12 Lead EKG Interpretation Stephanie Roberson NREMT-P, BS Virginia College of Osteopathic Medicine Disclaimer • This is intended to simplify some of the concepts introduced to us in lecture. • You should by all means still understand the concepts in the lectures provided by the faculty. • At any place should an opinion differ from something introduced by the faculty, defer to the opinion of the faculty (they write the tests). Objectives • Proper lead placement • Relevant cardiac anatomy • Interpreting the 12 lead EKG – Rate – Rhythm – Axis – Bundle branch blocks (BBB) – Ventricular Hypertrophy – Atrial enlargement – ST elevation • Ischemia, injury, and infarction – Pericarditis What is 12 lead? • Consists of 10 lead cables that generate 12 different views of the heart • Limb leads (look at the frontal plane) – I, II, III – aVR, aVL, aVF • Precordial leads/Voltage/Modified Chest leads (look at the horizontal plane) – V1, V2, V3, V4, V5, V6 12 Leads • Leads I, II, and III are bipolar • aVR, aVL, and aVF are unipolar leads • Leads V1-V6 are all positive leads with the reference point (negative pole) becoming the heart Proper Lead Placement Precordial Leads • V1 – right 4th ICS • V2 – left 4th ICS • V3 – between V2 and V4 • V4 – 5th ICS midclavicular • V5 - between V4 and V6, 5th ICS anterior axiallary line • V6 – horizontal to V4 mid-axillary, 5th ICS Precordial Leads are Unipolar Cardiac Conduction System Walls of the Heart Anterior/ septal lateral Inferior “I See All Leads” I aVR V1 V4 Lateral Septal Anterior II aVL V2 V5 Inferior Lateral Septal Lateral III aVF V3 V6 Inferior Inferior Anterior Lateral Coronary Artery Correlation to Leads I aVR V1 V4 LCX LAD LAD II aVL V2 V5 RCA LCX LAD LCX III III V3 V6 RCA RCA LAD LCX Right Coronary v. Left Coronary • RCA feeds: • LCA feeds: – Right ventricle – Anterior wall LV (LAD) – Inferior wall of LV (90% – Septal wall LV (LAD) of population) – Lateral wall – Posterior wall of LV (LCircumflexA) (posterior descending – Posterior wall LV artery) (LCircumflexA) Putting It All Together I aVR V1 V4 LCX LAD LAD Lateral Septal Anterior II aVL V2 V5 RCA LCX LAD LCX Inferior Lateral Septal Lateral III aVF V3 V6 RCA RCA LAD LCX Inferior Inferior Anterior Lateral System for Interpreting the 12 Lead • Rhythm • Axis • Bundle Branch Blocks (BBB) • Ventricular Hypertrophy • ST elevation Interpret the Rhythm • Rate? • Rhythm? • P wave? • PR Interval? • QRS Interval? • R-wave progression – R wave should appear smaller in V1 steadily progressing to the largest at V6 with the transition (equiphasic) at V3. • S-wave regression – S wave should appear largest in V1 steadily regressing to smallest in V6 with transition (equiphasic) at V3. Note that R waves progress nicely, but S wave regression is not steady. Assess the Axis • Axis is the term we use to define the net flow of electrical activity in the heart. • Axis deviation is when the net flow of electricity in the heart is not going in the normal direction due to either a physiological or pathological change. • Axis is used to help diagnose a hemiblock (Dr. Rawlins said he will not be teaching hemiblocks…so moving on) Assessing the Axis Lead I Lead aVF Interpretation Up Up All good! Up Down Left Axis Deviation Down Up Right Axis Deviation Down Down Extreme Right Axis 20 • P231 Dubin Quadrant Approach Bundle Branch Blocks • A new onset BBB indicates a severe MI carrying a 40-60% increase in mortality….however we do not always know if it is new. We need an old 12 lead to compare to. In the absence of an old 12 lead, we assume the worst and gain additional information via blood work and what the patient is telling us. • The bundle branches are supplied by the LAD • Bundle branches are divided into right and left, with the left further divided into anterior and posterior fascicles Cardiac Conduction System Anterior Fascicle Posterior Fascicle Bundle Branch Blocks • The bundle branches see to it that the ventricles are supplied with syncytium (or that they generate contractions at the same time) • A BBB causes the ventricles to contract out of sync either reducing preload (for the right) or force of contraction (for the left) • You cannot determine an MI in the presence of a LBBB by traditional means (but it can be done…way more advanced. For now, at this level, you cannot make the diagnosis) Recognizing a BBB • Different method than shown by Dr. Rawlins. • Defining a BBB must be done in V1 • Complex must be atrial in origin • QRS must be wide (> 0.12 sec) • Determine right or left BBB – Turn signal method • Find the J-point • Determine the direction of the deflection immediately preceding the J point • Use your “turn signal” to determine left or right • Notching of the QRS complex in V5 or V6 is additional proof of a LBBB J Point • Point on the EKG tracing where the S wave transitions to the ST segment • Not always easy to identify. Turn Signal??? • After identification of the J point, look at the deflection of the wave immediately preceding it. • Is it up or down? • Think about the turn signal on a car – Push down to signal left – Push up to signal right • If the wave immediate preceding the J point: – deflects downward left BBB – deflects upwards right BBB Right BBB Upward deflection J Point Left BBB J Point Downward deflection Notched QRS Bundle Branch Blocks • The turn signal method of determining BBB is different from Dr. Rawlin’s method. • BY ALL MEANS understand Dr. Rawlin’s way as well, but this is meant to show you another way to assist you in identifying a BBB. Why is it important to assess axis and BBB? • This is not a testable point per Dr. Rawlins. If you don’t care why, skip ahead to ventricular hypertrophy. • But since I’ve heard people asking why this is important…. • RBBB only the left bundle branch is providing an electrical pathway to the ventricles • What happens when one of the fascicles of the LBB is also blocked (ie, bifascicular block)? • Important point because bifascicular block leaves only one fascicle of the bundle branches left to depolarize both ventricles. Bifascicular Block Only this guy works RBBB Left posterior Only these guys RBBB fascicle work blocked Bifascicular Block • When only one fascicle of the ventricles is providing an electrical current, the ventricles will still contract, as the signal will propagate from the functioning fascicle through functioning ventricular cells. • However, contraction of the ventricles will not be coordinated as the electrical signal is delayed due to the distance it has to travel. • Synctium is lost. Ventricular Hypertrophy • Right VH • Left VH – Occurs when there is – Occurs when there is increased pressure or prolonged back pressure volume on the RV or increased volume on – Typically caused by the LV respiratory diseases – Caused by prolonged – Why? HTN, mitral or aortic valve problems, MI, cardiomyopathy Determining RVH • Right axis deviation • R-wave in V1 > 7mm tall • Again, Dr. Rawlins teaches a different technique. Still know his technique for the test. Right Ventricular Hypertrophy 15-16 mm high Determining LVH • This is one of three of the techniques Dr. Rawlins teaches. I find this one the easiest. • Measure the deeper of the S-waves of V1 or V2 • Measure the taller of the R-waves in V5 and V6 • Add the amplitudes of the deepest S-wave of V1 or V2 to that of the tallest R-wave of V5 or V6 • If the sum is >= 35 mm, then you have LVH. • Above criteria not applicable in presence of LBBB Left Ventricular Hypertrophy 15 mm + 22 mm = 37 mm LVH Approximately 22 mm Approximately 15 mm Right Atrial Enlargement • Look in Lead II, III, or aVF (Dr. Rawlins says just Lead II) • Tall, pointed P wave greater than 2.5 mm high. • 3 P’s – Pointed – Prominent – Pulmonary • Causes of RAE – Congenital heart disease – Tricuspid or pulmonary valve disease – Pulmonary HTN • Clinical Implications – Frequently seen with RVH – Pulmonary implications Right Atrial Enlargement P wave greater than 2.5 mm tall Left Atrial Enlargement • Lead II shows a widened (> 0.12 sec) P wave with a notched or m-shaped appearance (the “golden arches” McD’s sign) or the P wave is mooning you (use your imagination) • Lead V1 shows a broad, inverted P wave of > 0.4 sec wide • Causes of LAE – HTN – Pumonary Edema – Nitral or aortic valve stenosis – LVH – AMI • Clinical Implications – Clue to underlying disease process (see causes) Left Atrial Enlargement Lead II Lead V1 Broad, negative P wave > 0.4 sec wide M-shaped P wave > 0.12 sec wide Myocardial Infarction • Proceeds along a continuum: – Ischemia – temporary hypoxia in the cells – Injury – prolonged oxygen deprivation in the cells; cells will die if not corrected – Infarction – cell death from lack of oxygen; dead cells cannot generate or pass along electrical energy or provide mechanical pumping power Recognizing the Three I’s • Ischemia is represented on a 12 lead by peaked T- waves, however this in itself is not enough to confirm the beginnings of an MI • Early ischemia can also be recognized by T-wave inversion • ST segment depression can be either a reciprocal change for elevation or ischemia • Injury and early infarction is represented by ST segment elevation Progressive EKG Changes During an MI • Normal EKG • ST depression/peaked T-waves (seen in first hours) • ST elevation • Development of Q-wave (in some but not all MI’s); ST elevation may begin to decrease; this is typically seen in the first or second day of MI • Q-wave present (may or may not be significant); R-wave may be diminished or nonexistent; ST often baseline; possible T- wave inversion • Return of R-wave; Q-wave may or may not be present • Q-wave typically represents transmural infarction ST Elevation • The ST segment is considered elevated if the J point is > 1 mm above the isoelectric line in the limb leads (criteria from Dr. Power’s lecture) • the ST elevation must be >= 2 mm above the isoelectric line in precordial leads (criteria from Dr. Power’s lecture) • ST elevation must be present in 2 or more anatomically contiguous leads to definitively deduce infarction • ST elevation is often seen but not always indicative of MI resulting from hypoxia of cardiac cells “I See All Leads” I aVR V1 V4 Lateral Septal Anterior II aVL V2 V5 Inferior Lateral Septal Lateral III aVF V3 V6 Inferior Inferior Anterior Lateral Where is the ST Elevation? “I See All Leads” I aVR V1 V4 Lateral Septal Anterior II aVL V2 V5 Inferior Lateral Septal Lateral III aVF V3 V6 Inferior Inferior Anterior Lateral Where is the ST Elevation? “I See All Leads” I aVR V1 V4 Lateral Septal Anterior II aVL V2 V5 Inferior Lateral Septal Lateral III aVF V3 V6 Inferior Inferior Anterior Lateral • So, can the previous 12 lead be called a septal MI as well as an anterior MI? • By definition, no. To diagnose septal MI, the ST elevation MUST be in V1 AND V2. • HOWEVER, both the septal and anterior walls are fed by the LAD, thus it is logical that we would see changes in the septal leads as well. After all, the “walls” of the heart aren’t actual walls separate from one another. Anterior and septal MI’s often have what is termed “extension” into the wall sharing the same blood supply, the LAD. • The previous EKG would often be called an anterioseptal MI Where is the ST Elevation? “I See All Leads” I aVR V1 V4 Lateral Septal Anterior II aVL V2 V5 Inferior Lateral Septal Lateral III aVF V3 V6 Inferior Inferior Anterior Lateral Where is the ST Elevation? “I See All Leads” I aVR V1 V4 Lateral Septal Anterior II aVL V2 V5 Inferior Lateral Septal Lateral III aVF V3 V6 Inferior Inferior Anterior Lateral Pericarditis • Signs and symptoms: – Chest pain alleviated by leaning forward, exacerbated by lying back. – Described as sharp and severe, often radiating to back – Friction rub on auscultation • Diffuse ST elevation that appears concave (like a soup ladle) in all leads except aVR and V1. “soup ladle” concavity Pericarditis Diffuse ST elevation OTHER Causes of ST Elevation • Electrolyte changes • Rhythms of ventricular • Hypothermia origin • Increased ICP • Left Ventricular • LBBB Hypertrophy • Early Repolarization Treat the Patient, Not the Monitor! • Remember, all of these findings are relative to the presentation of the patient. • BBB, hemiblocks, and axis deviations can be established changes in an individual’s 12 lead. • These findings are only significant when they are new onset, or more importantly when they are accompanied by S&S (typical or atypical) of an MI. • Treat the patient, not the test! • Your patient will often tell you their diagnosis in their own way if you only take the time to listen to them.