Dawn's picture

How Do You Explain the Genesis and Significance of Ventricular Bigeminy to Your Students?

Submitted by Dawn on Sun, 03/18/2012 - 11:25

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.

 

Darlene Hutton, RN, BScN, MSN

 

 

 

 

Dawn's picture

How do you teach the concept of reentry in PSVT to students with only a basic understanding of dysrhythmias?

Submitted by Dawn on Sun, 03/04/2012 - 02:13

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:
PSVT is a reentry tachycardia. This arrhythmia carries many names, one of which is AVNRT = AV Nodal Reentry Tachycardia - recognizing that in the vast majority of cases, there is reentry occurring in or around the AV node. The AV node is not a homogeneous structure - instead functionally (and anatomically on a microscopic level) - there are 2 basic pathways. One of these conducts "fast" - and the other "slower". Conduction preferentially goes down the "fast" pathway (thereby 'blocking' and preventing conduction down the slow pathway). But if for any reason (like a PAC) the fast pathway is "blocked" - then conduction of the impulse will have to go down the "slow" pathway. If the timing is just right - conditions may be set up that allow "reentry" within the AV node - with the impulse going down the slow pathway and up the fast pathway. Less commonly, reentry within the AV node may be set up in which the impulse goes down the fast pathway and back up the slow pathway.

 

Think of the phenomenon of reentry as comparable to the situation when 50 young children are all holding hands and running around in a circle while holding hands. All it takes is for one disgruntled person to stick out their leg - and ALL 50 of the children who are holding hands will fall down. So it is with reentry - it is a circuit that is set up by fortuitous circumstances of conduction speed, refractory period duration, and usually a precipitating premature impulse. How do we treat AV Nodal Reentry Tachycardia (PSVT)? Either by vagal maneuvers or medication such as adenosine, diltiazem/verapamil, or beta-blockers - ALL of which at least transiently alter conduction properties within a portion of the AV node. Just like the disgruntled citizen who stuck out their leg and tripped up all 50 children - all it takes is brief alteration/interruption of the conduction circuit (by meds or vagal maneuver) to terminate an AV Nodal Reentry Tachycardia.

 

Simplistic illustration of the concept of reentry appears in the Figure below (excerpted from pp 567-574 of Grauer K, Cavallaro D: ACLS: Comprehensive Review [Vol 2] - 3rd Edition, Mosby Lifeline, St. Louis - 1993). For a more detailed look at reentry - visit: https://www.kg-ekgpress.com/reentry-svt/ - where you can download a pdf of the above 7 pages.

 

Ken Grauer, MD ([email protected])

 

 

Exerpted from pp 567-574 of Grauer  K, Cavallaro D: ACLS: Comprehensive Review (Vol. 2) - 3rd Edition, Mosby Lifeline, St. Louis - 1993.

 

 

 

 

Dawn's picture

How can I use laddergrams to teach my students?

Submitted by Dawn on Mon, 01/30/2012 - 13:49

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

 

 

Dawn's picture

Question: Does an extreme right axis (backward) always indicate a ventricular rhythm?

Submitted by Dawn on Sat, 01/21/2012 - 23:16

Today's expert is Jason E. Roediger, CCT, CRAT, who is a highly respected Cardiovascular Technician at the Dept. of Veterans Affairs, Hunter Holmes McGuire VA Medical Center in Richmond, VA. He is known for holding numerous certifications in all levels of ECG interpretation, and also for scoring 100% on the Level IV Advanced ECG Board Certification exam that is usually reserved for cardiologists.
 

Answer: Always? No. Usually, Yes.
There are exceptions to several "golden rules" in electrocardiography and this one is not exempt. One of the chronic issues contributing towards widespread confusion in understanding electrical axis is a lack of continuity in terminology. There is no general concensus on how to refer to an axis in the right upper quadrant. Depending on which author you are reading, it has traditionally been known by multiple names: Northwest axis. . . upper right quadrant. . . extreme right axis. . . right superior axis. . . "no-man's-land" (i.e., "N-M-L".). . . etc. Because my first exposure to electrical axis was through Dr. Marriott's textbooks and he prefered to use "N-M-L", I have personally latched on to that particular name as well. Even though some persist in calling it an "extreme left axis" or "far left axis deviation", this practice is frowned upon and discouraged. It's important to note that an axis in "N-M-L" is not synonymous with an "indeterminate" axis which occurs when the QRS is essentially isodiphasic or equphasic in all 6 limb leads and therefore the polarity of the QRS cannot be discerned in leads I and aVF.

Definition: An axis in "N-M-L" is recognized when the QRS complex has a predominantly or wholly negative deflection (i.e., down) in leads I and aVF. The axis is −90 to −180 degrees.

Irregardless of which descriptive name you prefer, in the context of a wide QRS complex tachycardia, this particular axis is highly predictive of ventricular tachycardia and is rarely encountered in "conducted" rhythms however some examples of aberrant SVT have been published with an axis in "N-M-L".

In summary: An axis in "N-M-L" implies (but is not proof of) an apical origin to the rhythm and should make one think of and exclude the possibility of ventricular tachycardia. As a general rule, until it is proven otherwise, assume any wide QRS complex tachycardia is ventricular tachycardia. Even though this one clue carries significant weight in supporting the interpretation of ventricular tachycardia, that conclusion can not be made based solely on this single criteria. This axis is just one of a long list of criteria and should be used in conjunction with all of them as they carry alot of strength when used collectively.
 

Dawn's picture

What Are The Criteria For Determining That A Wide-Complex Tachycardia Is V Tach?

Submitted by Dawn on Tue, 01/10/2012 - 23:13
Today's Answer is provided by Jason E. Roediger, CCT, CRAT, who is a highly respected Cardiovascular Technician at the Dept. of Veterans Affairs, Hunter Holmes McGuire VA Medical Center in Richmond, VA.  He is known for holding numerous certifications in all levels of ECG interpretation, and also for scoring 100% on the Level IV Advanced ECG Board Certification exam that is usually reserved for cardiologists.

Submitted 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/

Dawn's picture

How Do You Teach Assessing For QT Prolongation?

Submitted by Dawn on Mon, 12/12/2011 - 20:23

Today's Expert is Dr. 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:
 The QT interval is the period that extends from the beginning of ventricular depolarization - until the end of ventricular repolarization. Along with the PR interval and QRS duration - it is one of the 3 key intervals that we measure. Although severe hypercalcemia (usually only with serum levels exceeding 12 mg/dL) may produce QT interval shortening - this is rare (as well as being very difficult to recognize! ). So, for practical purposes - we really only need to concern ourselves with determining whether the QT interval is normal or long.
That said - accurate QT interval can be complex involving tables based on age, sex, and heart rate ... Fortunately - this isn't needed in most cases. Instead - a very handy "eyeball method" may be used to rapidly assess the QT. For practical purposes, the QT is prolonged - IF it clearly measures more than half the R-R interval. All you need do is select a lead where you can clearly see the end of the T wave. Measure the QT in the lead where the QT interval appears to be longest. If you don't have a pair of calipers handy - mark the QT you measure on a piece of paper, and see if the R-R interval is more than twice this amount. If it isn't - then the QT is probably prolonged. The principal exception to this "eyeball method" is when the heart rate is rapid (i.e.r., over 90-100/minute) - in which case it becomes more difficult to measure the QT and determine its clinical significance (CLICK HERE FOR ADDITIONAL RESOURCES.)
This of course brings up the question, "Why care if the QT is long?" We answer this question in the form of a LIST. Other than myocardial infarction/ischemia and bundle branch blocks (which will usually be obvious on the tracing) - there are 3 principal causes of QT prolongation where the only abnormality on the ECG may be the long QT. These 3 entities are conveniently remembered by the saying, "Drugs/Lytes/CNS". Thus, antiarrhythmic drugs/tricyclic antidepressants/phenothiazines - low potassium, magnesium, or calcium - AND - almost any CNS catastrophe (stroke, seizure, coma, intracerebral or brainstem bleeding) may cause QT prolongation.
 
SUMMARY: We assess the 3 intervals (PR/QRS/QT) early in the process of ECG interpretation, usually right after determining the rhythm. Assuming the heart rate is not overly rapid (under 100/minute) - We look to see if the QT measures more than half the R-R interval. If it doesn't - then the QT is normal. If it does - then the QT is probably long. Correlate clinically by looking for, "Drugs/Lytes/CNS" as a possible cause for the long QT.
 
Ken Grauer, MD
 

Dawn's picture

How Do You Teach the Hemiblocks?

Submitted by Dawn on Wed, 11/23/2011 - 17:01

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
 

Dawn's picture

Ask the Expert

Submitted by Dawn on Mon, 10/24/2011 - 09:06

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