PT School – Cardiovascular Physical Therapy – EKG Presentation (Schwirian)



1.     EKG basics (waves, segments, intervals)

2.     EKG events correspond to pressure & volume changes during the cardiac cycle

3.     Three unique properties of the heart the influence the EKG

a.      Automaticicty & rhythmicity

b.     Conductivity/Functional syncitium

c.     Conduction system

4.     EKG Leads and electrode placement

5.     Basic EKG analysis

a.      Rate

b.     Rhythm

c.     Axis

d.     Hypertrophy

e.      Ischemia/injury/infarction

6.     Recognizing basic arrhythmias

7.     Causes/consequences/treatment of basic arrhythmias

8.     Recognizing life threatening vs. benign arrhythmias

9.     Recognizing signs of ischemia/infarction

10. Be able to read a patient’s chart and understand clinical diagnosis


The following pages review some EKG basics.  Those of you who took human and exercise physiology lab here at OU will recognize these pages (hopefully).  Your Cardiopulmonary Physical Therapy text (Hileglass & Sadowsky) also covers most of these EKG basics fairly well.

Introduction to Electrocardiography

     Electrocardiography is a procedure to evaluate the electrical activity of the heart.  Electrocardiography results in the production of an electrocardiograph (EKG) or a graphic representation of the electrical activity of the heart.  The EKG demonstrates a very organized and reproducible sequence of electrical events that occur within the heart.  Examination of this sequence of electrical events can be useful to determine if the mechanical events (pressure and volume changes) of the heart are also occurring in the properly.  Abnormal electrical events in the EKG may result in abnormal mechanical events which could compromise cardiac output and normal delivery of oxygen to the heart,  brain and other tissues. 

     It is important to note that the EKG represents a complex depiction of all of the electrical activity of the heart; not individual action potentials.  The depolarization and repolarization of heart’s millions of cells give rise to these characteristic EKG waves.  In order to produce a productive contraction, some of the myocardial cells need to be stimulated sooner than others.  The heart has three important anatomical and physiological properties that can account for this very reproducible event.

1)  Automaticity - The cell membranes of most of the myocardial cells, especially pacemaker cells (such as the SA and AV nodes) , have an increased permeability to sodium.  These "leaky membranes" allow sodium ions to gradually leak into the interior of the myocardial cell, resulting in a slow depolarization of the membrane.  Because of the presence of voltage gated calcium channels, if the membrane depolarizes enough, the calcium channels open and allow an influx of calcium, causing further depolarization.  Thus, as sodium and then calcium ions leak in, the membrane depolarizes and eventually reaches threshold.  Once the cell reaches threshold an action potential will occur, and will ultimately result in depolarization and contraction of cardiac muscle cells.  Therefore the heart has the ability to stimulate itself without any outside influence (i.e. it automatically depolarizes itself).  Thus, unlike skeletal muscle, no neural input is required to initiate cardiac muscle contractions.  The heart is innervated by both branches of the autonomic nervous system.  However, these serve to increase the rate of depolarization (sympathetic nervous system) or decrease the rate of depolarization (parasympathetic nervous system), resulting in an increase or decrease in heart rate.    

2)  Functional Syncytium -  Due to the presence of gap junctions, specialized proteins located in the intercalated discs between cardiac muscle cells, once one cell in the heart reaches threshold a wave of depolarization and repolarization will spread from cell to cell through the entire myocardium.  This arrangement allows the heart to function collectively.  However, the heart contains a fibrous skeleton, which separates the upper atria from the lower ventricles.  How does the impulse move from the atria to the ventricles?

3) Conduction System – (see CPT text figures 9-3 to 9-7) Within the myocardium is specialized muscle tissue that exhibits very rapid conduction ability.  This tissue is arranged in such a way to allow the impulse to be rapidly distributed to different parts of the heart at different times.  This system is responsible for the order and timing of the electrical (and contraction) events within the heart.  Sino-atrial Node (SA), Internodal and Interatrial Bands, Atrioventricular Node (AV), The Common AV Bundle (of HIS), Right and Left Bundle Branches and the Purkinje Fibers. 

     Each portion of the conduction system exhibits the property of automaticity.  The SA node usually spontaneously depolarizes at a rate of about 70 times per minute. Each segment of the conduction system spontaneously depolarizes at a progressively slower rate If the SA node stopped having action potentials, or if each part of the heart was dissected and studied separately, the atrial muscle cells would depolarize approximately 60 times per minute.  In the absence of SA node, or atrial muscle initiation of depolarization in the heart the AV node could take over as the pacemaker.  The AV node depolarizes at an inherent rate of approximately 50 times per minute.  The purkinje fibers could take over as the pacemaker for the ventricles if the SA node, and AV node failed to take over as the pacemaker.  The purkinje fibers depolarize at an inherent rate of about 30 times per minute.  The inherent rate of depolarization in the ventricles is about 25 times per minute.  Due to the arrangement of the myocardial cell in a functional syncytium the cell that reaches threshold first will control the rest.  Thus, since the SA node normally depolarizes first, it usually serves as the pacemaker of the heart, depolarizing around 70 times per minute in an average individual.     

     If some other cell in the heart should depolarize before the SA node it would become the pacemaker, at least for that beat of the heart.  For example, if a myocardial cell in the atria should happen to depolarize before the SA node, it would result in a premature beat.  If the premature beat is initiated in the atria, they are referred to as premature atrial contractions (PAC). If a premature beat is initiated in the ventricles they are referred to as premature ventricular contractions (PVC). These (atrial or ventricular myocardial) cells that initiate a heart beat, but that are not normally the pacemaker are referred to as ectopic foci. These PAC’s and PVC’s alter the normal cardiac cycle and therefore result in an abnormal electrical rhythm.  An abnormal heart rhythm is referred to as an arrhythmia.  The normal electrical rhythm of the heart is referred to as Normal sinus rhythm.

     In addition to the myocardial properties listed above it is also important to understand that cardiac muscle cells (myocardial cells) do not produce a “typical” action potential.  This is due to the presence of slow calcium channels in the myocardium.  These channels are opened at the point of stimulus like the sodium channels; however, they open much slower and remain open much longer.  This produces a plateau phase in the action potential immediately following depolarization.  As the slow calcium channels close the potassium channels open and the cell repolarizes.  The end result is an action potential that usually is 0.25 to 0.3 seconds in duration, much slower than typical skeletal muscle.  This long action potential results in an extended refractory period.  This accounts for the inability of the heart to be tetanized (as we will see in our cardiac cycle lab).

     The normal function of these features results in the following sequence of electrical events in the myocardium (see diagram and CPT text figures 9-9 & 9-18).










P wave -  Represents depolarization of the myocardial cells in the atria, initiated by the SA node.

QRS complex - Represents depolarization of the myocardial cells in the ventricles. This also happens to coincide with the part of the cardiac cycle when the myocardial cells in the atria are repolarizing.  The impulse is slightly delayed at the AV node before entering the ventricles through the Common AV Bundle.

J-point  Is the end of the QRS complex and the beginning of the ST segment.

T wave -  Represents repolarization of the myocardial cells in the ventricles.

U wave -  If present, it represents repolarization of purkinje fibers and/or the ventricular septum.

Isoelectric line -  Is the flat parts of the EKG, for example between the T and P waves or between the P wave and the QRS complex.

R-R interval  - The RR interval represents the amount of time between heart beats.  Thus, the RR interval is heart rate dependent.  When heart rate increases, RR interval decreases and the opposite is true when heart rate decreases.  In fact, most of our methods for determining heart rate from the EKG are dependent on measureing the RR interval.  For example if there is 0.6 seconds between beats, and there are 60 seconds per minute, then the heart rate would be 100 beats per minute [(60 sec/minute / (0.6 sec/beat)].  The RR interval is measured from the peak of one QRS complex (R wave) to the peak of the next QRS complex.  Heart rate must be assessed in order to determine the subject’s electrical rhythm.  If all intervals are normal and all waves are present and if the subject’s heart rate is between 60 and 100 beats per minute, then they are in normal sinus rhythm.  Individuals with sinus arrhythmia have an RR interval that varies with the respiratory cycle.  Thus, it is necessary to measure the RR interval several places across the EKG.  If a subject’s heart rate is over 100 beats per minute they are said to be in sinus tachycardia. If their heart rate is below 60 beats per minute they are said to be in sinus bradycardia.  Recall from human physiology that the sympathetic nervous system causes an increase in heart rate and the parasympathetic nervous system causes a decrease in heart rate.  What effect would the sympathetic and parasympathetic nervous system have on the RR interval?

PR interval - This interval represents the time delay between the depolarization of the atria and the ventricles and is measured from the beginning of the P wave to the beginning of the QRS complex (not to the R wave as its name implies). This interval normally lasts 0.12 and 0.20 seconds.  It is used to evaluate the function of the AV node.  For example, if the PR interval is greater than 0.2 seconds every beat the subject has a first degree AV block, and represents a slowing of action potential propagation across the AV node.   There are several types of “AV blocks” that are clinically significant that will be discussed later.

QRS interval - This interval represents the time for the impulse to be distributed over the entire ventricular myocardium.  This interval usually lasts between 0.08 and 0.12 seconds.

QT interval - This interval represents the total time between the beginning of ventricular depolarization and the end of ventricular repolarization. It is measured from the beginning of the QRS complex to the end of the T wave.  At a heart rate of 70 beats per minute it is usually about 0.35 seconds in duration, but the duration of the QT interval is very heart rate dependent.  The lower the heart rate is, the longer the QT interval.  Individuals with a mutation in one of several ion channel genes may have long QT syndrome, which increases the possibility of sudden cardiac death (SCD)

ST segment - Is the segment between the J point (the end of the QRS complex) and the beginning of the T wave.  If this segment is significantly below the isoelectric line it is called ST segment depression and it suggests that part of the subject’s myocardium is not getting enough oxygen (myocardial ischema).  This segment is also frequently elevated (ST segment elevation) above the isoelectric line in the early stages of a myocardial infarction.  The ST segment is discussed in detail in the next lab. 

If you have assessed each of these intervals and have assessed each of the different waveforms on your subject’s EKG, you can now identify your subject’s rhythm and determine whether their heart in a normal, regular electrical rhythm (normal sinus rhythm) or if they have an abnormal rhythm (an arrhythmia).  When abnormal electrical rhythms are present the subject is said to have an arrhythmia (sometimes called a dysrhythmia, although these terms are not completely interchangable).  A very common arrhythmia occurs in conjunction with respiration.  During inspiration the large veins in the thoracic cavity fill with blood and during expiration this blood is forced into the heart.  If there is an increase filling of there will be an increase in heart rate, this reflex increase in heart rate is called the Bainbridge reflex.  Therefore heart rate is frequently seen to increase and decrease during the respiratory cycle and is referred to as a Sinus arrhythmia (or respiratory sinus arrhythmia).  To determine if your subject has sinus arrhythmia, measure the interval between two consecutive R waves.  Compare this interval with the next 5-8 R-R intervals; are they all the same or do they differ?  If the RR intervals are not all the same, your subject may have sinus arrhythmia.  However, if the RR interval is varying greatly and is switching between tachycardia and bradycardia for no particular reason they might have sick sinus syndrome, a potentially more serious dysrhythmia.  In general, arrhythmias can be grouped into four basic areas (see CPT text for details on each).

                        a) abnormal pacemaker function

                                    - Sinus arrhythmia, sick sinus syndrome

                        b) ectopic focus (originating from some point other than the SA node)

                                    - PACs, PVCs

                        c) conduction system blocks

                                    - Atrioventricular (1st, 2nd and 3rd degree) and bundle branch blocks

                        d) abnormal conduction pathways

                                    - flutter and fibrillation patterns

Recording the electrical activity of the heart

            EKGs are usually recorded on a standardized EKG paper resembling graph paper with red lines.  On EKG paper, each of the vertical thick red lines is separated from each other by a horizontal distance of 5mm and represents a time of 0.2 seconds.  Each thin red line is separated by a horizontal distance of 1mm and represents 0.04 seconds.  Thus, the PR interval, which is usually 0.12 to 0.2 seconds long, is usually 3 to 5 “small boxes” across and the QRS interval (0.08 to 0.12 seconds normally) is 2-3 “small boxes” across (NOTE: your CPT text uses a range of 0.04-0.1 and two other texts recommend ranges of 0.06 to 0.10, and .08 to 0.10).  A vertical distance of 10mm usually represents a deflection of 1mV on a standard EKG tracing.

            The electrical activity of the heart is recorded from the body by surface electrodes. The electrodes make up leads; with each lead depicting the electrical activity of the heart in a particular plane relative to the heart. Electrodes may serve as leads either alone or in combination with each other. In the unipolar (chest) leads, which are also called precordial leads, each electrode serves as a positive electrode. In each of the limb leads one electrode is designated as positive (+) and one is designated as negative (-).  In each of the augmented voltage leads one electrode is designated as positive (+) and two electrodes are designated as negative (-).  If the wave of depolarization (the spread of electrical activity) is moving toward the (+) electrode, it results in an upward deflection of the recording (see figure below).  A wave of depolarization moving away from the (+) electrode causes a downward deflection in the recording.  The opposite is true for a wave of repolarization.


     (+)                                           (-)                            (+)                                        (-)

                   Depolarization                                                            Depolarization



                                                    EKG                                                                      EKG                                                          




If the wave of depolarization is in some other direction the corresponding graphic

representation may appear as one of the following.








                 (+)                                                                                                                          (-)


            The mean electrical axis (the average direction of the wave of depolarization) of the heart is from the base toward the apex (down and to the left side of the subject). Thus, in limb lead II, because the electrical activity is spreading from towards the positive electrode (Left leg), the QRS complex is generally very positive (upwards). The mean electrical axis gives us a relative indicator of the direction and magnitude of the electrical activity in the heart.  Remember that in a normal human heart as the electrical impulse goes from the SA node to the AV node to the Common bundle to the right and left bundle branches to the Purkinje fibers and then into the ventricular myocardium the wave of depolarization tends to go from the right atrium towards the apex of the heart.  










Looking at the mean electrical axis of an individual’s heart can give us valuable information about possible hypertrophy and/or infarction of part of the myocardium.  If the myocardium is hypertrophied, the increase in the size of the myocardium in the hypertrophied area causes a relative increase in the electrical activity of that area.  This means that the mean electrical axis will tend to shift towards hypertrophy due to this increase in electrical activity.  On the other hand if the myocardium is necrotic (dead) in a particular area, such as is the case after a myocardial infarction, because these cells are no longer living they do not depolarize when an action potential reaches them.  The result of this lack of electrical activity is that the mean electrical axis will tend to shift away from infarction.  Some dysrhythmias, such as bundle branch blocks, may also shift the mean electrical axis.

            Other situations and conditions can alter the mean electrical axis.  The mean electrical axis of individuals who are severely obese or pregnant may be shifted to the left.  The reason for this is that the fatty deposits or the fetus are pushing up on the diaphragm, which is in turn pushing the apex of the heart towards the left.  It is also not uncommon in tall thin individuals to see a difference in mean electrical axis between the supine and standing positions. The cause of this difference is that when the individual is lying down many of the abdominal contents push up on the diaphragm, and thus on the heart.  When they stand up the heart shifts back.

            Utilizing these concepts and placing surface electrodes on standard areas of the body we can produce standard lead configuration with reproducible waveforms.  The placement of electrodes in different arrangements allows for different views of the same electrical event.  Some leads provide better information than others regarding a specific area of the heart.  For this reason several lead combinations are frequently used to give a comprehensive evaluation of the electrical activity of the heart.  A 12 lead EKG is a standard procedure that uses the combination of 10 different electrodes to provide 12 different lead configurations.  We will be using a standard 12 lead EKG in today's lab.  A standard 12 lead EKG includes: three limb leads, three augmented voltage leads, and six precordial leads.

            The limb lead configuration is based on Einthoven's Triangle.  This triangle surrounds the heart and is made up of three electrodes placed on the right and left arm and the left leg (an electrode is also placed on the right leg to serve as a ground wire).  Combinations of these three electrodes can be used to produce six different views of the heart in the frontal plane.  Limb leads I, II and III are demonstrated in the following diagram.  It is very important to note what

electrodes make up each of these leads and which electrode is positive or negative in each lead.

                                    (-)                         I                          (+)

                        RA                                                                         LA


                              (-)                                                                (-)



                                    II                                                   III



                                                      (+)               (+)



            The other three leads on the frontal plane are produced by combining two electrode locations to make the negative component of the lead.  These leads are referred to as augmented voltage (AV) leads.  There names correspond to the single electrode that is positive.  AVR - the right arm is positive and the left arm and left leg are negative.  AVL the left arm is positive and the right arm and left leg are negative, and in AVF (F is for the left foot or leg) the left leg is positive and the right and left arms are negative.  By combining two electrodes to serve as the negative pole of the lead reference of the lead goes half way between the two electrodes.

                                         RA                                        LA                                  


                                         AVR                               AVL       











The combination of all six frontal leads allows the heart to be evaluated from six different angles or views.














            The six precordial leads, or chest leads, are said to be on the horizontal plane relative to the heart.  They are arranged at various positions around the chest and are named V1 through V6.  V1 and V2 are frequently referred to as the right chest leads.  V5 and V6 are frequently referred to as the left chest leads, although they are also sometimes referred to as lateral chest leads, or apical chest leads because they are located near the apex of the heart.  V3 and V4 are approximately over the anterior wall of the heart and the interventricular septum.




12 lead EKGs require electrode placement on the right arm, left arm and the left leg (the right leg is also used for a ground) as well as various locations around the chest. Please note that for exercise measurements, the locations of the limb electrodes are modified to the anterior shoulder just below the clavicle (avoiding muscle mass) for the arm electrodes and the lower left intercostal space for the left leg electrode.  Before placement of electrodes, attachment sites should be rubbed thoroughly with an alcohol prep pad until the skin is slightly reddened.  It may be necessary to shave small areas around the chest for placement of the chest electrodes.  Further irritation of the skin with fine, medical grade sandpaper will also improve the electrical conductivity of your leads. 

Once the electrodes are in place, both 12 lead EKGs and rhythms strips can be printed.  The difference between a rhythm strip and a 12 lead EKG is that a rhythm strip records the same lead or leads all the way across the EKG paper.  A 12 lead EKG records information from all 12 leads across the EKG paper divided into short, 2.5 second periods so that all 12 leads can fit on one page.  In this course we will always analyze the EKG in the following order.  Rhythm strips are typically better for evaluation of the rate and rhythm (although these can be performed on a 12 lead EKG), and 12 lead EKGs are better for determination of electrical axis, hypertrophy, and for assessing signs of ischemia and infarction.

Each EKG contains a great deal of information.  In order to expedite your diagnosis and to make sure that your review of the EKG is appropriately thorough, it has been recommended that the EKG be analyzed in the following order:


a.     Determine HR

b.     Determine Rhythm

c.     Determine Axis

d.     Determine if there are any signs of hypertrophy

e.      Determine if there is any evidence of ischemia or infarction

I. Site preparation and electrode placement. 

The placement of the chest leads is fairly standard.  However, the placement of the electrodes for the limb and augmented voltage leads are slightly different depending on whether you are performing a resting or exercising EKG.  We will be using the exercise placement of these electrodes.  Prior to placing the electrodes on the subject prepare the skin with an alcohol prep pad, and by shaving if necessary.  Allow the alcohol on the skin to dry before placing the electrodes on the skin.  After the electrodes are attached to your subject's body, attach the electrical cords from the EKG machine to the surface electrodes.  The following are the locations of the 10 electrodes used in a 12 lead EKG.

Ground (or "reference") electrode

RL – placed on the lowest right intercostal space, approximately mid-clavicular

Limb electrodes

RA - placed half way across the right clavicle in the sub-clavicular fossa

LA - placed half way across the left clavicle in the sub-clavicular fossa

LL - placed on the lowest left intercostal space, approximately mid-clavicular

Chest electrodes*

V1  -  right sternal border in the 4th intercostal space

V2  -  left sternal border in the 4th intercostal space

V3  -  mid way between V2 & V4

V4  -  mid clavicular in the left 5th intercostal space

V5  -  mid way between V4 & V6 (around the left anterior axillary line, 5th intercostal space)

V6  -  left mid axillary line in the 5th intercostal space (or mid axillary and even with V4)

*The placement of some or all the chest electrodes may need to be slightly modified in women to avoid placing the electrodes over the fleshy part of the breast.


II. Evaluating the EKG

      After preparing the subject, hooking the subject up, and printing both a rhythm strip and a 12 lead EKG, use the following steps to evaluate the EKG.

A.  Determine the Heart Rate  in beats per minute.  Use the following four methods.

1.                              Count QRS complexes that are found in a 6 second interval and multiply by 10, this will give you the approximate HR.  This method is especially good if there is an arrhythmia.

2.                              Determine the amount of time between beats – count the number of small boxes between QRS complexes and multiply by 0.04 seconds/box.  60 seconds divided by the amount of time between beats will give you the HR.

3.                              Count the number of small boxes between QRS complexes (RR interval).  1,500 divided by this number will give you the HR.

4.                              Count big boxes between QRS complexes to determine HR as follows:

      boxes               rate                  boxes               rate

      1                      300                  4                        75

      2                      150                  5                        60

      3                      100                  6                        50

B.   Determining the electrical Rhythm of the heart and measuring intervals. 

1. RR interval and HR

      a. Is Heart Rate normal? ® Normal Sinus Rhythm, Bradycardia, or Tachycardia

      b. Is RR interval (and thus HR) consistently the same from beat to beat?  If not

          check for sinus arrhythmia or PACs

2. Presence or absence of normally observed waves

a. Is there a P before each QRS? ® if not check for PVCs, atrial fibrillation, 2° or 3° AV blocks

b. Is there a QRS after each P wave? ® if not check for 2° or 3° AV blocks, atrial            flutter
c. If P, Q, R, S, and T waves are all absent ® check for ventricular fibrillation or ventricular tachycardia

3. PR interval

      a. Is PR interval normal? Is PR interval always normal? ® if not check for Wolf-

          Parkinson-White syndrome or 1°, 2° or 3° AV blocks

4. QRS interval

      a. Is QRS interval normal? Is QRS interval always normal? ® if not check for PVCs

         or bundle branch block


C.  Determine electrical axis 

We will determine the mean electrical axis of the heart in two steps.  See the electrical axis worksheet to assist you with this part of the EKG analysis.

1.                              The first step is to determine which “quadrant” the mean electrical axis lies in.  This will allow us to know within 90 degrees the direction of the the mean electrical axis. This can easily be determined by observing leads I and AVF.  Observe each lead and determine if the QRS complex is more above the isoelectric line (positive) or more below the isoelectric line (negative).  Lead I is horizontal relative to the heart (and the subject’s body) and is positive on the left side of the body, if the QRS complex in this lead is more positive, then most of the electrical activity is going to the left (normal quadrant or left axis deviation) and if the QRS is more negative, then most of the electrical activity is going toward the right (right axis deviation or extreme right axis deviation).  Lead AVF is vertical relative to the heart (and the subject’s body) and is positive at the subject’s left foot.  If the QRS complex in AVF is more positive, then most of the electrical activity is going down towards the subject’s feet (normal quadrant or right axis deviation) and if the QRS is more negative, then most of the electrical activity is going upwards (left or extreme right axis deviation).  Thus, based on using only these two leads you can determine which quadrant the mean electrical axis lies in.

2.                              The second step in determining the mean electrical axis will allow us to determine the direction of the mean electrical axis to the nearest 30 degrees.   This step requires you to look at all three limb leads and all three augmented voltage leads.  Looking at these six leads, you need to find the most isoelectric lead.  The most isoelectric lead is the lead whose QRS complex has closest to a net deflection of zero.  To determine the net deflection of the QRS complex you simply count the number of small boxes from the isoelectric line to the peak of the QRS complex (the number of positive boxes) and count the number of small boxes from the isoelectric line to the bottom of the QRS complex (the number of negative boxes).  The net deflection of the QRS complex is determined by adding the number of positive and negative boxes.   For example, if the QRS complex in AVL goes up 6 small boxes from the isoelectric line (+6) and goes down 6 small boxes from the isoelectric line (-6), then the net deflection is zero.  The significance of the most isoelectric lead is that it lies approximately perpendicular to the mean electrical axis of the heart.  You can also think of it as the lead where there is just about as much electrical activity going away from the positive electrode as there is going towards the positive electrode. 

Once you have determined the most isoelectric lead, you go perpendicular from that lead (in the direction of the quadrant that you determined above) to determine the mean electrical axis.  For example, if AVL is the most isoelectric lead and the subject’s mean electrical axis is in the normal quadrant, their mean electrical axis is 60° (see electrical axis worksheet below).

D.  Determine if there is any evidence of myocardial hypertrophy

Several laboratory methods are available for assessing signs of myocardial hypertrophy.  For example, echocardiography can be used to directly take measurements of the heart's walls or chambers.  Assessing myocardial hypertrophy with EKGs is somewhat imperfect because it only allows for an indirect assessment of myocardial hypertrophy.  Myocardial hypertrophy specifically relates to the size of the heart wall or chamber and EKGs do not provide direct measurements of heart size or heart dimensions.  However, EKGs can provide some indirect evidence of cardiac hypertrophy.  In this course we will only discuss the most common type of cardiac (or myocardial) hypertrophy; left ventricular hypertrophy.  The following are considered electrocardiographic indicators of left ventricular hypertrophy. 

1.  A large, deep S wave in V1 and a large, tall R wave in V5.  It has been suggested that if the depth (in mm) of the S wave in V1 plus the height (in mm) of the R wave in V5 totals greater than 35mm, then the subject may have left ventricular hypertrophy.

2.  Asymmetric, inverted T waves in V5 or V6

3. Left axis deviation with a slightly widened QRS complex.

Electrical Axis worksheet
































            Normal             Left Axis                      Right Axis                     Extreme Right

            Quadrant                      Deviation                      Deviation                     Axis Deviation

            AVF = 0°                     AVF = 0°                     I        = + 90°               I       = - 90°

            III     = + 30°               II      = - 30°                AVR = + 120°             AVL = - 120°

            AVL = + 60°               AVR = - 60°                II       = + 150°             III     = - 150°

            I       = + 90°                I        = - 90°                AVF = + 180°             AVF = - 180°