heart author" faq
Resting Electrocardiogram (ECG)

The electrocardiogram is a recording of the electrical activity of the heart as it undergoes excitation (depolarization) and recovery (polarization) to initiate each beat of the heart.

This electrical activity is represented by a tracing showing the various phases of the activity above or below an isoelectric line (positive above and negative below) over time in a progressive fashion from the sinus node (the site of initiation of the electrical impulse in the cranial portion of the right atrium) to the AV node (in the right atrium) and then into the HIS-Purkinje bundle, where it spreads through both the left and right ventricular bundles (located on each side of the interventricular septum respectively). The activity spreads from these bundles out to each of the ventricles of the heart.

This activity is recorded using an electrocardiographic machine connected to the patient with four electric leads (labelled 1, 11 ,111, AVR, AVL, AVF) on the ankles and wrists and six on the front of the chest over the heart area (labelled V1-6).

The normal pattern of the ECG allows analysis to determine whether there is any abnormality in any particular patient's ECG (see fig 94).
The activity is classically represented by labeling the initial activity a P wave and in succession QRS, T and U waves. The P wave represents the electrical excitation of the atria, which causes contraction of both atria. The QRS complex represents the electrical excitation of the ventricles, which initiates the ventricular contraction (systole) shortly after the Q wave. The T wave represents the return of the ventricles from excitation to a normal state. The end of T wave marks the end of systole. The T wave represents the return to normal of the specialized muscle fibers, that make up the pacemaker, which spreads the electrical signal throughout the ventricles. The interval between the onset of the P wave and the onset of the QRS is called the PR interval, which usually does not exceed 0.20 seconds. The QRS duration is from 0.08-0.10 seconds. There is an isoelectric line separating the activity of the P wave from the QRS and the QRS from the T wave.

Counting the number of QRS complexes occurring per second gives the heart rate of the individual.
The electrical axis (EA) of the heart is a vector originating in the center of Einthoven's equilateral triangle and refers to the direction of the cardiac activation process as projected in the limb leads (1, 11, 111, AVR, AVL, AVF). The term "electrical axis" generally refers to the QRS complex.

A simple, though not precise,method of calculating the quadrant (or parts of a quadrant) in which the EA is located consist of using the maximal QRS deflection in leads 1 and AVF and if necessary, lead 11 (see figure 94-1).

Figure 94-1
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Figure 94-2
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Figure 94-3
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Figure 94-4
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Figure 94-5
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Figure 94-6
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In electrocardiographic language "injury" refers to abnormal ST-segment changes (see figure 94-2), "necrosis" implies abnormal Q waves, and "ischemia" implies symmetrical T-wave inversion (or elevation). According to current-of-injury theory, ST-segment elevation occurs when the injured muscle is located between normal muscle and the corresponding precordial electrode. On the other hand, ST-segment depression occurs when normal muscle is located between the injured tissue and the corresponding electrode.

Chronic ST-segment elevation indicates the existence of a large infarction, mainly anteriorly, usually with ventricular aneurysm.

Coronary artery disease (see definition on my website) is the most frequent cause of abnormal ST-segment changes.The latter, however, can be due to pericarditis (see definition and example of resultant ECG on my website) or to subendocardial injury resulting from the effects of drugs.


The ECG pattern of acut (generalized) pericarditis not due to MI is produced by the associated epicardial epimyocarditis, which in turn results in diffuse "epicardial injury". The ST segments can be elevated in all leads except AVR and rarely, in V I (see ECG in definition pericarditis). Symmetrical T- wave inversion (due to epicardial "ischemia") usually develops after the ST segments have returned to baseline (but can can appear during the injury stage). Neither reciprocal ST-segment changes nor abnormal Q waves are seen. In most cases of acute pericarditis, the PR segment is depressed in leads V 2-6. Average ECG resolution of acute pericarditis has to be differentiated from a normal variant cccurring in some normal young persons that is often referred to incorrectly as early repolarization. The latter consists, in the left chest leads, of normal ST-segment elevation associated with usually large R waves that have small r' deflections or notches starting above" the baseline (see figure 94-3 above).


Abnormal Q waves appearing several hours after total occlusion of a coronary artery result from the necrosis secondary to the decreased blood supply. The number of cells has to be large enough so as to produce changes reflected at the body surface. In general, the depth of the Q wave is proportional to the wall thickness involvement. Thus, in leads1 and V4-6, a QS complex reflects transmural necrosis. The duration of the Q wave is proportional to the extent of the area of necrosis parallel to the epicardial surface. If the latter starts in the subendocardium and extends toward (but not quite reaching) the epicardium, the corresponding leads will record QR or Qr complexes depending on the amount of living tissue located between thedead tissue and the recording electrode.

In the course of the clinical entity known as acute MI persisting Q waves are usually due to anatomia necrosis. Abnormal Q waves can occur in unstable angina, Prinzmetal's angina,coronary spasm (without chest pain), and exercise induced angina. Spontaneous recanalization of an occluded vessel, spontaneous reversion of the ischemia, or spasm and interventions that improve cellular metabolism and oxgenation can restoe the normal polarizatio. If these cells becomeexcitable, the abnormal Q waves may disappear or vanish.
Q waves that persist for more than one day may result from other causes than necrosis. Profound and prolonged ischemia can cause myocardial stunning with reversible functional, metabolic, ultrastructura, and electeophysiologic abnormalities. Thus, transient Q waves may be the electrocardiographic counterpart of the corresponding mechanical stunning. Myocardial hibernation refers to mechanical dysfunction of an ischemic area that is not transient but chronic.
Finally, abnormal Q waves may be due to primary (due to drugs or infection) cellular necrosis with normal coronary arterie and inother pathological processes such as myocardial infiltration and certain types of interventricular septal hypertophy.


Symmetrical T waves, upright or inverted as in figure 94-4 above, characteristic of electrocardiographic 'ischemia', are due to cellular affection resulting in prolongation of the action potential reflected in the QT interval.

The picture below, figure 94-4b, representing hyperacute ischemia shows tall, broad based T waves, which are not narrow and pinched together to a point at the apex or top of their height, as they are in hyperkalemia (see figure 94-28a).

hyperacute ischemia

Figure 94-4b


Alterations in the sequence of ventricular depolarization (as those produced by bundle branch block (see figure 94-5), ventricular pacing, ectopic ventricular impulse formation, preexcitation syndromes, and ventricular hypertrophy) result in a change in the sequence of ventricular repolarization. The latter causes nonischemic T-wave inversions (secondary T-wave changes) in leads showing a predominantly positive QRS deflection.


This is said to occr in around 50 to 75 percent of patients with the clinical diagnosis of acute MI.The initial changes also depend on the moment at which the ECG is recorded, in reference to the moment of occurrence of the infarction. Thus, the first ECG change is usually an abnormal T wave. The T wave may be increased in magnitude, prolonged, and either positive or negative. A straightening of the normal upward concavity of the ST segment also has been reported. In mostcases, the first ECG shows abnormal ST segment elevation and an increase in the R wave in leads exploring the affected area (figure 94-2). Subsequently, a Q wave appears, usually while the ST segment is elevated and generally before the T wave becomes negative. Thereafter the R wave becomes smaller and, as the ST segment returns to baseline, symmetrical T waves evolve.


Table 1 shows the location of the leads in which abnormal Q waves appears. It has to be understood, when classifying the location of an MI by the leads where abnormal Q waves occur, that the "affected" zone produced by the occlusion or spasm of a given vessel may and in fact does, extend beyond the the area of necrosis to one with injury alone. In other words, the region where normal Q waves and abnormal ST-sgment elevation are present is not one to which the necrosis or infarction is extended, but it is part of the originally affected zone.


In an inferior MI with abnormal Q waves and ST-segment elevation limited to this wall (that is without "affectation" of the posterobasal, or true posterior, wall), the reciprocal ST-segment changes will occur in diametrically opposed leads located in the same plane. For example, "indicative ST elevation in leads 1 and AVF, which record the electrical activity of the inferior (posteroinferior, or diaphramatic) wall, yields "reciprocal ST- segment depressionin leads 1 and AVL because they face the superior (anterolateral) wall (figs. 94-2 and 94-6, left).

For this reason, an inferior wall "injury" not affecting the posterobasal wall cannot produce "reciprocal" changes in a lead, such as V2, which is located in a plane perpendicular to the frontal plane. The perpendicularity between vertical lead AVF and horizontal lead lead V2 can best be seen in a left sagittal plane where lead AVF faces the inferior wall and leadV2 the anterseptal and posterobasal walls (fig. 94-6).


The "typical" pattern of non-Q-wave MI consist of abnormal ST-segment depression in all leads except AVR, which shows ST-segment elevation (fig. 94-7). These changes usually persist for several days rather than disappearing in minutes or hours, like in the transitory ST changes of syndromes of coronary ischemia.The diagnosis takes into consideration the clinical, enzymatic findings as well as the above plus the ischemic T-wave changes, nonspecific ST-T wave changes, or rarely a normal ECG.


An ST-segment elevation of at least 1mm in lead V4R in patients with acute inferior MI has a sensitivity of 100 percent, a specificity of 87 percent, and a predictive accuracy of 92 percent for the diagnosis of right ventricular infarction (fig. 94-8). These changes disappear within 10 to 18h after the onset of chest pain in 50 percent of patients and after 72h in the remaining patients.

The majority of patients with acute inferior infarction have abnormal regional function of the right ventricle. The incidence of right ventricular infarction in patients with obstruction of the right coronary artery and inferior infarction is in the 70 to 80 percent range. Occasionally, patients may have predominantly right ventricular involvement and exhibit right ventricular failure with signs of systemic congestion without pulmonary congestion. The infarction usually involves the posterior septum and posterior wall rather than the right ventricular free wall, which receives blood not only from the right coronary artery but also the conus artery and the septal branches of the left anterior descending artery.

These patients frequently require additional fluid to maintain adequate cardiac output. Diuretics and vasodilators may aggravate the volume status. Severe right ventricular dysfunction is uncommon.

Echocardiograhic studies may show a dilated right ventricle, which may have regional dysfunction, and abnormal motion of the atrial septum.


In left anterior fascicular block, the posteroinferior regions of the left ventricular endocardium are activated abnormally before the anterosuperior left ventricular area. After emerging from the posteroinferior division of the left bundle branch, the impulse first propagates in an inferior, rightward, and usually anterior direction for a short period of time. This orientation is responsible for the small q waves in leads1 and AVL and for the r waves in leads 11, 111, and AVF (fig. 94-9).

Occasionally, small q waves are not present in leads 1 and AVL. In the absence of MI, these initial QRS abnormalities have been attributed to "anatomic clockwise rotation of the heart" or to coexiting septal fibrosis or to incomplete LBBB. The latter cannot explain a similar orientation of the vectors when LAFB is present with "complete" right bundle branch block (RBBB) because ventricular activation cannot be a function of the "completely" blocked right branch. In these cases, diffuse septal fibrosis or anatomic clockwise rotation appear more probable. In pure LAFB, the general direction of the activation process (which determines the direction of the EA) occurs in a superior and leftward direction. Consequently, the fascicles of the left branch behave more as if they were "superior" and "inferior" rather than "anterior" and "posterior" (figs. 94-9, 94-10).

The degree of left axis deviation required for the diagnosis of complete LAFB is for the EA to be least -45 degrees or greater (fig. 94-10 tab2 and fig. 94-10 tab3 ).

When LAFB coexist with certain congenital types of right ventricular enlargement and extensive anterolateral MI, the EA can be shifted to the "undeterminate" (right superior) quadrant (fig. 94-11). Thus, the constant feature of the axis deviation produced by LAFB is its superior orientation, not its superior and leftward orientation (abnormal left axis deviation).

The appearance of LAFB does not increase QRS duration by more than 0.025s due to multiple interconnections between the fascicles of the left bundle. Thus, LAFB pattern with a prolonged QRS duration indicates the presence of additional conduction disturbances such as RBBB, MI, focal block, or a combination of these (fig. 94-12).


In pure left posterior fascicular block (LPFB), the impulse emerges from the unblocked anterosuperior division, thus producing small q waves in leads II, III, and aVF. Thereafter, the impulse moves through the electrically predominant left ventricle in an inferior and rightward direction, thus explaining the S waves in leads I and aVL as well as the R waves in leads II, III, and aVF. Radiologic studies of the human heart in situ have shown that the paraseptal regions of the posteroinferior (diaphragmatic) surface of the anatomic left ventricle are spatially located more to the right than certain (anterior) portions of the anatomic right ventricle. Since the portions of the left ventricle that are spatially located to the right are less than those located superiorly, the degree of right-axis deviation produced by pure LPFB is of lesser magnitude than that of left-axis deviation produced by LAFB. The hallmark of LPFB, therefore, is an "inferior" axis shift as much as "right" axis deviation (Figs.1LPFB to 3LPFB). Because a similar sequence of ventricular activation also can occur in right ventricular hyper-trophy, pleuropulmonary disease (acute or chronic), and extremely vertical anatomic heart positions due to a slender body build or chest wall deformities, it is evident that the diagnosis of "pure" LPFB cannot be made from the ECG alone. Additional clinical, radiologic, or pathologic information is required for this purpose.

See ECG findings below as a summary:

Left Posterior Fascicular Block (LPFB).... Very rare intraventricular defect!
Right axis deviation in the frontal plane (usually > +100 degrees)

rS complex in lead I

qR complexes in leads II, III, aVF, with R in lead III > R in lead II

QRS duration usually <0.12s unless coexisting RBBB

Must first exclude (on clinical grounds) other causes of right axis deviation such as cor pulmonale, pulmonary heart disease, pulmonary hypertension, etc., because these conditions can result in the identical ECG picture!

The changes imposed in LPFB by MIs of different locations are depicted in Figs. Figs.1LPFB to3LPFB below:

FIGURE 1LPFB Premature atrial beats showing increasing degrees of (incomplete and complete) LPFB aberration. The first beats in all panels are escape beats with the same morphology as that of sinus beats. The second, aberrantly induced ventricular complexes show different degrees of right-axis shift with an increase in size of the R waves in leads II and III. Note that the fundamental characteristic of LPFB was not right-axis deviation (beyond +90°) but an inferior-axis shift. (From Castellanos A, Myerburg RJ. The Hemiblocks in Myocardial Infarction. New York: Appleton-Century-Crofts; 1976. Reproduced with permission from the publisher and authors.

FIGURE 2LPFB. LPFB with RBBB. A. No MI. B. Anteroseptal MI (note q wave inin V2).C. Inferior MI (note ST-segment elevation and T-wave inversion in leads II and aVF with slight ST-segment depression in lead I).The differences in QRS complexes between A and C are not very marked because pure LPFB
may produce an almost abnormal Q wave in the inferior leads.

Figure 3LPFB: Pure (without RBBB) LPFB (third row) and LAFB (second row) occurring during acute anterior wall MI. Pre- and postfascicular block QRS morphologies are shown in the top and bottom rows, respectively.











Idiopathic Fascicular Ventricular Tachycardia

Indian Pacing Electrophysiol. J. 2004;4(3):98-103 Editorial

Johnson Francis, MD, DM*, Venugopal K, MD, DM†, Khadar SA, MD, DM‡, Sudhayakumar N, MD, DM§, Anoop K. Gupta MD, DM, DNB, FACCll


Idiopathic fascicular ventricular tachycardia is an important cardiac arrhythmia with specific electrocardiographic features and therapeutic options. It is characterized by relatively narrow QRS complex and right bundle branch block pattern. The QRS axis depends on which fascicle is involved in the re-entry. Left axis deviation is noted with left posterior fascicular tachycardia and right axis deviation with left anterior fascicular tachycardia. A left septal fascicular tachycardia with normal axis has also been described. Fascicular tachycardia is usually seen in individuals without structural heart disease. Response to verapamil is an important feature of fascicular tachycardia. Rare instances of termination with intravenous adenosine have also been noted. A presystolic or diastolic potential preceding the QRS, presumed to originate from the Purkinje fibers can be recorded during sinus rhythm and ventricular tachycardia in many patients with fascicular tachycardia. This potential (P potential) has been used as a guide to catheter ablation. Prompt recognition of fascicular tachycardia especially in the emergency department is very important. It is one of the eminently ablatable ventricular tachycardias. Primary ablation has been reported to have a higher success, lesser procedure time and fluoroscopy time.

Key words: Ventricular Tachycardia, Structural Normal Heart(as opposed to left posterior fascicular block discussed above), Radiofrequency ablation.


In general ventricular tachycardias have wide QRS complexes. One of the earliest descriptions of ventricular tachycardia (VT) with a narrow QRS complex was by Cohen et al in 1972.1 Their description was a left posterior fascicular tachycardia with relatively narrow QRS. In 1979, Zipes et al2 reported three patients with ventricular tachycardia characterized by QRS width of 120 to 140 ms, right bundle branch block morphology and left-axis deviation. These patients were young and had no major cardiac abnormalities. The arrhythmia could be induced by exercise, atrial and ventricular premature beats as well as atrial pacing and ventricular pacing. Belhassen et al observed that this tachycardia can be terminated by the calcium channel blocker verapamil3 This observation has been confirmed subsequently by others as well.4,5,6,7 Belhassen et al proposed that this is a specific ECG-electrophysiological entity.8 Fascicular tachycardia has also been called Idiopathic Left Ventricular Tachycardia (ILVT) by other authors, though left ventricular outflow tract VT also comes under the purview of this term.9,10 Fascicular tachycardia is usually paroxysmal, but a case which was persistent, leading to cardiac enlargement and complete resolution following therapy with verapamil has also been reported.4 Termination of idiopathic fascicular ventricular tachycardia by vagal maneuvers was noted in 4 cases by Buja et al.11 Successful radiofrequency catheter ablation was described by Klein et al.12 In this article we propose to review the current status of our knowledge regarding the genesis and treatment of idiopathic fascicular ventricular tachycardia.

Mechanism and Classification

Zipes et al postulated that the origin of the tachycardia was localized to a small region of reentry or triggered automaticity located in the posteroinferior left ventricle, close to the posterior fascicle of the left bundle branch.2 Response to verapamil suggested a role for the slow inward calcium channel in the genesis of the arrhythmia. Endocardial mapping during tachycardia revealed the earliest activation at the ventricular apex and mid septum.13 The tachycardia can be entrained by ventricular and atrial pacing. Entrainment by atrial pacing suggests easy access over the conduction system into the reentry circuit and hence a role for the fascicles in the reentrant circuit.14 Lau suggested the origin as reentry circuits involving the lower septum or posterior part of the left ventricle close to the endocardial surface in view of the response to radiofrequency ablation in these sites.15 Purkinje potential recorded in the diastolic phase during VT at the mid-anterior left ventricular septum in rare cases with RBBB pattern and right axis deviation suggested origin near left anterior fascicle in those cases.16
Recently Kuo et al has questioned the involvement of the fascicle of the left bundle branch in ILVT. 17 They studied two groups of patients with ILVT. One with left anterior or posterior fascicular block during sinus rhythm and the other without. They noted that the transition zone of QRS complexes in the precordial leads were similar during VT in both groups. New fascicular blocks did not appear after ablation. Therefore they concluded that the fascicle of the left bundle branch may not be involved in the anterograde limb of reentrant circuit in ILVT.
Fascicular tachycardia has been classified into three subtypes: (1) left posterior fascicular VT (Figure 1) with a right bundle branch block (RBBB) pattern and left axis deviation (common form); (2) left anterior fascicular VT with RBBB pattern and right-axis deviation (uncommon form); and (3) upper septal fascicular VT with a narrow QRS and normal axis configuration (rare form).18

Figure 1. 12 lead ECG of Idiopathic left ventricular tachycardia. It shows classical RBBB with leftward axis morphology suggestive of posterior fascicle origin.

Anatomical Substrate

Endocardial activation mapping during VT identifies the earliest site in the region of the infero-posterior left ventricular septum. This finding, along with VT morphology and short retrograde VH interval suggests a left posterior fascicular origin. Nakagawa and colleagues19 recorded high-frequency potentials preceding the site of earliest ventricular activation during the VT and sinus rhythm. These potentials are thought to represent activation of Purkinje fibers and are recorded from the posterior one third of the left ventricular septum. Successful RF ablation is achieved at sites where the purkinje potential is recorded 30 to 40 ms before the VT QRS complex.
Some date suggest that the tachycardia may originate from a false tendon or fibro- muscular band that extends from the posteroinferior left ventricle to the basal septum.20 Histological examination of false tendon disclosed abundant Purkinje fibers.

Electrophysiological Study

Fascicular tachycardia can be induced by programmed atrial or ventricular stimulation in most cases. Isoprenaline infusion may be required in certain cases; rarely there may be difficulty in induction despite isoprenaline infusion. Endocardial mapping identifies the earliest activation in the posteroapical left ventricular septum in patients with posterior fascicular tachycardia.
A high frequency potential with short duration, preceding the QRS has been described as the Purkinje potential (Figure 2). This has also been called P potential and diastolic potential. P potentials can be recorded both in sinus rhythm and during ventricular tachycardia. Pacing at sites manifesting the earliest P potential produces QRS complexes identical to that of the clinical tachycardia.19

Figures 2. Intracardia electrogram during tachycardia showing purkinje potential, which persisted after the ablation also (arrow).







Pharmacological Therapy

Intravenous verapamil is effective in terminating the tachycardia. However the efficacy of oral verapamil in preventing tachycardia relapse is variable. Good response and resolution of tachycardiomyopathy with verapamil treatment was noted by Toivonen et al4, while Chiaranda et al commented on the poor efficacy.21 Treatment with propranolol has also resulted in cure of arrhythmia and resolution of features of tachycardiomyopathy in another case with incessant fascicular VT.22 Though fascicular tachycardias do not generally respond to adenosine, termination of VT originating from the left anterior fascicle by intravenous adenosine has been documented.23

Catheter Ablation

The young age of most patients with need for long-term antiarrhythmic treatment and attendant side effects prompted the search for curative therapies. Fontaine et al (1987) described successful treatment of ILVT by application of a high-energy DC shock (fulguration) between the catheter tip and a neutral plate placed under the patient's back.24 Klein et al (1992) reported cure of ILVT by radiofrequency catheter ablation.25 Since then radiofrequency has remained the procedure of choice.
Different approaches for radiofrequency ablation have been described by various authors. Nakagawa et al preferred careful localization of the Purkinje potential in guiding ablation. They selected the area where a Purkinje potential precedes the QRS complex during tachycardia.19 Wellens et recommend pace mapping with a match between the 12 simultaneously recorded ECG leads during pacing and the clinical tachycardia for localizing the site of ablation.9 They hypothesize that pathways within the Purkinje network that are not included in the reentry circuit responsible for the tachycardia may also become activated. Ablation of those regions may not result in interruption of the tachycardia circuit.

Primary Radiofrequency Ablation

Since fascicular VT is sometimes difficult to induce despite pharmacological provocation, some workers (Gupta et al) prefer primary ablation. In a recent report, seven cases of incessant fascicular VT were successfully ablated with no recurrence.26 They reported a shorter procedure time, significantly lower fluoroscopy time and lesser number of radiofrequency energy deliveries in the primary versus elective groups. The longer procedural time during elective ablation was mainly due to the time spent in induction of fascicular VT.


1. Cohen HC, Gozo EG Jr, Pick A. Ventricular tachycardia with narrow QRS complexes (left posterior fascicular tachycardia). Circulation. 1972 May; 45(5): 1035-43.

2. Zipes DP, Foster PR, Troup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: reentry versus triggered automaticity. Am J Cardiol. 1979; 44:1-8.

3. Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil. Br Heart J. 1981 Dec; 46(6): 679-82.
4. Toivonen L, Nieminen M. Persistent ventricular tachycardia resulting in left ventricular dilatation treated with verapamil. Int J Cardiol. 1986; 13(3): 361-5.

5. Tai YT, Chow WH, Lau CP, Yau CC. Verapamil and ventricular tachycardias. Chin Med J (Engl). 1991 Jul; 104(7): 567-72.

6. Ward DE, Nathan AW, Camm AJ. Fascicular tachycardias sensitive to calcium antagonists. Eur Heart J. 1984;5:896-905.

7. Sethi KK, Manoharan S, Mohan JC, Gupta MP. Verapamil in idiopathic ventricular tachycardia of right bundle-branch block morphology: observations during electrophysiological and exercise testing. Pacing Clin Electrophysiol. 1986;9:8-16.

8. Belhassen B, Shapira I, Pelleg A, Copperman I, Kauli N, Laniado S. Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: an ECG-electrophysiologic entity. Am Heart J. 1984 Oct; 108(4 Pt 1): 1034-7.
9. Wellens HJJ, Smeets JLRM. Idiopathic Left Ventricular Tachycardia: Cure by Radiofrequency Ablation. Circulation. 1993; 88(6): 2978-2979.

10. Thakur RK, Klein GJ, Sivaram CA et al. Anatomic Substrate for Idiopathic Left Ventricular Tachycardia. Circulation. 1996;93:497-501.

11. Buja G, Folino A, Martini B et al. Termination of idiopathic ventricular tachycardia with QRS morphology of right bundle branch block and anterior fascicular hemiblock (fascicular tachycardia) by vagal maneuvers. Presentation of 4 cases. G Ital Cardiol. 1988 Jul; 18(7): 560-6.

12. Klein LS, Shih H, Hackett FK, Zipes DP, Miles WM. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease. Circulation. 1992;85:1666-1674.

13. German LD, Packer DI, Bardy GH, Gallagher JJ. Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac disease. Am J Cardiol. 1983;52:1202-1207.

14. Okumura K, Matsuyama K, Miyagi II, Tsuchlya T, Yasue H. Entrainment of idiopathic ventricular tachycardia of left ventricular origin with evidence for re-entry with an area of slow conduction and effect of verapamil. Am J Cardiol. 1988;62:727-732.

15. Lau CP. Radiofrequency ablation of fascicular tachycardia: efficacy of pace-mapping and implications on tachycardia origin. Int J Cardiol. 1994 Oct; 46(3): 255-65.

16. Nogami A, Naito S, Tada H et al. Verapamil-sensitive left anterior fascicular ventricular tachycardia: results of radiofrequency ablation in six patients. J Cardiovasc Electrophysiol. 1998 Dec; 9(12): 1269-78.

17. Kuo JY, Tai CT, Chiang CE et al. Is the fascicle of left bundle branch involved in
the reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia? Pacing Clin Electrophysiol. 2003 Oct; 26(10): 1986-92.

18. Nogami A. Idiopathic left ventricular tachycardia: assessment and treatment. Card Electrophysiol Rev. 2002 Dec; 6(4): 448-57.

19. Nakagawa H, Beckman KJ, McClelland JH, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation. 1993;88:2607-2617.

20. Kudoh Y, Hiraga Y, Iimura O. Benign ventricular tachycardia in systemic sarcoidosis--a case of false tendon. Jpn Circ J. 1988 Apr; 52(4): 385-9.

21. Chiaranda G, Di Guardo G, Gulizia M, Lazzaro A, Regolo T. Ital Heart J. 2001 Nov; 2(11 Suppl): 1181-6.

22. Anselme F, Boyle N, Josephson M. Incessant fascicular tachycardia: a cause of arrhythmia induced cardiomyopathy. Pacing Clin Electrophysiol. 1998; 21: 760-3.

23. Kassotis J, Slesinger T, Festic E, Voigt L, Reddy CV. Adenosine-sensitive wide-complex tachycardia: an uncommon variant of idiopathic fascicular ventricular tachycardia--a case report. Angiology. 2003 May-Jun; 54(3): 369-72.

24. Fontaine G, Tonet JL, Frank R et al. Treatment of resistant ventricular tachycardia by endocavitary fulguration associated with anti-arrhythmic therapy. Eur Heart J. 1987 Aug; 8 Suppl D: 133-41.

25. Klein LS, Shih H, Hackett FK, Zipes DP, Miles WM. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease. Circulation. 1992;85:1666-1674.

26. Gupta AK, Kumar AV, Lokhandwala YY et al. Primary radiofrequency ablation for incessant idiopathic ventricular tachycardia. Pacing Clin Electrophysiol. 2002 Nov; 25(11): 1555-60.

Complete RBBB

A " complete RBBB pattern (with QRS duration > 0.11s) does not necessarily reflect the existence of a total conduction block in the right branch. This pattern only indicates that the entire or major parts of both ventricles are activated by the impulse emerging from the left branch. Thus, a significant degree of conduction delay ("high-grade" or "incomplete RBBB) can produce a similar pattern.

In pure complete RBBB, the EA should not be deviated abnormally either to the left or to the right. These axis deviations reflect coexisting fasicicular block or right ventricular hypertrophy.

Causes of RBBB Pattern

BBB is rarely a clinical problem of any consequence except when the block occurs simulanteously in both branches.

Causes of the RBBB include the following:

1. Surgical trauma from a heart operation for congenital heart diseases like a ventricular septal defect, atrial septal defect and use of catheters etc.

2. A disease which interrupts the heart fibers like a prior heart attack (myocardial infarction) causing fibrosis.

3. Chronic lung disease (cor pulmonale)

4. Elongation of the right bundle due to a congenital volume overload of the right ventricle(stretched or dilated)

5. Age associated predisposition in the elderly to sinus node dysfunction, abnormal conduction in the AV node, His-Purkinje system, and inthe bundle branches.

6. Sarcoidosis, rheumatic fever, amyloiosis, systemic lupus erythematosis, gout, familial heart block etc.

Reference:Castellanos,A. and others,Hurst's The Heart 8th Edition,The Resting Electrocardiogram,321-356.

Incomplete RBBB Pattern

Incomplete RBBB patterns can be produced by the following mechanisms
(1) different degrees of conduction delays through the main trunk of the right bundle branch (fig. 94-17);
(2) an increased conduction time through an elongated right bundle branch that is stretched because of a concomitant enlargement of the septal surface (as in congenital volume overload of the right ventricle);
(3) a diffuse Purkinje-myocardial delay due to right ventricular stretch or dilatation;
(4) surgical trauma or disease-related interruption of the major ramifications of the right branch ("distal" RBBB or "right fascicular blocks"); or
(5) congenital variations of the distribution of the major ramifications resulting in a slight delay in the activation of the crista supraventricularis.

Reference:Castellanos,A. and others,Hurst's The Heart 8th Edition,The Resting Electrocardiogram,321-356.

Concealed RBBB

A conduction delay in the main trunk of the right bundle or in its major ramifications may be concealed (not manifested in the surface ECG) when there are coexisting (and of greater degree) conduction disturbances in the main left bundle branch, the anterosuperior division of the left bundle branch and/or the free left ventricular wall.

A RBBB can also be concealed in some patients with Wolff-Parkinson-White syndrome if the ventricular insertion of the accessory pathway causes preexcitation of the right ventricular regions that would be activated late because of the RBBB.

Reference:Castellanos,A. and others,Hurst's The Heart 8th Edition,The Resting Electrocardiogram,321-356.

Complete LBBB

This conduction disturbance is characterized by wide (greater than 0.11s) QRS complexes. The diagnostic criteria consist of prolongation of the QRS complexes (over 0.11s) with neither a q wave nor an S wave in lead V1 and in the "properly placed" V6. A wide R wave with a notch on its top ("plateau") is seen in these leads. In hearts with an electrical (and anatomic) vertical position a small Q wave may be seen in AVL in the absence of MI. Right chest lead V1 may or may not show an initial r wave, but the latter should be present in lead V2. Unfortunately, as mentioned in reference to complete RBBB, a complete LBBB form can be recorded in patients with high degree (not necessarily complete) LBBB. The direction of the electrical axis in patients showing QRS changes typical of complete LBBB has also been widely discussed.
In the majority of the human hearts, the site of exit from the right bundle branch does not seem to be at the lowermost right ventricular region (that called in pacemaker nomenclature the right ventricular apex). If this were the case, all complete LBBBs would show (as when the right ventricular apex is paced) abnormal left axis deviation whereas the electrical axis in "uncomplicated" complete LBBB block usually is not located beyond -30 degrees.

Reference: Castellanos, A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.

Complete LBBB with MI

Normally, in complete LBBB, the impulse emerges from the right bundle branch and propagates to the left and slightly anteriorly. This orientation of the initial forces tend to abolish previously present inferiorly and laterally located abnormal Q waves characteristic of inferior and lateral MI. If the infarction is anteroseptal, however, the impulse cannot propagate toward the left. Instead, the initial vectors point toward the free wall of the right ventricle because now the right ventricular free-wall forces are not neutralized by the normally preponderant septal and/or initial left ventricular free Thus, a -wall forces. Thus, a small q wave will be recorded in leads (1, V5, and V6) where it is not normally recorded in complete LBBB (Fig. 94-18).

The most sensitive sign to detect acute MI is ST-segment elevation in leads facing the affected region (Fig. 94-19).

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.

Incomplete LBBB Pattern

An incomplete LBBB pattern can be diagnosed in a heart with an electrically horizontal (or semihorizontal) heart position when leads 1 and V6 show an R wave with a slurring in its upstroke ( not on its top, as incomplete LBBB). Lead V1 shows Rs or QS complexes, and lead V2 shows Rs complexes. Although QRS duration usually ranges between 0.o8 and 0.11s , this pattern can be observed with QRS durations of 0.12 and 0.13s.

Not surprisingly, an incomplete LBBB pattern can be produced by various processes, including the following
(1) conduction delays in the main trunk of the left bundle branch,
(2) conduction delays (of more or less equal degree) in the fascicles of the left bundle branch,
(3) diffuse septal fibrosis,
(4) small septal infarcts,
(5) left ventricular enlargements (generally due to pressure overloading) in patients with congenital heart disease, and
(6) combinations of all of the above.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.

Wide QRS Complexes in Patients with Manifest Preexcitation Syndromes

The characteristic pattern of manifest Wolff-Parkinson-White syndrome consists of a short PR interval (reflecting faster than normal conduction through an accessory pathway of the Kent bundle type) preceding a wide QRS complex. The latter usually shows an initial slurring (delta wave) followed by a terminal, slender part. The classical ventricular complex is a fusion beat resulting from ventricular activation by two wave fronts. One, traversing the accessory pathway, produces the delta wave. The other, emerging from the normal pathway, is responsible for the terminal, more normal parts of the QRS complex.

The degree of preexcitation (amount of muscle activated through the accessory pathway) depends on many factors. Foremost among these are the distance between the sinus node and atrial insertion of accessory pathway and, more important, the differences in conduction time through the normal pathway and accessory pathway.

Other things being equal, a patient with rapid (enhanced) AV nodal conduction will have a smaller delta wave than a patient with slow conduction through the AV node. Moreover, if there is total block at the AV node or His-Purkinje system, the impulse will be conducted exclusively via the accessory pathway. When this occurs, the QRS complexes are no longer fusion beats, since the ventricles are then activated exclusively from the preexcited site. Consequently, the delta wave disappears and the QRS complexes are different than fusion beats, though the direction of the delta wave remains the same.

Moreover, the QRS complexes are as wide as (and really simulating) those produced by artificial or spontaneous beats arising in the vicinity of the ventricular end of the accessory pathway.

Also of importance are the characteristics of the QRS complexes of beats without preexcitation in relationship to the characteristics of beats resulting from exclusive accessory pathway conduction (which in turn depends on the location of the pathway). Not surprisingly, the EA can show marked changes when fusion beats are compared with pure peexcited beats (figure 94-20).

There are three major methods available for the anatomic localization of accessory pathways, namely intra operative mapping, catheter electrode techniques, analysis of the 12-lead ECG (least accurate but the easiest).

Left free-wall accessory pathways are characterized by negative or isoelectric delta waves in one of leads 1, AVL, V5 or V6. Lead V1 shows RS or R complexes (fig. 94-20). During sinus rhythm, the electrical axis may be normal, but when atrial fibrillation develops and elusive accessory pathway conduction occurs, the EA is deviated to the right and inferiorly (figure 94-20).

Posteroseptal accessory pathways show negative or ioselectric delta waves in two of LEADS 11, 111, or AVF and RS (or R) waves in V1,V2, or V3 (figure 94-21).

An Rs (or RS) wave in V1 suggests left paraseptal pathway; a QS complex in the same lead may correspond to a right paraseptal pathway.

Right free-wall accessory pathways display an LBBB pattern defined, for purposes of accessory pathway localization, by an R wave greater than 0.09s in lead 1 and rS complexes in leads V1 and V2 with an EA ranging between+30 degrees to - 60 degrees (fig. 94-22).

The most rare right anteroseptal accessory pathways show an LBBB pattern with an EA between +30 degrees and +120 degrees (fig. 94-23). A q wave may be present in lead AVL but not in leads 1 orV6.

Mixed patterns may result from the existence of two separate accessory pathways.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.


Clues to left atrial hypertrophy include (1) P-wave duration greater than 0.11 s and notched P wave with an interpeak interval in excess of 0.04 s and (2) negative phase of P in V1 longer than 0.04 s and greater than 1 mm in lead VI. These criteria apply to intraatrial block actually, and if found in patients with left ventricular enlargement or mitral stenosis, then left atrial hypertrophy is most likely present. The ECG pattern of left atrial hypertrophy results from a hypertrophy- induced intraatrial conduction delay.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.


As emphasized by Surawicz, since the advent of other noninvasive techniques, there has been a changing role for the ECG in the diagnosis of ventricular hypertrophy. Necropsy studies have exposed the superiority of echocardiography with respect to electrocardiography to detect LV hypertrophy. Echocardiography is also a better method for the serial follow-up of changes during progression or regression of LV hypertrophy. Multiple criteria have been proposed to diagnose LV hypertrophy using necropsy or echocardiographic information (Table 3 and Table 4). Of these, the Sokolow-Lyon criterion (SV1 + RV5,6 _35 mm) is the most specific (>95 percent) but is not very sensitive (45 percent) (see Table 4). The Romhilt-Estes score has a specificity of 90 percent and a sensitivity of 60 percent in studies correlated with echocardiography. The following are some of the other criteria49: The Casale (modified Cornell) criterion (Ravl + SV, >28 mm in men and >20 in women) is somewhat more sensitive but less specific than the Sokolow-Lyon criterion. The Talbot criterion (R _16 mm in avL) is very specific (>90 percent), even in the presence of MI and ventricular block, but not very sensitive. The Koito and Spodick criterion (RV6> RV5) claims a specificity of 100 percent and a sensitivity of more than 50 percent. According to Hernandez Padial, a total 12-lead QRS voltage of greater than 120mm is a good ECG criterion of LV hypertrophy in systemic hypertension and is better than those most frequently used. With echocardiography as the "gold standard," several authors postulated ECG criteria for diagnosis of LV hypertrophy in the presence of complete LBBB and LAFB . The high sensitivity and specificity reported by Gertsch et al. for diagnosis of LV hypertrophy with LAFB have not been corroborated in preliminary studies performed in the department of A.Castellanos and others,Hurst,s THE HEART,10ty Edition,Chpt.11,p.302.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.


Right ventricular hypertrophy is manifest in the ECG only when the right ventricular forces predominate over those of the left ventricle. Since the latter has, roughly, three times more mass than the former, the right ventricle may double in size (when the left ventricle is normal) or triple its weight (when there is significant LVH) and still not result in the necessary requirements to pull the electrical forces anteriorly and to the right. For these reasons, RVH cannot be recognized easily in adult patients.
The ECG manifestations of RVH or enlargement can be divided into the following three main types :
(1) the posterior and rightward displacement of QR forces associated with low voltage, as seen in patients with pulmonary emphysema (fig. 94-24);
(2) the incomplete RBBB pattern occurring in patients with chronic lung disease and some congenital cardiac malformation resulting in volume of the right ventricle (fig. 94-25);
(3) the true posterior wall myocardial infarction pattern with normal to low voltage of the R wave inV1 (fig. 94-26);
(4) and the classical right ventricular hypertrophy and strain pattern as seen in young patients with congenital heart disease (producing pressure overloading) or adult patients with high pressure ("primary " pulmonary hypertension) (fig. 94-27). False patterns of RVH may occur in patients with true posterior (basal) MI, complete RBBB with LPFB and Wolff-Parkinson- White syndrome resulting from AV conduction through the left free wall, or posteroseptal accessory pathways.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.


Because multiple factors can affect ventricular repolarization in diseased hearts, the finding characteristic of a specific electrolyte abnormality may be modified, and even mimicked, by various pathological processes and the effects of certain drugs. The major problem with the ECG diagnosis of electrolyte imbalance is not the negative ECG with abnormal serum values. But the production of similar changes by other conditions in patients with normal serum values.


The initial effect of acute hyperkalemia is the appearance of peaked T waves with a narrow base (Fig. 94-28a, left).The diagnosis of hyperkalemia is almost certain when the duration of the base is 0.20s or less (with rates between 60 and 110 per minute). As the degree of hyperkalemia increases, the QRS complex widens with the EA usually being deviated abnormally to the left, and rarely to the right (Fig. 94-28b). In addition, the PR interval prolongs, and the P wave flattens until it disappears (Fig. 94-28c).

The effect of hyperkalemia on cardiac rhythm is complex, and virtually any arrhythmia may be seen. Various bradyarrhythmias, including impaired AV conduction and complete AV block, may occur. If untreated, death ensues either due to ventricular standstill or coarse slow ventricular fibrillation.

Death can also result if wide QSR complexes (due to hyperkalemia) occurring at fast rates are diagnosed as ventricular tachycardia and the patient is treated with antiarrhythmic drugs.

In other circustances, tachycardias may result, including sinus tachycardia, frequent ventricular extrasystoles, ventricular tacycardia, and ventricular fibrillation.
The rate of K elevation appears to influence the type of arrhythmia produced. A slow elevation of K produces widespread block and depressed automaticity, and rapid infusions produce ventricular ectopic rhythms and terminally ventricular fibrillation.
Moderate hyperkalemia has been noted to suppress supraventricular and ventricular ectopic beats in about 80% of patients.

On the other hand, Class1A and ClassC drugs as well as large doses of tricyclic antidepressants (especially when ingested for suicide purposes) can also produce marked QRS widening. These processes, however, do not coexist with narrow-based, peaked T waves.

Rarely, hyperkalemia produces ( in the absence of coronary artery disease) a degree of ST-segment elevation in the right chest leads capable of suggesting anteroseptal myocardial injury (Fig. 94-28d). These constitute the "dialyzable currents of injury in potassium" reported by Levine et al.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram, 321-356.
Reference:Rardon,D.F. and Fisch,C.,Electrolytes and the Heart,Hurst's The Heart, 8th Edition ,Ch.37,759-774.


The abnormal and delayed repolarization that occurs in hypokalemia is best expressed as QU, rather than QT, prolongation, since at times it can be difficult to differentiate between notching of the T wave and T- and U- wave fusion. As the serum potassium falls, the ST-segment becomes progressively more depressed and there is a gradual blending of T wave into what appears to be a tall U wave (Fig. 94-29a). Decreased amplitude of the T wave, an increase in U-wave amplitude, and ST-segment depression produce a rather characteristic undulating appearance to the baseline very suggestive of hypokalemia (Fig. 94-29b). When hypokalemia is severe, the QRS complex may widen slightly in a diffuse manner. The P-wave amplitude may be increased and the PR interval is often slightly prolonged.

The changes in the ECG correlate with the plasma K level fairly well,being found in 78% of patients with plasma K below 2.7 meq/liter, in 35 % of those with K between 2.7 and 3.0 meq/liter, and in10% with K between 3.0 and 3.5 meq/liter.

Hypokalemia promotes the appearance of supraventricular and ventricular ectopic rhythms, being enhanced by increased automaticity and/or facilitation of reentry.

The effects of digitalis on the myocardium are modified by the extracellular K concentration. Digitalis glycosides inhibit the Na-K-ATPase, increasing intracellular Na and reducing K. This interrelationship between digitalis and K is manifest by
(1) depression of digitalis-induced ectopy by K,
(2) emergence of digitalis-induced ectopy during hypokalemia, and
(3) enhancement of digitalis-induced depression of conduction by K.

The major sign of digitalis toxicity is increased automaticity with extrasystoles or tachycardias (like nonparoxysmal junctional tachycardia and atrial tachycardia with block), both of which are potentiated by low serum K. The administration of K is safe and quite effective in suppressing these arrhythmias.

Because of the differing sensitivities of the Purkinje and AV junctional tissues to K, there is a significantly wide margin of safety between the antiectopic and the AV depressant effects of K. This margin of safety permits judicious administration of K for control of life-threatening arrhythmias, even in the presence of simple AV conduction delay.

An ECG pattern similar to that of hypokalemia can be produced by some antiarrthythmic drugs, especially quinidine. These quinidine-induced repolarization changes may appear in patients receiving therapeutic doses who do not have elevated serum levels. Although at times these changes simply reflect that the patient is taking the drug, they should be viewed with extreme caution. When repolarization is greatly prolonged, however, they lead to multiform ventricular arrhythmias, including the so-called torsades de pointes (Fig. 6, 7, 9b).

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.
Reference:Rardon,D.F. and Fisch,C.,Electrolytes and the Heart,Hurst's The Heart, 8th Edition ,Ch.37,759-774.


Hypomagnesemia does not produce QU prolongation unless the coexisting hypokalemia (with which it is almost invariably associated) is severe. Long-standing and very marked magnesium deficiency lowers the amplitude of the T wave and depresses the ST-segment. It is difficult to differentiate between the changes produced by magnesemia from those produced by potassium. Elevation of extracellular Mg to a level of 6 to 10 meq/l depresses AV and intraventricular conduction. Sinoatrial and AV block occur at 15 meq/l, and cardiac arrest may be expected at levels of 15 to 22 meq/l.
Hypomagnesemia may predispose to digitalis toxicity.

Administration of intravenous magnesium sulfate to patients with prolonged QT intervals and torsades de pointes, whether the initial Mg level is normal or low, may suppress the ventricular arrhythmia.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.
Reference:Rardon,D.F. and Fisch,C.,Electrolytes and the Heart,Hurst's The Heart, 8th Edition ,Ch.37,759-774.


During sinus rhythm with normal rates the QT interval is short (Fig. 94-29a bottom). If factors known to modify the QT are not present, it has been said that a reasonably accepted correlation exist between the duration of the interval and serum calcium levels. The primary manifestation of hypercalcemia is a marked decrease in the duration of the ST segment. The Twave may actually begin at the end of the QRS complex, and virtually no ST segment may be present. This change produces a decrease in the length of the QTc interval. There is a lack of correlation QTc and serum calcium. The interval from the qt to the apex of the T wave can be measured most precisely and shows the best correlation with the Ca level (Fig. 94-29c).
First degree AV block may be seen. Cardiac arrhythmias secondary to hypercalcemia are unusual.
Occasionally, the ST segment is depressed and the T waves may become inverted in the left and the right ventricular chest leads.

Digitalis also shortens the QT interval but produces its characteristiac "effects" in leads where the R wave predominate. The classical upward concavity of the ST segment is seen in the left chest leads in patients with LVH and in V1 and V2 when there is RVH (with predominantly positive deflections in these leads).

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.
Reference:Rardon,D.F. and Fisch,C.,Electrolytes and the Heart,Hurst's The Heart, 8th Edition ,Ch.37,759-774.


The typical ECG pattern of hypocalcemia consists of QT prolongation due to ST segment prolongation.The QTc rarely exceeds 140% of normal. If hte QT exceeds that number, the U wave is likely to be included in the measurement.
The T wave is usually of normal width but can be narrow based if there is coexistent (moderate) hyperkalemia (Fig. 94-30a), most often seen in patients with chronic renal failure (Fig. 94-30b). A very marked subendocardial ischemia (with the so-called hyperacute ST-T changes) can produce a similar pattern, but in those cases the T wave, though peaked, is not as narrow based.
Similarly, hypocalcemia in association with a terminal wave consisting of both the T and the U waves. While the ST segment is prolonged, the total QU interval remains normal.
It has been said that hypocalcemia per se does not produce T wave inversion. When present, the latter is usually a reflection of coexisting processes such as LVH and incomplete LBBB.
An ECG pattern similar to that of hypocalcemia can be produced by organic abnormalities of the central nervous system and by congenitally prolonged QT intervals such as the Jervell and Lange-Nielsen and Romano-Ward syndromes.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356
Reference:Rardon,D.F. and Fisch,C.,Electrolytes and the Heart,Hurst's The Heart, 8th Edition ,Ch.37,759-774.


Lithium is important in cardiac electrophysiology because of its wide use in the management of depressive disorders. Reversible T- wave changes are the most common ECG abnormality due to lithium. Dysfunction of the SA node is the characteristic and clinically significant complication of Li therapy. Disordered sinus node function may be manifested by sinus bradycardia, SA arrest, or exit block, either type 1 (Wenckebach) or type 11 (Mobitz 11) (see definition of sinus bradycardia, figures 16, 17, exit block, atrioventricular conduction disturbances, figures 84-92 on this website). These side effects occur most often within the therapuetic range. The effect of lithium on SA node appears to be selective as suggested by a normal PR, a normal QRS, and in the HIS electrogram, a normal AH with only slightly prolonged HV interval.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356
Reference:Rardon,D.F. and Fisch,C.,Electrolytes and the Heart,Hurst's The Heart, 8th Edition ,Ch.37,759-774.

Long QT syndrome (LQTS)

This is an inherited disorder ot cardiac repolarization, characterized by ECG
abnormalities, syncopal attacks and risk of sudden death due to ventricular
tachyarrhythmias such as torsade de pointes (figure 13, see definition of
ventricular tachycardia on this website). The LQTS may occur as an
autosomal dominantly inherited form (Romano-Ward syndrime, RWS), or as a
part of the autosomal recessively inherited Jervell and Lange-Nielson
syndrome (JLSN) in which prolongation of the QT interval is assoociated with
sensorineural deafness. The LQTS is associated with significant morbidity
and mortality, with estimated annual rates of 5% and 1% for syncope and
death, respectively. A recent study found a single missense mutation of the
KCNQ1 gene (a potassium channel gene) accounting for 30% of Finnish
cases with the LQTS, which may be associated with both the RWS and JLNS
phenotypes of the syndrome.

Reference:Piipo,K, and others,A founder mutation of the potssium
channelkcnq1 in long qt syndrome,JACC,Vol.,37,No.2,2001,562-567.


Although it is not always easy to differentiate between prolonged QT and QU intervals, determining the existince of prolonged repolarization is not difficult, especially if indeterminate (V3 and V4) chest leads are analyzed. For these reasons, it has been recommended that the single, more comphrensive, delayed depolarization syndrome be used (Table 5). In these cases, long strips should be obtained since the duration of the depolarization, though greater at slower rates (or longer cycle lengths) as well as under normal conditions, differs from the latter in the magnitude of its brady cardia dependency.

Reference: Castellanos,A. and others, Hurst's The Heart 8th Edition, The Resting Electrocardiogram,321-356.


Characteristic ECG changes develope when the body temperature drops to approsimately 30 degreesC. In addition, deflection, called the Osborn wave, appears in a place said to be located between the end of the QRS complex and the beginning of the ST segment (fig. 94-31). This deflection has been attributed to delayed depolarization. In leads facing the left ventricle, the deflection is positive and its is inversely related to body temperature.

Brugada Syndrome

Brugada syndrome, a primary electrical disease of the heart, is characterized by a pattern of RBBB and ST-segment elevation in electrocardiogram (ECG) leads V1-V3 (Figures 94-32, 94-33) and caused by a defect in ion channel genes, resulting in abnormal electropysiological activity in the right ventricle and propensity to malignant tachyarrhythmias. It occurs particularly frequently in Asian countries.

The mechanisms responsible for the arrhythmogenesis in this syndrome are currently unknown. Recent studies have linked the pathogenesis of the ECG manifestations of this syndrome to heterogeneous loss of the action potential dome, causing a marked epicardial and transmural disperion of repolarization, which may result in the production of ST-segment elevation, thus giving rise to phase 2 re-entry. These observations support the hypothesis that the mechanism of malignant ventricular arrhythmias (Figure 94-34) in this syndrome is caused by repolarization abnormality.

Another explanation of arrhythmogenesis in this syndrome is the presence of delayed conduction in the right ventricle,which may support the conduction abnormality hypothesis. It has been found that the late potential (LP) detected by signal average ECG (Figure 94-34) is a noninvasive risk stratifier in these patients.
Nevertheless, electrophysiologic testing--including provocative tests of induciblity of VT/VF and drug effects on:
1) the magnitude of the ST-segment elevation ,
2) induciblity of VT/VF--remain the tool most appropiate for confirmation of diagnosis and risk stratification in patients with BRS.

Reference:Ikeda,T.,MD,and others,Assement of noninvasive Markers in Identifying Patients at Risk in the Brigada Syndrome:Insight into Risk Stratification,JACC,Vol.37,No.6,2001,1630-1634.
Reference:Gussak,Ihor,MD,and others,Clinical Diagnosis and Risk Stratification in Patients with Brugada Syndrome,JACC,Vol.37,No.6,2001,1635-1638.