The basics of the normal ECG have been described in the first five chapters. From this point on, will be concerned primarily with abnormal ECG patterns, beginning in this chapter with a consideration of the effects on the ECG of enlargement of the four cardiac chambers.
Several basic terms must first be defined. “Cardiac enlargement” refers to either dilation of a heart chamber or hypertrophy of the heart muscle. In dilation of a chamber the heart muscle is stretched and the chamber becomes enlarged. In cardiac hypertrophy the heart muscle fibers actually increase in size, with resulting enlargement of the chamber. When cardiac hypertrophy occurs, the total number of the heart muscle fibers does not increase; rather, each individual fiber becomes large. One obvious ECG effect of cardiac hypertrophy will be an increase in voltage of the P wave or QRS complex. Not uncommonly hypertrophy and dilation occur together.
Both dilation and hypertrophy usually result from some type of chronic pressure or volume load on the heart muscle. We will proceed with a discussion of the ECG patterns seen with enlargement of each of the four cardiac chambers, beginning with the right atrium.
RIGHT ATRIAL ENLARGEMENT (RAE)
Enlargement of the right atrium (either dilation or actual hypertrophy) may increase the voltage of the P wave. To recognize a large P wave, you must know the dimension of the normal P wave.
When the P wave is positive (upward), its amplitude is measured in millimeters from the upper level of the baseline, where the P wave begins, to the peak of the P wave. A negative (downward) P wave is measured from the lower level of the baseline to the lowest point of the P wave.
Normally the P wave in every lead is less than or equal to 2.5 mm (0.025 mV) in amplitude and less than 0.12 second (three small boxes) in width. A P wave exceeding either of these dimensions in any lead is abnormal.
Enlargement of the right atrium may produce an abnormally tall P wave (greater than 2.5 mm). However, because pure RAE does not generally increase the total duration of atrial depolarization, the width of the Pwave in RAE is sometimes referred to as P pulmonale because the atrial enlargement is often seen with severe pulmonary disease. Fig. 6-2 shows an actual example of RAE with a P pulmonale pattern.
The tall narrow P waves characteristic of RAE can usually best be seen in leads II, III, aVF, and sometimes V1. The ECG diagnosis of P pulmonale can e made by finding a P wave exceeding 2.5 mm in any of these leads. Recent echocardiographic evidence, however, suggests that the finding of a tall peaked P wave does not always correlate with RAE. On the other hand, patients may have RAE and not tall P waves.
LEFT ATRIAL ENLARGEMENT (LAE); LEFT ATRIAL ABNORMALITY (LAA)
Enlargement of the left atrium (either by dilation or by actual hypertrophy) also produces distinct changes in the P wave. Normally the left atrium depolarizes after the right atrium. Therefore, enlargement of the left atrium should prolong the total duration o atrial depolarization, indicated by an abnormally wide P wave. LAE characteristically produces a wide P wave of 0.12 second (three small boxes) or more duration. The amplitude (height) of the P wave in LAE may be either normal or increased.
The characteristic P wave changes seen in LAE. Sometimes, as shown, the P wave will have a distinctive “humped” or “notched” appearance. The second hump corresponds to the delayed depolarization of the left atrium. These humped P waves are usually best seen in one or more of the extremity leads. The term “P mitrale” is sometimes used to describe these wide P waves seen with LAE because they were first described in patients with rheumatic mitral valve disease.
In cases of LAE, lead V1 sometimes shows a distinctive biphasic P wave. This biphasic P wave has a small initial positive deflection and a prominent wide negative deflection. The negative component will be of > 0.04 second duration or >1 mm depth. The prominent negative deflection corresponds to the delayed stimulation of the enlarged left atrium.
Some patients particularly those with coronary artery disease, may show broad P waves without actual LAE. The abnormal P waves in these cases probably represent an atrial conduction delay. Therefore, the more general term “left atrial abnormality” is used by some authors in preference to left atrial “enlargement” to describe abnormally broad P waves.
RIGHT VENTRICULAR HYPERTROPHY (RVH)
Although atrial enlargement (dilation or hypertrophy) produces characteristic changes in the P wave, the QRS complex will be modified primarily by ventricular hypertrophy. The ECG changes that will be described indicate actual hypertrophy of the ventricular muscle and not simply ventricular dilation.
The ECG changes produced by both right and left ventricular hypertrophy can be predicted on the basis of what you already know about the normal QRS patterns. Normally the left and right ventricles depolarize simultaneously and the left ventricle is electrically predominant because it is normally the larger chamber. As a result, leads placed over the right side of the chest, such as lead V1, record rS-type complexes, in which the deep negative S wave indicates the spread of depolarization voltages away from the right side and toward the left side. Conversely, a lead placed over the left chest, such as V5 or V6, records a qR-type complex, in which the tall positive R wave indicates the predominantdepolarization voltages that point to the left generated by the left ventricle.
Now, if the right ventricle becomes sufficiently hypertrophied, this normal electrical predominance of the left ventricle can be overcome. In such case of RVH, what type of QRS complex might you expect to see in the right chest leads? With RVH, the right chest leads will show tall R waves, indicating the spread of positive voltages from the hypertrophied right ventricle toward the right. Instead of the rS complex normally seen in lead V1, we now see a tall positive (R) wave, indicating marked hypertrophy the right ventricle.
How tall an R wave in lead V1 do you have to see to make a diagnosis of RVH? As a general rule, the normal r wave in lead V1 in adults is usually smaller than the S wave in that lead. An R wave exceeding the S wave in lead V1 is suggestive, but not diagnostic, of RVH. Sometimes, a small q wave precedes the tall R wave in lead V1 in cases of RVH.
Although with tall right chest R waves, RVH also often produces two additional ECG signs: right axis deviation and right ventricular strain T wave inversions.
The normal mean QRS axis in adult lies approximately between –300 and +1000. A mean QRS axis of +1000 or more in called right axis deviation. One of the most common causes of right axis deviation is RVH. Therefore whenever you see an ECG with right axis deviation, you should search carefully for other confirmatory evidence of RVH.
RVH not only produces depolarization (QRS) changes but also affects repolarization (the ST-T complex). Hypertrophy of the heart muscle alters the normal sequence of repolarization. In RVH the characteristic repolarization change is the appearance of inverted T wave in the right and middle chest leads. These right chest T wave inversions are referred to as a right ventricular strain pattern. (Strain is a descriptive term. The exact mechanism for the strain pattern is not understood)
The ECG changes produced by LVH, like as noted, the left ventricle is electrically predominant over the right ventricle and produces prominent S waves in the right chest leads and tall R waves in the left chest leads. When LVH is present, the balance of electrical forces is tipped even further to the left. Thus, when LVH is present, the chest leads will show abnormally tall R waves (left chest leads) and abnormally deep S waves (right chest leads).
The following criteria and guidelines have been established to help in the ECG diagnosis of LVH:
If the depth of the S wave in lead V1 (SV1) added to the height of the R wave in either lead V5 or V6 (RV5 or RV6) exceeds 35 mm (3.5 mV), then suspect LVH.
You should also realize that high voltage in the chest leads in commonly seen as a normal finding, particularly in young adults with thin chest walls. Consequently, high voltage in the chest leads (SV1 + R V5 or RV6 > 35 mm) is not a specific indicator of LVH.
In some cases LVH will produce tall R waves in lead aVL. And R wave of 13 mm or more in lead aVL is another sign of LVH. Occasionally a tall R wave in lead aVL may be the only ECG sign of LVH and the voltage in chest leads may be normal. In other cases the chest voltages may be abnormally high, with a normal R wave in lead aVL.
Furthermore, just as RVH is associated with a right ventricular strain pattern, so left ventricular strain ST-T changes are often seen in LVH. Notice that the ST-T complex has a distinctive asymmetric appearance, with slight ST-T segment depression followed by a broadly inverted T wave. In some cases these left ventricular strain T wave inversions may be very deep. The left ventricular strain pattern is seen in leads with tall R waves.
With LVH the electrical axis usually horizontal. Actual left axis deviation (axis –300 or more negative) may also be seen. In addition, the QRS complex may become wider. Not uncommonly patients with LVH will eventually develop complete left bundle branch block.
Finally, ECG signs of LAE (broad notched P waves in the extremity leads or wide biphasic P waves in lead V1) are often seen in patients with ECG evidence of LVH. Most conditions that lead to LVH ultimately produce LAE as well
A variety of clinical conditions are associated with LVH. In adults, three of the most common are (1) valvular heart disease, such as aortic stenosis, aortic regurgitation, or mitral regurgitation, (2) hypertension, and (3) cardiomyopathies.
VII. Ventricular Conduction Disturbances
Bundle Branch Blocks
The normal process of ventricular stimulation was outlined in Chapter 4. The electrical stimulus reaches the ventricles from the atria by way of the AV junction. As mentioned, the first part of the ventricles normally stimulated (depolarized) is the left side of the ventricular septum. Soon after, the depolarization spreads to the main mass of the left and right ventricles by way of the left and right bundle branches. Normally the entire process of ventricular depolarization is completed within 0.1 second. Therefore, the normal width of the QRS complex is less than or equal to 0.1 second (two and a half small boxes on the ECG graph paper). Any process that interferes with the normal stimulation of the ventricles may prolong the QRS width. In this chapter we will be concerned primarily with the effects of blocks within the bundle branch system on the QRS complex.
RIGHT BUNDLE BRANCH BLOCK (RBBB)
Consider, first, the effect of cutting the right bundle branch. Obviously this will delay right ventricular stimulation and widen the QRS complex. Furthermore, the shape of the QRS complex with a right bundle branch block (RBBB) can be predicted on the basis of some familiar principles.
Normally, as noted above, the first part of the ventricles to be depolarized is the interventricular septum. The left side of the interventricular septum is stimulated first (by a branch of the left bundle). This septal depolarization produces the small septal q wave in lead V6 seen on the normal ECG. Clearly, RBBB should not affect this first septal phase of ventricular stimulation, since the septum is stimulated by a part of the left bundle.
The second phase of ventricular stimulation is the simultaneous depolarization of the left and right ventricles. RBBB should not effect this phase either, since the left ventricle is normally electrically predominant, producing deep S waves in the right chest leads and tall R waves in the left chest leads.
The change in the QRS complex produced by RBBB is a result of the delay in the total time needed for stimulation of the right ventricle. This means that following the completion of left ventricular depolarization, the right ventricle continues to depolarize. This delayed right ventricular depolarization produces a third phase of ventricular stimulation. The electrical voltages in the third phase are directed to the right, reflection the delayed depolarization and slow spread of the depolarization wave outward through the right ventricle. Therefore a lead placed over the right side of the chest will record this third phase if ventricular stimulation as a positive wide deflection (R’wave). The same delayed and slow right ventricular depolarization voltages spreading to the right will produce a wide negative (S wave) deflection in the left chest leads. T wave inversions in the right chest leads are a characteristic finding in RBBB. These T wave inversions are referred to as secondary changes because they are related to the abnormal process of ventricular stimulation.
ECG criteria in RBBB
I, V5, V6 qRS, (slurred and wide S waves.)
QRS > or = 0.12”
ST segment slight depression, T waves inversion.
Complete vs Incomplete RBBB
RBBB can be further divided into complete and incomplete forms depending on the width of the QRS complex. Complete RBBB is defined by a QRS complex (rSR’ in lead V1 and qRS in V6) of 0.12 second or more width. Incomplete RBBB shows the QRS shape described in the preceding section but the QRS duration is between 0.1 and 0,12 second.
RBBB may be caused by a number of factors. First, some normal people will show an RBBB pattern without any underlying heart disease; therefore, RBBB per se is not necessarily abnormal. In many persons, however, RBBB is associated with organic heart disease. RBBB may be caused by any conditions that affect the right side of the heart. In some cases, individuals (particularly older people) develop RBBB because of chronic degenerative changes in the conduction system. RBBB may also occur with myocardial ischemia and infarction. Pulmonary embolism, which produces acute right-sided heart strain, may also produce RBBB.
The conduction disturbance does not, in itself, require any specific treatment.
LEFT BUNDLE BRANCH BLOCK (LBBB)
Left bundle branch block (LBBB) also produces a pattern with a widened QRS complex. However, the shape of the QRS complex with LBBB is very different from that with RBBB. The reason for this difference is that RBBB affects mainly the terminal phase of ventricular activation. LBBB, on the other hand, affects the early phase of ventricular depolarization as well.
Recall that the first phase of ventricular stimulation-depolarization of the left side of the septum-is started by a part of the left bundle branch. LBBB, therefore, will block this normal pattern of septal depolarization. When LBBB is present, the septum depolarizes from right to left and not from left to right. Thus the first major change on the ECG produced by LBBB will be a loss of the normal septal r wave in lead V1 and the normal septal q wave in lead V6. Furthermore, the total time for left ventricular depolarization will be prolonged with LBBB, resulting in an abnormally wide QRS complex. Lead V6 will show a wide entirely positive (R) wave. The right chest leads record a negative QRS (QS) complex because the left ventricle is still electrically predominant with LBBB and produces greater voltages than the right ventricle. The major change is that the total time for completion of left ventricular depolarization is delayed. Therefore, with LBBB, the entire process of ventricular stimulation is oriented toward the left chest leads-the septum depolarizing from right to left, with stimulation of the electrically predominant left ventricle prolonged.
Just as there are secondary T wave inversions with RBBB, so there are also secondary T wave inversions with LBBB. The T wave in the leads with tall R waves is inverted. This T wave inversion is characteristic of LBBB. However, T wave inversions in the right precordial leads cannot be explained solely on the basis of LBBB and, if present, reflect some primary abnormality, such as ischemia. Occationally an ECG will show wide QRS complexes that are not typical of an RBBB or LBBB pattern. In such cases, the general term intraventricular delay is used.
ECG criteria in LBBB
V1 QS or rS with a wide S wave
I, V5, V6 a notched, wide tall R wave without a preceding q wave.
QRS > or = 0.12”
ST segment depression, T waves inversion in leads with a predominant R wave.
Complete vs incomplete LBBB
As with RBBB, there are complete and incomplete forms of LBBB. With complete LBBB, the QRS complex has the characteristic appearance described previously, and the QRS complex is 0.12 second or wider. With incomplete LBBB, the QQRS complex is between 0.1 and 0.12 second.
Unlike, RBBB, which is occasionally seen n normal people, LBBB is usually a sign of organic heart disease. LBBB is often seen in elderly patients with chronic degenerative changes in their myocardial conduction system. LBBB may develop in patients with long-standing hypertensive heart disease, with valvular lesions or the different types of cardiomyopathy. LBBB is also seen in patients with coronary artery disease. Most patients with LBBB have underlying left ventricular hypertrophy. When LBBB occurs with an acute myocardial infarction it is often a forerunner of complete heart block. In rare instances some otherwise normal individuals will show an LBBB pattern.
We will conclude this chapter on ventricular conduction disturbances by introducing a slightly more complex but important topic, the hemiblocks. Up to now we have discussed the left bundle branch system as if it were a single pathway. Actually it has been known for many years that the left bundle subdivides into major two branches, or fascicles (fasciculus, latin, small bundle). The left bundle subdivides into an anterior fascicle and a posterior fascicle. The right bundle branch, on the other hand, is a single pathway and consists of just one main fascicle or bundle.
A block in either fascicle of the left bundle branch system is called a hemiblock. Recognition of hemiblocks on the ECG is intimately related to the subject of axis deviation, presented in chapter 5. Somewhat surprisingly, a hemiblock (unlike a full left or right bundle branch block) does not widen the QRS complex markedly. It has been found experimentally that the main effect of cutting these fascicles is to markedly change the QRS axis. Specifically, left anterior hemiblock results in a marked left axis deviation (- 450 or more); left posterior hemiblock produces a right axis deviation (+ 1200 or more).
Left anterior hemiblock. Left anterior hemiblock is diagnosed by finding a mean QRS axis of – 450 or more and a QRS width of less than 0.12 second. A mean QRS axis of – 450 or more negative can be easily recognized because left axis deviation is present and the S wave in lead aVF equals or exceeds the R wave in lead 1. rS wave in leads II, III, and aVF, S III > S II.
Left posterior hemiblock. Left posterior hemiblock is diagnosed by finding a mean QRS axis of + 1200 or more, with a QRS width of less than 0.12 second. However, the diagnosis of left posterior hemiblock can be considered only if other, more common, causes of right axis deviation (right ventricular hypertrophy, normal variant, emphysema, lateral wall infarction, and pulmonary embolism) are first excluded.
Left anterior hemiblock is relatively common, while isolated left posterior hemiblock is rare. We will discuss the clinical importance of the hemiblocks and bifascicular and trifascicular blocks further in the section on complete heart block. In general, the finding of isolated left anterior or left posterior hemiblock is not of much clinical significance.
VIII Myocardial Ischemia and Infarction-1
Transmural Infarct Patterns
Myocardial cells require oxygen and other nutrients to function. Oxygenated blood is supplied by the coronary arteries. If blood flow becomes inadequate due to severe narrowing or complete blockage of a coronary artery, ischemia of the heart muscle will develop. The term “ischemia” means literally “to hold back blood.” Myocardial ischemia may occur transiently. For example,. patients who experience angina pectoris with exercise are having transient myocardial ischemia. If the ischemia is more severe, actual necrosis (depth) of a portion of heart muscle may occur. The term “myocardial infarction” (MI) refers to myocardial necrosis caused by severe ischemia.
TRANSMURAL AND SUBENDOCARDIAL ISCHEMIA
The left ventricle can be subdivided into an outer layer, the epicardium, and an inner layer, the subendocardium. This distinction is important because myocardial ischemia or infarction is sometimes limited to just the inner layer (subendocardial ischemia and infarction) and sometimes affects the entire thickness of the ventricular wall (transmural ischemia and infarction).
Transmural infarction, as mentioned, is characterized by ischemia and ultimately, by necrosis of a portion of the entire thickness of the left ventricular wall. Not surprisingly, transmural infarction produces changes in both myocardial depolarization (QRS complex) and myocardial repolarization (ST-T complex.)
The earliest changes seen with an acute transmural infarction occur in the ST-T complex. There are two sequential phases to these ST-T changes seen with MI: the acute phase and the evolving phase. The acute phase is marked by the appearance of ST segment elevations and sometimes tall positive (hyperacute). T waves in certain leads. The evolving phase (occurring after hours or days) is characterized by the appearance of deep T wave inversions in those leads that previously showed ST elevations.
Transmural MI can also be described in terms of the location of the infarct: anterior means involving the anterior and/or lateral wall of the left ventricles (chest leads V1 to V6, limb leads 1 and aVL): inferior means involving the inferior (diaphragmatic) wall of the left ventricle.(leads II, III and aVF). For example, with an acute anterior wall MI the ST segment elevations and tall hyperacute T waves appear in one or more of the anterior leads.
One of the most important characteristics of the ST-T changes seen in MI is their reciprocity. The anterior and inferior leads tend to show inverse patterns. Thus in an anterior infarction with ST segment elevations in leads V1 to V6, 1, and aVL, leads II, III and aVF will characteristically show ST segment depression.
The ST segment elevation seen in acute MI is called a “current of injury” and indicates the acute injury to the epicardial layer of the heart, which occurs with transmural infarction. The ST segment elevations (and reciprocal ST depressions) are the earliest ECG signs of infarction and are generally seen within minutes of the infarct. As mentioned previously, tall positive (hyperacute) T waves may also have the same significance as the ST elevations. In some cases hyperacute T waves actually precede the appearance of ST elevation.
After a variable time lag of hours to days, the ST segment elevations start to return to the baseline. At the same time the T waves begin to be inverted in leads that previously showed ST segment elevations. This phase of T wave inversions is called the evolving phase of the infarct. Thus, with an anterior wall infarction the T waves become inverted in one or more of the anterior leads (V1 to V6, I, aVL). With an inferior wall infarction the T waves become inverted in one or more of the inferior leads (II, III, aVF).
QRS Changes: Q Waves of Transmural Infarction
Transmural infarction also produces distinctive changes in the QRS (depolarization) complex. The characteristic sign of a transmural infarct is the appearance of new Q waves. A Q wave in any lead simply indicates that the electrical voltages are directed away from that particular lead. When transmural infarction occurs, there is necrosis of heart muscle in a localized area of the ventricle; therefore the electrical voltages produced by this portion of the myocardium will disappear. Instead of positive (R ) waves over the infarcted area. Q waves will be recorded (either a QR or a QS complex).
LOCALIZATION OF INFARCTS
As mentioned, MIs are generally localized to a specific portion of the left ventricle, affecting either the anterior or the inferior wall. Anterior infarcts are sometimes considered as anteroseptal, strictly anterior, or anterolateral depending on the leads that show signs of the infarct.
Anterior wall Infarcts
The characteristic feature of anterior wall infarcts is a loss of the normal R wave progression in the chest leads. Normally there is a progressive increase in the height of the R wave as you move from the right to the left chest leads. An anterior infarct interrupts this normal R wave progression, resulting in pathologic Q waves in one or more of the chest leads.
Anteroseptal infarcts. Normally, as mentioned earlier, the ventricelar septum is depolarized from left to right. So leads V1 and V2 show small positive r waves (septal r waves), consider the effect of damaging the septum. Clearly, you would expect to see a loss of septal depolarization voltages; thus, in leads V1 and V2 the normal septal r waves will be lost and an entirely negative QS complex will appear.
The septum is supplied with blood by the left anterior descending coronary artery, and septal infarction generally suggests that there has been an occlusion of this artery or one of its branches.
Strictly anterior infarcts. Normally leads V3 and V4 show RS- or Rs-type complexes. If the anterior wall of the left ventricle is infarcted, then the positive R waves that reflect the voltages produced by this muscle area will be lost. Instead, Q wave, as part of QS or QR complexes, Q waves, as part of QS or QR complexes will be seen in leads V3 and V4. Strictly anterior infarcts generally also result from occlusion of the left anterior descending coronary artery.
Anterolateral infarcts. Infarction of the lateral wall of the left ventricle produces changes in the more laterally situated chest leads, for example, leads V5 and V6. With lateral wall infarction, abnormal Q waves, as part of QS or QR complexes, appear in leads V5 and V6. Lateral wall infarction is often caused by an occlusion of the left circumflex coronary artery but may also result from occlusion of the left anterior descending coronary artery or a branch of the right coronary artery.
Differentiating anterior wall infarctions. The above classification of anterior infarcts – as anteroseptal, strictly anterior, and anterolateral – is not absolute. Often there is overlap. You can simply describe Mis by calling any infarct that shows ECG changes in one or more of leads I, aVL, and V1 to V6 as “anterior” and then specifying which leads show Q waves and ST-T changes.
Inferior wall infarcts
Infarction of the inferior (diaphragmatic) portion of the left ventricle is indicated by changes in leads II, III, and aVF. These three leads, as shown in the frontal plane axis diagram, are oriented downward or inferiorly. Thus these leads will record voltages from the inferior portion of the ventricle. An inferior wall infarct will produce abnormal Q waves in leads II, III, and aVF.
Inferior wall infarction is generally caused by occlusion of the right coronary artery and, less commonly, by a left circumflex coronary obstruction.
The posterior (back) surface of the left ventricle can also be infarcted. This may be difficult to diagnose because characteristic abnormal ST elevations may not appear in any of the 12 conventional leads. Instead, a tall R wave and ST segment depression may occur in chest leads V1 and V2 (reciprocal to the Q wave and ST segment elevations that would be recorded at the back of the heart). During the evolving phase if such infarcts, when deep T wave inversions appear in the posterior leads, the anterior chest leads will show reciprocally tall positive T waves.
In most cases of posterior MI the infarct extends either to the lateral wall of the left ventricle, producing characteristic changes in lead V6, or to the inferior wall of the left ventricle, producing characteristic changes in leads II, III, and aVF. Because of the overlap between inferior and posterior infarcts the more general term “inferoposterior” can be used when the ECG shows changes consistent with either inferior or posterior infarction.
Right Ventricular (RV) Infarcts
A related topic is right ventricular (RV) infarction. Recent studies show that a high percentage of patients with an inferoposterior infarct have associated RV involvement. In one autopsy study RV infarction was noted in about one of four cases of inferoposterior MI but not in cases of anterior MI. Clinically patients with an RV infarct may have elevated central venous pressure (distended neck veins) because of the abnormally high diastolic filling pressures in the right side of the heart. If the RV damage is severe, hypotension and even cardiogenic shock may result. AV conduction disturbances are not uncommon in this setting. The presence of jugular venous distension in a patient with an acute inferoposterior MI should always suggest this diagnosis. In addition, many of these patients will show ST segment elevations in leads reflecting the right ventricle, such as V1 to V3 and V3R to V5R.
Recognition of RV infarction is of major clinical importance. Volume expansion may be critical in patients who are hypotensive and have a low or normal pulmonary capillary wedge pressure despite elevated systemic venous pressure. Patients with an acute RV infarct may also be at increased risk for the development of ventricular fibrillation during placement of a temporary pacemaker.
Subendocardial Ischemia and Infarct Patterns
Transmural myocardial infarction (MI) may be associated with abnormal Q waves and typical progression of ST-T changes described in Chapter 8. In other cases (described in this Chapter), however, myocardial ischemia with or without actual infarction may be limited to the subendocardial layer of the ventricle.
The most common ECG change with subcardial ischemia is ST segment depression. The ST segment depression caused by subendocardial ischemia nay be limited to the anterior leads or to the inferior leads, or may be seen more diffusely in both groups of leads. The ST segment depression seen with subendocardial ischemia has a characteristic squared-off shape. (ST segment elevations may be seen in lead aVR.)
ECG Changes with Angina pectoris
The term “angina pectoris” refers to transient attacks of chest pain caused by myocardial ischemia. Angina is a symptom of coronary artery disease. The classic attack of angina is experienced as a dull, burning, or boring substernal pressure or pain. angina is typically precipitated by exertion, stress, exposure to cold, and so on, and is relieved by rest and nitroglycerin.
Many patients with classic angina will show an ECG pattern of subendocardial ischemia, with ST segment depressions during an attack. When the pain disappears, the ST depressions generally return to the baseline. Not all patients with angina will show ST depressions during chest pain. The presence of a normal ECG does not rule out underlying coronary artery disease. However, the appearance of transient ST segment depression with chest pain is a strong indicator of myocardial ischemia.
Similar ST segment depressions may develop during exercise (with or without chest pain) in people with ischemic heart disease. Recording the ECG during exercise (stress electrocardiography) is a method of determining the presence of ischemic heart disease. ST segment depression of 1 mm or more, lasting 0.08 second or more, is generally considered a positive (abnormal) response. However, false-negative (normal) results can occur in patients with ischemic heart disease and false-positive results can occur in normal people.
If the ischemia to the subecdocardial region is severe enough, actual subendocardial infarction may occur. In such cases the ECG may show persistent ST segment depression instead of the transient ST depressions seen with reversible subendocardial ischemia.
Do Q waves appear with pure subendocardial infarction? The answer is that if only the subendocardium is infarcted abnormal Q waves are seen only with transmural infarction. Subendicardial infarction generally affects ventricular repolarization (ST-T complex) and not depolarization (QRS complex). However, exceptions may occur.
Another pattern sometimes seen in cases of nontransmural (non-Q wave) infarctions is T wave inversion with or without ST segment depressions.
ECG Changes Associated with Noninfarctional Ischemia
Prinzmetal’s angina occurs in patients who develop transient ST segment elevations, suggestive of epicardial or transmural ischemia, during attacks of angina. These patients have atypical chest pain, which occurs at rest or at night, in contrast to classic angina, which is typically exertional and is associated with ST segment depressions. Prinzmetal’s (variant) angina pattern is generally a marker of coronary artery spasm with or without underlying coronary obstructions.
The ST segment elevations of acute transmural MI can be simulated by the ST segment elevations of Prinzmeral’s angina as well as by the normal variant ST segment elevations seen in some healthy people (“early repolarization pattern”) and by the ST segment elevations of acute pericarditis.
The abnormal ST segment depressions of subendocardial ischemia or infarction can be simulated by the pattern of left ventricular strain, digitalis effect, or hypokalemia.
T wave inversions may be a sign of ischemia or infarction but may also occur in a variety of other settings, including normal variants, ventricular strain, pericarditis, subarachnoid hemorrhage, secondary ST-T changes due to bundle branch block, and so on.
x. Miscellaneous ECG Patterns
WOLFF-PARKINSON-WHITE SYNDROME (WPW)
The Wolff-Parkinson-White (WPW) syndrome is an unusual and distinctive ECG abnormality caused by pre-excitation of the ventricles. Normally the electrical stimulus passes to ventricles from the atria via the AV junction. The physiologic lag of conduction through the AV junction results in the normal PR interval of 0.12 to 0.2 second. Imagine the consequences of having an accessory conduction pathway between the AV junction and pre-excite the ventricles. This is exactly what occurs in the WPW syndrome: an accessory conduction fiber (the bundle of Kent) connects the atria and ventricles, bypassing the AV junction.
Pre-excitation of the ventricles in the WPW syndrome produces the following three characteristic changes on the ECG:
The PR interval is shortened (often but not always <0.12 sec) because of ventricular pre-excitation.
The QRS complex is widened, giving the superficial appearance of a bundle branch block pattern. The wide QRS in the WPW syndrome is caused not by a delay in ventricular depolarization but by early stimulation of the ventricles. The QRS complex will be widened to the degree that the PR interval is shortened.
There is slurring, or notching, of the upstroke of the QRS complex. This is called a delta wave.
The significance of the WPW syndrome is twofold. First, patients with this pattern are prone to atrial arrhythmias, especially paroxysmal atrial tachycardia and atrial fibrillation. Second, the ECG of these patients is often mistaken as indicating a bundle branch block or myocardial infarction.
The WPW syndrome predisposes to paroxysmal atrial tachycardia in particular because of the accessory conduction pathway. For example, an impulse traveling down the AV junction may recycle up the bundle of Kent and then back down the AV junction, and so on. This type of reentry mechanism (circus movement) may also account for other types of tachycardias.
Another type of pre-1excitation variant, the Lown-Ganong-Levine (LGL) pattern, is caused by a bypass tract (James fiber) that connects the atria and AV junction. Bypassing the AV node results in a short PR interval (less than 0.12 sec). However, the QRS width will not be prolonged because ventricular activation occurs normally. Therefore, the LGL pattern consists of a short PR interval with a normal-width QRS and no delta wave; the WPW syndrome consists of a short PR interval with a wide QRS and delta wave. Patients with the LGL pattern may also have “reentrant” paroxysmal atrial tachycardia (PAT).
NORMAL SINUS RHYTHM (NSR)
The diagnosis of normal, or regular, sinus rhythm (NSY) was already described in Chapter 3. When the sinus (SA) node is pacing the heart, atrial depolarization spreads from right to left and downward toward the AV junction. An arrow representing this atrial depolarization wave will point downward and toward the left. Therefore, as described earlier, with NSR, the P wave is negative in lead aVR and reciprocally positive in lead II.
By convention, NSR is defined as sinus rhythm with a heart rate between 60 and 100 beat/min. Sinus rhythm with a heart rate of less than 60 beat/min is called sinus bradycardia; one with a heart rate greater than 100 beat/min is called sinus tachycardia.
REGULATION OF THE HEART RATE
The heart, like the other organs, has a special nerve supply from the autonomic nervous system, which controls involuntary muscle action. The autonomic nerve supply to the heart consists of two opposing groups of never fibers: the sympathetic nerves and the parasympathetic nerves. The sympathetic fibers supply the sinus node, the atria, the AV junction, and the ventricles. Sympathetic stimulation produces an increased heart rate and also increases the strength of myocardial contraction. The parasympathetic nervous supply to the heart is from the vagus nerve, which supplies the sinus node, atria, and AV junction. Vagal stimulation produces a slowing of the heart rate as well as a slowing of conduction through the AV junction. In this way, the autonomic nervous system exerts a counterbalancing control of heart rate. The sympathetic nervous system acts as a cardiac accelerator, while the parasympathetic (vagal) fibers produce a braking effect. For example, when you become excited or upset, increased sympathetic stimuli (and diminished parasympathetic tone) result in an increased heart rate and increased contractility, producing the familiar sensation of a pounding heart (palpitations).
Sinus tachycardia is simply sinus rhythm with a heart rate exceeding 100 beats/min. Generally in adults the heart rate with sinus tachycardia is between 100 and 180 beats/min. in sinus tachycardia, each QRS complex is preceded by a P wave. Note that the P waves are positive in lead II. With sinus tachycardia at very fast rates, the P waves may merge with the preceding T wave and become difficult to distinguish.
The following conditions are commonly associated with sinus tachycardia:
Anxiety, emotion, and exertion
Drugs such as epinephrine, ephedrine, and isoproterenol (isoprel) that increase sympathetic tone
Drugs such as atropine that block vagal tone
Congestive heart failure (Sinus tachycardia caused by increased sympathetic tone is generally seen with pulmonary edema.)
Pulmonary embolism (Sinus tachycardia ia the most common arrhythmia seen with acute pulmonary embolism)
Acute myocardial infarction, which may produce virtually any arrhythmia (Sinus tachycardia persisting after an acute infarct is generally a bad prognostic sign and implies extensive heart damage.)
Hyperthyroidism (Sinus tachycardia occurring at rest is a common finding.)
Hypotension and shock associated with myocardial infarction, sepsis, or blood loss
With sinus bradycardia, sinus rhythm is present and the heart rate is less than 60 beats/min. It is commonly occurs in the following conditions:
as a normal variant (Many normal people have a resting pulse rate of less than 60 beats/min, and trained athletes may have a pulse rate as low as 35 beats/min.)
Drugs that increase vagal tone, such as digitalis or edrophonium (Tensilon), or that decrease sympathetic tone, such as propranolol (Inderal) or reserpine (In addition, calcium channel-blocking drugs such as diltiazem hydrochloride and verapamil may cause marked sinus bradycardia.)
Hypothyroidism (This is generally associated with a sinus bradycardia, just as hyperthyroidism produces a resting sinus tachycardia.)
“sick sinus syndrome” (Some patients, particularly among the elderly, will have marked sinus bradycardia without obvious cause, probably from degenerative disease of the sinus node.
Sleep apnea syndrome
Carotid sinus syndrome
Even in healthy persons the sinus node does not pace the heart at a perfectly regular rate. Actually, there is normally a slight beat-to-beat variation in sinus rate. Sometimes, when this beat-to-beat variability in sinus rate is more accentuated, the term “sinus arrhythmia” is used. Sinus arrhythmia, therefore, is sinus rhythm with an irregular rate. The variation of the P-P interval is grater than 0.12 seconds.
The most common cause of sinus arrhythmia is respiration. With inspiration the heart rate normally increases slightly; with expiration it slows slightly. This respiratory, or phasic, sinus arrhythmia is caused by slight changes in vagal tone occurring during the different phases of respiration.
Occasionally a nonphasic sinus arrhythmia occurs, and the heart rate varies from beat to beat without relation to the respiratory cycle.
Phasic sinus arrhythmia is a normal finding. Particularly in children. A nonphasic sinus arrhythmia, while not strictly normal, does not have any special pathologic or therapeutic significance.
SINUS ARREST AND ESCAPE BEATS
Suppose for some reason the sinus node fails to function for one or more beats. Such failure of the sinus node to pace is called sinoatrial block (SA block). SA block may occur intermittently, where there is simply a missing beat (no P wave or QRS complex) at occasional intervals, or it may be more extreme. Sinus pause or arrest is the sinus node fails to function altogether for a prolonged period. This type of block will lead to cardiac arrest with asystole unless the sinus node regains function or some other pacemaker (escape pacemaker) takes over. Fortunately, as mentioned earlier, other parts of the cardiac conduction system are capable of producing electrical stimuli and functioning as an escape pacemaker in these circumstances. Escape beats may come from the atria, the AV junction, or the ventricles.
SA block and sinus arrest can be caused by numerous factors, including hypoxia, myocardial ischemia, hyperkalemia, digitalis toxicity, and toxic reactions to other drugs such as the beta-blockers and calcium-channel blockers. In elderly people the sinus node may undergo degenerative changes and fail to function effectively. The term “sick sinus syndrome” is used to refer to this type of sinus node dysfunction.
SICK SINUS SYNDROME AND THE BRADY-TACHY SYNDROME
The term “ sick sinus syndrome” has been coined to describe patients who develop sinus node dysfunction that causes marked sinus bradycardia, sinus arrest, or junctional escape rhythms, which may lead to symptoms of light-headedness and even syncope.
In some patients with the sick sinus syndrome, these bradycardic episodes alternate with periods of tachycardia (for example, paroxysmal atrial tachycardia, atrial fibrillation, or even ventricular tachycardia). Sometimes the bradycardia will occur immediately after spontaneous termination of the tachycardia. The term “brady-tachy syndrome” has been used to describe this subset of patients with sick sinus syndrome who have tachyarrhythmias as well as bradyarrhythmia.
2. Supraventricular Arrhythmias – 1
Premature Atrial Contractions, Paroxysmal Atrial Tachycardia, AV junctional Rhythms The normal pacemaker of the heart is the sinus node, and normally it initiates each heartbeat. However, pacemaker stimuli can arise from other parts of the heart-the atria, the AV junction, or the ventricles. The terms “ectopy,” “ectopic pacemaker,” and “ectopic beat” are used to describe these nonsinus beats. Ectopic beats are often premature; that is, they come before the next sinus beat is due. Thus we may find premature atrial contractions (PACs), premature AV junctional contractions (PJCs), and premature ventricular contractions (PVCs). Ectopic beats can also come after a pause in the normal rhythm, as in the case of AV junctional or ventricular escape beats. Ectopic beats originating in the AV junction or atria are referred to as supraventricular (that is, coming from above the ventricles).
PREMATURE ATRIAL CONTRACTIONS (PACs)
Premature atrial contractions (PACs) are ectopic beats arising from somewhere in either the left or the right atrium but not in the sinus node. The atria, therefore, are depolarized from an ectopic site. Following atrial stimulation, the stimulus will spread normally through the AV junction into the ventricles. For this reason, ventricular depolarization (QRS) is generally not affected by PACs.
PACs have the following major features:
The beat is premature, occurring before the next normal beat is due. This is in contrast to escape beat, which come after a pause in the normal rhythm.
The PAC is often, but not always, preceded by a visible P wave. This P wave usually has a slightly different shape and/or slightly different PR interval from the P wave seen with the normal sinus beats. The PR interval of the PAC may be either longer or shorter than the PR interval of the normal beats.
Following the PAC there is generally a slight pause before the normal sinus beat resumes.(incomplete compensatory pause)
Occasionally, no clear P wave will be seen preceding the PAC. In such cases the P wave may be “buried” in the T wave of the preceding beat.
The QRS complex of the PAC is usually identical or very similar to the QRS complex of the preceding beats. Remember that with PACs the atrial pacemaker is in an ectopic location, but the ventricles are depolarized in a normal way. This contrasts with premature ventricular contractions where the QRS complex is abnormally wide because of abnormal depolarization of the ventricles. Occasionally, PACs will result in aberrant ventricular conduction so the QRS is wider than normal. Differentiation of such PACs “with aberration” from premature ventricular contractions may be difficult.
Sometimes, when the PAC is very premature, the stimulus will reach the AV junction shortly after it has already been stimulated by the preceding normal beat. Because the AV junction, like all other conduction tissue, requires time to recover its capacity to conduct impulses, this premature atrial stimulus may reach the junction when it is still refractory. In such cases the PAC may not be conducted to the ventricles and no QRS complex will appear. This situation will result in a blocked PAC. The ECG will show a premature P wave not followed by a QRS complex. Following the blocked P wave, there is a slight pause before the next normal beat resumes. The blocked PAC, therefore, produces a slight irregularity of the heartbeat. If you do not search carefully for these blocked PACs you will overlook them.
PACs may occur frequently (for example, five or more times/min) or sporadically. Two PACs occurring consecutively are referred to as “paired PACs.” Sometimes, each sinus beat is followed by a PAC. This pattern is referred to as atrial bigeminy.
PACs are very common. They may occur both in persons with normal hearts and in persons with organic heart disease. Finding PACs, therefore, does not imply that the person has cardiac disease. In normal subjects PACs may be seen with emotional stress, with excessive coffee drinking, or as a result of sympathomimetic drugs. PACs may produce palpitations-the patient may complain of feeling a skipped beat or an irregular pulse. PACs, as noted, may also be seen with any type of heart disease. Frequent PACs are sometimes the forerunner of atrial fibrillation or paroxysmal atrial tachycardia.
PAROXYSMAL ATRIAL TACHYCARDIA (PAT)
Paroxysmal atrial tachycardia (PAT) is the second tachyarrhythmia we shall discuss. The first was sinus tachycardia. PAT is simply a run of three or more consecutive PACs.
In some cases, the run of PAT may be brief and self-limited. In other cases, it may be sustained for hours, days, or even weeks.
PAT has the following characteristics:
The heart rate with PAT is generally between 140 and 250 beats/min. Recall that with sinus tachycardia the heart rate in adults did not generally exceed 160 to 180 beats/min.
PAT is usually extremely regular. Each beat falls exactly on time, and the RR intervals between beats do not generally show any variability. This also contrasts with sinus tachycardia, in which there is generally some slight but discernible beat-to-beat variability.
P waves may or may not be visible. When seen, they are generally different from the P waves in a patient with normal sinus rhythm. The PR interval may be the same as, greater than, or less than the patient’s usual PR interval.
The QRS complexes are usually of normal width, since intraventricular conduction is generally normal with PAT. (A wide QRS complex will be seen if the patient has an underlying bundle branch block or if the PAT induces a “rate-related” bundle branch block.)
PAT may be seen both in normal persons and in those with organic heart disease. It , therefore, does not necessarily imply that the patient has any significant heart disease. PAT may also occur with heart disease of any type. Occasionally, a run of PAT in a patient with limited cardiac reserve may precipitate angina pectoris or congestive heart failure.
AV JUNCTIONAL RHYTHMS
With PACs and PAT the ectopic pacemaker is located somewhere in the atria outside the sinus node. Under certain circumstances, the AV junction may also function as an ectopic pacemaker, producing an AV junctional rhythm.
AV junctional rhythm shows the following features:
The P, when seen, is negative (downward) in lead II and positive (upward ) in lead aVR, just the reverse of the pattern seen with normal sinus rhythm. These are called retrograde P wave.
These retrograde P waves may precede or follow the QRS complex.
In some cases, retrograde P waves may be buried within the QRS complex. If this occurs, then the baseline between the QRS complexes remains completely flat.
AV junctional rhythms can be considered in two general classes-slow escape rhythms and tachycardias-depending on the rate. The slow junctionl escape rhythms are less than 60 beats/min. The junctional tachycardias have rates between 100 and 250 beats/min.