of tradition. Drs. Wolferth and Wood first described the usages of additional chest leads for the diagnosis of myocardial infarction using the leads IV, V, and VI in 1932[1] and by 1938 the standard nomenclature and position of the V-leads was described in a joint paper from the American Heart Association and the Cardiac Society of Great Britain and Ireland[2].

Since 1938, there has been little focus in validating the classical precordial lead placement. Instead, efforts to improve the sensitivity and specificity of the 12-Lead ECG focused on adding new electrodes[3,4,5] or improving existing morphological and ST-segmental criteria[6].

In 1971, the concept of body surface potential mapping (BSPM) was introduced as an alternative to the standard 12-Lead ECG [7], and by the 1980's it was recognized as providing larger gains in sensitivity in acute myocardial infarction detection over the usage of the classical precordial leads[8]. However, BSPM relies on expensive recording and post-processing techniques, and is cumbersome in its requirement for a large electrode vest which envelops the chest of the patient.
Figure 1: 80-Lead body surface potential mapping locations.
In 1985 the first paper on improving the positions of the precordial leads using BSPM was introduced by Drs. Kornreich et al[9]. They explored electrode locations which provided higher degrees of sensitivity and specificity than the traditional precordial lead placement and continued their research into 2008 with a paper describing 4 additional leads which could be added to the traditional 10 electrodes to provide information similar to that of a BSPM[10].

Research in 2002 by Drs Kors and Herpen found that moving only two precordial electrodes (V4 and V6) was required to transform the 6 precordial electrodes into a viable interpolated BSPM[11]. Their paper was notable in it sought to find the minimal derangement of the classical positioning in order to obtain diagnostic results.

In 2007 and 2008, Drs. Finlay et al explored alternative precordial lead placement using a data driven approach which sought to improve the sensitivity and specificity of MI, LVH, and other ECG abnormalities[12,13]. As with prior research, they proved again that the classical precordial lead positions perform poorly when compared to interpolated BSPMs, however, they acknowledged their improved lead positions were not practical in clinical application. Also of note, Drs. Finlay et al commented that any change to the precordial lead placement would be, "unlikely to succeed because the familiar format of the 12-lead ECG coupled with the considerable amount of diagnostic criteria accumulated in the literature mean that it is a tool with which most clinicians are extremely comfortable and which they are therefore unlikely to relinquish."[14]

However, in 2011, Drs. Peter Scott et al demonstrated a simple repositioning of the precordial electrodes which not only improved sensitivity and specificity of acute myocardial infarction identification, but also could be performed in a practical manner[15]. Using data derived from 80-lead BSPM tracings, they performed analysis which found the most appropriate positions of the precordial leads to be located along a horizontal line beginning from V1 and V2 and extending along to the midaxillary.

Figure 2: Optimal location of the precordial leads V1-V6 for the detection of acute myocardial infarction.
This paper has a high potential to challenge the status quo in not only pre-hospital acquisition of 12-Lead electrocardiograms but also in-hospital. The electrode positions given are simple to apply, and could provide for a lesser degree of inter-operator variability in positioning. More importantly, this optimized placement provided for a higher sensitivity and specificity across all types of myocardial infarction.

In personal correspondence with Dr. Scott, I inquired as to the changes this presented to other common uses of the 12-Lead ECG--such as bundle branch block definitions or VT vs SVT algorithms--and he related that this research served to open the door to further research into the practical clinical benefits.
  • Does the evidence support challenging traditional precordial lead placement?
  • What possible limitations does this lead placement present?
  • What barriers exist to the adoption of this lead placement today?
  1. Wolferth CC, Wood FC. The electrocardiographic diagnosis of coronary occlusion by the use of chest leads. Am J Med Sci 1932;183:30-35.
  2. Barnes AR, Pardee HEB, White PD, et al. Standardization of precordial leads. Am Heart J 1938;15:235-239.
  3. Perloff JK. The Recognition of Strictly Posterior Myocardial Infarction by Conventional Scalar Electrocardiography. Circ 1964;30:706-718. [FullText]
  4. Erhardt LR, Sjogrn A, Wahlberg I. Single right-sided precordial lead in the diagnosis of right ventricular involvement in inferior myocardial infarction. Am Heart J 1976;91:571-6. [PubMed]
  5. Zalenski RJ, Cook D, Rydman R. Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9: The 15-lead ECG. Ann Emerg Med 1993;22:786-793. [PubMed]
  6. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circ 2013;127:e362-e425. [FullText]
  7. Barr RC. Selection of the Number and Positions of Measuring Locations for Electrocardiography. IEEE Trans Biomed Eng 1971;18(2):125-138.
  8. Kornreich F, Rautaharju PM. The missing waveform and diagnostic information in the standard 12 lead electrocardiogram. J Electrocardiol 1981;14(4):341-50. [PubMed]
  9. Kornreich F, Rautaharju PM, Warren J, et al. Identification of best electrocardiographic leads for diagnosing myocardial infarction by statistical analysis of body surface potential maps. Am J Cardiol 1985;56(13):852-6. [PubMed]
  10. Kornreich F, MacLeod RS, Lux RL. Supplemented standard 12-lead electrocardiogram for optimal diagnosis and reconstruction of significant body surface map patterns. J Electrocordiol 2008;41(3):251-6. [PubMed]
  11. Kors JA, van Herpen G. How many electrodes and where? A "poldermodel" for electrocardiography. J Electrocardiol 2002;35 Suppl:7-12. [PubMed]
  12. Finlay DD, Nugent CD, Kors JA, et al. Optimizing the 12-lead electrocardiogram: a data driven approarch to locating alternative recording sites. J Electrocardiol 2007;40(3):292-9. [PubMed]
  13. Finlay DD, Nugent CD, Donnelly MP, Black ND. Selection of optimal recording sites for limited lead body surface potential mapping in myocardial infarction and left ventricular hypertrophy. J Electrocardiol 2008;41(3):264-71. [PubMed]
  14. Ibid. 12.
  15. Scott PJ, Navarro C, Stevenson M, et al. Optimization of the precordial leads of the 12-lead electrocardiogram may improve detection of ST-segment elevation myocardial infarction. J Electrocardiol 2011;44(4):425-431. [PubMed]

Friday, July 27, 2012

Synchronized Cardioversion: What Happened?

EMS was dispatched for a 62 year old male with an altered mental status. Upon their arrival they found the patient to be non-communicative, responsive to verbal stimuli, in moderate respiratory distress, with pale, diaphoretic skin, and weakly palpable radial pulses. The patient was placed on the monitor during their initial assessment:

Wide complex tachycardia of unknown etiology.
A blood pressure was unobtainable, however a pulse of 150 was palpable at the carotid. Labored respirations were present, with clear breath sounds bilaterally. The patient had an extensive cardiac history, renal failure, and insulin dependent diabetes mellitus. The patient's blood sugar was 300 mg/dL.

A 12-Lead was obtained and interpreted as presumed ventricular tachycardia:

Wide complex tachycardia, interpreted as presumed ventricular tachycardia.
Differentials of a wide complex tachycardia at 150 bpm include: ventricular tachycardia, SVT with aberrancy, sinus tachycardia with aberrancy, and 2:1 atrial flutter with aberrancy. No previous 12-Lead was available for comparison.

Given the presence of a WCT with hemodynamic instability the patient was prepped for synchronized cardioversion. Combo-pads were placed anterio-laterally, the Sync button was pressed, and sync markers were noted with each QRS complex.

The patient was then synchronized cardioverted at 100J biphasic:

100J synchronized cardioversion.
A rhythm change was noted on the monitor:

Ventricular fibrillation post cardioversion.
With ventricular fibrillation present, the paramedic disabled synchronization and delivered a 200J biphasic shock:

200J defibrillation of ventricular fibrillation.
After defibrillation, the patient regained consciousness and palpable radial pulses were present. Emergency transport was initiated. During transport, a sustained run of ventricular tachycardia occurred and the patient was given 100 mg lidocaine IV with a subsequent conversion of a sinus rhythm (not captured). The patient experienced multiple episodes of non-sustained ventricular ectopy during transport.

In this case the paramedic did not appreciate that oversensing was present from the cardiac monitor's display. It was not until after the summary printed that the ineffective synchronization was discovered.

Oversensing during synchronized cardioversion--highlighted in red--resulting in therapy delivery during the vulnerable period.
As the ventricular myocardium repolarizes, it may not do so homogeonously. This window of non-uniformity, with both absolutely and relatively refractory myocardium present is known as the Vulnerable Period. Electrical stimulation during the vulnerable period of ventricular repolarization may result in ventricular tachyarrhythmias.

Illustration of the vulnerable period of ventricular repolarization. Adapted from Reilly et al. 1998 pp 188 Fig 5.19.
This is best appreciated during episodes of a prolonged QT interval. An early-cycle premature ventricular contraction may result in the so called "R-on-T" phenomenon initiating Torsades de Pointes.

A prolonged QT interval and an "R-on-T" PVC resulting in Torsades de Pointes. Used with permission from Dr. Ken Grauer's ECG Web Brain.
In this case, the electrical stimulation was provided by inappropriately synchronized biphasic shock. By default the synchronization used Lead II, which featured proportionately smaller negative complexes when compared to their T-waves. Sometimes atrial tachyarrhythmias, such as atrial flutter or atrial fibrillation, may produce deflections sufficient to trigger R-wave deflection as well.

Oversensing of atrial fibrillation. Adapted from Resuscitation 82 (2011):135-136,Fig.1.
Appropriate lead section is important when performing synchronized cardioversion in order to avoid delivering the therapy while the myocardium is vulnerable. If synchronization is not accurate the operator of the cardiac monitor should switch leads, increase the gain, or change pad placement.

  • Reilly J. Patrick. Applied Bioelectricity: From Electrical Stimulation to Electropathology. Springer-Verlag: New York (1998); pp 188.
  • Dr. Ken Grauer's ECG Web Brain. Accessed online 26 July 2012. []
  • Sodeck GH, Huber J, Stollberger C. Letter to the Editor: Electrical cardioversion - Misinterpretation of the R-wave. Resuscitation 82 (2011): 135-136. [PubMed]

Wednesday, July 18, 2012

Incidence of cardiac rhythms as determined by Paramedics on an ALS ambulance

The following are the incidence of various cardiac rhythms as determined by the treating Paramedic for an ALS ambulance from October 2007 to June 2012. Outlier data were examined for correctness, including all interpretations of rhythms with less than 2% incidence. Incomplete data for each record was added if available, otherwise the record was ignored. AV Nodal Blocks and Bundle Branch Blocks were not recorded in this data set.

  • Patients: 3528 (47% male)
  • Age: 8 hours - 110 years (avg 56 yr, median 60 yr)

  • First Contact Heart Rate (>0): 22-260 bpm (avg 91 bpm, median 90 bpm, stdev 29.5)

  • First Contact Rhythm:
Count Rhythm
184152.18%Normal Sinus Rhythm
99528.20%Sinus Tachycardia
1454.11%Paced Rhythm
1393.94%Sinus Bradycardia
1143.23%Atrial Fibrillation
681.93%Sinus Arrhythmia
671.90%Atrial Fibrillation w/ RVR
190.54%Pulseless Electrical Activity
180.51%Supraventricular Tachycardia
110.31%Ventricular Fibrillation
100.28%Atrial Flutter
50.14%Ventricular Tachycardia
40.11%Junctional Rhythm
20.06%Idioventricular Rhythm
10.03%Ectopic Atrial Tachycardia
10.03%Junctional Tachycardia

Thursday, July 12, 2012

EKG Myth - "Can't be Ventricular Tachycardia with that Axis"

This is part of a series of posts detailing common electrocardiogram myths.

Myth: Ventricular Tachycardia always has an extreme axis

When evaluating a wide complex tachycardia, many providers will look at the QRS axis to rule out ventricular tachycardia if an extreme axis is not present. An extreme right axis deviation, also known as No Man's Land, is easiest to appreciate when leads I, II, and III are almost wholly negative.

The absence of an extreme right axis deviation does not rule out ventricular tachycardia.

In fact, the sensitivity of an extreme right axis deviation may only reach 20%[1]. More commonly, VT features a left axis deviation[2].

In 70% (n=172) of VT cases studied by Brugada et al had a Left axis deviation[2].

As with any cardiac rhythm, the axis is dependent on the origin and subsequent activation of the myocardium.

VT origin and QRS axis. An apical origin results in a superiorly directed axis in the frontal plane. In contrast, a basal origin leads to an inferior QRS axis (lower panel)[3].

In VT arising from the left ventricle, a RBBB-like morphology is most common[4]. If the origin is in the apex of the left ventricle near the inferiolateral wall, the classic extreme right axis deviation (right superior axis) will be present. Whereas, if the origin is in the left free wall a right inferior axis deviation will be present[5].

Two cases of Ventricular Tachycardia with an (A) inferior axis and a (B) right axis deviation[6].

In VT arising from the right ventricle, a LBBB-like morphology is most common[7]. If the origin is closer to the septum, a right axis deviation will be present. If the origin is the Right Ventricular Outflow Tract (RVOT), an inferior axis will be present with characteristic broad, monomorphic R-waves in leads II, III, and aVF. RVOT-VT is a common ventricular tachycardia in patients without known cardiac disease[8]. In some cases, VT arising from the right ventricle will have a normal axis.

VT with a normal axis, misclassified as SVT[9].

Any approach to the diagnosis of a wide complex tachycardia should include ruling in Ventricular Tachycardia if an extreme right axis deviation is present. However, clinicians should be mindful that the absence of an extreme right axis deviation cannot rule out Ventricular Tachycardia.

  1. Vereckei A, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm 2008;5:89–98. [PubMed]
  2. Brugada P, et al. A New Approach to the Differential Diagnosis of a Regular Tachycardia with a Wide QRS Complex. Circulation 1991;83:1649-1659. [Full Text PDF]
  3. Wellens HJJ. Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart 2001;86:579-585. [Full Text]
  4. Surawicz B, Knilans TK. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric, 6th ed. Philadelphia, PA. Saunders, 2008.
  5. Pellegrini CN, Scheinman MM. Clinical Management of Ventricular Tachycardia. Curr Probl Cardiol. 2010;35:453-504. [PubMed]
  6. Ibid 2.
  7. Ibid 4.
  8. Ibid 5.
  9. Ibid 2.

Tuesday, February 7, 2012

J-waves after ROSC and Intra-arrest Therapeutic Hypothermia

The following is the post-resuscitation 12-Lead electrocardiogram of an 82 year old female who received intra-arrest therapeutic hypothermia, via chilled saline and ice packs, as part of a new protocol for cardiac arrest management. The patient also received three defibrillations and was administered epinephrine, naloxone, and amiodarone during the resuscitation.

12-Lead ECG obtained approximately 5 minutes after ROSC
The post arrest 12-Lead ECG shows a sinus rhythm with frequent premature atrial and ventricular ectopic complexes. The LifePak 12, which uses the GE Marquette 12SL algorithm, displayed the ominous *** ACUTE MI SUSPECTED *** message and suggested a lateral injury pattern.

Closer inspection of the lateral precordial leads reveals the ST-elevations present are actually giant J-waves, or Osborn waves.

J-waves--or Osborn waves--appreciated in the lateral precordial leads
Recognizing this finding is present, a closer look at the entire 12-Lead ECG shows that subtle J-waves are present in almost every lead group.

Subsequent 12-Lead ECG obtained 17 minutes after ROSC
A repeat 12-Lead ECG acquired 12 minutes later shows a sinus tachycardia with a single PAC, without the giant J-waves from the initial ECG, diffuse ST/T-wave changes consistent with ischemia are also present. However, small J-point elevation persists in the lateral precordials. The computerized interpretation no longer believes a STEMI-pattern is present and incorrectly identifies the rhythm as atrial fibrillation.

Comparison of the precordial leads between the first and subsequent 12-Lead ECG.
A side by side look at the precordial leads provides an interesting look at the near resolution of the giant J-waves post-ROSC.

One explanation for the normalization of the traditional electrocardiographic findings of hypothermia may be related to the management of the patient's ventilation both intra-arrest and post-arrest. As the patient's pH normalized with mechanical ventilation and a perfusing rhythm, so did the repolarization abnormalities (visualized as J-waves).

  1. Antzelevitch C, Yan GX. J Wave Syndromes. Heart Rhythm. 2010; 7(4):549-558. [FullText]
  2. Fenstad ER, et al. Therapeutic hypothermia in out of hospital sudden cardiac arrest: Significance of J-waves. J Am Coll Cardio. 2011; 57(14):Suppl 5, E1002. [PDF FullText]
  3. Edelman ER, Joynt K. J Waves of Osborn Revisited. J Am Coll Cardio. 2010; 55(20):2287. [PubMed]
  4. Dr. Smith's ECG Blog: Osborn Waves and Hypothermia.

Monday, December 26, 2011

Philips Healthcare's Sierra ECG format XLI Compression Scheme

One of the services I work for has recently acquired a Philips HeartStart MRx cardiac monitor. It came complete with Bluetooth transmission of 12-Lead and event data. At roughly the same time our service installed a computer, an MDT, into the cab of our unit to interface with our county's CAD software.

Naturally I linked our monitor and our MDT via Bluetooth, and transmitted a 12-Lead from a rhythm generator. When the file landed on the MDT, I looked for an application to view the 12-Leads and rhythm strips, however, none appeared to be able to use the file as-is.

For the non-technical, the ECGs are shipped compressed--somewhat like a ZIP file--which contains all of your monitored vital signs, printed rhythm strips, and your 12-Leads. The format of the 12-Leads is an Open Standard; Philips Healthcare provides most of the details needed to use the files. The 12-Lead data is also compressed to save space. Unfortunately, there is no documentation which tells you how to decompress the 12-Lead data.

The technically-faint-of-heart should skip these next bits.

For the technical, the ECGs are contained in a Gzip'd TAR archive. The 12-Leads are stored inside in an XML format known as the Sierra ECG format (currently at version 1.03 or 1.04, as far as I can tell). Inside this XML format is Base64 encoded, XLI compressed data comprising the acquired leads during a 12-Lead (up to 16 leads appear to be able to be stored).

I searched for a description of the XLI compression format, however, I was only able to find a reference implementation for Microsoft Windows which simply decoded the files. No code or description was provided, and the implementation itself is not portable. (ed: it appears this may be a reference to the HP PageWriter XLi which Philips acquired)

At this point I decided my only option was to reverse engineer the XLI Compression format, and began with simple guesses. I tried decompressing the data using Deflate, Zip, and RLE without any progress. I was able to determine that the first 8 bytes of the compressed data included a compressed length, some uncompressed data, and that each of the 12 to 16 leads were stored in a chunk with one of these headers:
offset   2        4        6        8  ...
| Size            |  Unk.  | Delta? | Compressed data...       |
+--------+--------+--------+--------+                          |
| ...                                             [Size bytes] |
| Next lead chunk ...                                          |
Once the simple guesses were ruled out, I began exploring the behavior of the reference implementation provided for the Sierra ECG format. Using OllyDbg I noticed certain code tells which made me believe the decompression algorithm read 10-bits at a time:
SHR   EAX, 16h   ; reduce EAX to the 10-bit code word
SHL   ECX, Ah    ; prepare to read 10 more bits from the input
The compressed data also did not appear to contain a compression dictionary referenced by the code. At this point I considered I was looking at a form of Lempel-Ziv-Welch, or LZW, compression. LZW is a popular, lossless compression scheme which creates its compression dictionary on the fly. It is used by the GIF and TIFF image formats, and was the subject of controversy when it was first introduced into the GIF format due to patent licensing requirements.

In my quest to quickly reach a conclusion I found an excellent LZW implementation from Mark Nelson in C and it successfully decompressed the data. In fact, the structure of the C code was so familiar, I realized the reference implementation from Philips used the exact same code!

If you've reached this step while following along at home, you'll notice the decompressed data seems front-loaded with 0's. This is a case of intelligently streaming the data to the compression algorithm to take advantage of data duplication.

The uncompressed data represents 16-bit delta codes, of which the majority include 0x00 or 0xFF in their most significant byte (MSB). This is because they are either small and positive or small and negative, and as ECG data is rhythmic the delta codes are likely to retain the same sign for numerous samples.

To take advantage of this fact during compression, the delta codes are first deinterleaved into two halves. The first half includes each MSB and the second half includes each LSB. The pseudo-code for interleaving the decompressed data looks like the following:
# input contains the decompressed data
# output will contain the interleaved 16-bit delta codes
fun unpack( input[], output[], nSamples )
    for i <- 1..nSamples
        output[i] <- (input[i] << 8) | input[nSamples + i]
At this point the delta compression scheme will need to be decoded to produce the actual signal data for each of the leads. The delta compression scheme is a simple recurrence relation (a second order difference relation) using the prior two delta codes:
# output contains the 16-bit delta codes
# first is the 16-bit delta code from the chunk header
fun deltaDecompression( output[], nSamples, first )
    x <- output[1]
    y <- output[2]
    prev <- first
    for i <- 3..nSamples
        z <- (2 * y) - x - prev
        prev <- output[i] - 64   # is -64 to 64 the range?
        output[i] <- z
        x <- y
        y <- z
Now that you have the actual, per signal data all you need to do is recreate leads III, aVR, aVL, and aVF. This is done using the data from leads I and II as on most ECG machines. I've omitted the actual formulas for brevity.

Using my reference implementation of the decompression algorithm I was able to feed the original acquired 12-Lead to the Philips ECG to SVG converter, with the following results:

If you'd like to start playing with my code I welcome you to join my Github Project: sierra-ecg-tools. I am also working on a C implementation, and likely an Android implementation. Stay tuned, and apologies for the technical post.

The author has no financial ties to Philips Healthcare and received no compensation for this work.

Tuesday, December 6, 2011

EKG Myth - Ventricular tachycardia must have concordance

This is part of a series of posts detailing common electrocardiogram myths.

Myth: Ventricular Tachycardia must have precordial concordance

When differentiating a regular, wide-complex tachycardia some will look for precordial concordance to rule-in, or more importantly to rule-out ventricular tachycardia.

The absence of precordial concordance is not a reliable method of ruling out ventricular tachycardia:
Although the specificity of concordance for VT is high (>90%), the sensitivity is low (~20%)1.
It is generally thought that positive concordance indicates a posteriobasal left ventricular origin and negative concordance indicates an anterioapical left ventricular origin. However, in the case of positive concordance, SVT with a left-posterior accessory pathway is a known cause.

Until recently, negative concordance has been thought to be "virtually diagnostic" of ventricular tachycardia2. Multiple case reports have shown that certain configurations of accessory pathways can also cause negative concordance3,4,5.

The key takeaway is while this criteria is a useful tool to rule-in ventricular tachycardia (i.e. high specificity), it is not a useful tool to rule-out ventricular tachycardia (i.e. low sensitivity).

Ventricular tachycardia without precordial concordance6.
Ventricular tachycardia without precordial concordance. (c) 2011 EMS 12-Lead Blog.
WPW and Atrial flutter with positive concordance7.
While positive or negative concordance may strongly suggest ventricular tachycardia, providers should not rule-out ventricular tachycardia in its absence.

  1. Pellegrini CN, Scheinman MM. Clinical management of ventricular tachycardia. Curr Probl Cardiol. 2010; 35(9):453-504. [PubMed]
  2. Goldberger ZD, Rho RW, Page RL. Approach to the Diagnosis and Initial Management of the Stable Adult Patient With a Wide Complex Tachycardia. Am J Cardiol. 2008; 101:1456-1466. [Full Text]
  3. Pappas LK, et al. Wide QRS complex supraventricular tachycardia with negative precordial concordance. Am Heart Hosp J. 2009; 7(1):67-8. [PubMed]
  4. Kappos KG, et al. Wide QRS Complex tachycardia with a negative concordance pattern in the precordial leads: Are the ECG criteria always reliable? Pacing Clin Electrophys. 2006; 29:63-6. [PubMed]
  5. Volders PGA, et al. Wide QRS complex tachycardia with negative precordial concordance: Always a ventricular origin? J Cardio Electro. 2003; 14:109-111. [PubMed]
  6. Garmel GM. Wide Complex Tachycardias: Understanding this Complex Condition Part 1 - Epidemiology and Electrophysiology. W J Emerg Med. 2008; 9(1):28-39. [Full Text]
  7. Ibid. 1, Figure 3.

Thursday, November 17, 2011

EKG Myth - "It's Too Fast for Ventricular Tachycardia"

This is part of a series of posts detailing common electrocardiogram myths.

Myth: Rate can help you rule out Ventricular Tachycardia

When differentiating a regular, wide-complex tachycardia some will look at the rate to rule out ventricular tachycardia. Studies have not found rate to be a predictive finding1.
...regarding ventricular rate, significant overlap unfortunately exists between VT and SVT such that rate is not a helpful criterion to differentiate origins2.
Ventricular tachycardia technically can range in rates from 100 bpm through 300 bpm. However, a practical definition of VT would place the lower bound around 120 bpm and the upper bound around 260 bpm3.

Common terminology includes rates slower than 120 as "Slow Ventricular Tachycardia", which most often is not true VT4. Rates upwards of 260 to 300 bpm are commonly termed "Ventricular Flutter"5.

Ventricular tachycardia at 130 bpm. (c) 2001 - 2011 Beth Israel Deaconess Medical Center.

Ventricular tachycardia at 206 bpm. (c) 2011 EMS 12-Lead Blog.

Ventricular tachycardia at 280 bpm. (c) 1994-2011 WebMD.

As a rule: a regular, wide-complex tachycardia should be treated as ventricular tachycardia in the field, until proven otherwise.

  1. Griffith MJ, et al. Multivariate analysis to simplify the differential diagnosis of broad complex tachycardia. Br Heart J (1991); 66:166-74. [PubMed]
  2. Hudson KB, et al. Electrocardiographic Manifestations: Ventricular Tachycardia. J Emerg Med (2003); 25:303-314. [PubMed]
  3. Surawicz B, Knilans TK. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric, 6th ed. Philadelphia, PA. Saunders, 2008. 
  4. Mattu A. ECG PEARLS: Beware the Slow Mimics of Ventricular Tachycardia. Emergency Physicians Monthly, 24 August 2010. Retrieved Online 8 November 2011. [Free Full Text]
  5. Gurevitz O, et al. Long-term prognosis of inducible ventricular flutter: not an innocent finding. Am Heart J (2004); 147(4):649-54. [PubMed]

Wednesday, June 22, 2011

Zebra Spotting

I'm sure we all received the following good advice at some point in our EMS education or careers:
"When you hear hoofbeats, think horses not zebras."
I propose we add the corollary:
"...but if you don't stay to watch, you won't know what you missed."
Remember, always err on the side of the patient.