Our expert today is Darlene Hutton. She has worked in CCU, ICU, PACU, and Emergency as a bedside nurse, educator, and manager. She is currently working as a Clinical Research Manager at Rouge Valley Metabolic Research Associates in Toronto. Darlene also is an Educational Consultant providing workshops, seminars, and conferences on such topics as ECG Interpretation, Dysrhythmia Interpretation, Acute Coronary Syndromes and Cardiology Drugs. She is also an ACLS Course Director and runs courses throughout the province. Her company, QRS Educational Services, founded 18 years ago, provides education to nurses and other health care professionals throughout Canada. She is also the Department Head for Emergency Preparedness in the O.R. in the American College of Plastic Surgical Nursing journal.

Answer:

I PERSONALLY WENT THROUGH THIS 8 YEARS AGO...FUN TIMES. WHEN I WENT TO MY FAMILY DOCTOR HE STATED THE POTENTIAL CAUSES, IN THIS ORDER WERE: ADRENAL TUMOR, CARDIAC DISEASE. THOSE WERE HIS ONLY 2 OPTIONS. NEEDLESS TO SAY, I AM NO LONGER WITH THIS PRACTITIONER. THE 24 HR URINE WAS NEGATIVE AND THE CARDIAC STRESS TEST DID NOT INDUCE THE BIGEMINY, SO THAT WAS ALSO NEGATIVE. IN MY CASE, THE CAUSE CAN BE ATTRIBUTED TO THOSE WONDERFUL HORMONES THAT ACT UP IN THE PERIMENOPAUSAL PERIOD OF OUR LIVES.  I TEACH STUDENTS THAT THE HEART DOESN'T NORMALLY THROW OFF BIGEMINY, OR MULTIFOCAL PVCS, OR COUPLETS. WHEN IT DOES, WE MUST ASK OURSELVES "WHY?"  COMMON CAUSES ARE: ISCHEMIA (DO AN ECG, THE PATIENT SHOULD HAVE A STRESS TEST AS ANOTHER TEST FOR ISCHEMIA), ELECTROLYTE IMBALANCE (CHECK THE LYTES - HYPERKALEMIA IS ALWAYS A FRONT RUNNER), DRUGS (ONE EXAMPLE IS RED BULL-INDUCED VT IN AN EMERGENCY NURSE WHO DRANKS 3 LARGE CANS DURING HIS 8 HOUR SHIFT).

The significance of ventricular bigeminy may be huge or of little consequence. First, it depends on how my patients looks right at this moment. Are they compromized? Some ventricular beats produce an output while others don't. So, when assessing this patient it is important to determine if there is output with these beats; otherwise what may look like a heart rate of 80 may only be one of 40. If all tests have deemed no significant cause of the bigeminy, then there is really nothing more to be done. Starting on an antiarrhythmic drug, such as amiodarone, would not be recommended as this drug may cause worse side effects that the treatment it's being given for; namely torsade des pointe from a prolongation of the QT interval.

Our expert today is Dr. Ken Grauer.  He is a frequent contributer to the ECG Guru. 

KEN GRAUER, MD  is Professor Emeritus (Dept. Community Health/Family Medicine, College of Medicine, University of Florida in Gainesville).
Dr. Grauer has been a leading family physician educator for over 30 years. During that time he has published (as principal author) more than 10 books and numerous study aids on the topics of ECG interpretation, cardiac arrhythmias, and ACLS (including an ongoing Educational ECG Blog).

Answer:  To see illustrated explanations of laddergrams, and how to use them, please use this link to his ECG Blog http://tinyurl.com/KG-Blog-69

Comprehensive list of criteria

PermalinkSubmitted by jer5150 on Tue, 01/10/2012 - 22:17

INTERPRETATION: Ventricular tachycardia (rate about 163/min) presumably originating from the left ventricle (LV).
Overwhelming evidence that this is ventricular tachycardia are as follows:
1.) The ventricular tachycardia is apparently dissociated from a sinus tachycardia at a somewhat slower rate of about 123/min (best seen in leads V1 and aVL; vertical arrows). While not nearly as clinically significant as those types of double tachycardia caused by digitalis intoxication, this example might technically qualify as a form of “double tachycardia” since both the upper and lower chambers of the heart are exceeding a rate of 100/min.
2.) The duration of the QRS interval is so-called “wide-wide” (i.e., > 0.14s) at about 0.19s to 0.20s.
3.) The predominantly negative rS complex in Lead I and wholly negative QS complex in aVF indicate an axis of roughly about -120 and would place it in the right upper quadrant (i.e., “No-Man’s-Land” or “N-M-L”). This is suggestive of an apical origin of the tachycardia.
4.) Brugada criterion # 1: There are no RS complexes in any of the V leads (here they’re either qR or QS complexes.) Brugada pointed out that if none of the V leads contained a diphasic RS complex, then there was no need for any further analysis, the tachycardia was unequivocally ventricular in origin. 2
5.) The presence of a monophasic QS complex in V6 is more diagnostic of ventricular tachycardia than just a rS complex; especially if associated with a QRS complex in V1 that is predominantly positive. By Dr. Marriott’s estimation, this combination only occurs in about 20% of all left ventricular tachycardias (LVT).
6.) Cogent evidence arguing against this being the result of conduction over an accessory pathway are threefold:
a. The wholly negative QS complexes from V4-6 are also suggestive of an apical origin of the tachycardia. Since all accessory pathways enter the ventricles at their base, accessory pathway conduction is effectively excluded; and . . . 1
b. . . . a qR complex in any of the five leads, V2-6 (here in V2-3) also excludes preexcited (W-P-W) tachycardia; and . . . 1
c. . . . the presence of more QRS complexes than P-waves (because in any form of preexcited tachycardia, the atria are involved in every beat). 1
7.) The QRS complex in V1 is not a monophasic R-wave. Rather it is a diphasic qR complex with very subtle notching / slurring on the downstroke (oblique arrow) of the R-wave (i.e., so-called taller left “rabbit-ear” equivalent.)
8.) The q-waves in V1-3 are superficially mimicking the negative component (i.e., nadir) of an atrial flutter wave but right-sided chest leads do not usually show the typical “saw-tooth” pattern so often seen in inferior leads II, III, and aVF. Atrial flutter waves in V1 usually take on the appearance of little positive “P-like” waves. What looks like a retrograde atrial impulse immediately following a QRS complex in V4 is actually part of the QRS complex itself.

References / Sources.
1.) Marriott, HJL. Emergency Electrocardiography. Naples, Fl.: Trinity Press, 1997, p. 60 - 71.
2.) Nelson's EKG Site: http://nelsonsekgsite.com/

Today's Expert is Dr. KEN GRAUER, MD   Dr. Grauer is Professor Emeritus (Dept. Community Health/Family Medicine, College of Medicine, University of Florida in Gainesville).
Dr. Grauer has been a leading family physician educator for over 30 years. During that time he has published (as principal author) more than 10 books and numerous study aids on the topics of ECG interpretation, cardiac arrhythmias, and ACLS (including an ongoing Educational ECG Blog) . For more information about Dr. Grauer, see his website: https://www.kg-ekgpress.com/
 
ANSWER:

Teaching the hemiblocks has often been an area that leads to confusion among those learning ECG interpretation. It is easy to understand why ... - even expert electrocardiographers don't agree on the definition as to what constitutes a hemiblock. I've always felt that when many equally correct answers exist to a question - Why not choose one of the answers that is easy to apply and easy to remember? So it is with the hemiblocks. All that a "hemiblock" is - is failed conduction down one of the two major fascicles of the left bundle branch.
Although there are millions of fibers within the conduction fascicles - for practical purposes, there are 2 main divisions to the left bundle branch (See accompanying PDF in RESOURCES  for explanatory figure and description). These 2 divisions of the left bundle branch are the left anterior and left posterior hemifascicles. A hemiblock entails failed conduction in one of these hemifascicles. If conduction fails in both hemifascicles (or if the defect in conduction is proximal to the level where the main left bundle branch divides into these 2 hemibranches) - then complete left bundle branch block (LBBB) will arise. For practical purposes - LPHB (left posterior hemiblock) is rare. This is because the left posterior hemifascicle is both much thicker as well as enjoying of dual blood supply from both left and right coronary arteries - vs the much thinner and singly supplied left anterior hemidivision. Although I've never seen a study quantifying the relative frequency of LAHB vs LPHB - in my experience LPHB is very rare (probably less than 1-2% of the hemiblocks). Even cardiologists often do not agree on whether or not LPBH is present - such that most noncardiologists would be none the worse if they never in their life diagnosed LPHB (suggestions for how to diagnose LPHB are included in the attached PDF). Thus, IF a hemiblock is present - it will almost always be LAHB.
 
How then to diagnose LAHB? For practical purposes - one can equate the diagnosis of LAHB with that of a "pathologic" left axis. LAD (left axis deviation) is defined as an axis that falls in the upper left quadrant (ie, between -1 to -90 degrees). We define "pathologic LAD" as an axis more negative than -30 degrees. Fortunately - this is EASY to determine on the ECG. We know that the axis lies perpendicular (90 degrees away) from a lead that is isoelectric (equal parts positive and negative). Therefore, assuming lead I is positive (so that the axis lies in the left hemisphere) - IF the QRS complex is isoelectric in lead II (at +60 degrees) - then the axis must lie 90 degrees away from lead II, or at -30 degrees. All one has to do to determine IF there is a pathologic left axis is look at lead II. If the net QRS deflection in lead II is more positive than negative - then the axis lies LESS than 90 degrees away from lead II, or between -1 and -30 degrees. On the other hand - IF the net QRS deflection in lead II is more negative than positive - then the axis must lie MORE than 90 degrees away = a "pathologic left axis" = LAHB.
 
Reasons to consider teaching the above approach for the hemiblocks is that it is equally accurate and far simpler than worrying about complex morphologic criteria or axis deviations exceeding other amounts. The beauty of the above approach is that it allows accurate determination of whether LAD is sufficiently negative to satisfy criteria for LAHB in less than 5 seconds.
 
 
 
Ken Grauer, MD