EKG of the Week: Primum Atrial Septal Defect

Characteristics
Patients with Atrial Septal Defects may have Atrial Fibrillation, Atrial Tachycardia, or Atrial Flutter, but these arrythmias are not usually seen until patients grow older. Features also seen on the EKG include Right Atrial Enlargement, PR prolongation and advanced AV block. When you suspect a patient has an ASD based on the findings of an incomplete Right Bundle Branch Block with a rSr' or rSR' the next thing you should do is examine the frontal plane QRS. The frontal plane QRS is the most helpful clue to help you differentiate Secundum ASD from Primum ASD. In Primum defects left axis deviation is seen in most patients with an axis of > -30 degrees and very few patients have right axis deviation. In contrast Secundum defects have an axis between 0 degrees and 180 degrees with most cases to the right of 100 degrees.

In the EKG above, you can see an example of the rSR' pattern in V1 with a R' greater than S with T wave inversion which is commonly seen in volume overload. See www.askdrwiki.com for more interesting EKGs

References
Pryor R, Woodwork MB, Blount SG: Electrocardiographic Changes in Atrial Septal Defects:Ostium Secundum versus Ostium Primum defect. Am Heart J 58:689, 1959.

EKG of the Week: Ashman's Phenomenon

Characteristics
Physiologic abberation of a complex on a EKG is called Ashman's Phenomenon and is seen in normal subjects. It occurs when the conduction system does not have time to recover and most commonly occurs in the Right Bundle because it is the segment of the conduction system that has the longest refractory period. Following the Right Bundle Branch the Left Anterior Fascicle is the next most common site of conduction delay resulting in a Left Anterior Hemiblock or a Left Anterior Fascicular Block on EKG. It is usually seen when there is a combination of a long cycle followed by a short cycle as seen above in the ninth complex that conducts with a Right Bundle Branch Block morphology after a long RR interval. See www.askdrwiki.com for more EKGs

References
Ashman R, Byer E:Aberration in the conduction of premature ventricular impulses. J La State Med Soc 8:62, 1946

EKG of the Week 2/11/2007

Characteristics
Normal activation of the left ventricle proceeds down the left bundle branch, which consist of two fascicles the left anterior fascicle and left posterior fascicle. Left Anterior Fascicular Block (LAFB), which is also known as Left Anterior Hemiblock (LAHB), occurs when a cardiac impulse spreads first through the left posterior fascicle, causing a delay in activation of the anterior and lateral walls of the left ventricle which are normally activated via the left anterior fascicle.

Although there is a delay or block in activation of the left anterior fascicle there is still preservation of initial left to right septal activation as well as preservation of the inferior activation of the left ventricule (preservation of septal Q waves in I and aVL and small initial R wave in leads II, III, and aVF). The delayed and unopposed activation of the remainder of the left ventricle now results in a shift in the QRS axis leftward and superiorly, causing marked left axis deviation. This delayed activation also results in a widening of the QRS complex, although not to the extent of a complete LBBB

Criteria for LAFB

1. Left axis deviation (usually between -45° and -90°), some consider -30° to meet criteria
2. QRS interval less than 120ms
   
3. qR complex in the lateral limb leads (I and aVL)
4. rS pattern in the inferior leads (II, III, and aVF)
5. Delayed intrinsicoid deflection in lead aVL (> 0.045 s)

Exceptions
It is important not to call LAFB in the setting of a prior inferior wall myocardial infarction which may also demonstrate left axis deviation due to the '''initial forces''' (Q wave in a Qr complex) in leads II, III, and aVF. As opposed to LAHB, the left axis shift is due to '''terminal forces''' (i.e., the S wave in an rS complex) being directed superiorly,

Effects of LAHB on Diagnosing Infarctions and Left Ventricular Hypertrophy
LAHB may be a cause of poor R wave progression across the precordium causing a pseudoinfarction pattern mimicking an anteroseptal infarction. It also makes the electrocardiographic diagnosis of LVH more complicated, because both may cause a large R wave in lead aVL. Therefore to call LVH on an EKG in the setting of an LAHB you should see the presence of a “strain” pattern when you are relying on limb lead criteria to diagnose LVH.

Clinical Significance

1. It is seen in approximately 4% of cases of acute myocardial infarction
2. It is the most common type of intraventricular conduction defect seen in acute anterior myocardial infarction, and the left anterior descending artery is usually the culprit vessel.
3. It can be seen with acute inferior wall myocardial infarction.
4. It also associated with hypertensive heart disease, aortic valvular disease, cardiomyopathies, and degenerative fibrotic disease of the cardiac skeleton.

References

1. Mirvis DM, Goldberger AL. Electrocardiography. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001:82–125.
2. Surawicz B, Knilans TK. Chou’s electrocardiography in clinical practice: adult and pediatric, 5th edn. Philadelphia: W.B. Saunders; 2001.

EKG of the Week 2/4/2007

Introduction
This EKG can be solved with the use of the Brugada criteria published in Circulation in 1991. The criteria were established because the conventional criteria used to differentiate a Wide Complex Tachycardia lacked specificity. The Brugada criteria consisted of four criteria established by the authors, which were prospectively analyzed in a total of 554 tachycardias with a widened QRS complex (384 ventricular and 170 supraventricular). The sensitivity of the four consecutive steps was 0.987, and the specificity was 0.965.

Four Brugada Criteria for Diagnosis of Ventricular Tachycardia
1. Lack of an RS complex in the precordial leads
2. Whether the longest interval in any precordial lead from the beginning of the R wave to the deepest part of the S wave when an RS complex is present is greater than 100 ms
3. Whether atrioventricular dissociation is present
4. Whether both leads V1 and V6 fulfilled classic criteria for ventricular tachycardia.

Diagnosis
Monomorphic Ventricular Tachycardia. See www.AskDrWiki.com for more info about the Brugada Criteria.

References
A New Approach to the Differential Diagnosis of a Regular Tachycardia With a Wide QRS Complex. Pedro Brugada, MD; Josep Brugada, MD; Lluis Mont, MD; Joep Smeets, MD; and Erik W. Andries, MD. Circulation 1991;83:1649-1659

EKG of the Week 1/27/2007

Background
Apical Hypertrophic Cardiomyopathy is a specific variant of Hypertrophic Cardiomyopathy. This disease has been first described in Japan by Yamagutchi where the prevalence is much higher than in the western world. It is characterized by hypertrophy that is confined to the apex which causes a ace of spades like configuration in RAO on the left ventriculogram.

EKG Characteristics
Giant negative T waves and tall R waves in the left precordial leads are the ECG hallmarks of the Japanese form of apical hypertrophy as seen on the EKG seen on the tracing above. Typically T waves in V4-V5 has the greatest degree of T wave depth possibly due to their proximity to the apex of the Left Ventricle which may result from the reversal in the direction of the vector of repolarization or myocardial ischemia due to hypoperfusion of the hypertrophied ventricle. Other findings on EKG include Left Atrial Enlargement, Right Atrial Enlargement, Left axis deviation, and First Degree AV Block.

See www.askdrwiki.com for more EKGs.

EKG of the Week 1/18/2007

This EKG shows marked right axis deviation (Negative vector in Lead I and Postive Vector in Lead aVF) as well as loss of voltage across the precordium seen in V1-V6. If you look closely you will notice there are negative or inverted p waves in lead I and aVL which is a clue to the diagnosis. The differential for inverted p waves in lead I and aVL is Dextrocardia or Reversed Arm Leads. Since there is loss of voltage across the precordium this is Dextrocardia. See more interesting EKGs on www.askdrwiki.com

EKG of the Week 1/5/2007

This EKG shows a slow wide complex tachycardia with intermittent narrow complex beats. The 5^th and 10^th beats are sinus rhythm and close examination of these beats will give you a clue to the cause of the wide complex rhythm. In Leads II and III you can appreciate ST elevation indicating an acute current of injury due to a myocardial infarction. The wide complex beats therefore represent an Accelerated Idioventricular Rhythm or AIVR which is usually seen following reperfusion after an acute infarct.

Accelerated Idioventricular Rhythms are ectopic ventricular rhythms at rates between 40 bpm and 100 to 120 bpm. The ventricular origin of this rhythm can be demonstrated by the usual EKG criteria which include AV dissociation, fusion, and capture complexes. In this EKG the 4^th beat represents a fusion complex and the 5^th beath represents a capture beat proving that these beats are ventricular in origin. The incidence of Accelerated Idioventricular Rhythms following acute MI is reported to be between 8 and 36 percent. This rhythm can also be seen in patients with primarily myocardial disease, hypertensive, rheumatic, and congenital heart disease. It can also be caused by digoxin. See more on www.askdrwiki.com