Cardiology Review Notes Cardiorespiratory Diagnosis Dr



Cardiology Review Notes Cardiorespiratory Diagnosis

Dr. Christy

Introduction

The study of cardiology is an interesting and provocative endeavor. The amount and depth of material far exceed the time limitations of a single course which also includes the study of respiratory conditions. Nevertheless, the time allotted for review of cardiac dysfunction is sufficient to familiarize the student with the majority of common ailments associated with cardiac disease. I have divided the presentation of these conditions into five major areas: Rate, Rhythm, Axis Deviation, Blocks, and Infarction.

As we discuss each area, ECG presentations will be emphasized. The electrocardiogram is noninvasive and reveals conduction patterns throughout the heart muscle during systole and diastole. The ECG is a universally accepted diagnostic tool with an established language shared by all professionals within the health care system. Even with the limitations of an ECG, the knowledge gained by its proper application and interpretation is invaluable.

I wish to point out that this class is not a class of electrocardiography. The best example I can give is the use of x'ray in a class of bone pathology. 1t simply makes sense to visualize on the radiograph the appearance of the bone pathology in question. Likewise, it makes sense to visualize the electrical changes which take place in cardiac pathology. I will not be requiring the student to "interpret" the ECG; assistance will be given in determining the wave morphology, the leads, the presence or absence of aberrations or artifacts on the strip, and essentially any question the student may have about the particular ECG. However, once all questions have been answered, the student must be responsible to understand what event is occurring in the heart muscle and where the lesion site is located.

A number of ECG worksheets will be provided during the course, and each strip will be analyzed and interpreted in class. These worksheets should solidify the knowledge base necessary to succeed in the cardiology portion of this course.

Please remember, these notes are meant to help, but they are not intended to replace class attendance and personal note taking and reading. (In other words, certain questions on the exam may not be answered on these pages!)

12 lead ECG

To begin, a definition of the word "lead" is in order. I prefer not to be extremely technical, so I suggest that a lead is a "view." Thus, a 12 lead ECG will give us 12 "views" of the heart. Some views will be from the right side, some from the left, some from the apex of the heart, and some from the anterior. What is often confusing is the fact that these 12 views are achieved with only 10 (ten) electrodes attached to the patient. Four of these electrodes are attached to the arms and legs (the so-called "limb" leads) and six electrodes are attached to the chest wall (the so-called "chest" leads). It is also true that the word "lead" is commonly used to refer to the electrodes themselves. Therefore, one must always be careful when reference is made to a particular "lead." Is the reference to the electrode or to the view?

I have provided each student with a normal ECG, so please refer to this as you read the following. On the ECG, locate the I, II, III, aVR, aVL, aVF, VI, V2, V3, V4, V5, and V6.

These are the names of the leads (views) which the standard ECG provides. Leads I, II, and III are called the "standard limb leads." Leads aVR, aVL, and aVF are "augmented leads (views). The "V" leads are the chest views. Remember that there are actually only 10 (ten) electrodes which are attached to the patient. The electrodes which are attached to the wrists and ankles are able to provide six views: I, II, III, aVR, aVL, and aVF. The six chest electrodes provide the six "V" leads (views). It is of no further benefit or interest to the student to discuss the electronics in these notes. Since this is not an ECG class, reference to bipolar or unipolar leads is inappropriate in these notes. Brief mention will be made in class to these matters, but the student is not held responsible to know the mechanisms behind the workings of the ECG itself. A laboratory experience will be available for those students who are interested in learning how to perform an ECG, and an opportunity will be provided to have an ECG performed on themselves.

Now, please refer back to the normal ECG. Find lead "I" which is located in the upper left portion of the ECG grid. You will see four heartbeats illustrated. Look down to lead "II and observe four heartbeats. Now look below lead "II" and find lead "III." There will be four heartbeats in lead III also. These four heartbeats are the same. In other words, the heart has beat four times and the ECG has observed these four heartbeats from three different "views" at the same time. After the fourth beat, the ECG has now changed to three new views (aVR, aVL, and aVF). Continue looking at the normal ECG --- there are three beats which were recorded in these leads (aVR, aVL, and aVF) before the "V" leads began. There are then three heartbeats recorded in V1, V2, and V3 before the final leads V4, V5, and V6 begin. There are four heartbeats recorded in these leads before the ECG was finished. There were fourteen heartbeats in all recorded on this particular ECG.

Rhythm Strip At the bottom of every standard ECG there is a view which is called the "rhythm strip." The reality is that this particular view is actually lead II. This particular lead (view) is considered to be the most revealing of the twelve, and it has been chosen as the one view which should continue throughout the entire ECG. Therefore, when the other leads cease to record, the lead II continues and is seen in its entirety at the bottom of the ECG. It is appropriately labeled as the "rhythm" strip because it does display to the examiner one single view which does not change throughout the entire ECG. This rhythm strip is the first image which most physicians examine when asked to read the ECG. From lead II we should be able to see the typical P, QRS, and T waves. The textbook pictures of a typical ECG recording are always from lead II. The rhythm strip also provides an uninterrupted view of cardiac activity so that the true rhythm pattern can be discerned. Essentially, the rate and rhythm of the heart are based upon the socalled "rhythm strip."

Why so many views??? I like to use the comparison of buying a car. How many views would satisfy you that there is no damage? One side view? One view from the top? One view from the front? One view from the back? One view from the bottom? The same parallel can be applied to the heart. The truth is that electrical activity can become aberrant in one specific site of the cardiac wall while the remaining portions of the heart appear to be normal. It is absolutely expected that a major pathology can be spotted in one or two views of the ECG while, at the same time, the remaining views (leads) are normal. For example, when one considers the coronary circulation (coronary arteries), it is understandable that one particular coronary artery could be occluded and create major problems in the tissue perfused by it. However, the other areas of the heart could be normal. Knowing which lead(s) show the abnormality is one of the means by which the physician can determine the lesion site. The student will have to learn the exact area of the myocardium which is being viewed by each "lead." The heart has been divided into areas such as the inferior, lateral, and anterior. There are three leads (views) which examine the inferior portion of the heart, two leads which examine the lateral, and six leads

which examine the anterior. There remains one lead (view) which examines exclusively the right side of the heart. Add them all up and you get twelve!

Reading the ECG Wave Patterns

Positive and Negative For the purpose of definition, any part of the ECG tracing which rises above the isoelectric (base) line is considered to be "positive" or a "positive deflection." Likewise, any part of the tracing which goes below the isoelectric line is considered to be "negative." What does that mean? This is quite simple, so do not panic. If the wave of cardiac depolarization is toward a particular viewpoint (lead), then the wave deflections will go up (positive) in that lead. If the wave of depolarization is going away from a particular lead, then the wave deflections will go down (negative) in that lead. Obviously, the traditional ECG tracing which we have seen in our physiology texts have all been from lead 11. When we look at a typical lead II, we see that the majority of waves go above the isoelectric line. That is, most wave deflections are positive. Let's put it another way. The "P" wave is positive in lead II, so that means that atrial depolarization (P wave) must be in a direction which goes toward lead 11. Also, ventricular depolarization (QRS) is almost all positive, so ventricular depolarization must be in a direction toward lead 11. Likewise, the T wave is positive, so ventricular repolarization must be in a direction toward lead II also. Conclusion: Lead II must be from some viewpoint that is directly positioned in the "line of fire" for atrial depolarization, ventricular depolarization, and ventricular repolarization. All of these events are headed directly toward lead 11.

On the other hand, look at aVR on the normal ECG. Note that all of the events are recorded as below the isoelectric line (negative). Thus, atrial depolarization, ventricular depolarization, and ventricular repolarization must be in a direction going away from aVR. This is true, because lead aVR is the only lead which is exclusively from the right side of the heart. All myocardial electrical activity is essentially from the right to the left. Therefore, all of the events actually do occur while going away from lead aVR, and that explains why all of its wave deflections are negative. Notice that the fifth heartbeat on the normal ECG is negative from the point of view of lead aVR but is positive from the point of view of lead 11. Lead aVL (below aVR on the ECG) is half positive and half negative, so it must be in a position which is somewhat between the lead aVR and lead 11. Picture a clock face on the chest wall. Lead aVR is approximately at the 10 position, lead aVL is approximately at the 2 position, and lead II is at the 5 position. Cardiac depolarization heads toward the 5:00 position, away from the 10:00 position. This would make the 2:00 position somewhat in the middle. Thus, it is recorded as half positive and half negative. (Pretty neat, huh?)

The lead which records the tallest QRS will be the lead most in the direct line of depolarization. The height of the wave pattern is a measurement of the energy (amplitude) of the depolarization wave headed toward that particular lead. The more a view is in the "direct line of fire" of the wave of depolarization, the taller the wave pattern. On the normal ECG, please note that lead II has the tallest QRS. Thus, ventricular depolarization must be headed toward lead II more than toward any other lead. This is one of the reasons why lead II has been chosen as the "rhythm strip" lead. Let's assume, however, that a particular ECG demonstrates that aVL has the tallest QRS. This would mean that ventricular depolarization is headed more toward the two o'clock position (remember the clock analogy) than toward the five o'clock direction. In other words, the direction of ventricular depolarization is more toward lead aVL than toward lead II. This would be an abnormal observation.

Let's suppose for a moment that lead aVR demonstrated a positive QRS and lead II demonstrated a negative QRS; this would be a startling finding on the ECG. This would indicate that ventricular depolarization was occurring in a direction toward the right side and away from

the left. This is, of course, completely contradictory to the normal and expected direction of cardiac depolarization which is known to occur from right to left, not left to right. Therefore, such a finding would have to be explained by one of the following: (1) the electrodes have been reversed when being placed on the patient; (2) the patient's heart is placed backwards in the chest cavity, a very rare condition known as "dextrocardia"; or, (3) there is a pathological condition in this patient's heart.

The most likely conclusion would be #3 above unless proven otherwise. The ECG would be carefully analyzed to determine the presence of other pathological findings which could explain the change in the direction of depolarization. Thus, knowing which leads should be positive and which should be negative is of all importance to the detection of ECG abnormalities. This will be emphasized later. The purpose of this part of the notes is to familiarize the student with the mechanics behind the ECG - the fact that there are twelve views provided on the standard ECG, the fact that wave patterns go up (positive) when the depolarization occurs toward the lead and go down (negative) when the depolarization occurs away from the lead, the fact that there are major anatomical areas of the heart which are viewed by certain ECG leads, and the fact that lead II is the worldwide accepted view of the heart by which we have all learned the P/QRS/T wave formations and what they mean.

Understanding the Various Leads (Views)

As described above, it is helpful to visualize a clock face on the chest of the patient. The circle is situated above the heart with the apex of the heart facing somewhat toward the 5:00 position on the clock face. There will be six leads (views) possible on the standard ECG which include leads I, II, III, aVR, aVL, and aVF. These leads have been internationally standardized to be viewing the depolarization of the heart from established positions. For the purpose of simplicity, let me explain the views using the clock face analogy. Lead aVL is a view from the 2:00 position; lead I is at the 3:00 position; lead II is at the 5:00 position; lead aVF is at the 6:00 position;

lead III is at the 7:00 position; and lead aVR is at the 10:00 position. It becomes more confusing when the student is told that only four electrodes provide these _six views, but this is true. There are only ten electrodes which will be attached to the patient. Four of them are attached to the limbs (limb leads) and six are attached to the chest wall (chest or precordial leads). The four limb leads will provide the six views mentioned above (I, II, III, aVR, aVL, aVF). The mechanism behind this is very complex and involves the changing of polarities (from positive to negative) of each of the limb leads. This changing of polarity will allow the electrodes to pick up the cardiac depolarization differently, thus giving us different views of the depolarization process. It is essential that the student understand that only the four limb leads participate in the six "clock face" views of the heart. The chest leads do not play a role in providing these six views. Instead, the chest leads are unipolar, and these give the VI - V6 views on the ECG.

The heart has been somewhat "compartmentalized" and specific views have been assigned to view different compartments. For example, leads I and aVL are said to provide views of the "lateral" portion of the heart. Leads II, aVF, and III provide views of the "inferior" or "diaphragmatic" portion of the heart. The V1 - V6 leads provide views of the "anterior" portion of the heart. Thus, when one reads, "ischemia of the inferior leads," this means that leads 11, aVF, and III are showing signs of ischemia in that portion of the heart. If the chest leads and leads I and aVL show evidence of an infarction, we would say that the "anterolateral" leads are positive for MI. Stated differently, an "inferior myocardial infarction" is diagnosed on the basis of ECG evidence provided by leads II, aVF, and 111.

Blood Supply to the Various Compartments

Very generally speaking, each of the three compartments (lateral, inferior and anterior) can be said to be perfused by a very specific coronary artery. The inferior portion of the heart is known to receive its major blood supply from the right coronary artery. The anterior portion of the heart (essentially the left ventricle) receives its blood supply from the left anterior descending coronary artery, while the lateral portion of the heart receives it blood supply from the circumflex. Remember that the left anterior descending and the circumflex arteries come from the left main coronary artery. Therefore an occlusion of the left main coronary artery could result in both an anterior and lateral myocardial infarction (anterolateral MI). This, of course, would be visualized in the "V" leads and leads I and aVL.

Note that the lead aVR is not considered to view a specific compartment. It remains the only view that should be completely negative because of the fact that all depolarization of the heart occurs "away from" its position on the right side of the body.

The SA Node

The sinoatrial node serves as the "pacemaker" of the heart. Please remember that conduction travels throughout the heart by means of specialized muscle cells, not by means of nerve cells. In other words, the SA node is not a cluster of neurons, it is a cluster of specialized muscle cells which have the property of intrinsic early depolarization. Once the SA node depolarizes, a wave of depolarization is sent throughout the atria in a wave-like (ripple) pattern. Because the atria are separated by a septal wall, depolarization does not routinely cross through a septal wall unless a specific pathway permits it. In this case, specialized muscle cells known as "Bachman's Bundle" carry the signal through the septal wall from the right atrium into the left atrium. Once the atria have depolarized, the signal is now in the AV (atrioventricular) node. The AV node will hold the signal for a few milliseconds in order to allow the atria to empty as much blood as possible into the ventricles. This time delay is known as the "AV delay" and will become an important part of the ECG to examine.

The "P" Wave

The first deflection visualized on a normal ECG is the "P" wave. The "P" wave represents atrial depolarization and should not be equated with SA firing. It must be understood that unless the atrial wall actually depolarizes, there will not be a "P" wave. If the atrial contraction is initiated by a source other than the SA node, there will still be a "P" wave, but the wave pattern will be different in its appearance. When we first look at the ECG (rhythm strip), we try to find the "P" wave. We then look at all of the "P" waves in one lead to see whether or not they look reasonably alike. (See next paragraph for further clarification.) We check out such things as their height (amplitude) and their width (time factor) as well as their general appearance. We know that when the SA node is the initiating site atrial depolarization starts in the upper right corner of the right atrium and spreads through the atrial wall from right to left. Therefore, the P wave should be positive (rising above the isoelectric line) in all of the leads except aVR (see previous explanation). If they all appear as expected, we assume that they represent atrial depolarization which has been initiated by the SA node. We then would use the word "sinus" to describe the contractions and rhythm. In other words, we would say that the heart is

demonstrating "sinus rhythm." In fact, the use of the word "sinus" always refers back to the SA node sinoatrial). We often see this word used in expressions such as "sinus tachycardia," "sinus bradycardia," "sinus arrest," "sinus arrhythmia," "sinus block," etc.... all of which have direct reference to the SA node. In other words, "sinus tachycardia" means that the heart is beating more than 100 beats per minute because the SA node is firing more than 100 times per minute.

"Sinus arrest" would mean that the SA node has ceased firing. The same analogy holds true every time you see the word "sinus" placed in front of a condition or event.

I mentioned that it may be confusing to say that "all P waves should be similar." What is meant by this is the fact that in any lead you may be viewing, all the P waves in that lead should look alike. If the shape and direction (positive or negative) of the P wave change within a lead, the evidence is clear that there must be a source of atrial depolarization other than or in addition to the SA node. When a pebble is dropped into a bucket of water at the eleven o'clock site, the ripples (depolarization) are different from those created when a pebble is dropped into the bucket at the seven o'clock site. (See "Wandering Pacemaker" later in the notes.)

The rate of the heart would also be observed. If, for example, the rate were below 60 beats per minute, the patient would be experiencing bradycardia. If the "P" waves all appeared to be similar (within each lead) and reasonably normal, we would assume that the signals were coming from the SA node. Thus, we would say that "sinus bradycardia" is demonstrated on the ECG. The use of the word "sinus" is used to describe the condition which follows (sinus bradycardia, sinus tachycardia, sinus contraction, sinus arrest, sinus arrhythmia, etc ... ) and means that the condition is the result of the SA node. When the heart beat appears to be under the control of the SA node (normal P wave prior to each ventricular contraction) we say that the heart displays "normal sinus rhythm."

Sinus Rhythm

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Wandering Pacemaker

Sometimes a part of the atrial wall may become irritated and initiate a depolarization signal which is more frequent or powerful than that coming from the SA node. Any signal not coming from the SA node is defined as "ectopic" (off the normal site). Thus, an ectopic focus (site) can establish itself in the atrial wall and essentially take over as the pacemaker for long periods of time or for only one or two contractions. When we use the expression "wandering pacemaker," we generally are referring to an ectopic focus which demonstrates numerous simultaneous contractions. For example, we might see a normal sinus rhythm pattern and then suddenly see six or more contractions with an unusual looking "P" wave. In this case, the ectopic focus actually assumed the role of pacemaker (not just one beat) and created a temporary rhythm which was not "sinus." Often, sinus rhythm reestablishes itself after several moments of ectopic rhythm.

Irritation of the atrial wall can cause such a mishap. One might consider the innervation of the atrial wall by the sympathetics and rationalize that increased sympathetic

output (sympatheticotonia) could lead to such ectopic sites. This is a reality and is treated with beta-blockers medically if such irritation begins to lead to difficulty in rhythm patterns. We really prefer to have everything under SA control (sinus). Please look at the following ECG strip to visualize a classic case of wandering pacemaker.

Wandering Pacemaker

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P pulmonale

Whenever the word "pulmonary" or similar words (pulmonale) are used, the reference is always to the lungs. In this case, the "P" wave is unusually shaped which represents some aberration of the atrial wall. The morphology of this particular "P" wave is tall and peaked. Generally speaking, the "P" wave should not be taller than 3-4 tiny boxes and should not be longer than approximately 1/z of one large box. In conditions involving the lungs, especially chronic obstructive pulmonary disease, the pressure in the lungs dramatically increases due to loss of capillary surface area. The right side of the heart is responsible to pump blood to the lungs, so it is the right ventricle which will first undergo strain as it attempts to pump blood to the lungs. This condition of increased resistance to pulmonary blood flow is known as pulmonary hypertension, and over time this will seriously damage the right ventricle. The right ventricle will enlarge and expand, thus decreasing its pumping capacity. As a result, blood will "back up" into the right atrium. Now the right atrium will enlarge. When this occurs, the P wave (which measures atrial depolarization) will become very tall, demonstrating that the atrial wall has enlarged and is exhibiting increased amplitude (energy) during its depolarization. Please remember that the greater the size of the cardiac wall, the greater the amplitude which will be recorded by the ECG during depolarization. Occasionally, the P wave will become tall and peaked for reasons other than pulmonary hypertension. For example, stenosis of the pulmonary or tricuspid valves will also cause back pressure on the right atrium and subsequent enlargement of the atrial wall. Again, the P wave will demonstrate a significant increase in its height.

Chronic obstructive pulmonary disease (emphysema) is the most common condition associated with P pulmonale. This particular disease will demonstrate swollen ankles, liver, and neck veins as blood is unable to enter the right side of the heart.

P-pulmonale

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Sick Sinus Syndrome/Sinus Arrest/SA Block

All of the above terms are essentially synonymous. They indicate that the SA node has failed to fire. During the time of sinus arrest, the heart is experiencing asystole (lack of contraction of the ventricles). Obviously, this will result in sudden loss of consciousness (syncope) and death. The heart will have three choices when failure of the SA node occurs. The first choice would be to wait for the SA node to reawaken and initiate a signal. The second would be for another area within the atrial wall to assume the role of the SA node. The third option would be for the ventricles themselves to develop an ectopic site which would then fire and create a contraction. At first, the heart would elect to wait for the SA node to resume its pacemaker activity. During this waiting period of several seconds, the patient is likely to faint (syncope). These episodes of loss of consciousness are called "Stokes-Adams" attacks. While there are multiple reasons for a person to experience "Stokes-Adams" episodes, the most common cause is "sick sinus syndrome." The ECG should readily discover these "skipped beats" and be able to attribute them to interruption of the SA node. If the SA node fails to fire, there would not be a P wave, and the distance between beats would be greatly exaggerated during times of the sinus arrest. Anytime a person suddenly loses consciousness and emergency personnel are called, an ECG will be performed. Especially among the elderly, the incidence of sinus arrest is high. The cause may be attributed to increased vagal tone (vagotonia). I trust that you do not think that loss of sympathetics plays any role in this condition. The sympathetic nervous system provides exclusive innervation to the ventricles but only minimal innervation to the atria, while the right Vagus directly innervates the SA node and the left Vagus directly innervates the AV node. The Vagus (parasympathetic) will cause an inhibition to the SA node which can actually prevent its firing. Does the term "parasympatheticotonia" sound familiar? Could an upper cervical subluxation relate to this phenomenon?? Ischemia of the SA node is also a possible etiology of this condition. Drugs may also contribute to sick sinus syndrome.

When another atrial site assumes the role of pacemaker during times of SA block, the new site would be considered as "supraventricular" and "ectopic." The most common site would be the AV node itself. When the AV node fires, the signal will immediately enter the ventricles resulting in a contraction (QRS) followed by the traditional repolarization vector (T wave). In other words, the QRS would look the same as if the signal had come from the SA node. When the AV node initiates the signal, there will not be a visible "P" wave before the QRS. The signal will proceed into the atria in a retrograde manner from the AV node, but the signal will reach the ventricles before it stimulates the atrial wall. The atrial contraction (P wave) will be lost under the QRS. When this ectopic heartbeat comes as a result of SA block, it is considered to be an "escape" beat. The escape beat is an emergency event designed to keep the heart beating and blood circulating until the SA node recovers and the heart returns to sinus rhythm. Sometimes, there may be several escape beats in a row before the SA node resumes its activity. It it is reasonably clear that the escape beat came from the AV node, this is traditionally called a "nodal escape beat" or a "junctional escape beat" (the AV node is commonly referred to as the AV junction). If it not clear whether or not the escape beat came from the AV node, it may be referred to as a "supraventricular escape beat."

Sometimes, the AV node or atrial wall ectopic sites do not assume the role of pacemaker during times of sinus arrest. Occasionally, the ventricular wall develops an ectopic site during times of sinus arrest, and this site fires into the ventricles. This site does not allow the depolarization vector to assume the standard pathways of common bundle and bundle branches for ventricular depolarization. As a result, the contraction of the ventricles is accomplished in a bizarre and irregular manner. The ECG appearance is usually wild and without recognizable morphology. In other words, it does not look anything like the normal QRS pattern we are accustomed to seeing. This would then be considered as a "ventricular escape beat." The word "ventricular" merely means that the signal originated in the ventricle. Any beat which is "ventricular" is cause for alarm. Should a number of ventricular beats occur in a row, there is a risk of ventricular tachycardia developing followed by ventricular fibrillation - a potentially fatal outcome.

See below for ECG examples of sinus arrest and escape beat phenomena.

Sinus Arrest / Sick Sinus Syndrome / SA Block

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Sinus Arrest With Escape Beat

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Atrial Fibrillation/Flutter

A serious condition known as atrial fibrillation is of epidemic proportion among cardiac patients. In this situation, the atrial wall develops multiple sites of irritation which fire randomly. The atrial wall does not beat in a synchronous or rhythmic fashion, rather it assumes a "quivering" action which is not an effective pumping chamber. Increased sympathetic stimulation to the atrial wall is considered to be strongly sugestive as the etiology of the multiple sites of irritation. Consequently, beta blockers are provided to reduce the sympathetic stimulation. In addition, the removal of all stimulants such as nicotine and caffeine is recommended. When the condition does not respond after substantial time (weeks/months), a conversion may be attempted by shocking the heart muscle with a defibrillator. Once all cardiomyocytes have depolarized simultaneously, it is hoped that the SA node signal will resume its role as pacemaker and restore a normal sinus pattern ( P waves ). Unfortunately, the traditional medical solutions have not been reliable and often unsatisfactory. Perhaps one should look into why the sympathetic nervous system is stimulated. Did somebody say "subluxation?"

Of major concern with atrial fibrillation is the collection of blood in the wall of the atria. When the blood is not pumped from the atria to the ventricle, there tends to be a residual amount of blood which commonly collects along the wall and may form a clot. Should this clot break free and enter the ventricle, a pulmonary embolism or stroke is likely. This likelihood is why patients with atrial fibrillation are advised to be on anticoagulant therapy.

The ECG appearance is classic, with a "quivering" base line without recognizable "P" waves. The QRS complexes are arrhythmic, because the AV node is protecting the ventricles from receiving the hundreds of signals bombarding it. However, although the AV node successfully protects the ventricles from the barrage of signals being received, the node still has difficulty maintaining a steady and rhythmic pattern.

When the atrial signals total greater than 350 per minute, the "P" waves are not visible and the base line (isoelectric line) of the ECG is very shaky and with a "quivering" appearance. When the atrial signals total between 250 and 350 per minute, the "P" waves are visualized as a series of "bumps" before each QRS complex. This is called atrial flutter when the atrial signals are less than 350 per minute but greater than 250. Traditionally, atrial flutter is said to give a "picket fence" appearance.

See below for ECG examples of atrial fibrillation/flutter.

Atrial Fibrillation

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Understanding Axis Deviation

The words "axis" and "vector" are synonymous. They both refer to a "direction" of depolarization. Remember from the early pages that the normal heart depolarizes from right to left, generally directed toward the five o'clock spot on the imaginary clock face on the chest wall. (Remember that lead II is sitting at approximately the five o'clock position.) When the direction of depolarization is toward a lead, the ECG will show the signal as "positive" or above the line. When the direction of depolarization is awa, fro a lead, the ECG will show the signal as "negative" or below the line. The student is referred to the previous section entitled "Reading the ECG Wave Pattern" for a review of this concept.

I ask you to now examine the circle below.

[pic]

Please note that the center horizontal line is labeled as 0° on the right and 180° on the left. All number below the center horizontal line are considered as "positive" while all numbers above the center horizontal line are considered to be "negative." A center perpendicular line is labeled as negative 90° at the top and positive 90° at the bottom. These two lines thus provide four quadrants. This circle is to be considered as an imaginary image on the chest wall (much as the clock face we used previously). The heart will sit in the middle of this circle. Please note that the six leads (aVL, I, II, aVF, III, and aVR) which are derived from the four limb electrodes have been assigned a number of degrees. Lead aVL is -30°; lead I is 0°; lead II is 60°; lead aVF is 90°; lead III is 120°; and lead aVR is -150°. It has been established that lead II at 60° sits in the direct "line of fire" of cardiac depolarization. That is why lead II has been the standard for showing students what a "typical" ECG looks like. That is also why lead II has been selected for the rhythm strip at the bottom of the ECG.

The ideal situation is when the atrial depolarization vector and ventricular depolarization vector and the ventricular repolarization vector all occur between 0° and 90°. In other words, the axes of atrial and ventricular contraction should all be toward the left lower quadrant (using the patient's left side as reference). How do we know if the axes are between 0° and 90°? This is actually very simple. Look at the normal ECG in the upper left hand corner. You will see an

area labeled -AXIS-. Under this you see P, QRS, T with a number following each. After the "P" you will see the number 35. This refers to 35° on the circle (see above). In other words, we can now know that atria] depolarization (P wave) has occurred toward 35° which is quite normal since it is between 0° and 90°. Now look at the QRS axis (vector). You will see that it is at 67°. Again, this is quite normal for ventricular depolarization. The T axis is at 44°, and this is also a normal vector. Since all axes (vectors) are between 0° and 90°, we can state confidently that there is no axis deviation demonstrated on this ECG.

If the QRS axis would be -42°, that would be alarming. This would mean that the ventricles are depolarizing toward the patient's left shoulder, and this would be called "left axis deviation." On the other hand, if the QRS axis were given as 126°, this would mean that the ventricles are depolarizing toward the patients right side and would be labeled as "right axis deviation." The most common cause of an axis deviation is hypertrophy of the ventricular wall. In the case of left axis deviation, the left ventricle may be thicker and hypertrophied as a result of chronic systemic hypertension. Or, possibly, the aortic valve could be stenosed with a resultant left ventricular hypertrophy. At any rate, the QRS vector would be somewhere in the upper left quadrant. In cases of chronic obstructive pulmonary disease (emphysema), the blood pressure in the lungs has risen (pulmonary hypertension) thereby creating pressure on the right ventricular wall. This will result in hypertrophy of the right ventricle and subsequent right axis deviation. In this case, the QRS vector would be somewhere in the lower right quadrant. Stenosis of the pulmonic valve could also lead to right ventricular hypertrophy. When the right ventricle hypertrophies and weakens, the patient is said to be in congestive heart failure. In this case, the ankles will become edematous, etc...

A glance at the QRS patterns of leads I, II, and III can also provide clues to the nature of the axis. The closer the lead (view) is to the direction of depolarization, the taller the QRS pattern will be. The height of the image on the ECG strip relates to the amount of energy (amplitude) being sensed. Lead II is positioned at 60° which is directly in the "line of fire" of atrial and ventricular depolarization; therefore, lead II should have the tallest QRS pattern. It is also true that leads I, II, and III should all be positive. Lead I and lead III should not be as tall as lead II. What if lead II is not the tallest??? What if lead III is the tallest??? In this particular case, if lead III has the tallest QRS, that would indicate that ventricular depolarization must be headed more toward 120° than toward 60°. Indeed, if the ventricular depolarization vector is greater than 90° to a significant amount, often lead I is negative! The only way to know is to look at the QRS axis as provided on the ECG itself. If lead III is the tallest and Lead I is negative, I would predict that the QRS axis is going to be somewhere around 120° or more (right axis deviation).

On the other hand, if lead I has the tallest "R" and lead III demonstrates a negative vector, it is likely that the QRS axis is going to be around -30° or more. This would then be defined as "left axis deviation." One could also look to aVL to confirm suspicions about left axis deviation. If

lead I has a very tall QRS, what about lead aVL? Obviously, lead aVL should also demonstrate a very tall "R" wave if lead I has a tall "R". If the QRS axis is -30° or higher, the "R" wave of aVL will be even taller than the "R" wave of lead 1.

The deviation of the axis is a finding of likely importance. As mentioned previously, the most common cause of this event is chamber hypertrophy. However, another common cause is scarring of the myocardium. Suppose, for example, that a previous infarction resulted in scarring of the ventricular wall - since scar tissue does not conduct (depolarize), the direction of depolarization will be deflected away from the scar and in an opposite direction. This will be discovered by the ECG analysis of the vectors as given in the upper left hand corner. Another potential cause is ectopic site firing. For example, if the ventricle experiences several "ventricular" contractions (PVC), these vectors will be bizarre and will be factored into the more nearly normal QRS vectors. The end result may be a QRS axis which is not between 0° - 90°.

In the atrial wall, ectopic sites may develop and excite the heart to contract. These signals will not be coming from the SA node and may very well not depolarize in the same direction as the SA node. Cases such as "wandering pacemaker" commonly demonstrate an unusual "P" axis. Knowing this, the deviation of the axis is simply a way of noting the potential problem. The deviation becomes a `red flag' which should cause us to investigate the ECG further for indications of pathology. The deviation of the axis does not diagnose any specific condition per se, but in conjunction with other findings, it may lead the clinician toward a general diagnosis.

There are also physiological axis deviations; that is, deviations created by the anatomical position of the heart in the chest. For example, a patient with a protruding stomach ("beer belly" or pregnancy) will generally have a heart which is placed in a more horizontal position than normal. Short stocky people tend to demonstrate a more horizontally positioned heart. This anatomical variation will cause a more pronounced left axis deviation. Likewise, tall thin individuals tend to have a more perpendicular heart, and this will give a slight right axis deviation. Neither of these examples is pathological and merely reflects body type differences and the anatomical positioning of the heart in the chest cavity.

Evidence of Right Axis Deviation

I II III F L

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Conduction Blocks

This unit of study will focus on the following blocks: SA block, AV block, Bundle Branch Block. The SA block has already been discussed on previous pages and is synonymous with "sick sinus syndrome' and "sinus arrest." We shall not elaborate further on this particular conduction block.

Blocks involving the AV node are divided into lst degree, 2"d degree, and 3rd degree categories. As mentioned in class, the naming of these blocks as "AV" is a misnomer, for many of these lesions are found distal to the AV node (infranodal). Nevertheless, let's begin with the first degree (or primary) block. This particular problems is actually localized to the AV node itself or

perhaps more correctly to the influence of the vagus nerve on the AV node. Remember that the AV node is designed to receive the signals from the SA node and to hold the signal for a few milliseconds. This will permit atrial depolarization to complete the task of emptying the contents into the ventricles prior to ventricular contraction. This time delay is known as "AV delay" and is referred as the P-R interval on the ECG. The first degree (1') AV block is demonstrated on the ECG by a lengthening of the P-R interval. This increase of the AV delay can be due to several circumstances, commonly vagotonia (parasympatheticotonia). Taken as an individual finding, this condition is of little consequence. However, more than 50% of first degree blocks degenerate into second degree blocks. A first degree block may also result from ischemia to the AV node (perfused by the right coronary artery); compromised blood flow from the right coronary artery will generally cause other dysfunctions of the cardiac conduction system as well. As is often the case, a primary block becomes an incidental finding along with other problems of greater magnitude.

First Degree AV Block

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This leads us into a study of second degree (2°) AV blocks. The second degree block must be subdivided into two types, Type 1 and Type 2. The proper nomenclature would be, "second degree, Type 2 AV block," for example. First of all, what defines a second degree block? The defining feature of any second degree block is the non-conducted "P" wave. What this means is that the SA node is firing correctly, but the signal is not being conducted into the ventricles. Therefore, the ventricles are not contracting even though there is a viable "P" wave. A second degree block is always a serious condition, but Type 1 is less worrisome than Type 2. The Type 1 second degree AV block is often termed "Wenckebach" which refers to its predictable nature. In other words, we will be able to see on the ECG when there will be a non-conducted "P" wave. We can see this by observing the widening P-R interval. Whenever the word "Wenckebach" is used as a descriptor, it always refers to the predictable nature of the condition. The Type 1 second degree block is a lesion of the AV node itself. Apparently, the node will fire in a normal fashion and then become fatigued. The fatigue will manifest as an. increased AV delay (prolonged P-R interval). Eventually, after several beats with an ever-widening P-R interval, the "P" wave will occur without a "QRS" following. In other words, the "P" wave will be nonconducted. After the non-conducted "P" wave, the AV node will be essentially normal again and begin sending signals to the ventricles but will rapidly fatigue. On and on this same cycle will be repeated. (See ECG illustration below)

Second Degree AV Block, Type 1(Wenckebach)

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The second degree AV block, Type 2, is considered to be much more life-threatening. Its lesion site lies below the AV node (infranodal) and is likely in the region of the common bundle. The consequences of this particular block are often fatal. A sudden blow to the chest, or increased demand on exercise, will suddenly cause all supraventricular signals to be blocked from entering the ventricles. Obviously, asystole will result causing immediate collapse of the patient. The lesion is not in the AV node; it is not a matter of excessive vagal tone or AV fatigue. Instead, the atrial signals are working (continuous "P" waves) but are not followed by ventricular contraction (QRS) complexes. Because the lesion is within the common bundle itself (allegedly), the common bundle will not become the pacemaker and will not send signals into the ventricles. Therefore, the likelihood is that the ventricles will not receive any signal to beat and the heart will enter a period of asystole.a deadly consequence of this particular type of block. It is possible that the ventricles themselves will begin to generate focal sites which will fire and stimulate the ventricles to beat. Of course, these will be classified as "ventricular" beats since the signals originate in the ventricles. These type of ventricular beats are dangerous, because the multiple signals may collide and send the heart into ventricular fibrillation. As you can well understand, the possibility of a lethal asystolic episode is ever present with second degree AV block, Type 2. Some authorities credit this type of block with causing the sudden collapse of young athletes during competition or collision events on the field. Only an ECG is capable of determining this particular conduction block. Once determined that such a block exists, the patient requires immediate referral for complete cardiac work-up and likely pacemaker therapy.

Second Degree AV Block, Type 2

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The "third degree" AV block is often termed "AV dissociation." It is commonly called a "complete heart block" and results from scarring between the atria and ventricles. As a result, no signals from the atria (supraventricular) will enter the ventricles. Such occurrences often follow serious myocardial infarctions, while others are found incidentally without the patient's awareness of its existence. A complete heart block is considered, for obvious reasons, to be very serious. The pumping of the atria ("P" waves) and the pumping of the ventricles ("QRS" ) are not synchronized. The ventricles are receiving their signal to beat from several possible sources, including the common bundle, bundle branch, or a focal site on the ventricular wall. The ECG pattern is very curious and demonstrates multiple "P" waves and "QRS" complexes, but careful analysis indicates that the two are not related to each other at all. There will be a rhythmic patter to the "P" waves and a rhythmic pattern to the "QRS" complexes, but the two patterns simply lie on top of each other. A trained observer becomes aware of the typical appearance of this phenomenon on the ECG, but many incorrect ECG interpretations have been made by inexperienced clinicians. Some people believe that it looks like atrial flutter, while others believe that it resembles a second degree block with escape beats, etc..... I will provide an example of this below, but you will not be held responsible to recognize such an event for the purposes of this class. The patient will need to be provided a pacemaker to insure that the ventricles beat with sufficient rate and under the influence of a predictable signal.

Third Degree AV Block/AV Dissociation/Complete Heart Block

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The Bundle Branch Block is very common and should become familiar to the student. Essentially, the bundle branches include one right bundle branch and two left bundle branches. The ultimate consequence of a bundle branch block is the prolonged time required for the ventricles to contract. Since one (or more) of the bundle branches may be blocked, the signal will take longer to work its way around the heart and accomplish both right and left contractions of the ventricles. On the ECG, this will create a very "sloppy" and prolonged "QRS" image.

The usual appearance of the QRS is very pointed and brief. The bundle block appearance gives a rounded look with a wide base. Sometimes the "rabbit ear" appearance occurs which we would label as "R" and "R’" (R prime). We would be actually seeing both ventricles as they contract, whereas we usually see only the left ventricle. Again, this prolongation of time results from the fact that one or more of the bundle branches is blocked and the signal takes longer to get to both ventricles.

It is not the purpose of this class to discuss the ECG differences between a left or right bundle branch block. It is sufficient to recognize that the development of a bundle branch block in a patient who previously did not demonstrate such a block is a significant finding. It probably occurred as a result of scarring on the cardiac wall. If such an event occurs following a myocardial infarction, it would be considered significant. However, many healthy people are born with a right bundle block appearance on the ECG. It is important to see this early on an ECG and to be aware of its existence. Subsequent ECG's can then be compared with earlier ones to confirm the existence of this right bundle branch block appearance when the patient was much younger. However, the left bundle branch block is never considered to be benign and always demands investigation. Also, the sudden appearance of a right bundle branch block in a patient who did not demonstrate such a block previously is equally worthy of investigation. Again, it not essential for us to be able to determine the difference between the right and left bundle branch blocks. Simply recognize the wide QRS appearance associated with both the left and right bundle branch blocks and understand that loss of a bundle branch prolongs the contraction of the ventricles.

Bundle Branch Block

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Ventricular Contractions

As we leave the area of conduction blocks, I want to review the concept of "ventricular" beats. The adjective "ventricular" refers to the fact that the signal originates in the ventricular wall rather than from the atrial wall. The atrial signal is generally assumed to be coming from the SA node and is referred to as "sinus." Therefore, all "sinus" beats are "atrial" but not all "atrial" beats are necessarily "sinus." For example, if the beat originates from the AV node, the contraction of the ventricles will be designated as "atrial," "supraventricular," "nodal," or "junctional." The contraction will not be considered "sinus" since it did not originate from the SA node. Obviously, the term "atrial" covers a large territory of possibilities and so does the term "supraventricular". Combinations of terms may also be used, such as "supraventricular ectopic" or "atrial ectopic". In any event, these contractions are considered to have originated from a signal in the atrial wall.

When a contraction is considered to be "ventricular," the assumption is that the signal originates from somewhere within the ventricular wall, from an ectopic focus. These events do occur in healthy individuals and commonly called "Premature Ventricular Contractions" (PVC). Stress, too much caffeine, cigarettes, over the counter cold medications, etc... will contribute to an occasional premature ventricular contraction. The patient often complains of sensing a "pounding" in his chest, or will say that his heart feels like it "skipped a beat." These sensations are often amplified at night when the patient is lying down. The appearance of a ventricular contraction on the ECG is dramatic and produces a bizarre morphology. In the midst of an otherwise normal ECG with obvious P, QRS, and T waves there will appear a sudden and unidentifiable up and down "mark" on the ECG with no identifiable wave pattern. The reason that the contraction looks so strange is that the signal does not follow the regular SA-AVCommon Bundle-Bundle Branch-Purkinje Fiber pathway. Rather, it is like dropping a stone in bucket of water from the corner and watching the ripples go in a direction completely different from when the stone is dropped in the center of the bucket. An occasional PVC is of no concern to the clinician, but if there are six or more per minute further investigation is warranted. A ventricular contraction can be an issue when the heart is ischemic. Lack of sufficient blood to ventricular cells may cause them to become somewhat excited and fire, resulting in a ventricular contraction. If a number of ectopic sites develop on the ventricular wall, as commonly occurs following myocardial infarction, there is a serious risk of ventricular fibrillation. If several ectopic sites fire simultaneously, their signals may "collide" and result in a totally disruptive and asynchronous firing of ventricular cells (fibrillation). Anytime there is more than one site from which ventricular contractions occur (multifocal PVC), this is considered very serious. Generally, an occasional PVC is treated by adjustment to the upper thoracic spine and reduction of stress-causing factors.

Premature Ventricular Contraction

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Myocardial Ischemia/Injury/Infarction

This section will review the above three events and demonstrate the customary ECG changes associated with each. Beginning with ischemia, please understand that it is not unusual for a patient to experience ischemia for years while other patients may have only one or two anginal episodes prior to experiencing an infarction. Essentially, an area of the myocardium is not being sufficiently perfused. Please review the coronary artery circulation as discussed previously in these notes. Be certain to study the specific artery and its anatomical area of perfusion as well as which leads view these areas. Coronary artery disease (CAD) is the most common cause of ischemia. The most common symptom is angina and is quickly relieved by nitroglycerin compounds which dilate the coronary arteries. In times of complete occlusion of the artery, however, the dilation will not be sufficient to relieve pain or prevent infarction. The most notable dysfunction of the heart during ischemia is its inability to re polarize appropriately. The heart muscle (ventricle) will depolarize normally, but repolarization will be difficult and the cells will repolarize in a direction opposite to the direction of depolarization. Imagine a cell on the left side of the heart depolarizing first and the cells on the right side of the heart depolarizing first. It makes sense that the left side should repolarize first; however, if the myocardium is ischemic, insufficient oxygen will make repolarization difficult. As a result, the right side will initiate repolarization before the left, and thus the repolarization vector will occur in a direction opposite to that of depolarization. In these cases, a look at the -AXIS- section on the ECG will confirm your suspicions. The QRS vector may be something like 65° and the T vector may be 140°. On the ECG itself, the QRS will be positive and the T wave will be negative (inverted). Thus, the proverbial "inverted T wave" has come to mean that the heart is ischemic.

Often, a patient will complain of angina on exertion such as climbing steps. When the resting ECG is done, there is no evidence of ischemia. The Dr. may request a stress test in which the patient will be asked to walk on a tread mill while attached to the ECG. As the stress begins to place demands on the heart muscle, it will beat faster and harder, thereby requiring additional oxygen. When perfusion cannot keep up with the demand, the T wave will begin to invert. Once the cardiac personnel observe the inversion of the T wave, the test will be stopped. We now have sufficient evidence to state that specific areas of the heart are ischemic.

As you may remember, if leads H, III, and aVF demonstrate the inverted T wave, we can be certain that the "inferior" portion of the heart, perfused by the right coronary artery, is ischemic. If the V leads demonstrate inverted T waves, then we can know that the left anterior descending coronary artery is compromised. This usually results in severe angina when the left ventricle is involved with ischemia. This area of the heart is known as the "anterior" portion. Likewise, if leads aVL and I show the inversion of the T wave, then the "lateral" portion of the heart is ischemic. The lateral portion is perfused by the circumflex artery which is derived from the left main coronary artery. Occlusion of the left main coronary artery will involve the anterior and lateral portions of the heart and is called the "anterolateral" portion.

Ischemia of the Anterior Wall

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The injury will occur next, but this particular event will not last forever. Either the heart will recover or the tissue will not survive (infarction). During the first six hours (or so) of this injury appearance, the heart tissue has its best chance of survival provided appropriate intervention is done. For example, angioplasty, TPA (clot buster), bypass surgery, etc.... may be the recommended approach to restore circulation. During this time of injury, the situation is considered to be "acute," and the injury pattern will last for only a few days before resolving. Please remember that during ischemia, the heart experiences difficult repolarization. During injury, the heart will have difficulty depolarizing. The ECG is very obvious in demonstrating an "elevated" S-T segment. As the heart continues depolarizing, the site of injury will be unable to depolarize and will "drag it out." Therefore, the wave will be pulled away from the normal QRS thereby extending the S-T segment dramatically. The "R" does not return to the base line. At any rate, the appearance on the ECG is quite obvious and familiar to emergency room personnel who routinely see acute heart attack victims experiencing chest pain.

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Myocardial infarction is the end of the line event for ischemia. If the ischemia leads to injury and the circulation is not restored, infarction will result. In this event, cardiac tissue has died and will be replaced by connective tissue. This tissue does not depolarize, so the area will be electrically "dead." Depolarization vectors heading toward the infarcted area will be diverted away from the infarcted tissue, and this will be a negative deflection on the ECG in any lead viewing the event directly. In other words, leads which are in the vicinity of the infarction will not demonstrate the normal QRS pattern; instead, there will be a deep "Q" wave where there used to be a normal QRS. This will also give a very significant axis deviation. The deeper the "Q" wave, the closer the lead is to the dead tissue.

Inferior Myocardial Infarction

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