IMD420D: Introduction to the Cardiovascular System: ECG Syllabus Learning Objectives: This syllabus is designed to fill the needs of students who desire the ability to interpret the resting normal and abnormal ECG, as well as provide an overview of heart anatomy, function and neurophysiology. This should be considered to be an introduction to electrocardiography that will provide a basis for continuing study of this subject. This ECG syllabus is a supplement to the Lilly textbook. 1. Review of the heart anatomy and the cardiac cycle as they relate to the electrical conducting system 2. An understanding of cardiac muscle contraction 3. A comprehensive overview of EKG interpretation involving the recognition of the most common abnormalities NOTE: Many changes of serious abnormalities (e.g ST elevation) can be caused by less serious conditions (e.g early repolarization). The ECG can only react in a limited number of ways to innumerable clinical conditions. Therefore, we always interpret the ECG in the clinical context at hand.

Additional Reading Resources Malcolm S. Thaler’s The Only EKG Book You’ll Ever Need. (LWW, 4th Edition or 5th Edition) ECG Interpretation Cribsheets by G. Thomas Evans, Jr., M.D. Marriott’s Practical Electrocardiography by Galen Wagner (10th edition – LWW, 2001)

Online Resources

There are numerous sites with examples, definitions as well as quizzes. Especially good ones are:

12leadecg.com library.med.utah.edu/kw/ecg emedu.org/ecg I. INTRODUCTION TO THE CONDUCTING SYSTEM

The heart's pacemaker-conducting system consists of the sinoatrial node (SA node), atrioventicular node (AV node), the bundle of His, the bundle branches and the Purkinje fibers.

The electrical impulse that causes rhythmic contraction of heart muscles arises in the SA node which is the intrinsic pacemaker of the heart. From the SA node, the impulse spreads over the atrial muscles causing atrial contraction. The impulse is also conducted to the atrioventicular (AV) node.

From the AV node, the electrical impulse is conducted to ventricular muscles via the bundle of His, the bundle branches and the Purkinje fibers. The bundle branches and the Purkinje fibers are collectively called the ventricular conduction system.

A. Sinoatrial Node (SA node) Location The sinoatrial node (SA node) consists of a cluster of specialized cells that have pacemaker activity (automaticity). These cells are responsible for initiating the electrical impulse that stimulates the heart muscles to contract rhythmically. The SA node is located high on the right atrium close to where the superior vena cava enters the right atrium. Sinus rhythm The SA node is the normal pacemaker of the heart, firing at about 60-100 beats per minute. A heart controlled by the SA node is said to be in normal sinus rhythm. The electrical impulse from the SA node spreads over the right and left atria and causes atrial contraction. The impulses are also conducted to the atrioventicular (AV) node. It takes about 0.03 seconds for the impulse to travel from the SA to AV node.

Innervation by the Autonomic Nervous System

The SA node is under the influence of the autonomic nervous system. The sympathetic system innervates the heart and causes increases in the heart rate via B1 adrenergic receptors, for instance in fight or fright. The parasympathetic system, via the vagus nerve, slows the heart rate and establishes the resting heart rate of about 60-70 beats per minute. If parasympathetic activity is blocked by anti-cholinergic drugs or the vagus nerve is cut, the heart rate increases. If parasympathetic stimulation is increased, for instance by massaging the carotid sinus (baroreceptors), the heart rate decreases.

B. The Atrioventicular Node Location and activity Atrioventicular node (AV node) is located on the interatrial septum close to the tricuspid valve. It receives impulses from the SA node and conducts them to the bundle of His. Conduction through the AV node is slow providing a deliberate delay that allows the ventricles to fill (after atrial contraction) before the ventricles contract. The electric impulse from the SA node must be conducted though the AV node because the atria and ventricles are separated by a fibrous connective tissue septum that has poor conductivity. The AV node provides the path of least resistance for the impulse to proceed to the ventricles. AV rhythm The AV node, together with the bundle of His make up the AV junctional tissue. The AV junctional tissue has its own intrinsic pacemaker activity at of 40-60 beats per minute. If the SA node is injured, AV junctional tissue can take over control of heart rate and rhythm. Why must the electric impulse be conducted though the AV node? The electric impulse from the SA node is conducted though the AV node because the atria and ventricles are separated by a fibrous connective tissue ring that has negligible conductivity. The AV node provides a path for the impulses to proceed from the atria to the ventricles. In pathological circumstances involving rapid rhythms such as atrial fibrillation, the impulses arrive at the AV node at a very high rate (≥350 impulses a minute). Since the AV node has a long refractory period, some of these impulses find the AV node refractory and are not conducted to the ventricles. Therefore, the AV node functions in a protective role, preventing excessive ventricular rates which can result in hemodynamic dysfunction or serious ventricular arrhythmias which can be quickly fatal.

Bundle of His The bundle of His is located in the proximal interventicular septum. It emerges from the AV node to begin the conduction of the impulse from the AV node to the ventricles. The Bundle of His branches into the right, left anteriosuperior and left posterioinferior bundle branches. The AV node, together with the bundle of His make up the AV junctional tissue. The AV junctional tissue is considered supraventicular (above the ventricles). The AV junctional tissue has an intrinsic rate of 40-60 beats per minute. If the SA node is injured AV junctional tissue can take over control of heart rate and rhythm, albeit at a lower intrinsic rate (40-60/min) which may or may not be adequate. C. Bundle Branches & Purkinje Fibers The bundle of His branches into the three bundle branches: the right, left anteriosuperior and left postrioinferior bundle branches that run along the interventicular septum. The three bundle branches comprise the trifascular conducting system The bundles give rise to thin filaments known as Purkinje fibers. These fibers distribute the impulse to the ventricular muscle. Collectively, the bundle branches and Purkinje network comprise the ventricular conduction system. It takes about 0.03-0.04s for the impulse to travel from the bundle of His to the ventricular muscle. The ventricular conducting system is capable of intrinsic pacemaker activity at a rate of 30-40 impulses per minute. If the SA and AV nodes are injured the ventricular conducting system can take over control of heart rate and rhythm. The bundles give rise to thin filaments known as Purkinje fibers. These fibers distribute the impulse to the ventricular muscle. Collectively, the bundle branches and Purkinje network comprises the ventricular conduction

system. It takes about 0.03-0.04s for the impulse to travel from the bundle of His to the ventricular muscle. The ventricular conducting system is capable of intrinsic pacemaker activity at a rate of 30-40 impulses per minute. If the SA and AV nodes are injured the ventricular conducting system can take over control of heart rate and rhythm. I. Analysis of the ECG EKG Leads There are 12 leads on a standard ECG. Six of the leads are considered "limb leads" since they are placed on the arms and/or legs of the person. The other six leads are considered "precordial leads" since they are placed on the person's torso (precordium).

A. Reading the ECG

The SA node spontaneously depolarizes to initiate an action impulse that is rapidly propagated through the atria (causing atrial contraction), then slowly through the AV node and rapidly via the bundle branches and Purkinje system to the ventricles, causing ventricular contraction.

The electrical activity of the heart can be recorded at the surface of the body using an electrocardiogram. The electrocardiogram (EGG) is simply a voltmeter that uses up to 12 different leads (electrodes) placed on designated areas of the body.

The electrocardiogram is composed of waves and complexes. Waves and complexes in the normal sinus rhythm are the P wave, PR Interval, PR Segment, QRS Complex, ST Segment, QT Interval and T wave (shown below).

P Wave

P waves are caused by atrial depolarization. In normal sinus rhythm, the SA node acts as the pacemaker. The electrical impulse from the SA node spreads over the right and left atria to cause atrial depolarization. The P wave contour is usually smooth, and of uniform size. Its polarity depends on the lead in which it is being recorded. The P wave duration is normally less than 0.12 sec and the amplitude is normally less than 0.25 mV. A negative P-wave in leads in which the P wave is normally positive can indicate depolarization arising from the AV node.

Note that the P wave corresponds to electrical impulses not mechanical atria contraction. Atrial contraction begins at about the middle of the P wave and continues during the PR segment. PR INTERVAL

The PR interval is the time (in seconds) from the beginning of the P wave (onset of atrial depolarization) to the beginning of the QRS complex (onset of ventricular depolarization). The normal PR interval duration range is from 0.12 sec - 0.20 sec, measured from the initial deflection of the P-wave to the

initial deflection of the QRS complex. The PR interval is longer with high vagal tone. A prolonged PR interval can correspond to impaired AV node conduction.

Although electrical activity begins at the P wave, actually atrial contraction begins later at about the middle of the P-wave and continues during the PR segment. In terms of electrical activity, the PR segment is a time lag to allow atrial systole to occur, filling the ventricles before ventricular systole. Most of the delay occurs in the AV node. The AV node is slow conducting, causing a delay in conduction of about 0.1 seconds. Atrial repolarization (electrical impulse) is usually hidden by the QRS complex and atrial muscle relaxation occurs after the QRS complex and is accompanied by a decrease in atrial pressure.

The PR Segment PR segment is the portion on the ECG wave from the end of the P wave to the beginning of the QRS complex, lasting about 0.1 seconds. The PR segment corresponds to the time between the end of atrial depolarization to the onset of ventricular depolarization. The PR segment is an isoelectric segment, that is, no wave or deflection is recorded. During the PR segment, the impulse travels from the AV node through the conducting tissue (bundle branches, and Purkinje fibers) towards the ventricles. (Note a wave will be recorded only after the impulses exits the conducting systems and activates the ventricular muscle to give the QRS complex). Most of the delay in the PR segment occurs in the AV node. Although the PR segment is isoelectric, the atrial are actually contracting, filling the ventricles before ventricular systole The QRS Complex In normal sinus rhythm, each P wave is followed by a QRS complex. The QRS complex represents the time it takes for depolarization of the ventricles. Activation of the anterioseptal region of the ventricular myocardium corresponds to the negative Q wave. The Q wave is not always present. Activation of the rest of the ventricular muscle from the endocardial surface corresponds to the rest of the QRS complex. The R wave is the point

when half of the ventricular myocardium has been depolarized. The normal QRS duration range is from 0.08 sec to 0.12 sec measured from the initial deflection of the QRS from the isoelectric line to the end of the QRS complex. Normal ventricular depolarization requires normal function of the right and left bundle branches. A block in either the right or left bundle branch delays depolarization of the ventricles, resulting in a prolonged QRS duration. The QRS complex precedes ventricular contraction.

The shape of the QRS complex shape changes depending on which recording electrodes are being used. The shape will also change when there is abnormal conduction of electrical impulses within the ventricles. The figure to the right summarizes the nomenclature used to define the different components of the QRS complex.

The ST Segment The ST segment represents the period from the end of ventricular depolarization to the beginning of ventricular repolarization. The ST segment lies between the end of the QRS complex and the initial deflection of the T-wave and is normally isoelectric. It is clinically important if elevated or depressed as it can be a sign of clinical processes such as ischemia, injury current and hyperkalemia. The QT Interval The QT interval begins at the onset of the QRS complex and to the end of the T wave. It represents the time between the start of ventricular depolarization and the end of ventricular repolarization. It is useful as a measure of the duration of repolarization. The QT interval will vary depending on the heart rate, age and gender. It increases with bradycardia and decreases with tachycardia. Men have shorter QT intervals (0.39 sec) than women (0.41 sec). The QT interval is influenced by electrolyte balance, drugs, and ischemia.

The T Wave The T wave corresponds to the rapid ventricular repolarization. The wave is normally rounded and positive depending on the lead. The T wave can become peaked or flattened due to electrolyte imbalance, hyperventilation, CNS disease, ischemia or myocardial infarction.

B. Determining Heart Rate and Rhythm

The EKG paper is made of a grid of big boxes and small boxes. Each big box is 10 mm in length has five small boxes and is 0.20 sec. Each small box is 1 mm and represents 0.04 sec. The EKG paper moves at a standard speed of 25 mm/sec. At standard speed, the heart rate can be determined by either of the following methods.

Method 1

Examine the distance between QRS complexes and determine if the peaks (RR intervals) are regularly spaced.

The EKG below shows regular RR intervals. If the RR distances are regular, count the number of "small boxes" from the beginning of one QRS complex to the beginning of the next QRS complex. Then divide 1500 by the number of "small boxes" to obtain the heart rate in beats per minute.

Heart Rate = 1500

No. small boxes

The EKG on the bottom right shows irregularly spaced RR intervals. If the distances are irregular, count the number of QRS complexes within 30 large boxes (which each represent 0.2 seconds) and multiply this number by 10 to obtain the heart rate in

Method 2

If the peaks are regular, the heart rate can be estimated using the ECG grid. To do this, locate a QRS complex on a bold line. If the next QRS complex is separated by:

i. One large box, the heart rate is 300 BPM (300/1) ii. Two large boxes, the heart rate is 150 BPM (300/2) iii. Three large boxes, the heart rate is 100 BPM (300/3) iv. Four large boxes, the heart rate is 75 BPM (300/4) ...and so on. The ECG grid used to rapidly estimate the heart rate

The heart rate calculated using the RR intervals is the venticular rate. In sinus rhythm, the venticular rate corresponds to the atrial rate. The atrial rate

can be determined from the PP interval using either of the two methods above.

Fast and slow sinus rhythm

In sinus rhythm, every P-wave is followed by a QRS complex, the R-R interval is regular and the P-R interval is less than 0.2 seconds (one big box on the EKG paper). A fast sinus rhythm, faster than 100 beats a minute, is known as sinus tachycardia while a slow rhythm, slower than 60 beats a minute, is known as sinus bradycardia.

C. Determining Axis

Direction of depolarization (vector) of the QRS complex.

1. The left ventricle is thicker so the mean QRS vector is down and to the left. (The origin of the vector is the AV node with the left ventricle being down and to the left of this).

2. The vector will point toward hypertrophy (thickened wall) and away from the infarct (electrically dead area).

Fig 1: Axis Determination

Normal axis -30 to +90 degrees Left axis deviation -30 to -90 degrees Right axis deviation +90 to +/-180 degrees Indeterminate (extreme) axis deviation -90 to +/-180 degrees

Since lead I and aVF are perpendicular to each other, you can use those two leads to quickly determine axis.

Lead I runs from right to left across a patient's body, positive at the left hand: (See fig 1).

If the QRS in lead I is positive (mainly above the baseline), the direction of depolarization will be in the positive half (right half) of the circle above. You can make a diagram and shade in the positive half of the circle.

Lead aVF runs from top to bottom across a patient's body, positive at the feet: (See Fig 1)

If the QRS in lead aVF is positive (mainly above the baseline), the direction of depolarization will be in the positive half (lower half) of the circle above. You can make a diagram and shade in the positive half of the circle:

To find the axis overlap the two circles. The common shaded area is the quadrant in which the axis lies. In this example, the axis lies in the normal quadrant, which on a patient, points down and to the left.

You can repeat this process for any two leads, but I and aVF are the classic places to look. If you realize that there are two leads to consider and a positive (+) or (-) orientation for each lead, there would be four possible combinations. Memorize the following axis guidelines.

Lead I Lead aVF

1. Normal axis (0 to +90 degrees) Positive Positive 2. Left axis deviation (-30 to -90) Also check lead II. To be true left axis deviation, it should also be down in lead II. If the QRS is upright in II, the axis is still normal (0 to -30).

Positive Negative

3. Right axis deviation (+90 to +180) Negative Positive 4. Indeterminate axis (-90 to -180) Negative Negative

Figure 2: Normal axis

Figure 3: Left axis deviation.

Figure 4: Right axis deviation

The bottom line is, if the axis is shifted out of the normal quadrant, evaluate the reasons for this.

Differential Diagnosis Left axis deviation LVH, left anterior fascicular block, inferior wall MIRight axis deviation RVH, left posterior fascicular block, lateral wall MI

D. Hypertrophy

Below is the criteria used to establish enlargement of any of the four chambers.

1. LVH: (Left ventricular hypertrophy). Add the larger S wave of V1 or V2 (not both), measure in mm, to the larger R wave of V5 or V6. If the sum is > 35mm, it meets "voltage criteria" for LVH. Also consider if R wave is > 12mm in aVL. LVH is more likely with a "strain pattern" which is asymmetric T wave inversion in those leads showing LVH.

2. RVH: (Right ventricular hypertrophy). R wave > S wave in V1 3. Atrial hypertrophy: (leads II and V1). Right atrial hypertrophy - Peaked P wave in lead II > 2.5mm amplitude. Left atrial hypertrophy - Notched wide (> 3mm) P wave in lead II. V1 has increase in the terminal negative deflection.

Figure 5: Left ventricular hypertrophy (S wave V2 plus R wave of V5 greater than 35mm) and left atrial enlargement (II and V1).

E. Bundle Branch Blocks

I. Left Bundle Branch Block. The ECG criteria for a left bundle branch block (LBBB) include: 1) QRS duration of > 120 milliseconds. 2) Absence of Q wave in leads I, V5, and V6. 3) Monomorphic R wave in I, V5, and V6. 4) ST and T wave displacement opposite to the major deflection of the QRS complex. Note: If the QRS duration is between 100-119 milliseconds with criteria 2, 3, and 4 of the above, an incomplete left bundle branch block is present. Traditionally it has been taught that myocardial infarction is not able to be diagnosed via ECG in the presence of a left bundle branch block (LBBB), however Sgarbossa et al in 1996 described some ECG changes seen in those with LBBB and concomitant myocardial infarctions and devised a point scoring system. 1) ST elevation > 1 mm and in the same direction (concordant) with the QRS complex. 5 points 2) ST depression > 1 mm in leads V1, V2, or V3. 3 points 3) ST elevation > 5 mm and in the opposite direction (discordant) with the QRS. 2 points

Fig 6: Left bundle branch block II. Right Bundle Branch block The ECG criteria for a right bundle branch block include: 1) QRS duration of > 120 milliseconds 2) rsR' "bunny ear" pattern in precordial leads 3) Slurred S waves or wide terminal S wave (greater than 0.02 sec) in leads I, V5, and V6. Remember that T wave inversions and ST segment depression is normal in leads V1 - V3 in the presence of a RBBB, thus technically myocardial ischemia can not be easily determined in these leads. However, unlike in the presence of a left bundle branch block, myocardial ischemia and infarction can easily be detected on ECG when a RBBB is present.

Fig 7: Right Bundle Branch Block

F. Infarct

Accurate ECG interpretation in a patient with chest pain is critical. Basically, there can be three types of problems:

- ischemia is a relative lack of blood supply (not yet an infarct) - injury is acute damage occurring right now - infarct is an area of dead myocardium

It is important to realize that certain leads represent certain areas of the left ventricle; by noting which leads are involved, you can localize the process. The prognosis often varies depending on which area of the left ventricle is involved (i.e. anterior wall myocardial infarct generally has a worse prognosis than an inferior wall infarct).

V1-V2 anteroseptal wall V3-V4 anterior wall V5-V6 anterolateral wall

II, III, aVF inferior wall

I, aVL lateral wall

V1-V2 posterior wall (reciprocal)

1. Ischemia

Represented by symmetrical T wave inversion (upside down). The definitive leads for ischemia are: I, II, V2 - V6.

2. Injury

Acute damage - look for elevated ST segments. (Pericarditis and cardiac aneurysm can also cause ST elevation; remember to correlate it with the patient.

3. Infarct

Look for significant "patholgic" Q waves. To be significant, a Q wave must be at least one small box wide or one-third the entire QRS height. Remember, to be a Q wave, the initial deflection must be down; even a tiny initial upward deflection makes the apparent Q wave an R wave.

Figure 8: Ischemia: Note symmetric T wave inversions in leads I, V2-V5.

Figure 9: Injury: Note ST segment elevation in leads V2-V3 (anteroseptal/anterior wall).

Figure 10: Infarct: Note Q waves in leads II, III, and aVF (inferior wall).

For the posterior wall, remember that vectors representing depolarization of the anterior and posterior portion of the left ventricle are in opposite directions. So, a posterior process shows up as opposite of an anterior process in V1. Instead of a Q wave and ST elevation, you get an R wave and ST depression in V1.

Figure 9: Posterior wall infarct. Notice tall R wave in V1. Posterior wall infarcts are often associated with inferior wall infarcts (Q waves in II, III and aVF).

Two other caveats: One is that normally the R wave gets larger as you go to V1 to V6. If there is no R wave "progression" from V1 to V6 this can also mean infarct. The second caveat is that, with a left bundle branch block, you cannot evaluate "infarct" on that ECG. In a patient with chest pain and left bundle branch block, you must rely on cardiac enzymes (blood tests) and the history.

III. Systematic Guideline for ECG Interpretation

A. RATE Rate calculation Common method: 300-150-100-75-60-50 Mathematical method: 300/# large boxes between R waves Six-second method: # R-R intervals x10

B. RHYTHM Rhythm Guidelines: 1. Check the bottom rhythm strip for regularity, i.e. - regular, regularly irregular, and irregularly irregular. 2. Check for a P wave before each QRS, QRS after each P. 3. Check PR interval (for AV blocks) and QRS (for bundle branch blocks). Check for prolonged QT. 4. Recognize "patterns" such as atrial fibrillation, PVC's, PAC's, escape beats, ventricular tachycardia, paroxysmal atrial tachycardia, AV blocks and bundle branch blocks. C. AXIS

Lead I Lead aVF

1. Normal axis (0 to +90 degrees) Positive Positive 2. Left axis deviation (-30 to -90) Also check lead II. To be true left axis deviation, it should also be down in lead II.

Positive Negative

3. Right axis deviation (+90 to +180) Negative Positive 4. Indeterminate axis (-90 to -180) Negative Negative Left axis deviation differential: LVH, left anterior fascicular block, inferior wall MI. Right axis deviation differential: RVH, left posterior fascicular block, lateral wall MII

D. HYPERTROPHY 1. LVH -- left ventricular hypertrophy = S wave in V1 or V2 + R wave in V5 or V6 > 35mm or aVL R wave > 12mm. 2. RVH -- right ventricular hypertrophy = R wave > S wave in V1 and gets progressively smaller to left V1-V6 (normally, R wave increases from V1-V6). 3. Atrial hypertrophy (leads II and V1) a. Right atrial hypertrophy -- Peaked P wave in lead II > 2.5 mm in amplitude. V1 has increase in the initial positive direction. b Left atrial hypertrophy -- Notched wide (> 3mm) P wave in II. V1 has increase in the terminal negative direction. E. INFARCT

Ischemia Represented by symmetrical T wave inversion (upside down). Look in leads I, II, V2-V6.

Injury Acute damage -- look for elevated ST segments.

Infarct "Pathologic" Q waves. To be significant, a Q wave must be at least one small square wide or one-third the entire QRS height.

Certain leads represent certain areas of the left ventricle: V1-V2

anteroseptal wall

II, III, aVF inferior wall

V3-V4 anterior wall I, aVL lateral wall

V5-V6

anterolateral wall V1-V2 posterior wall

(reciprocal)