THE PHYSIOLOGICAL BASIS OF THE EKG

THE PHYSIOLOGICAL BASIS OF THE EKG
Dr. Guido E. Santacana Professor Dept. of Physiology

After this section you should be able to:
Differentiate between an intracellular action potential and the electrocardiogram as an extracellular recording. Recognize the concept of the dipole and electrical potential vector and how it applies to the heart and EKG recording. Recognize that the cumulative electrical activity of the heart forms dipoles or electrical potential vectors in different directions as the activation of the heart progresses. Recognize that the multiple dipoles or electrical potential vectors generated by the heart produce the EKG recording. Learn the 12 EKG Leads and their projection of the lead vectors in three orthogonal planes. Understand how each EKG wave is generated using Lead I as an example. Perform a simple sequential analysis of the EKG. Learn the standards of the EKG recording paper. Understand the origin of the Mean QRS Axis concept. Using the Electrical Axis Circle of the heart learn to estimate Mean Electrical Axis. Calculate the Mean QRS Axis by vector analysis using three or two standard leads. Recognize the effect of left or right hypertrophy on the Mean QRS Axis. Recognize the effect of left or right Bundle Branch Block on the Mean Electrical Axis. Understand the concept of current of injury and its clinical implications. Learn to estimate the site of an ischemic injury using the concept of the J Point.

The Conduction System of the Heart
In terms of electrical activity you can view the heart as being composed of three types of cells: -PACEMAKER CELLS (SA Node) (AV Node) CONDUCTING CELLS- The wires MYOCARDIAL CELLS- The contracting ones. The SA nodes originates the pacemaker activity of a normal heart. This activity is propagated from the right atrium into the left atrium and then through the AV node into the interventricular septum, endocardium and epicardium. The figure above illustrates the direction of the propagation. This is the activity that eventually generates the electrocardiogram. All cells of the heart are able to generate automatic activity but the AV node rules due to its innate higher firing frequency.

The ECG is not an action potential but
Action Potentials = Change in membrane potential occurring in nerve, muscle, heart and other cells The electrocardiogram shown at the bottom of the graph above is a reflection of the electrical events that occur in the heart during each beat. The intracellular recorded action potentials that originate in the SA node are distributed through the heart by a conducting fiber network. As the wave of depolarization traverses the heart different areas become depolarized creating electrical dipoles or electrical force vectors in different directions. These electrical dipoles can be recorded from the surface of the skin by very sensitive apparatus. Originally they were recorded with a galvanometer. It is the direction and amplitude of these electrical dipoles that creates the EKG recording with its typical wave pattern. The ECG is not an action potential but reflects their cumulative effect at the level of the skin where the recording electrodes are located.

THE DIPOLE CONCEPT METER C -2 +2 JAR + - - B + - + A D POS BATTERY NEG
+2 JAR + - - B + - + A D POS BATTERY The drawing above shows a battery connected to a small bar. The battery produces a positive pole and a negative pole in the bar and creates a dipole. This specific dipole is submerged in an electrolytic solution inside a round jar. Electrodes B and A record the electrical activity at a specific position in the jar. The meter allows us to observe this electrical activity. If the bar is placed so that the + pole points toward A and the negative pole toward B a potential difference is established between A and B with A positive. Under this condition the meter points toward the positive side. If the bar is rotated and placed perpendicular to B and A, no potential difference is recorded in these electrodes and the meter points to 0. Rotation of the bar so that the negative pole points toward A moves the meter to the negative side. If the bar starts to rotate continuously then the meter will oscillate between negative and positive. If we make the needle of the meter a marking pen and a paper is moved under this pen so that the pen leaves a tracing you can see that the tracing produced by the oscillating pen will be a biphasic wave. This is a good analogy of what happens during the recording of an EKG. The heart becomes the dipole and our body is the jar. The electrodes are those of the EKG recorder and a needle records in paper the electrical potential differences between two electrodes that could be located in the left and right arms. NEG

EINTHOVEN’S TRIANGLE AND LIMB LEADS
Willem Einthoven codified the analysis of the electrical activity of the heart by proposing that certain conventions be followed. The heart is considered to be at the center of a triangle where each corner serves as the location of one recording electrode. Since two electrodes are needed to record a potential difference, this arrangement leaves three alternatives. There is an electrode in the left arm (A) and one in the right arm (B) with two wires to the electrocardiography recorder. This is the Standard Lead I of the EKG. Another recording site can be established between the right arm B(-) and left leg A(+). This is the Standard Lead II of the EKG. Standard Lead III is then established by placing the electrodes in the left arm B(-) and left leg A(+). The three resulting Standard Limb Leads are I, II and III. By convention the electrode marked A (+) will cause an upward deflection of the recorder pen when it is under the influence of a positive charge relative to the other electrode marked B(-). Notice that now the body becomes the electrolyte jar and the depolarization of the heart during each beat will create electrical dipoles in different directions. The dipoles which are also electrical force vectors will be recorded by each standard EKG Lead. Each Lead will then record on paper the deflections of the EKG pen. These deflections will then produce an EKG recording for each Lead. As an example notice that the position of the recording electrodes in Lead I (A and B) correspond to those we had in the jar example of the last page. You can see that each EKG Standard Lead records the electrical activity of the heart from a different perspective in a vertical plane. Notice also that in the drawing to your right there are three QRS complexes recorded from each standard lead. The QRS complex of Lead II has more amplitude than that of Leads I and III. We will study the reason for these discrepancies in QRS amplitudes in the next pages.

Einthoven’s Original EKG Recorder
The string galvanometer was invented and used, among other purposes to amplify electrical signals being transmitted thousands of miles via the transatlantic undersea communications cable. Einthoven saw in this system a promising model for the recording of the EKG. He developed a very sensitive galvanometer using an extremely thin and light weight quartz "string" silvered to reflect a beam of light, which was deflected by the passage of a fluctuating current in a powerful magnetic field. This galvanometer was sufficiently sensitive to detect the extremely small electrical events generated by the heart. The movable part of a string galvanometer is a microscopic thread of quartz called a "string," which is suspended vertically in a strong magnetic field. When a minute current is passed through it, the "string" is deflected, or really bent laterally. As the string is supported at both ends, has a very small mass, and moves only a fraction of a millimeter, it has very little inertia, and can record impulses up to many hundred times per minute. These records are obtained by making the string opaque with a coating of silver, placing it in a beam of light which throws a vertical shadow, magnified by a microscope, onto a metal plate in which there is a horizontal slot. This slot allows only a point of shadow to pass through to a moving photographic plate or film, on which the point of shadow writes in a continuous curve. Einthoven won the Nobel Prize in Medicine and Physiology. String Galvanometer Schematic. String Galvanometer Based EKG Recorder. Patient with hands submerged in strong salt solution.

What are we looking at in the EKG waves?
VOLTAGE!! As amplitude in Millivolts. Baseline at 0mv The wave illustrated above could be any wave of an EKG. One important fact to recognize here is that the EKG is mainly a reflection of the electrical activity of the myocardial cells with an insignificant component of the electrical activity from pacemakers and conducting cells. Remember that myocardial cells comprise most of the mass of the heart. The wave above has three characteristics: Amplitude- the height of the wave tells us how many millivolts were generated. 2. Duration- tells us how much time the electrical event lasted in milliseconds. 3. Configuration- how the wave looks. Remember these characteristics as we follow the steps in describing how each electrocardiographic wave of the EKG is generated. In the next pages we will be recording only from Lead I. If you already forgot about Lead I, go back and study page 6. TIME!! Duration in fractions of a second

Atrial Depolarization P wave (Lead I)
B A Zero potential - Before the atria depolarizes the EKG recorder shows zero potential. As the first region of the heart depolarizes in the SA node of the right atrium, there is another region that remains at rest or polarized. This creates two areas, one of negative charge in the region were the tissue has depolarized plus one of positive charge in the rest of the heart. We have a dipole or an electrical force that has direction or an electrical force vector. In atria depolarization the dipole generated by the combination of depolarized/polarized regions points in the direction illustrated above. Due to the fact that the positive pole of this dipole projects more toward the A electrode, the needle of the recorder deflects toward the positive side or up. If a paper is passed under the needle at 25mm/sec a small upward deflection is recorded. This is the P wave or atrial depolarization wave. As the atrial depolarization progresses and more atrial muscle is depolarized we reach a peak in the potential difference. As the whole of the atria depolarizes the potential falls until the whole atrial muscle is depolarized and the potential difference ceases to exist. Thus, the recording goes back to baseline or zero potential. ends the wave is completed and voltage goes back to baseline as seen is the next page. If we divide the P wave in two, the left side is considered to represent mainly right atrial depolarization while the right side represents left atrial depolarization. Remember that atrial depolarization starts in the right atrium. Notice that the positioning of the A and B recording electrodes above correspond to Lead I. Go to page 6 if you forgot. P + - + Peak Potential

Ventricular Conducting System
AV Node Bundle of His Left Bundle Branch Right Bundle Branch Left Posterior Fascicle P This is a good time to focus on the conduction system of the ventricles since from now on the electrocardiogram will reflect the effect of this system. The directions of the next EKG waves follow the pattern dictated by this conduction system. As the wave of depolarization leaves the atria it encounters the AV node where the wave is delayed for a few milliseconds. Afterwards the wave is rapidly and almost simultaneously propagated to the right and left ventricles of the heart following the route dictated by the conducting system illustrated above. Notice that due to the bigger myocardial mass in the left ventricle, the conducting system is more complex on this side of the heart being divided into anterior and posterior components. Notice also that there is a small septal fascicle. The depolarization of the ventricles proceeds from endocardium to epicardium with the first depolarization occurring in the interventricular septum and the last one in the base of the left ventricle. Lets see how the next set of waves of the EKG are generated. From now on the waves will reflect ventricular depolarization and repolarization. Septal fascicle P Left Anterior Fascicle P= Purkinje Fibers

Ventricular Septal Depolarization- the Q Wave
B A After the atria completely depolarize, they acquire a negative charge and for a period of time the dipole disappears and the recorder needle goes to 0mv or zero potential. Before the next dipole is generated the depolarization wave has to pass through the AV node and in doing so conduction slows and a physiologic delay is produced. The depolarization wave now passes to the Bundle of His and from here to the left and right bundle branches and the Purkinje fibers through which it propagates almost simultaneously through both ventricles from endocardium to epicardium. The first area to depolarize in the ventricles is the Interventricular Septum. Sometimes this depolarization starts in a small left area of the septum and runs toward the left. This produces a small dipole in the direction shown above. The dipole or electrical potential vector generated is small and the positive pole points towards the B(-) recording electrode of Lead I. Since the negative pole is pointing toward the A(+) recording electrode, the needle of the recorder deflects to the negative side or downward. In the paper this looks like a small downward deflection or the Q wave. This wave does not always appear in the EKG especially in Lead I. NOTE: Only the first deflection downward in an electrocardiogram is called a Q wave. Any other deflection downward is called an S wave. Now go back to page 7 and review the dipole for the P wave. + - + Q -

Ventricular Depolarization-the R Wave
B A 3 - 4 + The next dipole forms from the depolarization of that occurs deep in the endocardium of the interventricular septum. Initially this depolarization runs toward the epicardium and the apex of the heart. This is a powerful dipole or electrical potential vector formed as the endocardial mass depolarizes toward the epicardium. The positive pole of the dipole or electrical potential vector is inclined toward A and is registered in Lead I as a large positive deflection. This is the R wave of the QRS complex. The strong dipole is formed because at this time almost half of the ventricular muscle is depolarized or negative while about half remains polarized or positive. As the depolarization wave moves toward the apex more muscle is depolarized and less remains polarized especially toward the epicardium at the base of the ventricles. This reduces the magnitude of the potential difference and the R wave begins to decline toward zero potential. - +

Ventricular Depolarization-The S Wave
B. A B. + As the endocardial mass completely depolarizes toward the apex the depolarization wave now runs toward the epicardial surface in the direction of the base of both ventricles. The right ventricle having a lower tissue content depolarizes more rapidly. This leaves a small area at the base of the left ventricle that remains polarized. The electrical potential vector or dipole that results runs from right to left as shown above the depolarization wave continues to travel toward the epicardium in the direction apex. This creates a smaller dipole with the negative pole toward A. A downward deflection of the needle is produced representing the S wave. Go back to page 11 to see how the dipole rotated. As the ventricular mass completely depolarizes no other dipole is formed and the recorder returns to the 0 mark neutral point. At this point the whole ventricular mass is depolarized or negative outside. This condition lasts only milliseconds. + - - S A

QRS Configurations RSR’ QRS RS QR QS
The configurations for the QRS wave shown above are the most common. The rules to follow and memorize are : First deflection downward is a Q wave. First deflection upward is called an R wave. The first downward deflection following an upward deflection is an S wave. If only a downward deflection is observed, it is called a QS wave. RS QR QS

Ventricular Repolarization- the T Wave
+ S B A Repolarization of the ventricles runs from epicardium to endocardium as shown above. This is the reverse of what happens in depolarization. The arrow that represents the dipole appears in the direction shown above with the positive end pointing toward the epicardium at the apex which is the first area to repolarize and become positive. As the wave of repolarization moves from epicardium to endocardium more muscle is repolarized. When about half of the cardiac muscle is repolarized, the dipole or electrical potential vector is highest. As more muscle repolarizes the dipole diminishes in magnitude and finally disappears leaving the heart repolarized and at the zero potential level. Due to the fact that the repolarization dipole always projects its positive end toward the recording electrode A a positive deflection or upward movement of the recorder needle is observed. This deflection is the T wave or ventricular repolarization wave. Remember that we cannot see atrial repolarization because it occurs at the same time as the QRS complex. Now, go back and review the whole process once more. + - T - +

Review of the Sequence in the Formation of the EKG
Study this sequence of EKG formation again and notice how each dipole or electrical vector formed is projected against each of the Standard Limb Leads. This projection indicates how much positive or negative deflection the specific dipole will produce in each lead. For example, in atrial depolarization, the dipole or electrical vector produced is small. In Lead III this dipole will produce a very small projection that translates into a very small P wave for this Lead as compared with Leads I and II. Now go through each dipole or electrical vector produced during ventricular depolarization and observe how they project in each Lead. Remember that the size of the projection indicates the potential difference that the recording electrodes of the Lead will register. The bigger the projection the larger the potential and consequently a larger deflection will be observed in the EKG paper. We will go through this again later.

Intervals and Segments of the Normal EKG
The figure above shows the intervals and segments of the electrocardiogram plus the main waves. Notice that a segment is always a straight line that connects two waves while the interval can encompass one or two waves. Example: PR interval is the time from start of atrial depolarization to start of ventricular depolarization. ST segment is the time from the end of ventricular depolarization to the start of ventricular repolarization. QT interval is the time from start of ventricular depolarization to the end of ventricular repolarization. You are required to memorize these intervals and segments now.

INTERVALS AND SEGMENTS !
PR Interval- Onset of P wave to onset of QRS. ( sec or 3-5 small squares) QRS Interval-Beginning and end of QRS wave.(<.12sec duration or 3 small squares) QT interval- Beginning of QRS to end of T wave.( Calculated as corrected QT = .42 sec) ST segment ( no elevation or depression) The main intervals and segments are defined above. You should be able to recognize them and calculate them. Remember that each interval and segment represent an electrophysiological event in a region of the heart. For example, an increase above normal of the QRS Interval is observed in conditions such as ventricular hypertrophy and is due to the fact that it takes more time for a stimulus to travel through more muscle mass. It is also seen in Bundle Branch Block. The ST segment may be elevated or depressed after a coronary infarct and is an important element in localizing the infarcted area of the heart.

Limb Leads=Frontal Plane B A B B 60° 0° 120°
- B + + A A -150° 90° B - - -30° B A + Chest Leads = Horizontal Plane You can see above the main electrocardiograph leads. Notice that they basically register the same electrical event from a different perspective. See the B and A electrode placement for Leads I,II and III. Lead I- Created by making left arm + and right arm -. Angle of orientation is 0 degrees. Lead II- Created by making left leg + and right arm -. Angle of orientation is 60 degrees. Lead III- Created by making left leg positive and left arm negative. Angle of orientation is 120 degrees. Augmented Leads- for these a single lead is + and all others are averaged as negative. Lead AVL- Left arm + and other leads -. Angle of orientation is -30 degrees Lead AVR- Right arm positive and the other leads negative. Angle of orientation 150 degrees. Lead AVF-Left leg positive and other leads negative. Angle of orientation is 90 degrees. Leads I, II and three are also called the Standard Leads. Leads aVR, aVL, and aVF are the augmented or Wilson Leads. Remember this nomenclature. B A

The Chest or Precordial Leads
V1 V2 V3 V4 V5 V6 Over right ventricle Over Interventricular Septum Over the Left Ventricle The six precordial leads look at the heart in the transverse plane. In other words they register electrical forces moving anterior and posterior. Each lead is made positive and the body as a whole serves as the negative electrode. The arrow head for the dipole or electrical vector of each precordial Lead is positive. This means that a positive potential in the arrow head will produce a positive deflection and vice versa for a negative potential. Like the limb leads and augmented leads, each precordial leads looks at the heart in a particular direction as indicated above. You must learn the areas of the heart that each lead represents. The precordial leads are also unipolar. Each recording electrode is an exploring electrode and an indifferent electrode is kept at zero potential by connecting all the three limbs to a central terminal through 5000 ohm resistances.

Projection of the 12 Lead EKG Vectors in Three Orthogonal Planes
The figure above clearly demonstrates the ability of the EKG to register electrical events in the heart in three planes. This makes the EKG a powerful tool in the hands of an experienced clinician since it provides data from a three dimensional look at the heart. The heart in this model is considered a theoretical perfect sphere in the center of the Electrical Axis Circle.

Review of what each EKG Lead looks at.
Y Z X Anterior Leads V1,V2,V3,V4 Left lateral Leads I, AVL,V5 V6 As you can see the precordial leads look at the heart in a horizontal plane while the limb leads and the augmented leads look at the heart in the vertical plane. Leads V1,V2,V3 and V4- Anterior Leads Leads III,II and AVF- Inferior Leads-View the inferior surface of the heart that rests on the diaphragm. Leads I and AVL plus V5 and V6- Left lateral Leads- View best the left lateral wall of the heart. Lead AVR- Looks more at the right side of the heart. If you look at the drawing and imagine the heart at the center in a three dimensional format, then all these leads are really registering the electrical phenomena of the heart in the three dimensions or X, Y and Z. Inferior Leads II,III,AVF

MEAN QRS AXIS BASICS NORMAL RANGE= -30 TO +90 DEGREES
WHAT IS THE MEAN QRS AXIS? IT REPRESENTS THE AVERAGE DIRECTION OF THE INSTANTANEOUS FORCES GENERATED DURING THE SEQUENCE OF VENTRICULAR DEPOLARIZATION. NORMAL RANGE= -30 TO +90 DEGREES NORMAL VALUE= 59 DEGREES MORE - THAN -30 = LEFT AXIS DEVIATION MORE + THAN +90 = RIGHT AXIS DEVIATION The normal Mean electrical axis of the heart responds to the fact that the left ventricular mass produces a larger electrical effect than the right ventricular mass under normal conditions. In fact most of the QRS complex is a reflection of left ventricular depolarization. Thus, if we look at the average electrical forces of the heart in the vertical plane, there is a normal small inclination of the Mean Electrical Axis to the left. This inclination is a reflection of greater cardiac muscle mass and more time for the stimulus to depolarize this mass versus the right ventricle. So remember that the two reasons why the normal QRS axis has a leftward tilt are: More cardiac muscle mass in the left with more electrical representation. More time for the electrical stimulus to propagate through more tissue.

Instantaneous and Mean Vectors of Ventricular Depolarization
-90° +90° 180° 0° A B C D E F G The drawing shows the so called mean electrical axis circle with the heart in its center and the instantaneous vectors generated by ventricular depolarization. The A vector indicates septal depolarization followed by a progressive depolarization of the ventricles from A to D. The fact that they tend to move leftward is due to the much bigger left ventricular mass. At the end there is a Mean Vector that represents the sum of all the ventricular depolarization forces. The direction in which this vector is pointing is the MEAN ELECTRICAL AXIS. As you can see we have placed the heart inside an imaginary circle with angular measurements that have been agreed upon and that do not correspond to the mathematical reality. This is the Electrical Axis Circle and in the next pages we will see where does it come from. Mean Vector

The Electrical Axis Circle Where does it come from?
Lead I Lead II Lead III REMEMBER EINTHOVEN Lead I Lead II Lead III 0° 60° 120° Moving each standard lead of the Einthoven triangle toward a common center generates for us the Electrical Axis Circle in which an imaginary heart is at the center. Here we can see the effect of moving the three main leads of Einthoven;s triangle toward a common center. Now, if we trace a circle around these arrows, the positive recording electrode of each lead (represented by the point of the arrows) will point toward a specific angle of the circle. These angles have been divided by agreement into an unconventional format with Lead I at 0° as seen in the next slide.

The three Leads with a Common Center
Lead I Lead II Lead III 0° 60° 120° Here we can see the effect of moving the three main leads of Einthoven;s triangle toward a common center. Now, if we trace a circle around these arrows, the positive recording electrode of each lead (represented by the point of the arrows) will point toward a specific angle of the circle. These angles have been divided by agreement into an unconventional format as seen in the next slide. Make sure that you memorize the angles pertaining to the three limb Leads.

THE ELECTRICAL AXIS CIRCLE!
-90° -120° -60° aVR ° aVL ° +180° I- 0° Normal Range The complete QRS axis circle is shown above and includes the augmented leads. The normal range of the Mean Electrical Axis is indicated. Notice that the placement of degrees in this circle has been done by convention and does not follow the mathematical norm. NEXT PARAGRAPH SHOULD BE READ AFTER YOU PROCEED TO THE NEXT THREE PAGES! Ok so you found that the isoelectric QRS was in the aVL lead. Find this lead above. Now find the lead that is perpendicular to aVL. This is Lead II. Since the deflection of Lead II is positive and the positive side of the Lead II dipole points toward 60 degrees, this is your best estimation of the Mean Electrical Axis. +30° +150° III- +120° II - +60° aVF- + 90°

Using the Circle to Estimate MEA
-90° Lead II QRS UP TO ESTIMATE QRS AXIS -30° +180° I-0° +150° Lead I QRS UP +90° II - +60° If the QRS complexes observed in the ECG recording for Leads I and II are positive then the average electrical forces generated by Lead I and II provide a broad estimation of Mean Electrical Axis indicating that it can be in the normal range. Notice that in the drawing above a positive deflection of Lead I covers -90 to +90 degrees while a positive deflection of Lead II covers from -30 to +150 degrees. On average, Leads I and II cover from -30 to +90 degrees. This range is well within normal values of the Mean QRS axis. This is why both leads can be used to evaluate if the Mean QRS axis lies in the normal ranges. Note: Other books on the subject use Lead I and AVF for estimating if the QRS axis lies within the normal range. In this case the normal range is considered to be 0 to +90 degrees. In reality most cardiologists extend the normal range to -30 degrees validating the use of leads I and II as done above. -30° NORMAL AXIS +90°

The Isoelectric QRS and its use!
aVL -30° Look at the limb leads and find out which one is more biphasic or isoelectric (R wave and S wave have more similarity in magnitude). In the specific case of our ECG this similarity is found in the aVL Lead. NOW GO BACK TO THE QRS AXIS CIRCLE IN PAGE 24 FOR A MOMENT. This is a method for the estimation of Mean Electrical Axis in the heart. Note that the lead aVL has the more biphasic QRS. The lead perpendicular to this one is lead II. +60 II Lead perpendicular to the isoelectric QRS

Why is a Wave Biphasic? C B A - - - Lead ++++ ------- ---------- +++++
- + Cardiac Muscle Meter Lead +++++ ++++ - + Cardiac Muscle Meter + - Cardiac Muscle Lead Meter The occurrence of a biphasic wave in the EKG depends on the position of the recording electrode or Lead. In the example above the recording electrode is marked as Lead with the other electrode being the reference electrode. If the electrodes are placed over a cardiac muscle mass at rest (A) they will record no potential difference since the surface of the muscle cells will be positively charged everywhere. As one region of the muscle mass becomes depolarized (B) a negative charge will develop in the surface of the cells near one of the electrodes while the other electrode, in this case the Lead will be over an area at rest with positive charge outside. The meter will record a potential difference and move toward the positive electrode. As the depolarization continues to move it reaches the Lead (C). Now the area below the Lead is negative while the area below the reference electrode is positive because it has repolarized. The meter will now move toward the reference electrode. As the depolarization ends and the whole muscle mass is repolarized we return to (A). If the meter needle was placed over a moving piece of paper it would have recorded the biphasic wave that you see in (C). Electrode Perpendicular to Direction of Depolarization

Why is Lead aVL Biphasic?
+ RA LA RV LV - + Lead I + Mean QRS If the Mean QRS Axis of the schematic heart above indicates the direction of all the electrical forces during ventricular depolarization, then as you can see, the aVL Lead electrode will be positioned in the middle of the muscle mass that is being depolarized. Using the example from the last page you can clearly see why this electrode will record a biphasic QRS wave. The wave will also be very small and quasi isoelectric. It is then logical that the Lead perpendicular to aVL is the one located approximately near the Mean QRS Axis in our EKG of page 34. This is Lead II. In the next page you can see this analysis. Lead II +

Quick Estimation of Axis Deviation
AVF I Extreme Right axis deviation deviation. Normal axis Left axis I AVF 0° Lead I Looking at the QRS complexes of Leads AVF and Lead I also serves as a means of estimating the QRS Axis when the normal range is considered to lie between +90 and 0 degrees. Thus, if the QRS is mainly positive in Leads AVF and I then the QRS Axis must fall between normal limits. Just remember that for most cardiologists a range of -30 to +90 degrees is accepted. The figure above shows the different axis deviations and the associated QRS complexes in Leads I and AVF. Since ventricular axis deviations are usually associated to left or right ventricular hypertrophies, let’s see an example of each one and the criteria used to evaluate them. AVF I I AVF +90° Lead AVF

Ventricular Hypertrophy 1
Limb Leads Precordial Leads Using the figure on page 35 or the analysis of the QRS complexes in Leads I and II coupled to the biphasic lead which in this case is Lead II, you can see that there is a right axis deviation in this EKG. If this deviation is greater than +100° a diagnosis of right ventricular hypertrophy is considered. A negative QRS complex in lead one is also believed to be paramount in the diagnosis of right ventricular hypertrophy. The precordial leads above do not show the normal progression of an R wave amplitude that increases from Lead V1 to Lead V5. Instead we find a large R wave in V1 coupled to a small S wave and the R wave in V6 almost equal to the S wave. V5 shows a larger S wave than R wave. This is the pattern of right ventricular hypertrophy.

Ventricular Hypertrophy 2
Precordials S wave R exceeding 18mm R exceeding 26mm The figure above shows an EKG taken from the precordials only. It shows higher than normal R waves in both V5 and V6. This is in agreement with a diagnosis of left ventricular hypertrophy. In left ventricular hypertrophy we should expect to find increased R wave amplitude in the leads that overlie the left ventricle and increased S wave amplitude in leads overlying the right ventricle. Thus, an increase of R wave amplitude in leads that are overlying the left ventricle (V5 and V6) form the basis for the diagnosis of left ventricular hypertrophy. In this matter the precordial leads are more sensitive in detecting left ventricular hypertrophy than the limb leads. Four criteria for Left Ventricular Hypertrophy -R Wave in V5 or V6 plus S wave amplitude in V1 or V2 exceeding 35mm -R wave amplitude in V5 exceeds 26mm -R wave amplitude in V6 exceeds 18mm - R wave amplitude in V6 exceeds that of V5

Review of Vectors and Vectorial Analysis of the EKG
Guido E. Santacana Ph.D. Professor Department of Physiology

Basis for Vectorial Analysis
The Boat example!!! Actual Direction (Resultant Vector) y x Graphical Representation Wind 10 knots From your basic physics course remember the use of vectorial analysis to calculate the actual direction and velocity of a boat that is moving at 20 knots but is being buffeted on its starboard side by a constant wind at 10 knots. The force vector provided by the wind has both magnitude and direction. The force vector provided by the boat velocity has also magnitude and direction. The resultant vector is the sum of the wind velocity and boat velocity vectors and reflects the effect of force and direction of the original vectors on the boat’s movements. The sum can be done using simple Cartesian coordinates and plotting the boat velocity in the Y axis and the wind velocity in the X axis. From the tip of each arrow representing the vectors we draw perpendicular lines. Then we draw a line from the origin to the point of intersection of the two perpendicular lines. This is the resultant vector. It has both direction and magnitude. Another way to add the vectors is by using the Pythagorean theorem. 20 knots

Vectorial Analysis of the Mean Electrical Axis
The reference system above illustrates the Electrical Axis Circle. Notice that each line in the circle represents an electrocariographic lead with one negative electrode and one positive electrode. The line connecting the two electrodes for each lead is the axis for that specific lead with the point of the arrow always pointing toward the positive electrode of the lead. Thus if you see Lead I this is the horizontal lead of the circle with the negative electrode on the right arm and positive electrode on the left arm (remember that the circle is projected into the heart of a person that is in front of you with the heart in the center of the circle). Remember also that the positive end of Lead I is the 0° reference point. From here the scale into which the circle is divided rotates clockwise to 90° in Lead III, 180° in the negative electrode of Lead I and -90° in the negative electrode of Lead aVF. You MUST MEMORIZE this circle and angles if you want to really understand what follows. At least the three bipolar Leads I, II, III.

EKG (LEAD I): Projected Vectors for different Mean Electrical Axes
Tilted Mean Vectors Partial Voltage Reading - + Parallel Mean Vectors LEAD I Higher Voltage Reading + - Perpendicular Mean Vectors No Voltage Reading The figure shows how different ventricular Mean Electrical Vectors would be registered in Lead I of the EKG. The uppermost left MEV is in the normal 60° direction and produces a projected vector in Lead I that shows only a partial reading of the total voltage. In the bottom left the MEV is perpendicular to Lead I and shows no reading or projected vector. The right drawing shows a MEV almost parallel to Lead I. Under this condition almost maximal voltage reading will be observed in Lead I. The rule is, if the MEV is perpendicular to the recording electrode there is no reading, if parallel there is almost maximal reading. This applies to all EKG leads. LEAD I + - LEAD I NO PROJECTED VECTOR!!!!!

The Concept of the Projected Vector
A=Mean Vector B=Projected Vector Figure A In the figure above we are registering only using Lead I. In figure A the ventricles are partially depolarized and have formed an instantaneous depolarization vector with the positive pole toward the left ventricle and the negative pole toward the right atrium. This vector or dipole produces a potential difference that is measured by Lead I. Now, Lead I will not be able to measure the total voltage of this vector simply because it is not pointing in the exact direction of the Lead. In other words it is not parallel to the Lead. In order then to measure how much voltage the lead will measure, we project the vector to the lead by drawing a line perpendicular to Lead I that touches the positive end of the vector. The point in Lead I where the line intersects represents the positive end of the projected vector. The size of the projected vector represents how much voltage from the instantaneous vector was really measured by Lead I. As you can see not all of the voltage was measured. Look at what happens in figure B where the instantaneous depolarization vector is tilted to the right and almost perpendicular to Lead I. If the instantaneous vector were exactly perpendicular to Lead I we would not have a projected vector. In other words, Lead I would not register any voltage from this depolarization. By the same token when the instantaneous heart vector has the same axis as the lead axis then the entire voltage of the vector is recorded. Figure B

Projected Vectors for theThree Standard Leads
The instantaneous depolarization potential depicted above by the axis A could be one from a normal partially depolarized heart. Using the three standard Leads we can produce the projected vectors for each lead. Each vector indicates how much voltage each lead will register from A. As you can see Lead III will register a small positive voltage because A is more perpendicular to this lead. Lead II will register the highest voltage because A is almost parallel to this lead. We will then see a higher R wave in Lead II, a small one in Lead III and the one in Lead I which is not as small as that in Lead III and not as large as that in Lead II. Notice that since each of the projected vectors point toward the positive electrodes of the three leads, the record in the EKG will be up or positive. Now you will do this: Take A and draw it in any other direction that you want, then draw the projected vectors and note how the voltages will be registered in the EKG. Repeat again and again until you understand it. Remember that you are only using the three standard leads.

Ventricular Depolarization Analysis Using the Projected Vectors
.01 sec .02 sec .05 sec .035 sec What you see above is the sequence of ventricular depolarization as it occurs in a normal heart. We will analyze it piece by piece using the projected vectors. Now, look at A. You already know that the sequence of ventricular depolarization begins deep in the interventricular septum. As the septum depolarizes in the first .01sec an area of the septum becomes negative (darker) while the rest of the ventricles are positive (lighter). This creates a depolarization vector inclined a bit toward the left and almost in the same direction as Lead II. The projected vectors indicate that there will be a positive deflection in the three standard leads at this moment or the beginning of the R wave. As we move to B a lot of the ventricles have depolarized producing a bigger depolarization vector. When this vector is projected to the three standard leads we reach the peak of the R wave. This occurs about .02sec after the start of ventricular depolarization. After .035sec in C the remaining positive areas of the heart are in the epicardium and most of the endocardium and apex of the heart are depolarized. The resultant depolarization vector is smaller and we are registering a lower positive voltage in the three leads. After .05 sec in D the right ventricles are totally depolarized and just a small area in the base of the left ventricle remains with positive charge. The axis of the depolarization vector now points toward the left. The depolarization vector now is small because almost all of the ventricles are depolarized and the projected vectors in this instant indicate a small positive deflection in Lead I and negative deflections in both II and III. At .06 sec the ventricles are totally depolarized and no depolarization vectors are present. In all leads there is no deflection and we are at zero voltage. Basically what we have done here is to construct the QRS complexes for the three standard leads. Note that Lead I usually shows no Q or S wave. Leads II and III show the S wave but usually do not show the Q wave. Sometimes the Q may show up. Now go back and review this until you can fully understand it and even dream about it. .06 sec

Ventricular Repolarization Analysis Using the Projected Vectors
Now we analyze ventricular repolarization also using the projected vectors. Repolarization begins about .15 sec after depolarization and is completed in about .35 sec. The epicardial surfaces of the heart near the apex repolarize first. As these surfaces become positive a resultant overall ventricular vector is produced as seen in the figure above. Since the repolarized epicardial mass is not large the vector is small and so are the resultant vectors. This vector reaches its maximum when half of the heart is repolarized. This would be the tip of the T wave. As the repolarization continues the vector is reduced until zero voltage is reached. Note that the repolarization vector produces projected vectors in the three standard leads that point toward the positive side of each lead. This means that the resultant deflection will be positive for the three leads. So the repolarization wave of the EKG is positive. Go back and review this until you fully understand it.

What is the Vectorcardiogram?
The vectorcardiogram is simply a graph that shows the continuous changes in the size and direction of the different overall vectors that form during ventricular depolarization. If we plot these changes we create a bean shaped elliptical graph like the one above. Another one can be plotted for repolarization. This can be done using oscilloscopes and can provide information as to the condition of the heart. They can also be used to visualize the generation of the EKG as a three-dimensional process. It is simply the path marked by the positive ends of The depolarization vectors.

How to Plot the Mean Electrical Axis Using Two EKG Leads
R wave only = 6mm or .6mv 6mm 6mm RS waves R= 8mm S= -2mm Total = 8-2=6mm or .6mv We already know what the Mean Electrical Axis of the ventricles means. This is just another way of determining the MEA using the standard limb leads of Einthoven. As you can see in the figure above we have used only Leads I and III to determine the MEA of the heart whose QRS is depicted for the three limb leads to the right. To do this we measure the size of the R wave in I and III. We also see that in I there are no Q or S waves just R. The size of the R wave in Lead I is 6mm. Since each mm is .1 millivolts then we have a total of .6 millivolts in Lead I. Lead three has no Q wave but has an S wave that is negative. The negative voltage of the S wave must be subtracted from the positive voltage of the R wave to obtain the net voltage for this lead which in this case is 6 millivolts. Now we plot the voltages (or mm) for both Lead I and III in their respective axes. The plots are toward the positive electrodes of each lead because the net QRS deflections for the leads are positive. Now all we need to do is to draw a line from the positive apices of the arrows representing the voltages in leads I and III. The lines will be drawn perpendicular to the arrow tips. At one point these lines (dashed lines above) will intersect. Now f from the point of intersection of Leads I and III (center of the graph) we will draw a line toward the point of intersection of the two dashed lines. This line is the resultant vector and indicates the direction and magnitude of the MEA for this heart. In this case the MEA is 59° which is normal. Note: Usually we subdivide the axes for the leads into millimeters with each millimeter representing .1 millivolts. The EKG recording is divided also in millimeters so all we have to do is to measure and calculate the net QRS waves. Note also that if the net QRS for Lead III were negative, lets say -6mm we would have plotted the potential for this lead toward the negative side. In other words the same arrow as the one above but pointing toward -60°. Why don’t you try an exercise and do the whole MEA calculation using a net QRS for Lead III of -6mm (-.6mv)? What if both Leads I and III were -6mm(-6mv)? Mean Electrical Axis

Abnormal Ventricular Conditions That Cause Axis Deviation
Change in position of the heart in the chest. Hypertrophy of one ventricle. Bundle Branch Block. If the heart shifts or is angulated toward the left, the Mean Electrical Axis shifts left. This occurs at the end of deep expiration, when lying down because abdominal contents press against the diaphragm and in stocky fat people because the abdominal contents press toward the diaphragm. A shift or angulation of the heart to the right causes the Mean Electrical Axis to shift to the right. This occurs during deep inspiration, when a person stands up and in tall skinny people whose hearts hang downward. There are two reasons why the Mean Electrical Axis shifts toward an hypertrophied ventricle. 1. A much greater quantity of muscle is present in the hypertrophied side allowing excess generation of electrical potential on that side. 2. More time is required to depolarize the hypertrophied ventricle. The normal ventricle depolarizes much faster and this causes a strong vector to form from the normal into the hypertrophied side that has remained positively charged. The axis deviates toward the hypertrophied ventricle. The left and right branches of the Purkinje system transmit the cardiac impulse to the two ventricular walls at almost the same time. If one branch is blocked, then the impulse spreads through the normal ventricle faster. As a result depolarization of the ventricle is not as simultaneous and strong axis deviation occurs. In Left Bundle Branch Blocks deviations of the Mean Electrical Axis are intense because the right ventricle depolarizes faster than the left ventricle leaving the left ventricle positive at a time when the right ventricle is very negative. The vector points strongly toward the left. In Right Bundle Branch Blocks the opposite occurs with strong right axis deviation.

Vectorial Analysis of Ventricular Hypertrophy
-15° Hypertrophy of the left ventricle is a condition that produces deviation of the normal MEA of the heart. Using the same analysis as we did before with Leads I and III and plotting the net QRS potentials for the heart above we get an MEA of -15°. This indicates left axis deviation. The left axis deviation occurs because there is more muscle on the left side of the heart that generates more electrical potentials and more time is required for the electrical potential to travel through more muscle. This means that the right side will depolarize first and faster thus creating a strong vector with the positive apex toward the left. This is evident from the analysis of the EKG above for Leads I and III. Although Lead I is positive it is larger than usual. Lead III normally positive is negative. This type of axis deviation may be caused by hypertension. It can also be caused by aortic valve stenosis, aortic valve regurgitation, aortic coarctation and other congenital conditions. Left ventricular hypertrophy in a hypertensive heart. Reasons for deviation are LV mass and conduction time.

Vectorial Analysis of Right Ventricular Hypertrophy
Notice also the High voltage EKG in Lead I The EKG above shows a typical right axis deviation caused by congenital pulmonary valve stenosis. Plotting the net QRS potentials for Leads I and III results in a MEA that is very right shifted. The net QRS in Lead I is negative while that of Lead III is positive although higher than usual. Tetralogy of fallot and interventricular septal defects are also causes of right axis deviations. 170° 170° RV Hypertrophy caused by Pulmonary Valve Stenosis

Vectorial Analysis in Bundle Branch Block
Prolongued QRS due to Slower Conduction Time Through Block -50° left deviation In a Left Bundle Branch Block (LBBB) the ventricular depolarization occurs 3 times more rapidly in the right than in the left ventricle. The right ventricle is electronegative as the left ventricle remains electropositive during much of the ventricular depolarization. The resulting MEA is very shifted to the left as analyzed above from the net QRS potentials of Leads I and III. You can also notice the greatly prolonged duration of the QRS complex. This is due to the fact that the branch block also provokes an obligatory conduction of the impulse through the myocardial cells since the Purkinje system is blocked. This conduction is much slower and is the cause of the long duration of the QRS. The prolonged QRS duration can help to differentiate between Bundle Branch Block and hypertrophy. Left axis deviation caused by a Left Bundle Branch Block

Vectorial Analysis in Bundle Branch Block
In the figure above we see the vectorial analysis of RBBB. Basically the physiological basis for the shift in the MEA is the same as that for LBBB but in the opposite direction. Again observe the prolonged duration of the QRS. Right Bundle Branch Block producing a right axis deviation. Again observe the longer QRS interval. Longer QRS intervals Can distinguish axis deviations due to BBBs vs. hypertrophies.

Low Voltage EKG Normal voltage between R wave and S wave should
be from .5 to 2mv If the sum of the voltages in the QRS of leads I,II,III is greater than 4mv the EKG is considered as high voltage. A reduction in muscle mass due to myocardial infarctions is probably one of the most common causes of low voltage EKG reflected as low voltage QRS waves. Local delays in impulse conduction cause the prolonged durations of the QRS observed above. Pericardial effusion also reduces the QRS voltage by basically shortcircuiting the EKG voltages reaching the skin. The same thing may happen with pleural effusions. In emphysema the lungs tend to produce an insulating effect on the heart that reduces the EKG level in the skin. Low voltage EKG due to myocardial infarction. Low voltage EKG is also caused by pericardial effusion, pleural effusion and pulmonary emphysema.

The Current of Injury Cardiac abnormalities specially those that damage the heart muscle cause part of the heart to remain partially or totally depolarized all the time. The current that flows even between heartbeats from the pathologically depolarized area to the normal area is the CURRENT OF INJURY.

Causes of the Current of Injury
Mechanical Trauma. Infections Ischemia caused by coronary occlusions. (Most common cause)

The Current of Injury Current of injury remains after the heart has
Repolarized. Ischemia of parts of the heart muscle caused by coronary occlusion can leave parts of the heart continuously depolarized. This means that even after normal ventricular repolarization if part of the ventricle is ischemic, it can remain electronegative. Thus we will have most of the ventricles repolarized or electropositive while an area remains electronegative. This creates a flow of current between the depolarized and repolarized areas at a time when no such current should be present. This is the current of injury and depending on the area where the ischemia is localized, the current will generate an electrical potential with an axis that will point away from the damaged area. This is the situation we have above where the base of the left ventricle is ischemic and even before the the P wave of the EKG occurs we can see that the voltage is not at zero in any of the three leads. It is negative in Lead I and positive in both Leads II and III. A plot of these voltages in the axes of the three limb leads produces a resultant vector with the axis pointing toward the right. Since the axis of the vector is positive, we then know that the depolarized area must be opposite the axis of the vector or toward the left. In this case it points toward the negative side of Lead III or toward the base of the left ventricle. The total effect of the current of injury on the EKG in the 3 limb leads can be observed as the ventricular depolarization wave progresses. In this heart the last area de depolarize is the right ventricle. Not that zero potential is only reached when depolarization is complete. This is the only time in which this heart is at zero potential. OK go back an read again and again…..

EKG Generation in Normal vs. Infarcted Heart
Ok, what I want you to do here is to carefully study the progression of ventricular depolarization in a normal heart and compare it with that of the heart in which the ischemia is present. Notice that in the normal heart the QRS complex starts from zero potential. Not so in the ischemic heart where the injury current is present. Notice also the abnormal QRS complexes of the heart with the injury current. It is very important that you understand that the heart with the injury current will only be at zero potential after ventricular depolarization. This point of zero potential when there is an injury current present is called the J Point. After the J point is passed the heart repolarizes but since the ischemic area remains depolarized the injury current appears. So the injury current is measured between the J point and the point just before the P wave. If this is done in the three limb leads it will give resultant potentials that can be plotted in the respective axes and used to calculate the direction and magnitude of the mean potential for the current of injury. This will indicate not only the approximate location of the ischemia but also the magnitude of the damage. INFARCTED NORMAL

The J Point and the Current of Injury Vector Analysis
J Point is the zero potential line from which the direction of the injury current is determined Using only Leads I and III above we can calculate the injury potential in each lead. In Lead I as the QRS ends zero potential is reached, this is the J point. After repolarization and just before the P wave we can measure a voltage. For this Lead it is positive and is plotted toward the positive side in Lead I axis. For Lead III you can see that the injury potential is negative and it is plotted as such in the lead axis. The mean vector points toward the left. This means that the ischemic or damaged area is toward the right. In this case the lateral wall of the right ventricle. Remember that the negative end of the mean vector for the injury potential is the one that points toward the injured area. Now go back and analyze this graph and results again.

Injury Potential in Anterior Wall Infarction
Respective J Points In Leads I and III J point in V2 an anterior Lead Allright now lets analyze this one. I have indicated where the J point is located in Leads I and III. When each injury potential is plotted for the respective leads the mean injury potential points toward the right. This means that the ischemic area is toward the left. Now V2 has been added here and we can see that the injury potential in V2 calculated from the J point is negative. This means that the positive side of the injury potential points away from V2 and the negative is toward V2. Since V2 is an anterior lead and we already know from the standard leads that the mean injury potential is to the left, then the ischemic area must be in the anterior wall of the left ventricle. Notice that the key to pinpointing the area was the precordial lead.

Injury Potential in Posterior Wall Apical Infarction
J Points of Leads II & III. J point of V2 In this case the injury potential appears clearly in Leads II and III so we use these leads to calculate the mean injury potential. The mean injury potential indicates damage to the apical region of the heart. V2 shows a positive injury potential. The negative injury potential is away from V2 so we can say that the infarct is in the posterior wall toward the apex. Review this analysis very carefully.

Cardiac Arrhythmias Result from disturbances of IMPULSE INITIATION
PROPAGATION INITIATION Conduction Blocks Reentry rhythms SA Node Ectopic Foci

Alteration of SA Rhythm
Autonomic nervous system usually involved. P, QRS, T waves normal. Duration of Cardiac Cycle P-P interval shortened or prolonged. Sinus Bradycardia- Slow Rhythm. Sinus Tachycardia- Fast Rhythm. Cardiac frequency changes gradually.

Bradycardia Normal Rhythm Bradycardia
The symptoms of sinus bradycardia include dyspnea, dizziness, and extreme fatigue. Bradycardia may be accompanied by an increase in stroke volume due to greater end diastolic pressure (preload). The pulse volume may be greater due to a greater stroke volume and an increased diastolic run-off time (longer time for blood to flow away from the heart). Sinus bradycardia may occur due to any of the following: a.Increase in parasympathetic (vagal) tone, for instance, due to training in athletes. This is a normal response. The heart rate increases with exercise or atropine.b. Parasympathetic (vagal) stimulation, for instance, with carotid sinus stimulation. Stimulation of carotid sinus baroreceptors results in increased parasympathetic stimulation that decreases the heart rate. c. Sick sinus syndrome or sinoatrial (SA) node disease. These are rhythm disorders that occur if the SA node loses its ability to initiate or increase the heart rate. If the SA node is unable to properly function due to sick sinus syndrome, the AV node (or ventricular tissue if the AV node is also not functioning) take over the initiation of the heart beat, but at a rate that is slower than the sinus rhythm. d. Heart block which occurs when the signal from the SA node is slowed or stopped at the AV node or in the ventricular conducting system. Heart block is described as first, second, or third degree. The decrease in the heart rate depends on the degree of heart block.e. Acute myocardial infarctions.f. Drugs like digitalis and beta-blockers. bradycardia occurs when the hearts rate is slower than 60 beats per minute.

Tachycardia Normal Rhythm Tachycardia
Sinus tachycardia may be accompanied by a decrease in stroke volume because the ventricles do not have enough time to fill (after atrial systole) before ventricular contraction.. The pulse pressure may decrease due to a lower stroke volume and decreased time for diastolic run-off. Sinus tachycardia results from increased automaticity of the SA node, for instance, due to increased sympathetic stimulation of the heart, fever or cardiac toxicity. Sinus tachycardia occurs when the sinus rhythm is faster than 100 beats per minute

AV Transmission Blocks
Impulse transmission through conduction tissue blocked. His Bundle Electrogram may be used to localize block.

His Bundle Electrogram
V Atrial Wave His Bundle Wave Ventricular wave Prolongation of either the A-H or H-V interval indicates block above or below the Bundle of His

Paroxysmal Tachycardia
Abrupt onset and termination. Origin is ectopic site. Reentry circus movements most frequent cause. High frequency. Can cause lightheadedness or syncope. Rapid contractions reduce ventricular filling.

Paroxysmal Supraventricular Tachycardia
Originate in atria or AV tissue. Usually from a reentry loop in atrial, AV tissue or both.

Paroxysmal Ventricular Tachycardia
From ectopic foci in the ventricles. From considerable ischemic damage. Bizarre QRS complexes May be a precursor of Ventricular Fibrillation Results from digitalis toxicity. Ventricular tachycardia occurs when electrical impulses originating either from the ventricles cause rapid ventricular depolarization ( beats per minute) Ventricular tachycardia is often due to some form of heart disease. Ventricular tachycardia can occur rarely in response to exercise or anxiety. In this case, the electrical impulses and rhythmic beats is similar is a normal beat but at a much faster rate. During ventricular tachycardia pumping blood is less efficient because the rapid ventricular contractions prevent the ventricles from filling adequately with blood. As a result, less blood is pumped to the body. The reduced blood flow to the body causes weakness, dizziness, and fainting. If left untreated, ventricular tachycardia may lead to a more life-threatening condition. Note, because of the decreased diastolic time, coronary blood flow is decreased, increasing the chances of a myocardial infarction.

Fibrillation Arrhythmia that is ineffectual in pumping blood.
Atria or Ventricles may be involved. Is due to fragmentation of reentry loop into multiple irregular circuits.

Atrial Fibrillation Atria do not contract and relax sequentially.
Atrial fibrillation occurs when the atria depolarize repeatedly and in an irregular uncontrolled manner usually at at atrial rate greater than 350 beats per minute. As a result, there is no concerted contraction of the atria. No P-waves are observed in the EKG due to the chaotic atrial depolarization. The chaotic atrial depolarization waves penetrate the AV node in an irregular manner, resulting in irregular ventricular contractions. The QRS complexes have normal shape, due to normal ventricular conduction. However the RR intervals vary from beat to beat. The ventricular rate may increase to greater than 150 beats per minute if uncontrolled. The irregular ventricular contractions cause the systolic arterial pressure to vary from beat to beat as ventricular filling time changes. The pulse pressure also may vary from beat to beat because the diastolic runoff time varies from beat to beat. Atrial fibrillation often involves microreentry. Atrial fibrillation is most common in individuals with atrial enlargement, often associated with valve diseases, sick sinus syndrome, pericarditis, lung disease and congenital heart defects. The incidents of atrial fibrillation increase with age and are slightly more frequent in men than women. Atria do not contract and relax sequentially. No contribution to ventricular filling. No P waves. Irregular fluctuations or f waves. Normal QRS complexes but irregular rhythm. Compatible with life and full physical activity. 20-30% reduction in ventricular pumping.

Ventricular Fibrillation
Irregular continuous twitching of the ventricular muscle. No pumping of blood possible. Loss of conciousness occurs rapidly Irregular fluctuations in the EKG Often initiated by a premature impulse arriving in the vulnerable phase. Vulnerable phase coincides with downslope of the T wave. Electric shock used to treat VF by leaving the ventricles temporarily refractory and allowing the SA node to take over again. Ventricular fibrillation occurs when parts of the ventricles depolarize repeatedly in an erratic, uncoordinated manner. The EKG in ventricular fibrillation shows random, apparently unrelated waves. Usually, there is no recognizable QRS complex. Ventricular fibrillation is almost invariably fatal because the uncoordinated contractions of ventricular myocardium result in ineffective pumping and little or no blood flow to the body. There is lack of a pulse and pulse pressure and the patients lose unconsciousness rapidly. When the patient has no pulse and respiration the patient is said to be in cardiac arrest. A person in cardiac arrest must receive CPR immediately. Electrical defibrillation, by passage of current at high voltage, may be successful in restoration of a normal regular rhythm. The electrical current stimulates each myocardial cell to depolarize simultaneously. Following synchronous repolarization of all ventricular cells, the SA node assumes the role of pacemaker and the ventricular myocardial cells can resume the essentially simultaneous depolarization of normal sinus rhythm. Ventricular fibrillation is associated with drug toxicity, electrocution, drowning and myocardial infarction.

Mechanism of Ventricular Fibrillation
Causes of reentry Circus movements Long Pathway= dilated hearts Decreased velocity of conduction=blockade of Purkinje System Greatly shortened refractory period= Epinephrine

60 Hz AC Induced VF 60Hz 120VAC Applied here End result

Atrial Flutter F wave Normal EKG
Atrial flutter occurs when the atria are stimulated to contract at beats per minute usually because electrical impulses are traveling in a circular fashion around and around the atria. Often the impulses are traveling around an obstacle like the mitral valve, tricuspid valve or the openings of the superior or inferior vena cavae. The atrial flutter waves, known as F waves, are observed. F waves are larger than normal P waves and they have a saw-toothed waveform. Not every atrial flutter wave results in a QRS complex (ventricular depolarization) because the AV node acts as a filter. Some flutter waves reach the AV node when it is refractory and thus are not propagated to the ventricles. The ventricular rate is usually regular but slower than the atrial rate. A whole number fixed ratio of flutter waves to QRS complexes can be observed, for instance 2:1, 3:1 or 4:1.Atrial flutter is usually associated with mitral valve disease, pulmonary embolism, thoracic surgery, hypoxia, electrolyte disturbances and hypercalcaemia. Atrial flutter results in poor atrial pumping since some parts of the atria are relaxing while other parts are contracting. Cardiac output decreases because the ventricles do sufficiently fill (as they would normally) before ventricular contraction. Ablation of some of the heart tissue to stop impulses from travelling around can be used to treat this condition Normal EKG

Wolf Parkinson-White Syndrome
Normal Wolf Parkinson White Normally, the AV node is the only conduction pathway for impulses from the atria to the ventricles. Wolff-Parkinson-White syndrome is characterized by the presence of an accessory atrioventicular pathway located between the wall of the right or left atria and the ventricles, known as the Bundle of Kent. This pathway allows the impulse to bypass the AV node and activate the ventricles prematurely. Consequently, an initial slur to the QRS complex, known as a delta wave may be observed. The QRS complexes are wide, more than 0.11 sec, indicating that the impulse did not travel through the normal conducting system. The PR is shortened, to less than 0.12 sec, because the delay at the AV node is bypassed. The accessory pathway can cause a reentry circuit to be established. Reentry is initiated by a premature atrial or ventricular beat coupled with a unidirectional block in one of the pathways (because the normal impulse gets to pathway when it is refractory after the premature beat). The result is a continuous impulse conduction. Reentry causes two kinds of tachycardia. 1.Orthodromic AV reentrant tachycardia which occurs when the impulse is conducted through the AV node with retrograde return to the atria via the Bundle of Kent. The heart rate is usually BPM. The QRS complexes are narrow and delta waves are not observed. 2.Antidromic AV reentrant tachycardia which occurs when the impulse is conducted through the Bundle of Kent with retrograde return to the atria via the AV node. The QRS complexes are wide. Wolff-Parkinson-White syndrome is commonly associated with congenital heart abnormalities like Tetrology of Fallot, coarctation of the aorta, tricuspid atresia and transposition of the great vessels. In severe cases, treatment would involve surgical removal or ablation of one of the pathways. Alternate Conduction Pathway Bundle of Kent

SEQUENTIAL APPROACH TO THE EKG
Gain familiarity with the normal EKG. Evaluate the rhythm. Calculate rate. Evaluate each P wave, QRS, ST segment and T wave in each lead. Mean QRS Axis Abnormalities of the P wave Abnormalities of the QRS ST and T wave abnormalities. The sequence above shows a way in which you can analyze the ECG recording in order to obtain valuable clinical information from it.

The Normal EKG - 12 lead The above shows a normal tracing of an EKG that includes the augmented and precordial leads. Notice the biphasic P wave in lead V1. It is usally also biphasic in lead III although it doesn’t show well in this specific EKG. Leads II and AVR have the most positive and negative P waves respectively. Also note the progression of the QRS complex in the precordial leads from negative in V1 to positive in V6. Could you explain this progression in terms of how ventricular depolarization occurs normally?

Reading the EKG Paper BASICS
Each individual horizontal and vertical line is ruled in 1 mm Each horizontal space represent a time interval of 0.04 sec Each vertical space represents a voltage change of 0.1 mv 0.5 mv Values in the standard ECG paper like the example above should be memorized. The dark lines that run in the EKG paper delineate spaces of 5 x 5 mm while the lighter lines delineate spaces of 1 x 1 mm. REMEMBER!!! – The horizontal axis measures TIME (duration) and the vertical axis measures VOLTAGE (amplitude). Memorize this NOW. You will have to do it anyway! 0.2 sec.

HEART RHYTHM Every P wave followed by a QRS.
Every QRS preceded by a P wave P wave upright in leads I, II, III PR interval greater than .12 sec P wave rate BPM with < 10% variation. < 60 - sinus bradycardia, >100sinus tachycardia. Variation of more than 10% = Sinus arrhythmia The above shows a simple analysis of heart rhythm with normal values.

CALCULATE HEART RATE HEART RATE = 25MM SEC X 60SEC/MIN MM/BEAT
STANDARD EKG PAPER SPEED OF 25MM SEC HEART RATE = 25MM SEC X 60SEC/MIN MM/BEAT OR!! = 1500 # of small boxes between 2 beats This is a simplified formula for the calculation of heart rate from standard ECG recordings.

Example There are 23 mm between the two QRS complexes, therefore:
Heart rate = 1500/23 = 65 beats/min Example of heart rate determination by using the formula.

Analyzing The Normal EKG
Look at the QRS complex in Leads I and II. They point upward so they are positive. The Mean QRS Axis probably lies in the normal range of -30 to +90 degrees. Look carefully at Lead AVL and you will see that it is the most isoelectric and biphasic. Now go to the next page to see why this lead is isoelectric and biphasic. We will use this lead later to do a more precise calculation of the Mean Electrical Axis.

Left Atrial Enlargement
Left atrial enlargement is best observed in the P waves of Leads II and V1. In V1 P is biphasic due to the position of the lead over the heart. Remember that the right side of the P wave represents the right atrial component and the left side the left atrial component. In figure B you can see that in both P waves the left atrial component has increased. In Lead I a notch has appeared in the left atrial component and in Lead V1 the left atrial component which is negative in more prominent.

Right Atrial Enlargement
In figure A the normal P waves of Leads II and V1 are shown. Figure B shows that the right atrial component of the P waves are more prominent in both leads. This is an indication of right atrial enlargement also called P pulmonale due to its relation to pulmonary disease.

Sample Abnormality of the P wave
MITRAL STENOSIS Go ahead and estimate the Mean Electrical Axis for this ECG and see if it agrees with some of the clinical findings shown above. P waves not visible random rhythm right ventricular hypertrophy atrial fibrillation

AV BLOCK Exercise Intolerance Ventricular Escape Rythm
You should be able to recognize a complete AV block like the one above. Estimate Mean Electrical Axis. Exercise Intolerance Ventricular Escape Rythm

Hyperkalemia Small or absent P waves Atrial Fibrillation Wide QRS
You should be able to recognize the main electrocardiographic characteristics of hyperkalemia. Again estimate Mean Electrical Axis. Small or absent P waves Atrial Fibrillation Wide QRS Shortened or absent ST segment Wide and tall T waves Ventricular fibrillation (sometimes) Haemodialysis

Hypokalemia Small or absent T waves 1st or 2nd degree heart AV block
This is another ECG that you should be able to recognize related to hypokalemia. Can you relate this ECG with the electrophysiological events that happen in cardiomyocytes under low K+ conditions? If not, go back and review your Cardio Manual ! Small or absent T waves 1st or 2nd degree heart AV block slight depression of ST segment Vomiting (prolonged)

Like in Music, with the EKG only Practice Makes Perfect

THE PHYSIOLOGICAL BASIS OF THE EKG

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THE PHYSIOLOGICAL BASIS OF THE EKG

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