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Blood Pressure and You
Medical tests

Main Content: Electrocardiogram (ECG) and high blood pressure

ECG (electrocardiogram) and high blood pressure

ECG (electrocardiogram) and high blood pressure

An electrocardiogram (ECG) is a test which measures the electrical activity of your heart to show whether or not it is working normally.

An ECG records the heart’s rhythm and activity on a moving strip of paper or a line on a screen. Your doctor can read and interpret the peaks and dips on paper or screen to see if there is any abnormal or unusual activity.

What can an ECG (electrocardiogram) show?

An electrocardiogram can be a useful way to find out whether your high blood pressure has caused any damage to your heart or blood vessels. Because of this, you may be asked to have an ECG when you are first diagnosed with high blood pressure.

Some of the things an ECG reading can detect are:

  • cholesterol clogging up your heart’s blood supply
  • a heart attack in the past
  • enlargement of one side of the heart
  • abnormal heart rhythms

How is an ECG carried out?

An ECG (electrocardiogram) is a safe and painless test which normally only takes a few minutes.

Leads from an electrocardiograph machine are attached to the skin on your arms, legs and chest using sticky patches. These leads read signals from your heart and send this information to the electrocardiograph. The machine then prints the reading on a paper strip or on a screen.

There are three main types of ECG: 

  • Resting ECG – if your doctor is interests in how your heart is working while you are at rest, you will be asked to lie down and relax while the heartbeat is being recorded.
  • Exercise ECG – your doctor may be interested in how your heart reacts to activity and you will be asked to walk or run on a treadmill or cycle on an exercise bike while your heartbeat is recorded.
  • 24-hour ECG – sometimes it can be helpful to monitor your heartbeat throughout the day, in which case you will be asked to wear a small electrocardiograph machine. The recordings from the machine are then read by your doctor when you return the machine.

Who will carry out my electrocardiogram?

You may be able to have your ECG in your GP surgery. However not all surgeries have this equipment so you may be referred to a local hospital to carry out the test.

Is there anything I need to do before an ECG (electrocardiogram)?

If you are having a resting ECG, there is no need to do anything different before having the test.

If you are having an exercise ECG, make sure that you are wearing comfortable clothes and shoes that you can exercise in. It is also helpful to avoid eating a meal or drinking a caffeinated drink for two hours before the test because these can affect your heart’s rhythm.

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heart author" faq

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

to enlarge

Figure 94-2

to enlarge

Figure 94-3

t o

enlarg e

Figure 94-4

to enlarge

Figure 94-5

to enlarge

Figure 94-6

to enlarge



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



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


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


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



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


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








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


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

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


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


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


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

(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


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

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

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

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


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.