Today's Expert is Dr. KEN GRAUER, MD Dr. Grauer is ProfessorEmeritus (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/
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 RESOURCESfor 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.