This week has been an exciting week for Brian Jefferson and I since the Plain Dealer article by Zachary Lewis was published on the front page. We have had an enormous number of visitors because of this article and we have received some great suggestions from visitors as well as from blogs. Over the next week we will start implementing some of these changes in the hopes of making a medical wiki that provides safe and up to date information.
Some changes and suggestions that we will implement.
1. Creation of an editorial policy as per the suggestion of David Rothman
2. Create a list of all contributing editors with their pertinent credentials
3. Creation of a New Logo
4. Protection of Pages on the Wiki that contain any medication dosages so these pages can not be altered.
5. Addition of a clinical pharmacist to the editorial board.
6. Addition of a AskDrWiki page on Wikipedia.
7. Addition of a General Surgery, ENT, Vascular Surgery, Dermatology, Emergency Medicine, and Basic Science Editors
We would also like to thank Ves Dimov from Clinical Cases and Images , David Rothman from davidrothman.net, and Bertalan Mesko from scienceroll.com for their advice.
Other comments this week on AskDrWiki include:
eHealth and The Krafty Librarian
Monday, April 2, 2007
Ask Dr Wiki in the News
Sunday, March 18, 2007
EKG of the Week:Non Reentrant Fast/Slow Supraventricular Tachycardia
Characteristics:
This is an extremely rare tachycardia which occurs when a single sinus impulse conducts down an AV node with both a slow and fast pathway. When most impulses reach the AV node they conduct down both the slow and fast pathway. Since conduction is faster down the fast pathway it beats out the slow pathway conduction and depolarizes the ventricle. The impulse traveling down the slow pathway either collides with the impulse from the fast pathway that is now traveling back up the slow or the impulse traveling down the slow pathway reaches the ventricle and finds the ventricle refractory. In the above EKG the sinus impulse represented by the P wave in the beginning of the rhythm strip conducts down the fast pathway resulting in the first QRS complex; the impulse from the slow pathway also depolarizes the ventricle seen as the second QRS complex. You will notice that there is no p wave between the first and second QRS complexes. Therefore the first sinus beat results in a doubling of the ventricular sinus rate. This sequence is repeated again in the 7th and 8th QRS complex. It is an extremely rare tachycardia and is resistant to multiple antiarrhythmic medications. The above patient underwent ablation of their slow pathway and no further episodes were observed. See www.askdrwiki.com for more interesting EKGs.
Wednesday, March 7, 2007
Ask Dr Wiki Will Now Require Proof of Credentials
Since Brandon Keim published his article in Nature Medicine titled WikiMedia, the subject of crendentialing has been a topic that has been discussed on DavidRothman.net and meredith.wolfwater.com. After hearing their arguments we have decided that they are correct. In order to create an expert medical wiki we need to prove that future users have real medical credentials. We will now require users to submit their real names, degree, and hospital or medical school and will then confirm their credentials before we allow them to create or edit articles. The comments and suggestions from everyone who weighed in are appreciated!
Reference:
Brandon Keim: WikiMedia; News@Nature 13, 231-233
Monday, February 26, 2007
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.
Sunday, February 18, 2007
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
Sunday, February 11, 2007
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
- Left axis deviation (usually between -45° and -90°), some consider -30° to meet criteria
- QRS interval less than 120ms
- qR complex in the lateral limb leads (I and aVL)
- rS pattern in the inferior leads (II, III, and aVF)
- 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
- It is seen in approximately 4% of cases of acute myocardial infarction
- 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.
- It can be seen with acute inferior wall myocardial infarction.
- It also associated with hypertensive heart disease, aortic valvular disease, cardiomyopathies, and degenerative fibrotic disease of the cardiac skeleton.
- 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.
- Surawicz B, Knilans TK. Chou’s electrocardiography in clinical practice: adult and pediatric, 5th edn. Philadelphia: W.B. Saunders; 2001.
Sunday, February 4, 2007
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