Hypertrophies and Intraventricular Conduction Defects

Hypertrophies and Intraventricular Conduction Defects Causes, Presentation, and Significance

Linda Josephson, MS, RN, CCRN-CMC

There is an increasing need for nurses to interpret a 12-lead electrocardiogram, both in critical care units and in other areas. This can be a challenging task, especially in the presence of hypertrophies, bundle-branch blocks, and fascicular blocks. This article reviews the pathophysiology of intraventricular blocks and hypertrophy, characteristics found in the 12-lead electrocardiogram, and discusses what the significance of these findings may be. Keywords: , Hypertrophies, Intraventricular conduction defects, Ischemic changes

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There is an increasing need for nurses to be able to cardiodynamic conditions or changes. Hypertrophy of the accurately interpret a 12-lead electrocardiogram (ECG). different chambers place patients at increased risk The accurate detection of ischemic changes and the con- for cardiovascular events and may be a contributing cause firmation of arrhythmic changes all require the accurate of intraventricular conduction defects themselves.3,4 Epi- interpretation of a 12-lead ECG.1 However, there has demiological studies on the prevalence of BBBs and hy- traditionally been less emphasis placed on nurses being pertrophies demonstrate that the prevalence of both these able to interpret a 12-lead ECG and a greater expectation conditions increases with age.3,5 As the population of the that nurses would be adept at detection using United States continues to age, there will be an increased a 1- or 2-lead monitoring system. Because of that, many prevalence for cardiac disturbances. The presence of both nurses who are currently in practice may not have re- these conditions indicates that the individual has a higher ceived instruction in nursing school on how to read a 12- risk of other cardiac comorbidities.6 lead ECG. Some nurses may not get all the education they This article reviews the pathophysiology of intraven- need in their critical care orientation program. As a result, tricular blocks and hypertrophy, characteristics found in nurses may not feel confident or comfortable in the in- the 12-lead ECG, and discusses what the significance of terpretation of a 12-lead ECG. Even for nurses who have these findings may be. taken a formal ECG course, interpreting an ECG may not always be done accurately.2 This may be especially chal- ANATOMY OF THE HEART’S ELECTRICAL lenging for some arrhythmias such as bundle-branch CONDUCTION SYSTEM blocks (BBBs), fascicular blocks, and hypertrophies. The sinoatrial node (SA node) is the pacemaker of the These conduction defects and hypertrophies can have heart. It is located high in the left atrium near the superior considerable clinical significance as precursors to other vena cava. The SA node is connected to the right atrium

DOI: 10.1097/DCC.0b013e3181f0be8d November/December 2010 259

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via Bachman bundle and to the atrioventricular (AV) node TABLE 1 Blood Supply to the Cardiac via internodal pathways that travel down the left atrium. Conduction System The AV node is located in the right atrium also, but low in the atrial wall just above the . It serves to Coronary slow the impulse SA node, to allow the atria to contract Structure Blood Supply Artery and push the last of the blood from the atria into the SA node RCA RCA ventricles just before the ventricular systole (Figure 1). AV node AV nodal artery from RCA RCA Conduction of the impulse continues down through Left anterior descending via septal LCA the bundle of His, which is a continuation of fibers from perforator arteries the AV node. The bundle of His continues for a short distance, and then it bifurcates, forming the right and left Right bundle branch Left anterior descending artery LCA bundle branches (LBBs). The right side of the bundle Left anterior fascicle Left anterior descending artery LCA becomes the right bundle branch (RBB), which is long and Left posterior fascicle Left anterior descending and LCA, RCA slender. It travels down the right side of the intraventricu- posterior descending artery lar septum to the base. At the base of the septum, the RBB diverges into the Purkinje fibers, which serves to stimulate Abbreviations: AV, atrioventricular; LCA, left coronary artery; RCA, right coronary the right to contract. artery; SA, sinoatrial. On the left side, the left common bundle continues for a short distance before it also bifurcates into the left anterior Normally, the bundle of His receives a dual blood fascicle (LAF) and the left posterior fascicle (LPF). The supply; the bundle receives blood from the left anterior LAF, like the RBB, is long and thin. It travels down the left descending (LAD) artery and the posterior descending ar- side of the intraventricular septal wall and runs toward the tery (PDA) (Table 1). anterior-superior papillary muscle. The RBB conducts the The RBB is supplied by the LAD artery. Because the impulse from the bundle of His to the anterior and lateral left RBB is a long and slender structure, it is vulnerable to ventricular (LV) wall. The posterior fascicle travels down the damage. However, this structure has many bifurcations posterior wall of the intraventricular septum in the direction that may be less turbulent. The LBB is much more robust of the posterior-inferior papillary muscle. It is responsible for than the RBB. The anterior and medial fascicles receive stimulating the posterior ventricular wall to contract.7,8 their blood supply from the LAD artery via the septal perforating branches of the LAD artery. The posterior fas- BLOOD SUPPLY TO THE CONDUCTION SYSTEM cicle, like the bundle of His, has a dual blood supply from 9,10 The right coronary artery (RCA) provides the blood sup- both the LAD artery and PDA (Figure 2). ply to the SA node in 55% of the population, and the left circumflex artery provides the blood supply to the SA VECTOR DEVELOPMENT OF THE QRS COMPLEX node in the remaining 45% of the population. The blood During depolarization of the heart, many vectors develop supply to the AV node is commonly supplied by the RCA as the myocardium contracts. However, to simplify the in the vast majority of the population, 90% or so. In the concept, the depolarization of the ventricles can be divided 10% of the population that does not have this arrange- into a 2-phase event.7,11 The first vector is developed when ment, the AV node is supplied by the left circumflex artery. the septal wall of the ventricles depolarizes. The septum

Figure 2. Blood supply to the conduction system. Courtesy of Figure 1. Conduction system. Abbreviation: AV, atrioventricular. ecgpedia, Rob Kreuger, medical illustrator; C. Carl Jaffe, MD, car- Courtesy of Wikimediacommons, drawing by Madhero88. Licensed diologist. Licensed under creative commons. http://creativecommons. under creative commons: http://creativecommons.org/licenses/by/2.5/. org/licenses/by/2.5/.

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Copyright @ 2010 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Hypertrophies and Intraventricular Conduction Defects depolarizes from the left side to the right. This creates a outflow tract of the left ventricle, exposing it to additional vector that travels in a rightward and slightly anterior stress. It is not uncommon to see a of the direction. On the surface ECG for leads that are on the RBB and the LAF. Both the RBB and LAF usually have a right side, such as aVR, and V1-V2, the first part of the single blood supply, usually from the LAD artery. The QRS complex is positive, and a small r wave is inscribed. single blood supply also makes them vulnerable to damage.

For leads that are on the left side, such as I, aVL, V5-V6, A block of the LPF is relatively rare. This is due to the because the septal vector moves away from the positive LPF being stronger and more robust fascicle, than either the electrode of the leads, the first part of the QRS complex is RBB or the LAF. Additionally, the LPF also has a dual blood negative and inscribes a small q wave. This is sometimes supply from both the right and left coronary artery system.8,9 called a septal q wave.9-11 The second phase of the ventricular depolarization is Right Bundle-Branch Block the activation of the free wall of the right and left ventricle. When a right BBB (RBBB) occurs, the septum continues to The free walls of both ventricles contract simultaneously. depolarize normally. The impulses from the SA node travel However, because the left ventricle has the greatest muscle to the AV node and then continue through the bundle of mass, it generates the greatest electrical force and domi- His and down the LBB as usual. The impulse depolarizes nates the morphology of the QRS complex. The contrac- the septum in the normal fashion, from left to right, and tion of the free wall of the ventricles produces the main then the left ventricle depolarizes.7 Then the impulses vector of the heart, which travels from right to left and travel from the left ventricle to the right ventricle, across somewhat downward.9-11 the septal wall and through the myocardium to stimulate The result of this is that in leads that are right-sided, aVR, the right ventricle and cause depolarization (Table 2).

V1 and V2, the deflection is seen primarily as a negative one On the surface ECG, the first portion of the QRS com- after the small initial r wave. The opposite is seen in those plex appears normal, reflecting that the initial vector is leads that are left-sided, I, aVL, V5 and V6;afterasmall caused by the septum depolarizing normally from right to initial q wave, the main deflection is positive.7,10 left. This produces a small r wave in right-sided leads: aVR

This causes the ‘‘r’’ wave of the QRS complex to and V1-V2, and a small q wave in the left-sided leads: I, become increasingly taller as the ECG is recorded across aVL, and V5-V6. The last portion of the QRS, however, the precordium. The electrical activity of the right ventricle appears quite different. Instead of the 2 ventricles depo- is overpowered by the activity of the larger and more mus- larizing simultaneously as would normally occur, in RBBB cular left ventricle. The right ventricle has a minimal impact the left ventricle depolarizes first and then the right ven- on the configuration of the QRS complex on the ECG. It is tricle. As a result of the right ventricle depolarizing last, it only when there is right ventricular (RV) hypertrophy or becomes the ventricle that has the greatest influence on the RBB that the right ventricle has much influence on the shape of the QRS complex. This has been referred to as shape of the QRS complex9,10 (Figure 3). an ‘‘unmasking’’ of the RV forces11 (Figures 4 and 5). The electrical vector produced by the right ventricle is PATHOPHYSIOLOGY OF BUNDLE BRANCH in the opposite direction to the vector produced by the left AND FASCICULAR BLOCKS ventricle. The result is the typical triphasic complex that is Because of its relatively small size, the RBB is particularly seen in the right-sided leads. In the left-sided leads, there is a vulnerable to lesions that can result in a block; the same is terminal S wave that tends to be deep and broad caused by true of the LAF. Additionally, the LAF travels across the the depolarization of the right ventricle. Because there is a delay in the depolarization, the QRS complex is broader than usual.7,10-12 When the duration of the QRS complex is greater than 0.12, the RBBB is referred to as complete. When the duration is less, typically 0.10 to 0.11 milli- seconds, the block is referred to as incomplete.9,11 An incomplete RBBB is a fairly common finding and may also be a normal variant. It tends to be associated with RV hypertrophy (RVH) or dilatation. If the dilatation is acute and transient, then the incomplete RBBB may also be transient. Although patients who develop an incom- plete RBBB have a greater likelihood of progressing to full RBBB, the great majority of these patients do not. There does not seem to be an increase in risk for cardiovascular Figure 3. Showing normal R progression across the precordium. death associated with an incomplete RBBB.11

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TABLE 2 Electrocardiographic Characteristics of Right Bundle Branch7,9,11,12 Duration of & 0.12 ms in complete right bundle-branch QRS complex block (RBBB) & 0.10-0.11 ms in incomplete RBBB Morphology of & The classic hallmark of an RBBB in the right

QRS complex facing precordial leads (V1-V2) is a triphasic complex or an rSR¶ pattern & In the left facing leads, there is usually a deep terminal S wave that may be slurred (leads I,

aVL, V5-V6) QRS axis & Should be in the normal range & If there is-axis deviation present, then this should Figure 5. Depolarization sequence for right . prompt a review for the presence of a fascicular, Courtesy of escapedia, Rob Kreuger, medical illustrator. Licensed under usually a left anterior fascicle block creative commons. http://creativecommons.org/licenses/by/2.5/. ST-T segments & Usually discordant (in the opposite direction) to the main QRS complex in the right-sided leads. (MI): RBBB complications in 13,14 However, in the left-sided leads, the ST-T 3% to 7% of patients with MI segments are usually concordant, or in the same direction as the QRS complex CLINICAL VIGNETTE Mrs N is an 84-year-old woman who comes to the emergency department (ED) of her local hospital with Although it is possible to develop RBBB in a normal a 2-day history of epigastric discomfort and increasing heart, it is far more usual for RBBB to develop in people shortness of breath. She thought her epigastric who have organic heart disease.8,9 The prognosis of RBBB discomfort was due to indigestion, but it has not is dependent on the underlying heart disease. Some of the responded to antacids. She is also short of breath. On 7,9,10,13 the second day, she develops left-sided jaw pain. At conditions that can cause an RBBB are as follows : this point, Mrs N calls her daughter, who then brings & chronically increased RV pressure her to the ED. cor pulmonale RVH On arrival to the ED Mrs N has the following vital hypertension (HTN) signs: blood pressure, 175/80 mm Hg; heart rate, 110 beats/min; respiratory rate, 24 breaths/min; and & Sudden increase in RV pressure pulse oximetry is 88% on room air. Physical pulmonary embolism examination shows an elderly woman in some distress; she is alert and oriented, complaining of epigastric & myocardial , infarction, or inflammation distress and left-sided jaw pain. Bibasilar crackles are heard bilaterally, and a systolic murmur at the apex. The abdominal examination is negative. Mrs N has a medical history of HTN that is not well controlled, diabetes mellitus, and dyslipidemia. Electrocardiogram reading of Mrs N is shown in Figure 6).

Do Mrs N’s clinical presentation and ECG represent high-risk , and should she be treated with fibrinolytics or percutaneous coronary intervention (PCI)? Whenever the ECG is distorted by a BBB, it makes it more difficult to identify the usual markers that are normally used to recognize ischemic changes. In the case of an anterior MI in the presence of an RBBB, if there is a Q wave that develops, the RBBB usually does not interfere Figure 4. Right bundle-branch block versus normal configuration in the recognition of the Q wave. The QRS complex will be of V1 and V6. abnormally wide, and there will also be a loss of the

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Figure 6. Electrocardiogram showing right bundle-branch block changes with ischemia in the inferior leads.

R-wave progression across the precordium if a Q-wave RBB. So a blockage in the LAD artery can also affect the anterior MI is present. If there is an inferior wall MI functioning of the RBBB. Right BBB in the setting of an present, then the Q wave will appear in the inferior leads acute anterior MI indicates a poorer prognosis. These (leads II, III, and aVF)14 (Figure 7; Table 3). patients have an increased risk for morbidity and mortal- Trying to detect a nonYST-elevation MI in the presence ity. When an RBBB occurs in conjunction with an anterior of an RBBB can be difficult. The ST segment and T waves MI, it signals a more extensive infarct size and poorer LV are distorted because of the abnormal depolarization and functioning. These patients tend to develop repolarization that the RBBB causes. In leads with an R¶ more frequently and complete . Some studies wave, typically leads V1,V2,andV3, there tends to be an have indicated that the mortality rate is 3 times higher for inverted , which can make detection of nonYST- patients with RBBB and AMI than it is for patients with- elevation MI in these leads difficult.14 out RBBB in the presence of an AMI.6,8,14-16 It has also

Leads that have a terminal S wave (V5-V6) usually have been noted that patients who do develop RBBB in com- an upright T wave. If ST-segment depression and T-wave bination with anterior MIs are more apt to be older and inversion occur in these leads, the possibility of ischemia female and to have a history of diabetes, , previous should be considered.14 MIs, and heart failure.6 Patients who have RBBB in the When an RBBB does appear in the presence of an setting of AMI should be considered for PCI or fibino- acute MI (AMI), the most common scenario is that it is an lytics, if no cardiac catheterization laboratory is available. infarction of the anterior wall of the left ventricle. The left In the prefibrinolytic era, RBBB was extensively stud- anterior descending artery provides the blood supply to ied, and its ability to indicate a worse outcome is well both the anterior wall of the left ventricle and also to the appreciated. In the postthrombolytic era, RBBB has been less studied. But it seems to remain an independent predictor of increased mortality and morbidity for patients despite reperfusion therapies.16 This may not be as well appre- ciated in the postfibrinolytic era. None of the commonly used risk stratification algorithms for predicting mortal- ity for AMIs include RBBB as a factor to be included.17

TABLE 3 Changes Associated with RBBB and Anterior MI

& V1 with Q-wave anterior myocardial infarction (MI) and right bundle-branch block shows an absence of any R wave, and there is only a large Q wave followed by the R wave.

& In V6, there is minimal disturbance to the morphology of the QRS. & However, if anterior Q wave MI is present, look for the absence of the Figure 7. Right bundle-branch block with acute myocardial R-wave progression across the precordium. infarction present.

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However, this does seem to be a subpopulation of AMI patients who should be closely monitored.

RIGHT BUNDLE-BRANCH BLOCK AND PULMONARY EMBOLUS Right BBB has also been associated with another condition that is potentially life-threatening: pulmonary embolus (PE)and other forms of pulmonary compromise. When a PE develops, one of the hemodynamic consequences that occur is that the vascular resistance for the pulmonary bed increases. This, in turn, causes an increase in the afterload for the right ventricle and can result in work overload for the right ventricle with dilatation occurring. Right ven- tricular dilatation can inhibit blood flow to the RBB and cause a complete or incomplete RBBB. Although not di- Figure 8. Normal versus left bundle-branch block, V1 and V6. agnostic for PE, it may be a marker for the presence of a pulmonary artery embolus. The presence of a complete or cal presentation and/or in patients with hemodynamic incomplete RBBB pattern is associated with an adverse compromise that may increase the risk of embolus in outcome from the PE.18 In a retrospective study, the re- other great vessels. cords of 20 patients who had autopsy confirmed main pulmonary trunk embolism. Ten subjects presented with LEFT BUNDLE-BRANCH BLOCK a new-onset complete RBBB. Another 6 subjects had a When an LBBB is present, the septum depolarizes abnor- new-onset incomplete RBBB. This was in contrast to a mally. The LBBB prevents the septum from being stimulated control sample of 30 patients who had peripheral PEs as usual. Instead of depolarizing from left to right, the septum who did not present with new-onset RBBB or incomplete is depolarized from right to left as the electrical impulses RBBB.19 The implication this has for nursing is that for make their way from the right ventricle across to the septum patients who are suspected of having a PE or are at high and left ventricle (Table 4; Figures 8 and 9) The sequence of risk for developing PE, the appearance of a new-onset depolarization in the presence of LBB is as follows7: complete or incomplete RBBB should raise the suspicion 1. The right ventricle depolarizes in the normal pattern, of a PE and should be correlated with the patient’s clini- from left to right. TABLE 4 Electrocardiographic Characteristics 2. The septum depolarizes abnormally from right to left. of Left Bundle-Branch Block 3. Then the left ventricle depolarizes afterward, in a right- to-left direction, as is normal. Duration & QRS interval is Q0.12 ms 4. The main vector direction in an LBBB is leftward, & QRS morphology In the right-sided leads of V1-V2, a small downward and toward the front. r wave is usually seen, followed by a wide, terminal S wave & There are no septal q waves seen in the

usual leads: leads I, V5, and V6

& In the left-sided leads of I, aVL, V5, and V6, there is a broad, monophasic R wave & The R waves are frequently slurred or notched. & There is poor R-wave progression seen across the precordium (see Figures 8 and 9) QRS axis & QRS axis should be within normal ST segment and T wave & In an LBBB, the ST-T direction is usually discordant to that of the QRS complex in the precordial leads and in leads I and aVL & This discordance of the ST-T segment causes serious difficulty in being able to distinguish Figure 9. Sequence of depolarization in left bundle-branch block. Courtesy ECG markers of ischemia of escapedia and ecgpedia, Rob Krueger, medical illustrator. Licensed under creative commons. http://creativecommons.org/licenses/by/2.5.

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Figure 10. Electrocardiogram 3 showing the changes typical of an left bundle-branch block.

Depolarization of the left ventricle is delayed with an with LBBB also developed another type of cardiovascular LBBB, and the complex is wider than normal, but the complex disorder, it showed that within 10 years of the diagnosis of may look more normal than it does when an RBBB is present. the LBBB, more than 50% of the affected individuals had The depolarization of the left ventricle has the major influence died of various cardiovascular causes.20 A study published on the morphology of QRS complexes across the precordium. in 2003 showed that LBBB also was associated with a Because of this effect, an LBBB has been described as an ex- higher mortality rate in patients with heart failure. This aggeration or distortion of a normal QRS complex.9 This is study used the Italian Network on Congestive Heart commonly described as rabbit ears or notched (Figure 10). Failure (CHF) Registry, which enrolled 5517 patients with congestive heart failure for a 1-year period.21 Of the 659 CLINICAL VIGNETTE patients who had LBBB, 11.9% died during the course of Mr M is a 58-year-old man who presents to the ED the study, with almost half of the deaths being classified as complaining of retrosternal chest pressure that radiates to his sudden cardiac death (SCD). When compared with those left shoulder and arm. The pain woke him up at 5 AM, but resolved after 2 hours. However, the pain returned within patients who did not have LBBB, the all-cause mortality 21 an hour and was worse. His wife then called emergency was significantly higher for those patients with LBBB. medical services and Mr M was brought to the ED. He has a medical history of HTN, type 2 diabetes mellitus, and dyslipidemia. His first troponin I level is normal. Should this patient receive fibrinolytics or be brought to the cardiac catheterization laboratory (Figure 11)?

CLINICAL CORRELATION OF LEFT BUNDLE-BRANCH BLOCK It has long been noted that the development of an LBBB has an adverse prognosis for patients.13,20,21 The data from the Framingham Heart Study concerning increased adverse affects associated with LBBB were published in 1979. Not Figure 11. Electrocardiogram 4 showing left bundle-branch block 24 only did these data show that almost 90% of individuals with ischemic changes in V4-V6.

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In patients who present with an AMI and a BBB, the developed by Sgarbossa and colleagues.24 Usingasample prognosis is also more compromised than it is for patients of 131 North American patients who demonstrated without a BBB.6,22-27 In a retrospective study done in the presence of LBBB, from the 26 000 (0.5%) who par- late 1990s, the records of 297 832 patients who were ticipated in the GUSTO 1 (Global Utilization of Strepto- treated for AMI were reviewed.6 Of these patients, the kinase and Tissue Plasminogen Activator for Occluded prevalence of LBBB was found to be 6.7%, and that of Coronary Arteries) trial, Sgarbossa and colleagues showed RBBB was 6.2 %. This study found that the presence of that 3 criteria had independent values to detecting AMI in LBBB with AMI was associated with a 33% increase in thepresenceofLBBB.The3criteriaareasfollows: mortality, as compared with patients with AMI but no ST-segment elevation greater than or equal to 1 mm LBBB. (It was also shown by this study that the presence of that was concordant with (in the same direction as) the an RBBB and an AMI presented a greater, independent QRS complex predictor of in-hospital mortality.) This study also showed ST-segment depression of 1 mm or more in leads V , that patients who do have an LBBB with an AMI tended to 1 V ,orV older, were more likely to be woman, had a greater oc- 2 3 ST-segment elevation that was 5 mm or more that currence of preexisting congestive heart failure and other was discordant with (in the opposite direction of) comorbid conditions, and received significantly less treat- the QRS complex ment with thrombolytics than did patients with an AMI andnoBBB.6 To appreciate this approach for evaluating the ECG for signs of an AMI in the presence of an LBBB, the concept of DETERMINING PRESENCE OF AMI WITH ‘‘appropriate discordance’’ needs to be reviewed.29 LBBB: A CHALLENGING ASSESSMENT In a normal ECG, the ST segment and the T wave tend When an LBBB is present, the usual signs on the ECG that to share the same direction as the main part of the QRS would indicate the presence of an AMI are concealed by the complex. This is concordant (Figure 12). However, when distortion of the ST and T waves.9,10 This can create an ECG demonstrating the presence of LBBB is viewed, difficulties in deciding how to treat patients with symptoms the ST segment and T wave tend to go in the opposite that indicate they may be having an MI.8,23-27 Of concern direction of the main part of the QRS complex. This is is that these patients may be exposed to the dangers of discordant. The discordant direction of the ST-T segment thrombolytics when they are experiencing either unstable in relationship to the main QRS direction is due to the angina or a nonYQ-wave AMI.28 The question of when to abnormal repolarization that occurs following the abnor- treat patients with an LBBB and suspected AMI has long mal depolarization of an LBBB. This has been termed been of concern and precedes the thrombolytic era.23-25 appropriate discordance; it is expected to have abnormal 29 Over time, various strategies for using the ECG to repolarization following abnormal depolarization. How- identify which patients with LBBB were experiencing AMI ever, when an AMI is present, this appropriate discordance 24 have been proposed. One method to identify these was is disrupted. This is described as the Sgarbossa criteria.

Figure 12. Appropriate and inappropriate discordance.

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Not all the Sgarbossa criteria have the same weight in Clinical Significance of Left Anterior predicting the presence of AMI in the setting of an AMI. Fascicular Block Criteria 1 and 2 have the most value in detecting ischemic The finding of a left anterior fascicular block (LAFB) on changes, whereas criteria 3 has the least value. However, the ECG is a relatively common occurrence and does not the Sgarbossa criteria are very sensitive to detecting AMI carry much prognostic value8 (Table 5; Figures 13-15). in the presence of LBBB; that is, when the criteria present Left anterior fascicular block is seen in a several cardiac on the ECG in the setting of suspected AMI, there is high diseases, most commonly ischemic heart disease and reliability that there is indeed ischemia present.30,31 hypertrophy due to HTN.8 The placement of the LAF The most recent practice guideline for the management across the outlet track of the left ventricle exposes it to of ST-elevation MI from the American College of Cardiol- the potentially damaging effects of the turbulence of the ogists (ACC) continues to recommend that patients pre- blood leaving the left ventricle.8 Some authors have pro- senting with history suggestive of AMI who have new or posed that LAFB may be a function of an aging heart32,33 presumed new LBBB should be treated with either Left anterior fascicular block is the most commonly fibrinolyticsorPCI.32 Although there is always the fear encountered associated with AMI. of exposing a patient to the dangers of thrombolytic ther- It is usually seen with an anterior AMI, and the LAD apy unnecessarily, the patients who benefit the greatest artery is generally the culprit artery. However, an LAFB from such therapy during an AMI are patients with an can appear with an inferior AMI also. When an LAFB LBBB.30,31 These patients have a high mortality rate, and develops along with an inferior MI, it is indicative of a earlytherapycandomuchtoimprovetheiroutcome. patient with multivessel disease and significant stenosis of Despite the recommendation by the ACC/American Heart the LAD artery.34 Association, there are physicians who feel that without better tools for diagnosing AMI, administering thrombo- LEFT POSTERIOR FASCICULAR BLOCK lytics to all suspected AMI with new or presumably new When a left posterior fascicular block (LPFB) occurs, the LBBB would result in overtreatment and possibly increased conduction impulses travel from the SA node through mortality in this group of patients.29 Because of this con- the AV node and down the bundle branches as usual. troversy regarding treatment, this group of patients has However, because the posterior fascicle is blocked, the been shown to be significantly undertreated.6,31 impulses are not able to be conducted to the left portion of the septal wall or posterior wall of the left ventricle. The LEFT ANTERIOR FASCICULAR BLOCK impulses, however, do travel down the right bundle as The LAF receives only a single blood supply from the LAD usual and then enter the septum. Simultaneously, the im- artery and is a slender fascicle, predisposing it to be pulses travel down the anterior fascicle to the lateral and damaged much more likely than the LPF. When an LAF is anterior wall of the left ventricle. The depolarization se- blocked, ventricular depolarization precedes in an abnor- quence of the heart is as follows: the septum is still the first mal fashion. The impulse travels from the SA node to the AV node and into the AV bundle in a normal fashion. The TABLE 5 ECG Characteristics of Left impulse then travels down the RBB and the LPF simulta- Anterior Fascicular Block neously. In this situation, the septum is depolarized by the impulse when it travels down the LPF. The right ventricle QRS pattern Normal appearance, there is no notching. Change and the posterior portion of the left ventricle depolarize in terminal vector causes some of the QRS simultaneously. As the impulse makes it way to the an- complexes to appear differently in some leads terior and lateral wall of the left ventricle, they contract Q waves Small q waves appear in leads I and aVL but are just slightly behind the right ventricle and posterior left absent from the inferior leads of II, III, and aVF ventricle. This changes the main axis of the heart so that it R waves Initial small r waves are present in II, III, and aVF is more leftward and anterior than normal. Because the S waves Are typically larger and deeper than the r waves in delay in the contraction of the anterior and lateral wall is the inferior leads so slight, the QRS complex remains within a normal du- Duration of QRS The delay in depolarization due to the block is not ration.7,9,10,13 But the change of direction in the terminal complex as long as when it occurs in the whole bundle vectors changes the normal axis for the heart and causes branch, so the complex is usually within normal some of the complexes to appear differently. In the limits, tends to be G0.10 ms inferior leads, the QRS complex displays a small r wave, QRS axis The change in the terminal vectors causes a change followed by a deep S wave, and the opposite appears in in axis; it is usually deviated to the left between leads I and aVL where there is a small septal q wave and 30 and 60 degrees a tall R wave.

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BIFASCICULAR AND TRIFASCICULAR BLOCKS In dealing with blockage of the various bundle branches and fascicles, it is important to define what is meant by bifascicular and . Bifascicular block is used whenever there is a blockage of 2 of the 3 fascicles. For this purpose, the fascicles are considered to be the RBB, the LAF, and the LPF. Bifascicular block is commonly seen as an RBBB and an LAFB. This condition can be diagnosed using a conventional 12-lead ECG.13 Trifascicular block, however, is much less seldom seen and may require ad- vanced electrophysiology studies to truly document it.32 The absolute definition of a trifascicular block is docu- mented blockage in all 3 fascicles whether simultaneously or at various times. Under this designation, an alternating LBBB and RBBB pattern seen on successive ECGs is suspected to be a trifascicular block.13 If one ECG shows Figure 13. Normal vs left anterior fascicular block V1 and V6. an RBBB and LAFB and a successive ECG shows an RBBB and LPFB, this will also fulfill the criteria for a trifascicular block.32 Trifascicular block has also been part of the ventricles to depolarize, but in an abnormal used to describe the situation in which a first-degree AV 35 way from the right to the left.9,13 Next, the right ventricle block is seen in the presence of an RBBB and LAFB. depolarizes simultaneously with the lateral and anterior Although various fascicular blocks usually precede wall of the left ventricle, and the last to depolarize, al- third-degree block, because the progress is slow and there is though it lags by only an instant, is the posterior wall of the no clinical or laboratory indicator that can accurately ventricle. Because the posterior wall depolarization is de- predict when third-degree heart block will occur, prophy- layed by only milliseconds, the QRS complex remains lactic permanent pacing for asymptomatic, chronic bifas- 35 within a normal duration. However, because of the abnor- cicular block is not recommended by practice guidelines. mal depolarization sequence, the vectors are changed and Patients with underlying cardiac disease and various com- are directed right and downward, instead of the usual left binations of fascicular block are at a high risk of SCD, but and downward direction. This causes the appearance of the the cause of the SCD is due to arrhythmias and not the 35 QRS complexes to be different in some of the leads.9,13 third-degree block. Because of this, insertion of a per- manent pacemaker may alleviate the common symptom of that these patients have, but will not reduce the Clinical Significance of LPFB risk of SCD from arrhythmia development (unless of An LPFB is seldom seen. This is due to the fact that the posterior fascicle is much more resistant to being damaged because of its sturdier, more robust structure than the RBB or LAFB.9 Also, the fact that the LPFB receives a dual blood supply, from both the left coronary artery via the LAD artery and from the RCA via the PDA in most people (85%), helps to isolate the LAFB from damage. By the time an LPFB is present on the ECG, the heart has suffered from a significant disease process.13 This increases the risk of extension to complete heart block and results in the patient requiring a pacemaker35 (Table 6; Figures 16/18). Patients with ischemic heart disease and BBBs of any description are at high risk for SCD, the mechanism of which seems to be due more to an arrhythmia than it does to progressive blockage of the conduction system.35 How- ever, although the progression of blockage within the conduction system occurs slowly, there are certain cir- Figure 14. Depolarization sequence during left anterior fascicle block. cumstances that do require pacing if complete heart block Courtesy of ecgpedia, Rob Kreuger, medical illustrator. Licensed under and syncope are to be avoided.35 creative commons. http://creativecommons.org/licenses/by/2.5/.

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Figure 15. Electrocardiogram 5 showing a left anterior fascicular block. course these patients have a pacemaker with defibrillating ment is usually the result.4 Chamber enlargement includes properties inserted). In the setting of various fascicular the concepts of both dilation and hypertrophy.7 When blocks then, the ACC/American Heart Association/North there is too much fluid (volume overload), this is referred American Society of Pacing and Electrophysiology guide- to as diastolic overload. Dilation of the heart chamber is lines rate the following conditions as a class I indication usually the result. Diastolic overload can be the result of for permanent pacemaker insertion (Table 7).35 either chronic or acute conditions. Acute cause of diastolic overload is classically associated with PE for the right side HYPERTROPHIES of the heart.4,10 Whentheheartisfacedwithanincreasedworkload,dueto Resistance overload, an increase in afterload, results in an increase in either volume or resistance, chamber enlarge- hypertrophy. Hypertrophy is the increase in muscle mass for the heart. This is also called systolic overload. Although it starts out as a coping mechanism, to allow the heart to TABLE 6 Electrocardiographic Characteristics deal with the increased workload, hypertrophy over the of Left Posterior Fascicular Block7,9,13 QRS pattern Remains within normal duration, QRS G0.10 ms There is no notching Q waves Small initial q waves are found in the inferior leads, II, III, and aVF

Q waves are absent from lateral leads of I, aVL, V5,andV6 R waves Small initial r waves are present in the lateral

leads I, aVL, V5, and V6 Tall R waves are found in leads II, III, and aVF QRS axis Terminal vectors due to block cause a right-axis deviation, usually between 110 and 180 degrees Figure 16. Hallmarks of left posterior fascicular block.

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for the work of the heart, to a more spherical shape, which is not efficient for the work of the heart.4 Hypertrophy most commonly occurs in response to increased afterload that is chronic, such as occurs with untreated or poorly treated HTN. However, for most chronic conditions, hy- pertrophy and dilation are observed together.7

RV Hypertrophy Afterload for the right ventricle is caused by the resistance of the pulmonary vascular bed. Therefore, anything that increases the resistance of these blood vessels can cause an increased resistance for the right ventricle and can result in RV resistance overload7,10 (Table 8). Other causes are from valvular or congenital heart disease.

Figure 17. Depolarization sequence for left posterior fasicular block. Main Features of RV Hypertrophy on the ECG Courtesy of ecgpedia, Rob Kreuger, medical illustrator. Licensed under The main feature seen when an RVH is present on the ECG creative commons. http://creativecommons.org/licenses/by/2.5/. is the reversal of the usual precordial pattern. Instead of a progression of R waves seen across the precordium, there long term is damaging. When hypertrophy occurs, there is are tall R waves seen in the right-sided precordial leads of an increase in the size of the myocardial cells (myocytes). As V1 and V2 (sometimes also in V3 as well). the individual myocytes increase in size, the intracellular In the left-sided precordial leads of V5 and V6,insteadof matrix that supports the myocytes also undergoes changes the typical tall R waves, deep S waves are seen.9-11,36 There to accommodate the larger myocytes. This results in the are few scoring systems for aiding in the diagnosis of RVH formation of scar tissue.10 via ECG. Electrocardiographic findings do not have a high As the myocytes change shape, the shape of the entire sensitivity of detecting RVH.11 However, familiarity with ventricular chamber also changes shape. The ventricle the findings associated with RVH will help to support the becomes less elliptical in shape, which is an efficient shape clinical assessment of this diagnosis and help prevent the

Figure 18. Electrocardiogram 6 showing a left posterior fascicular block.

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TABLE 7 Indications for Insertion of Pacemaker TABLE 9 Electrocardiographic Characteristics of Right Ventricular Class I indications for & Alternating bundle-branch block Hypertrophy9-11,36-38 pacemaker insertion & Intermittent third-degree block & Type II second-degree block P wave Right atrial abnormalities: tall, peaked P waves, height 92mm Class IIa indications for & Incidental finding during electrophysiology pacemaker insertion study of a pacing induced infra-His QRS duration/axis Right incomplete bundle-branch block block commonly seen (QRS G0.12 ms) and right-axis deviation 9110+ & Syncope that cannot be attributable to atrioventricular (AV) block, when other Morphology of QRS complex R 9 SinV1;S9 RinV6 probable causes have been ruled out, ST segment/T wave with concave ST-segment most notably VT depression and inverted T wave seen in V1

Class IIb indications for & Whenever there is any degree of fascicular and V2 leads and II, III, aVF leads pacemaker insertion block present along with certain neuromuscular diseases, because the ECG, then the natural balance of power between the left progression of the block can not be and right ventricles has been overcome. At this point, other predicted. clinical signs may be present. Although the 2 chambers & Some of the neuromuscular diseases are continue to depolarize simultaneously, the right ventricle, myotonic muscular dystrophy, Kearns-Sayre because of its size, takes longer to complete depolarization. syndrome, Erb dystrophy (limb-girdle), and This causes the terminal electrical forces on the ECG to be peroneal muscular atrophy directed rightward.7,9,36,37 The ECG shows a reversal of Class III indications for & Fascicular block without AV block the usual pattern in the precordial leads. No longer is pacemaker insertion or symptoms. thereseentheprogressionoftheRwaveacrossthepre- & Fascicular block with first-degree AV block cordium; instead, there are large R waves seen in the without symptoms right-sided leads with deep S waves seen in the left-sided leads.10 As RVH occurs, the R waves over the right-sided Abbreviation: VT, ventricular . chest leads increase in height, and the S waves in the left chest leads deepen. The result is an increase in the R to S findings from being misinterpreted as changes associated ratio. (If this ratio exceeds 1:1, then RVH can usually be with ischemia.11 Electrocardiographic findings associated diagnosed.)11 RV hypertrophy strain pattern appears with with RVH are shown in Table 9. long-standing hypertrophy. A strain pattern is an abnor- mality in the repolarization of the myocardium and is a Clinical Significance of RVH secondary feature to the chamber enlargement that has Most of the criteria for recognizing RVH center on the occurred. When a strain pattern is present, the ST segment QRS pattern in the right chest leads. When the right appears with a down-sloping depression and inverted T ventricle hypertrophies to the point that it is evident on the wave. It is typically seen in right-sided leads, that is, V1 9-11,37 and V2,leadsIIandIII,andaVF. The fully developed RVH pattern is seen less than that TABLE 8 Causes of Right of LV hypertrophy (LVH) because the etiology of RVH is 7,10 less common than that of LVH. Also, a greater workload Pulmonary conditions (either resistance or fluid) is required to produce a mature pattern of RVH.9,10 Usually, the right ventricle has to & Chronic obstructive pulmonary disease undergo hypertrophy to a severe degree before a mature & Status asthmaticus RVH pattern is seen. The right ventricle is at a disadvan- & Pulmonary embolism tage to assume the dominant terminal vectors, compared & Pulmonary edema with the naturally dominant left ventricle. The right ventricle has a fair amount of ground to cover to overtake the left Valvular problems ventricle and then surpass it, to be seen as the dominant & Pulmonary stenosis ventricle and be recognized as such on the ECG.10 & Tricuspid valve insufficiency & stenosis LV Hypertrophy When the left ventricle is exposed to an increase in work- & Mitral valve insufficiency load, either from an increased preload volume or pressure

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over time, the chamber will respond by dilating or increasing TABLE 10 4,38 Electrocardiographic Characteristics muscle size (hypertrophy) or both. The increase in the of Left Ventricular Hypertrophy size of the left ventricle has an effect on the usual pattern of & the ECG. Because the left ventricle is normally the pre- P wave May show signs of P mitral-notched P waves, P waves broader than normal dominant ventricle, the effect of hypertrophy is to exaggerate the usual ECG pattern.9,10 As the left ventricle & P waves may appear to be biphasic in increases in size, the depolarizing impulse has a longer way some leads to travel through the enlarged wall of the ventricle, in- QRS duration and axis & Usually normal duration of the complex and creasing the natural dominance of the left ventricle on the normal axis pattern of the ECG. The hallmarks of LVH on the ECG QRS morphology & Tall R waves are present in left facing are (1) a complex that may exceed the normal duration leadsVleads I, aVL, and V5-V6 9 ( 0.10 seconds); (2) a delayed intrinsicoid deflection in V5 & Deep S waves are present in the right or V6; (3) increased voltage of the QRS, with deeper S precordial leads of V1-V2 and lead III wavesovertherightventricle;(4)tallerRwavesoverthe ST segment and T wave & Will frequently have an abnormal repolarization left ventricle; and (5) an abnormal repolarization pattern pattern characterized by a downsloping ST 7,9,10,39-41 called a strain pattern. segment and a T-wave inversion pattern. This The mechanism that produces the strain pattern is not is referred to as a strain pattern precisely known.7,41 It appears to develop in individuals whohaveexhibitedLVHforsometime.9,10 The strain pattern intensifies when dilation and failure occur. The sultant subendocardial ischemia may cause changes or be strain pattern correlates with increasing LV mass, as con- apparent in the ST segment and T waves.7 However, the firmed by echocardiography.41 The LV myocardium may strain pattern has also been strongly associated with in- become so enlarged that some portions of the ventricle do creases in LV mass without being not receive adequate perfusion. Because the myocardium is present41 (Table 10; Figure 19.1 The changes associated with perfused from epicardium to (or from the a strain pattern are considered ‘‘secondary’’ changes; pri- outside to the inside), the subendocardium is the most mary ST- and T-wave changes would be caused by myocar- vulnerable portion of the myocardium to ischemia.7 Re- dial ischemia due to coronary artery blockage or spasm.7,9,10

Figure 19. Electrocardiogram 7 showing typical changes associated with left hypertrophy.

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Clinical Significance of LV Hypertrophy the simpler the criteria, the better for today’s busy clini- The identification of LVH has long been associated with an cians. However, a study by Hsieh et al45 showed that increase in mortality and morbidity and has been identified among the 17 different ECG criteria used for determining as an independent marker for increased cardiovascular LVH, voltage-only criteria such as the Cornell and risk.4,39,42,43 Patients with HTN, particularly severe HTN, Sokolow-Lyon criteria, although simpler to use, had a are especially prone to developing LVH. This condition lesser ability to predict cardiovascular mortality than did is also more prevalent with advancing age. It is found in composite criteria. The study showed that criteria that more than 43% of the population older than 70 years. included negative P terminal forces and strain patterns Some studies have estimated that the increased risk for had a better ability to predict cardiovascular mortality those individuals with LVH is increased by 3-fold for coro- (Table 11). nary events, increased by 4- to 7-fold for all cardiovascular events and increased by 3- to 5-fold for SCD.42 SUMMARY Given these increased risks of adverse cardiovascular The ECG, although not a perfect screening tool for car- events, there has been interest in determining if aggressive diovascular disease, does have the merit of being readily therapy, particularly for HTN, can have an impact on the regression of LVH and, if so, if the cardiovascular risk 4,43 factors are then reduced. The initial studies were done TABLE 11 Comparison Between Different in the late 1990s with small sample sizes, but were pro- Criteria for Diagnosing Left mising and seemed to indicate that a reduction in LV mass Ventricular Hypertrophy (LVH) 45 is associated with a decrease in risk factors for future car- by Electrocardiogram (ECG) 43 diovascular events and to decrease afterload. To date, Criteria for Diagnosing LVH by ECG the largest study to deal with this problem is the Losartan Intervention for Endpoint reduction in HTN (LIFE) Sokolow-Lyon Rohmhilt-Estes Cornell criteria (voltage Study. In this study, 9193 subjects with ECG LVH, were voltage criteria criteria) randomized to either the angiotensin receptor blocker, & S wave; this was & R or S wave in a limb & Size of R wave in losartan, or the "-blocker, atenolol. The study followed the first criteria lead Q20 mm lead aVL the subjects for up to 5 years and found that the losartan proposed for treatment group had the greater regression of ECG LVH detecting LVH by both the Cornell product and the Solkolow-Lyon volt- by ECG & Q & age measurements and a lower incidence of cardiovas- SinV1-V3 25 mm Plus the depth of the S 44,45 Q cular events. wave in V3 28 mm Q Using the ECG for diagnosing LVH is an unsatisfac- or 20 mm in women tory test. Echocardiography provides a more accurate and & R wave in & Can make diagnosis Q sensitive assessment of ventricular hypertrophy. The ECG V4-V6 25 mm of LVH has a low sensitivity for detecting LVH (meaning that the & IftheSwaveinV1 + & ST-TYwave changes

ECG can miss diagnosing patients with LVH). However, the R wave in V5 or consistent with a strain 9 the ECG does have a high specificity for LVH (ie, when the V6 35 mV = LVH pattern, if the patient ECG criteria for LVH are present, there is a high likelihood is on that LVH is present). However, patients are much more apt & Digitalis, then only to have an ECG done than an echocardiograph, so that the 1 point is scored for ability of the registered nurse to recognize the ECG signs the strain pattern 40,41,44 indicating LVH can help to detect this condition. & Left-axis deviation The ECG is a readily available and inexpensive test; this 915 degrees is makes it an attractive, if less than ideal, tool for screening 2 points patients at risk. & QRS complex duration In an attempt to be able to better identify which pa- 90.09 seconds is tients may have LVH, there have been several systems 1 point. developed for evaluating the ECG. None of the systems are & P mitrale is assigned ideal, and research studies done to try and determine which 3 points system has the highest sensitivity and specificity have & An intrinsoid deflection presented conflicting results.40,43 None of the criteria have in V5-V6 that is 90.05 shown consistent specificity across sexes and ages. This is 1 point makes it difficult to know which criteria to use. Ideally,

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Copyright @ 2010 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Hypertrophies and Intraventricular Conduction Defects available and inexpensive. Reviewing ECGs can provide a 15. Melgarejo-Moreno A, Galcera-Tomas J, et al. Incidence, clinical characteristics and prognostic significance of right fairamountofinformationthatcanthenbeusedtohelp bundle-branch block in acute myocardial infarction: a study in guide treatment for patients. Increasingly, it is becoming an the thrombolytic era. Circulation. 1997;96:1139-1144. expectation that nurses will be able to decipher ECGs. 16. Arslan U, Balcolu S, Tavil S, Ozdemir M, Cengel A. Clinical and angiographic importance of right bundle branch block in Knowing what to look for can help to direct further testing the setting of acute anterior myocardial infarction. Anatolian J and treatment for patients. Intraventricular conduction Cardiol. 2008;8:123-127. defects and hypertrophy when present on the ECG can 17. Elizari MV, Acunzo RS, Ferreiro M. Hemiblocks revisited. Circulation. 2007;115:1154-1163. indicate that the patient is at greater risk for cardiovascular 18. Petrov D. Appearance of right bundle branch block in electro- events and cue nurses concerning which patients may have cardiograms of patients with pulmonary embolism as a marker a greater potential for becoming unstable. for obstruction of the main pulmonary truck. J Electrocardiol. 2001;34:185-188. Because nurses were not traditionally expected to be 19. Kucher N, Walpoth N, Wustmann K, Noveanu M, Gertsch M. proficient at reading ECGs and many nurses did not QR in V1an ECG sign associated with right ventricular strain receive this instruction in their basic program, it may be and adverse clinical outcome in pulmonary embolism. Eur Heart J. 2003;24:1113-1119. necessary for them to gain a knowledge base concerning 20. Abnash JC, Mehta MC. Etiologies of ECGs, particularly for those dysrhythmias that may not be and correlations with hemodynamic and angiographic find- seen as commonly. Intraventricular conduction defects ings. Am J Cardiol. 2003;91:1375-1378. 21. Baldasseron S, Opasich C, Gorini M, et al. Left bundle branch and hypertrophies can indicate an ominous future event block is associated with increased 1-year sudden and total for patients, but they can also provide the opportunity for mortality rate in 5517 outpatients with congestive heart failure: nurses to help intervene to change that outlook. a report from the Italian network on congestive heart failure. Am Heart J. 2002;143:393-405. 22. Schneider JF, Thomas HE, Kreger BE, McNamara PM, References Kammel WB. Newly acquired left bundle branch block: the 1. The American Heart Association in Collaboration with the Framingham Study. Ann Intern Med. 1979;90:303-310. International Liaison Committee on Resuscitation. Guidelines 23. Francia P, Balla C, Paneni F, Volpe M. Left bundle branch 2000 for cardiopulmonary resuscitation and emergency car- blockVpathophysiology, prognosis and clinical management. diac care. Circulation. 2000;109(suppl I) I-1-I-11. Clin Cardiol. 2007;30:110-115. 2. Stephens KE, Anderson H, Carey MG, Pelter MM. Interpret- 24. Sgarbossa EB, Pinsik SL, Barbagelata A, et al. Electrocardio- ing 12-lead electrocardiograms for acute ST-elevation myocar- graphic diagnosis of evolving acute myocardial infarction in dial infarction: what nurses know. J Cardiovasc Nurs. 2007; the presence of left bundle branch block. N Engl J Med. 1996; 22:186-193. 334:481-487. 3. Levy D. Garrison RJ, Savage DD, Kannel WB, Castelli WW. 25. Wellens JJ. Acute myocardial infarction and left bundle branch Prognostic implications of echocardiographically determined blockVcan we lift the veil? N Engl J Med. 1996;334:450-451. left ventricular mass in the Framingham Heart Study. N Engl J 26. Shlipak MG, Lyons WL, Go AS, Chou TM, Evans GT, Med. 1990;322:1561-1566. Browner WS. Should the electrocardiogram be used to guide 4. Frey N, Katus H, Olson E, Hill J. Hypertrophy of the heart: a therapy for patients with left bundle branch block and new therapeutic target? Circulation. 2004;109:1580-1589. suspected myocardial infarction? JAMA. 1999;281:714-719. 5. Eriksson P, Hansson P, Eriksson H, Dellborg M. Bundle-branch block 27. Li SF, Walden PL, Marcilla O, Gallagher EJ. Electrocardio- in a general male population. Circulation. 1998;98:2494-2500. graphic diagnosis of myocardial infarction in patients with left 6. Go AS, Barron HV, Rundle AC, Ornato JP, Avins AL. Bundle bundle branch block. Ann Emerg Med. 2000:36:561-565. branch block and in-hospital mortality in acute myocardial 28. Moreno R, Garcia E, Lopez E, et al. Implications of left bundle infarction. Ann Intern Med. 1998;129:690-697. branch block in acute myocardial infarction treated with 7. Huszar RJ. Basic Dysrhythmias: Interpretation and Manage- primary angioplasty. J Am Coll Cardiol. 2002;90:401-403. ment. St Louis, MO: Mosby Inc, A Harcourt Health Sciences 29. Brady WJ, Lentz B, Barlotta K, Harrigan RA, Chan T. ECG Company; 2002. patterns confounding the ECG diagnosis of acute coronary 8. Rubart M, Zipes DP. Genesis of cardiac arrhythmias: electro- syndrome: left bundle branch block, right ventricular paced physiological considerations. In: Braunwald: Heart Disease: A rhythms and left ventricular hypertrophy. Emerg Med Clin North Textbook of Cardiovascular Medicine. 6th ed. Philadelphia, Am. 2005; 23: 999-1025. PA: WB Saunders Co; 2001. 30. Madias JE. Serial ECG recordings via marked chest wall 9. Marriott HJL. Marriott’s Practical . 10th landmarks: an essential requirement for the diagnosis of myo- ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001. cardial infarction in the presence of left bundle branch block. 10. Conover MG. Understanding Electrocardiography. 8th ed. St J Electrocardiol. 2002;35:299-302. Louis, MO: Mosby-Year Book, Inc; 2003. 31. Knontos MC, McQueen RH, Jesse RL, Tatum JL, Ornato JP. 11. Harrington RA, Pollack ML, Chan TC. Electrocardiographic Can myocardial infarction be rapidly identified in emergency manifestations: bundle branch blocks and fascicular blocks. department patients who have left bundle branch block? Ann J Emerg Med. 2003;25:67-77. Emerg Med. 2001;37:431-438. 12. DaCosta D, Brady WJ, Edhouse J. ABC of clinical electro- 32. ACC/AHA guidelines for the management of patients with ST- cardiography: and atrioventricular conduction elevation myocardial infarction. 2009. http://www.americanheart. block. BMJ. 2002;324:535-539. org/presented.jhtml?identifier=3004542. Accessed June 15, 2010. 13. Harrigan RA, Jones K. ABC of clinical electrocardiography: 33. Gallagher JE. Which patients with suspected myocardial conditions affecting the right side of the heart. 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35. Gregorators G, Brams J, Epstein AE, et al. ACC/AHA/NASPE cardiovascular risk: findings from a 40-to-69-year-old cohort 2002 guideline update for implantation of cardiac pacemakers in general practice. Fam Pract. 2004;21:63-65. and antiarrhythmia devices: a report of the American College 43. Verdecchia P, Schillaci G, Borgioni C, et al. Prognostic value of of /American Heart Association Task Force on a new electrocardiographhic method for diagnosis of left Practice Guidelines. 2002. www.acc.org/clinical/guidelines/ ventricular hypertrophy in essential hypertension. J Am Coll pacemakers/pacemaker.pdf. Accessed July 23, 2009. Cardiol. 1998;31:383-390. 36. Goldberger AL. Clinical Electrocardiography: A Simplified 44. Verdecchia P, Schillaci G, Borgioni C, et al. Prognostic significance Approach. St Louis, MO: Mosby Inc; 1999. of serial changes in left ventricular mass in essential hypertension. 37. Mirvis DM, Goldberger AL. Braunwald: Heart Disease: A Text- Circulation. 1998;97:48-54. book of Cardiovascular Medicine. Used Braunwalds 8th ed. 45. Hsieh BP, Pham MX, Froelicher VF. Prognostic value of elec- Philadelphia, PA: WB Saunders Company; 2007. trocardiographic criteria for left ventricular hypertrophy. Am 38. Magdic KS, Saul LM. ECG of chamber enlargement. Crit Care Heart J. 2005;150:161-167. Nurse. 1997;17:49-59. 39. Vakili B, Okin P, Devereux R. Prognostic implications of left ventricular hypertrophy. Am Heart J. 2001;141:334-341. ABOUT THE AUTHOR 40. Verdechhia P, Angeli F, Reboldi G, et al. Improved cardiovas- Linda Josephson, MS, RN, CCRN-CMC, nurse education specialist cular risk stratification by a simple ECG index in hypertension. Am J Hypertens. 2003;16:646-652. for Cardiac Care Unit at UMass Memorial Medical Center. Provide 41. Okin PM, Devereux RB, Neiminem MS, et al. Electrocardio- orientation to new staff for the cardiac care unit and staff development graphic strain pattern and prediction of cardiovascular morbid- for RNs caring for medical cardiac patients. ity and mortality in hypertensive patients. Hypertension. 2004; 44:48-54. Address correspondence and reprint requests to Linda Josephson, MS, 42. Ciardullo AV, Azzolini M, Bevini M, et al. A diagnosis of left RN, CCRN-CMC, UMass Memorial Medical Center, 55 Lake Ave North, ventricular hypertrophy on ECG is associated with a high Worcester MA 01605 ([email protected]).

Letter to the Editor

To the editor: After reading your closing word in Dimensions of Critical Care (May/June 2010), I was reminded of some words a close friend of mine told me during a hockey game after watching a Manitoba Nurses Union advertisement that reminded the general public ‘‘Always a nurse, always caring.’’ (He is an accountant, not a nurse.) ‘‘The problem with nursing is how you have branded yourselves. A commercial like that makes easy to make fun of nurses. Boy, Jason, I could sure use some caring right about now.’’ In Canada, we see commercials and ads reminding the public about the caring we provide (not unimportant). I have never seen an ad in Canada or the United States showing a registered nurse making an important decision, performing a critical lifesaving intervention, or aggressively advocating for a patient in need, all things I or colleagues have had to do during our careers. Perhaps our professional bodies and collective bargaining units should focus on selling and promoting these attributes to local media. Once we rebrand ourselves and change our own mind-set regarding what a nurse provides to the public, Hollywood, and ourselves, and change our own mind-set regarding what a nurse provides to the public, perhaps the national networks will take notice. Until we rebrand, we need to prepare for more of the same.

Jason Trottier, BN Winnipeg, Manitoba, Canada Editor’s response: Thank you, Mr Trottier, for taking the time to write about the editorial concerning how nurses are portrayed on television. While we are taking steps to improve the situation, we have a long way to go. DOI: 10.1097/0.1.DCC.000035162.20335.e9

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