The 12-Lead EKG

Ben Taylor, PhD, PA-C Good Starting Place

• A man calls an ambulance after his 79 year old spouse passes out while they were walking in the park. She has no significant medical history.

• No tobacco, alcohol, or drugs.

• Atrial with a rapid ventricular response. • Right axis deviation. • Intraventricular conduction delay. • Right (RVH). • This patient has severe mitral stenosis with pulmonary congestion, pulmonary hypertension, and right .

• A qR in lead V1 is one of the most specific signs for right ventricular hypertrophy. Other causes of a qR in V1 include a right (RBBB) in patients with an anterior or normal patients who have a QS in V1 and subsequently develop a RBBB. This patient has right axis deviation in addition to the qR in V1 which suggests RVH. Given and RVH one should strongly consider mitral stenosis. IVCD

RAD Poor R-wave progress = RVH

Atrial Fib Course Objective

• To systematically analyze the 12-lead ECG. But First… A-fib

Junctional PAC

PJC Idioventricular Rhythm

Wandering Pacemaker Normal Sinus Rhythm

Bigeminy Sinus

Sinus Tachycardia

3rd Degree AV Block 1st Degree AV Block

Ventricular Tachycardia Accelerated

Supraventricular Tachycardia Atrial Fibrillation (again)

2nd Degree AV Block type I (Wenchebach) Sinus Rhythm with Unifocal PVC’s

Torsade de Pointes Sinus Rhythm with Artifact

Junctional Escape Rhythm So now we can begin our Journey……… Leads Used

Modern ECG's utilize 12 leads which are composed of 6 limb leads and 6 precordial leads.

• Limb leads are: I, II, III, aVR, aVL, and aVF. – (The lower case "a" in this notation refers to "augmented" in the sense that the person who developed the augmented leads discovered that he had to augment or amplify the voltage in the EKG machine to get a tracing that would be of similar magnitude as leads I, II, and III.)

Precordial leads

• V1, V2, V3, V4, V5, and V6. • These measure the amplitude of cardiac electrical current in an anterior-posterior aspect with regard to the heart as opposed to the chest (limb) leads which record in the coronal plane.

1. Assess the rate (atrial and ventricular) and regularity of the underlying rhythm. a) Assess the usual intervals and widths: PR interval, QRS width, QT interval. b) Interpret the rhythm itself. 2. Determine the axis. 3. Grouped lead analysis a) Look for signs of infarct vs. in all grouped leads 4. Look for any other abnormality Grouped Lead Analysis

2. Lateral leads 3. Anterior leads

1. Inferior leads Step II (Axis Step IV (Lateral lead Step V (Anterior determination) analysis lead analysis)

Step III (Inferior lead analysis)

Step I (Rhythm strip Step VI (find analysis) everything else) Assessing the EKG Rhythm

Tip: the rhythm strip portion of the 12-lead ECG is a good place to look at when trying to determine the rhythm because the 12 leads only capture a few beats.

Atrial Rhythm? fibrillation

Lead II

Rhythm strip Assessing the EKG Rate

If you use the rhythm strip portion of the 12-lead ECG the total length of it is always 10 seconds long. So you can count the number of R waves in the rhythm strip and multiply by 6 to determine the beats per minute. Rate? 14 (R waves) x 6 = 84 bpm Assessing the Axis

Axis refers to the mean QRS axis (or vector) during ventricular depolarization. As you recall when the ventricles depolarize (in a normal heart) the direction of current flows leftward and downward because most of the ventricular mass is in the left ventricle. We like to know the QRS axis because an abnormal axis can suggest disease such as pulmonary hypertension from a pulmonary embolism. The QRS axis is determined by overlying a circle, in the frontal plane. By convention, the degrees of the circle are as shown.

The normal QRS axis lies between -30o and +90o.

o A QRS axis that falls between -30 o o -90 and -90 is abnormal and called left -120o -60o axis deviation. -150o -30o A QRS axis that falls between +90o o o and +150o is abnormal and called 180 0 right axis deviation. o 150o 30 o A QRS axis that falls between +150 o 120o 60 and -90o is abnormal and called 90o extreme right axis deviation. Assessing the Axis

• Causes of • Causes of right axis deviation include: include: – Left ventricular hypertrophy – Right ventricular hypertrophy – Inferior wall MI – Lateral wall MI – – Right bundle branch block – Left anterior fascicular block – Pulmonary hypertension -90o

180o 0o

90o Assessing the Axis

We can quickly determine whether the QRS axis is normal by looking at leads I and aVF. If the QRS complex is overall positive in leads I and aVF, the QRS axis is normal.

In this ECG what leads have QRS complexes that are negative? equivocal? Assessing the Axis

The thumb method Always go with the positive thumb!!!!

Normal Axis Right Axis

Left Axis Extreme Right Axis Normal, Right or Left Axis?

Normal Normal, Right or Left Axis?

Right Normal, Right or Left Axis?

Left Normal, Right or Left Axis?

Extreme Right Normal, Right or Left Axis?

Left Assessing the Axis

Is the QRS axis normal in this ECG? No, there is left axis deviation.

The QRS is positive in I and negative in aVF.

• Region of myocardium dies  becomes…. – Electrically silent. • As a result of this, the rest of the electrical forces are directed away from this area of infarction. • Electrode overlying this area will record a deep negative deflection – Q-wave. • Significant Q wave is one millimeter (one small square) wide, which is .04 sec. in duration… • … or is a Q wave 1/3 the amplitude (or more) of the QRS complex. • Note those leads (omit AVR) where significant Q’s are present * A Q wave in lead III alone is not diagnostic of infarction, even if it is otherwise “significant” in size and width. Qs in III are ignored unless other abnormalities are seen b/c they usually represent….. • Old infarcts: significant Q waves (like infarct damage) remain for a lifetime.

Q Wave Summary

• Causes: Septal, Infarction • Septal: I, AVL, V5-V6, occasionally inferior leads Significant: Q > 1/3 QRS, or Q > 1 box wide and NOT in lead III Significant or Not? Any Significant Q’s?

Yes in leads III & AVF only ST Elevation

• Signifies an acute process, ST segment returns to baseline with time. • ST elevation associated with significant Q waves indicates an acute (or recent) infarct. • ST depression (persistent) may represent “subendocardial infarction,” which involves a small, shallow area just beneath the lining the left ventricle. This is also a variety of “non-Q wave infarction. ST Segment Elevation • Earliest reliable sign that myocardial infarction has occurred

Causes of ST Elevation

• Infarction Vasospastic Early repolarization Is this ST Elevation? ST Depression Significance

• ST segment depression is considered significant if the ST segment is at least two boxes below baseline. • With infarction, the location of the ischemia is reflected in the leads in which the ST depression occurs. Flat ST Segment Depression • Results from subendocardial infarction Common Causes of ST Segment Depression

• Ischemia • "Strain" in LVH • Digitalis effect • Bundle branch block • Hypokalemia/Hypomagnesemia • Reciprocal ST elevation • Any combination of the above • The specific cause of ST segment depression in a given tracing may be suggested by the appearance of the ST segment and itself. For example, “strain" (for LVH) is suggested by asymmetric ST depression in lateral leads, especially if voltage criteria are met. • "RV strain" is suggested if the tracing depicted in the figure is seen in right-sided leads in a patient with RVH. • Ischemia is suggested by symmetric T wave inversion, especially when seen in two or more leads of a group (i.e., in II, III, and aVF). • Digoxin ("Dig effect") may produce either ST "scooping" or a "strain"-like pattern or no change at all. • Can be seen in levels greater than 2.5mg/ml Dig Toxicity A = Normal ST segment B = Junctional ST segment depression (frequently a normal variant - physiological) C = Upward-sloping ST segment depression D = ST segment elevation suggestive of or AMI injury pattern E = Flattening of the ST segment with a sharp-angled ST-T wave junction suggesting ischemia F = Depression of the ST segment with U wave inversion G = Sagging ST segment depression H = Downward-sloping ST segment depression Not depressed

Or you could see flipped T-waves

Way depressed What is your Dx? YOU’RE WRONG!!!! It’s early repolarization • Notching or slurring of the terminal portion of the QRS wave • Symmetric concordant T waves of large amplitude • Relative temporal stability (when patients are followed over time there will often be some variation in the degree of ST segment elevation but generally the change persists for years). • Most commonly present in the precordial leads V2-5, but often associated with pronounced ST segment elevation in the limb leads II, III, & AvF Early Repolarization • Normally the R wave becomes progressively taller as one moves across the precordial leads. • A number of conditions may be associated with "poor" R wave progression, in which the R wave in leads V1 through V3-V4 either does not become bigger, or only increases very slowly in size. Causes of Poor R Wave Progression

LVH RVH Pulmonary disease (i.e., COPD, chronic asthma) Anterior or anteroseptal infarction Conduction defects (i.e., LBBB, LAHB) Chest wall deformity Normal variant Lead misplacement Good R-Wave Progression

Our Clientele in the ER • Only two main areas of the heart that do this: – Inferior and lateral ones – Septal and posterior ones. • A set of inferior ST elevations in II, III and AVF can produce lateral ST depressions in I, AVL, V5 and V6. You’d think that this would mean lateral ischemia, but no – it’s a reflection, bouncing electrically across the heart from the inferior injury, showing up in reverse.

• Results if ischemia progresses unresolved or untreated Death of myocardial cells

Notice tall R wave in V1. Posterior wall infarcts are often associated with inferior wall infarcts (Q waves in II, III and aVF).

Now we search for everything else of importance. • All forms of bundle branch block involve delays or electrical blockages within the ventricles, they are all types of intraventricular conduction deficits (IVCD). Bundle branch blocks may also be categorized as either partial (incomplete) or complete, depending on which patterns of electrical activity are detected on an EKG.

• When the criteria for BBB are partially met (e.g. < 0.12 sec), this is termed “incomplete bundle branch block” • Widened QRS complex • RR’ configuration in chest leads • Degenerative effects of aging • Hypertension • Past heart attack that damaged the heart muscle • Past viral infection • , particularly calcific • One of several heart or lung conditions that could have affected the ventricles (e.g., heart failure or chronic obstructive pulmonary disease) • Congenital condition • Past injury to the chest • When the right bundle branch is blocked, activation of the right ventricle begins when electrical activity “spills over” from the left ventricle. Depolarization of the right ventricle is delayed. • The QRS is prolonged (over 0.10 sec) in right bundle branch block (RBBB). This extra length of the QRS is caused by late activation of the right ventricle, which is then seen after the left ventricle activity. Normally, right ventricle activity is not seen, as it is overshadowed by the larger left ventricle. • In RBBB, a typical RsR’ wave occurs in lead V1. Also, a wide S wave is seen in leads I, V5, and V6, along with a broad R in lead R. When RBBB occurs in a patient with old or new septal infarction, the initial septal R wave may not be seen in lead V1. Instead, a wide QR complex is seen. Look for RR’ in leads V1 or V2

• LBBB usually indicates widespread cardiac disease. When the left bundle is blocked, activation of the left ventricle proceeds through the muscle tissue, resulting in a wide (>. 12 msec) QRS complex. • In left bundle branch blockage (LBBB), the QRS usually has the same general shape as the normal QRS, but is much wider and may be notched or deformed. Voltage (height of the QRS complex) may be higher. • In LBBB, look for wide (possibly notched) R waves in I, L, or V5-V6, or deep broad S waves in V1-V3. There is left axis deviation. “Septal Q waves” sometimes seen in I, L, and V5-V6 disappear in LBBB. • T waves in LBBB are usually oriented opposite the largest QRS deflection. That is, where large R waves are seen, T waves will be inverted. ST segment depression may occur. Look for RR’ in leads V5 or V6

• The two major branches of the left bundle may be blocked individually. When only one branch is blocked, this is called hemiblock — either “anterior hemiblock” or “posterior hemiblock” depending on whether the anterior or posterior fascicles are involved. • Hemiblocks are commonly due to loss of blood supply to either the anterior or posterior division of the Left Bundle Branch. • An occlusion of the Anterior Descending Coronary Artery will produce an Anterior Infarction, which often causes Anterior Hemiblock. • Left posterior hemiblock is less common than left anterior hemiblock since the bundle is much thicker and has a double blood supply (left and right coronary arteries). Anterior Hemiblock Posterior Hemiblock

Left axis deviation Right axis deviation

Q waves in lead I Q waves in lead III

Wide or deep S wave Wide or deep S wave in lead III in lead I

A block of both the right and the left bundle branch is a complete AV block LAD RBBB Q1, S3, So….. LAHB + RBBB = • Right (RAE) is diagnosed by the presence of a P wave 2.5 millimeters or greater in height. The P wave often has a sharp, peaked appearance. This increased voltage is caused by hypertrophy or acute strain of right atrial tissue. • The lead most likely to show the is lead II. • Causes of right atrial enlargement include COPD, mitral stenosis, mitral regurgitation, or pulmonary emboli. Because RAE is so frequently seen in chronic pulmonary disease, the peaked P wave is often called “P pulmonale.” P pulmonale in II, III, aVF P pulmonale in V1

Classic finding in Severe Right Atrial Enlargement (RAE) Tall Peaked and Pointed P waves in the Pulmonary leads (II, III, aVF). If the P wave looks "uncomfortable to sit on", think RAE!!! SR, RAE, PJC • Dilation or hypertrophy of the left atrium may increase the DURATION of the P wave. (Recall that right atrial enlargement causes an increase in the HEIGHT or amplitude of the P wave.) The P wave is normally less than 0.11 msec (just under three small boxes). • The long or abnormally shaped P Left atrial enlargement often wave occurs because of delay in occurs in disease electrical activation of the enlarged (either stenosis or insufficiency). left atrium, as electricity moves Because of this association, a leftward from the SA node. A P broad notched P wave is often wave longer than 0.11 milliseconds called “P mitrale.” In addition LAE is diagnostic of left atrial often occurs with any cause of left ventricular hypertrophy. enlargement (LAE). P mitrale in II, III, aVF P mitrale in V1

• Diagnosed by finding an m-shaped (notched) and widened P wave ( > 0.12 second) in a "mitral" leads (I, II, aVL) and/or a deep negative component to the P in lead V1. • Caused by conditions that increase either pressure or volume loading on the atria leading to enlargement and/or hypertrophy. – Longstanding hypertension – Obstructive cardiomyopathy – Aortic stenosis – Aortic regurgitation

• Atrial Enlargement Criteria P > 2.5mm height = RAE P > 0.11 sec or P notch > 1 box width or P biphasic > 1 box square = LAE • Right ventricular hypertrophy (RVH) increases the height of the R wave in V1. An R wave in V1 that is greater than 7 boxes in height, or larger than the S wave, is suspicious for RVH. Other findings are necessary to confirm the ECG diagnosis. – Other findings include right axis deviation, taller R waves in the right precordial leads (V1-V3), and deeper S waves in the left precordials (V4-V6). The T wave is inverted in V1 (and often in V2). • True posterior infarction may also cause a tall R wave in V1, but the T wave is usually upright, and there is usually some evidence of inferior infarction (ST-T changes or Qs in II, III, and F). • A large R wave in V1, when not accompanied by evidence of infarction, nor by evidence of RVH (right axis, inverted T wave in V1), may be benign “counter-clockwise rotation of the heart.” This can be seen with abnormal chest shape. RVH may occur with any process that raises the ejection work in the right ventricle. This may be volume overload such as atrial septal defect or tricuspid regurgitation, or may be pressure overload such as pulmonary stenosis. Examples of pressure- load causes of RVH include pulmonary stenosis or primary pulmonary hypertension, pulmonary disease (COPD or pulmonary emboli), large ventricular septal defect, or pulmonary hypertension due to mitral valve disease. SR, RAD, RVH with Strain • Left ventricular hypertrophy is caused by increased loads on the left ventricle. Examples are hypertension, aortic stenosis or regurgitation, mitral regurgitation, or subaortic stenosis. • Left ventricular hypertrophy (LVH) may be difficult to diagnose with certainty from the ECG. Different scoring criteria have been recommended. One of the simplest uses five criteria, with the certainty of diagnosis based on the number of criteria present. If one is present, diagnose “possible LVH”; if two, “probable LVH”; if three are found, “definite LVH.” LVH Criteria #1: Increased limb lead QRS voltage: R in lead I plus S in lead III greater than 25 mm. LVH Criteria #2: Increased precordial QRS voltage: S in lead V1 plus R in either V5 or V6 greater than 35 mm. LVH Criteria #3: Typical ST and T abnormalities: ST depression or T wave inversion (or both) in the “lateral” leads (I, L, V4-V6)

LVH Criteria #4: Large leftward voltage: R wave in lead AVL greater than 11 mm. LVH Criteria #5: Left atrial enlargement: Wide (greater than 0.11 msec) P wave. This criterion is used IN SUPPORT of the diagnosis, not alone.

• Strain is usually associated with ventricular hypertrophy since a ventricle that is straining against some kind of resistance (e.g. increased resistance from a narrowed valve or from hypertension) will become hypertrophied in its attempt to compensate. • The changes seen in the EKG are called secondary repolorization abnormalities • Ventricular strain depresses the ST segment, which generally humps upward in the middle of the segment. • Look for these changes when hypertrophy is present to determine if there is strain present: – Downsloping ST segment depression – T-wave inversion

LVH with strain, possible LAE • RVH Criteria • LVH Criteria R in V1 > 7 mm or > S 1) R-I + S-III >25 mm wave 2) S-V1-2 + R-V5-6 T in V1 inverted >35 mm Right axis deviation 3) ST-Ts in left leads S waves in V5-V6 4) R-L >11 mm 5) LAE + other criteria • Positive Criteria: 1=possible 2=probable 3=definite • This is difficult, but not necessarily impossible. Look for ST-T wave changes or new Q waves in left-sided leads (I, aVL, V6) with LBBB. • New onset of LBBB is typically representative of an MI which you must now R/O. • Evidence of infarction (Q waves, ST-T changes) is easier to see with RBBB. • Suspect LVH with LBBB if there is LAA and/or very deep S waves (>30 mm) in V1, V2 or V3. • LVH is probably present with RBBB if the R in aVL is >12 and/or R in V5 or V6 is >25. • ECG findings noted during the acute phase of pulmonary embolism can include any number of the following: – “S1Q3T3” - prominent S in lead I, Q and inverted T in lead III – Right bundle branch block (RBBB), complete or incomplete, often resolving after acute phase – Right shift of QRS axis – shift of transition zone from V4 to V5-6 – ST elevation in VI and aVR – generalized low-amplitude QRS – , atrial fibrillation/flutter, or right-sided PAC/PVC – T wave inversion in V1-4, often a late sign.

S 1

Inverted T Low voltage QRS throughout

Q 3 pacemakers send electrical impulses to one or more chambers of the heart. These signals make the heart contract in a more regular rhythm than the chamber would otherwise. Pacemakers are designed to treat cardiac conditions that involve A pulse generator, which contains both the battery and the intelligent circuits, can be very small, as seen here. This device can be connected to a lead which makes contact with either the atrium or the ventricular muscle. • Shown here are two leads. The one on the top is a lead with a "J" shape, which is used for optimal positioning in the atrium. It is "unipolar", and therefore smaller, and is a "tined" lead which makes passive contact with the atrial muscle. • In contrast, the lead on the bottom is larger because it is a bipolar device which has more wire within it. It has a small screw at the end so that it can be actively fixated to the muscle. • Here, a pulse generator is shown which is connected to two leads, for dual- chamber pacing.

Anti- chambers chambers modes of programmable tachycardia paced sensed response functions functions 1 2 3 4 5

V = Ventricle V = Ventricle T = Triggered R = Rate Modulated O = None

A = Atrium A = Atrium I = Inhibited C = Communicating P = Paced

D = Dual (A & D = Dual (A & D = Dual M = S = Shocks V) V) Triggered/Inhibited multiprogrammable

P = Simple O = None O = None O = None D = Dual (P & S) Programmable

------O = None --- • Chamber paced - ventricle • Chamber sensed - ventricle • Response to sensing - Inhibits • Program functions - multiprogrammability • Antiarrhythmia functions - pacing • Sick sinus Syndrome (most common) if symptomatic • 3rd degree AV block • Recurrent • Chronotropic incompetence (inability to increase the heart rate to match a level of exercise) • Long QT syndrome • Sends out electrical signals to the upper part of the heart which are passed down the usual intrinsic conduction system to the lower chamber. – Only if the A-V node and the lower portions of the electrical system are intact. • Recommended so that the upper chambers can initiate a heartbeat much like the natural heartbeat. • Atrial pacing is commonly seen in patients that have damaged atrial pacing ability, but normal ventricular conduction. • Notice that the pacing spikes stimulate a P wave. Atrial Pacemaker with 100% sensing & capture • Seen in patients with damaged ventricular ability • Ventricularly paced rhythms generally have a wide (> 0.12 secs) ORS complex following the ventricular pacing spike.

Ventricular pacemaker with 100% sensing & capture

• A dual chamber pacer can sense and pace both atrial and ventricular activity as programmed. • Coordinates an electrical signal to the upper part of the heart with a signal to the lower part of the heart. • When an individual requires a heartbeat similar to a normal heartbeat, two wires are placed. One wire detects the signal and/or stimulates the upper chamber - atria. The other wire detects the signal and/or stimulates the lower chamber - ventricle.

• Ventricular inhibited • Most commonly used type of pacemaker • Sends out continuous, regular signals if needed. Can turn itself off when the individual’s heart sends out a competitive beat. • Fires when the pt’s own intrinsic HR falls below a threshold level. • Ventricular synchronous • Sends out continuous, regular signals if needed. If competitive heartbeats or electrical interference occurs, responds up to maximum of 150 beats per minute • Recommended when individual will have contact with special types of electrical machinery that can lead to faster pacemaker activity. • Upper pacemaker rate of 150 beats per minute prevents unusually rapid heart rate during close contact with machinery • Characterized by pacing impulses (singly or in groups) that are not followed by QRS complexes and produce an irregular rhythm. • Patient may or may not be symptomatic.

• Commonly caused by a damaged sensing lead that causes the pacemaker to misinterpret the patient’s native rhythm • Characterized by inappropriate pacing spikes that can occur within ALL phases of the cardiac cycle

Infarct in the antereoseptal and anterior wall (Q waves in V2-V4 there is also a probable inferior infarct (Q waves in II, III, and aVF)). Ischemia across the entire anterior and lateral wall (T wave inversions in V2-V6, I and aVL). Also note, the injury pattern in V2-3 of ST elevation, the prominent Q waves in V2 and V3 show that some of the myocardium has also reached the infarct stage. Left anterior hemiblock (left axis deviation and Q1, S3). LAD, Poor R-wave progression Left posterior hemiblock (right axis deviation and S1,Q3).

What Do you See? What Do you See? What Do you See? What Do you See? If you forget what I taught you