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ELECTROCARDIOGRAPHY

The electrocardiogram (ECG) is a graphic representation of the electrical activity generated by

the heart during the cardiac cycle. The electrical activity starts from the SA node, bundle of

His, right and left bundles, Purkinje fibers to stimulate the ventricles.

Waveforms: The waveforms and intervals of the ECG are: The P wave = atrial depolarization.

The QRS complex = ventricular depolarization. The Q wave is the initial downward deflection,

the R wave is the initial upward deflection, and the S wave is the second downward deflection.

The interval from the beginning of the P wave to the beginning of the Q wave is the PR

interval.

The T wave = ventricular repolarization. The interval from the end of ventricular

depolarization to the beginning of the T wave is termed the ST segment. The interval from the

onset of ventricular depolarization to end of T is the QT interval.

STANDARD APPROACH TO THE ECG: Normally, standardization is 1.0 mV per 10

mm, and paper speed is 25 mm/s (each horizontal small box = 0.04 sec)

Heart Rate: divide 1500 by number of small boxes between each QRS.

Rhythm: Sinus rhythm is present if every P wave is followed by a QRS, PR interval > 0.12 s,

and the P wave is upright in leads I, II, and III.

Intervals: PR (0.12 - 0.20 s). QRS (0.06 - 0.10 s).

QT 0.43 s;

ST-T WAVES: ST elevation : Acute MI, coronary spasm, pericarditis (concave upward), LV

aneurysm.

ST depression: Digitalis effect, strain (due to ventricular hypertrophy), ischemia, or

nontransmural MI.

Tall peaked T: Hyperkalemia; acute MI ("hyperacute T").

Inverted T: Non-Q-wave MI, ventricular "strain" pattern, drug effect (e.g., digitalis),

hypokalemia, hypocalcemia, increased intracranial pressure (e.g., subarachnoid bleeding).

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Fig 1: The magnified ECG wave is presented with the principal time intervals indicated.

Fig 2: The pathways of Conduction

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CARDIAC ARRHYTHMIAS

An arrhythmia is any disturbance in the normal sequence of impulse generation and

conduction in the heart.

Anatomy of the conduction system: The conduction system of the heart consists of the sinus

node, internodal tracts, atrioventricular node (AVN), bundle of His, bundle branches (right and

left), and Purkinje fibers.

General considerations: Normal cardiac impulses arise from the automatic (pacemaking)

cells of the sinus node and are conducted through the atria to the AV junction then the His-

Purkinje system to the ventricular muscle. Normally the sinus node discharges at a rate of 60-

100/min.

Mechanisms of arrhythmias

A- Disturbance of impulse formation: may result from either:

1- Disturbed normal automaticity:

2- Triggered activity: Myocardial damage can result in oscillations (afterdepolarizations) at the

end of the action potential. These oscillations may reach threshold potential and produce an

arrhythmia.

B- Disturbance of Impulse conduction:

1- Reentry: A wave of depolarization may be forced to travel in one direction around a ring of

cardiac tissue. The majority of paroxysmal tachycardias are produced by this mechanism.

Classification of arrhythmia:

Clinical classification:

- Rapid, regular. Sinus tachycardia, supraventricular tachycardia, atrial flutter, ventricular

tachycardia.

- Rapid, irregular. Sinus arrhythmia, multiple ectopic beats whether atrial or ventricular,

atrial fibrillation.

- Slow, regular. Sinus bradycardia, nodal rhythm, complete heart block.

- Slow, irregular. Slow atrial fibrillation.

Anatomical classification: it stratifies arrhythmia according to the site of origin; SA node,

atrial, AV node, abnormal pathways, bundles and ventricular.

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Mechanismal classification: This depends on the pathogenesis of the arrhythmia. It is

divided into disturbance in the formation of the impulse, propagation of the impulse or

combined.

SPECIFIC ARRHYTHMIAS

Sinus node

Sinus tachycardia

Cardiac impulses arise in the sinus node at a rate more than 100/min.

Etiology:

A- Physiological: Infancy, childhood, exercise and excitement.

B- Pharmacological: Sympathomimetic drugs such as epinephrine and isoproterenol.

Parasympatholytic drugs such as atropine. Thyroid hormones, nicotine, caffeine,

alcohol.

C- Pathological: Fever, hypotension, heart failure, pulmonary embolism, hyperkinetic

circulatory states as anemia.

Treatment: 1- Treatment of the underlying etiology. 2- Propranolol.

Sinus Bradycardia

Cardiac impulses arise in the sinus node at a rate less than 60/min.

Etiology:

A- Physiologic: Athletes, sleep, and carotid sinus compression.

B- Pharmacologic: Digitalis, propranolol, verapamil and diltiazem.

C- Pathologic: Convalescence from infections, hypothyroidism, obstructive jaundice,

rapid rise of the intracranial tension, hypothermia and myocardial infarction

(particularly inferior wall infarction).

Treatment:

1- Treatment of the underlying etiology is usually all that is needed.

2- If the patient is hemodynamically compromised, Atropine 0.6 – 1.0 mg IV may be

given and repeated every 3 hours (maximum 2.5 mg in two hours).

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Sinus Arrhythmia

Cardiac impulse arises in the sinus node with alternating periods of slowing and

acceleration. The condition is common in young age and has no pathological significance.

Respiratory sinus arrhythmia: The heart rate increases with inspiration and slows with

expiration. The inspiratory increase is secondary to the increased venous return.

FIG 3. Normal intracardiac electrograms.

SICK SINUS SYNDROME

This term is applied to a syndrome encompassing a number of sinus nodal abnormalities that

include: 1- persistent spontaneous sinus bradycardia not caused by drugs, and inappropriate for

the physiological circumstance, 2- apparent sinus arrest or exit block, 3- combinations of SA

and AV conduction disturbances, or 4- alternation of paroxysms of rapid regular or irregular

atrial tachyarrhythmias and periods of slow atrial and ventricular rates (bradycardia-tachycardia

syndrome).

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PREMATURE BEATS (EXTRASYSTOLES)

These are cardiac impulses of ectopic origin occurring earlier than expected in the

prevailing rhythm. The ectopic focus may be: 1- Atrial resulting in atrial premature beat. 2- AV

junctional (arising from bundle of His) resulting in AV junctional premature beat. 3-

Ventricular resulting in ventricular premature beat.

Etiology:

A- Physiological: Emotions, exercise and fatigue.

B- Pharmacological: Coffee, alcohol, tobacco, catecholamines, digitalis and hypoxia.

C- Pathological: Various infections, digestive disturbances, hyperthyroidism and all

cardiovascular disorders.

SUPRAVENTRICULAR TACHYARRHYTHMIAS

All tachyarrhythmias that originate above the bifurcation of the bundle of His are

classified as supraventricular arrhythmias. The atrial rate must be 100 or more beats per minute

for a diagnosis.

SVTs may be separated into three groups based on duration: brief paroxysms, persistent,

and chronic (permanent).

Arrhythmias that are paroxysmal in onset and offset (e.g., paroxysmal SVT due to AV

nodal reentry or WPW syndrome, paroxysmal atrial fibrillation, paroxysmal atrial flutter) tend

to be recurrent and of short duration; i.e., seconds to hours.

Persistent tachycardias (e.g., sinus tachycardia, ectopic atrial tachycardia

(nonparoxysmal), multifocal atrial tachycardia, longer episodes of PSVT or atrial flutter or

fibrillation) may persist for days or weeks.

Longstanding or chronic SVTs (chronic atrial flutter, chronic atrial fibrillation) do not

revert if untreated, often fail to revert even with attempted treatment, and if reverted will

frequently recur despite therapy.

Supraventricular tachyarrhythmias include; atrial tachycardia, atrial flutter, atrial

fibrillation and nodal tachycardia.

ATRIAL FLUTTER

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Atrial flutter is a rapid regular atrial tachyarrhythmia that is less common than the PSVTs

or atrial fibrillation. It is observed infrequently in normal individuals, but may occur at any age

in the presence of underlying atrial abnormalities such as those secondary to mitral valve

disease, congenital heart disease, cardiomyopathies, and, less frequently, coronary artery

disease.

Untreated atrial flutter usually has atrial rates between 240 and 340 per minute,

commonly very close to 300 per minute. The ventricular rate in atrial flutter is usually a

defined fraction of the atrial rate 2: 1 conduction generating a ventricular rate of 150 per minute

and 4:1 conduction at 75 per minute. The mechanism of the atrial activity is macroreentry.

Clinically, atrial flutter may occur in brief, persistent, or chronic forms, and therapeutic

approaches are influenced by the clinical pattern.

Electrocardiographic Features

Atrial flutter generates a defined pattern of atrial activity in the ECG. Classically, a saw-

tooth pattern is identifiable in leads II, 111, and aVF. A narrow QRS complex tachycardia at a

rate of 150 per minute should always lead to the consideration of atrial flutter. Carotid sinus

massage will not interrupt atrial flutter but nonetheless may be very helpful in distinguishing

flutter from other mechanisms, impairment of AV nodal conduction causes an abrupt change

from a rate of 150 per minute to 75 per minute or less. The unmasking of hidden flutter waves

at the slower ventricular rate will make the diagnosis evident.

Management of atrial flutter:

- If the patient is hemodynamically compromised, D.C. cardioversion using low energies

(around 50 joules) should be instituted.

- For many years, standard treatment consisted of administering a Class IA antiarrhythmic

agent (i.e., quinidine, procainamide, or disopyramide). However, recent studies indicate that

the type IC antiarrhythmic drugs, flecainide and propafenone, are as effective, if not more

effective than Class IA drugs. Class III antiarrhythmic agents (i.e., amiodarone, sotalol)

may also be quite effective. In general, atrial flutter is quite difficult to suppress completely

with drug therapy.

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- The ventricular rate is slowed by digitalis and/or propranolol or verapamil before

antiarrhythmics are instituted to avoid very rapid rates associated with drug induced 1:1 AV

conduction.

- At present, catheter ablation provides the best hope of cure.

FIG 4. A 12-lead ECG of a typical case of type 1 atrial flutter.

FIG 5. Atrial flutter with AV block varying between 2: 1 and 4: 1.

AV Nodal Reentrant Tachycardia

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Electrocardiographic Features

PSVT due to AV nodal reentry is characterized by an abrupt onset and termination and

usually has a narrow QRS complex without clearly discernable P waves. The rate is commonly

in the range of 150 to 250 per minute (commonly 180 to 200 bpm in adults) and with a regular

rhythm.

Management of PSVT Due to AV Nodal Reentry

The acute attack: Management depends on the underlying heart disease and how well the

tachycardia is tolerated. For some patients, rest, reassurance, and sedation may be all that are

required to abort the attack. Vagal maneuvers serve as the first line of therapy.

Table: Simple procedures to terminate paroxysmal SVT

- Carotid sinus massage: If effective the rhythm is abruptly stopped; occasionally only

moderate slowing occurs

- Cold water splash on face (to mimic the diving reflex)

- Performance of Valsalva's maneuver (often effective)

Intravenous adenosine, Ca channel blockers (verapamil), digoxin or B-blockers are the

choices for managing the acute episodes.

Adenosine, 6 mg given intravenously, followed by one or two 6-mg boluses if necessary,

is effective and safe for acute treatment.

A 5-mg bolus of verapamil, followed by one or two additional 5-mg boluses 10 min apart

if the initial dose does not convert the arrhythmia, has been an effective regimen in up to 90

percent of patients with PSVT due to AV node reentry. Intravenous digoxin, 0.5 mg infused

over 10 min and repeated if necessary may convert the arrhythmia. An additional 0.25 mg

every 4 h to a maximum dose of 1.5 mg in 24 h may be used. The class IA antiarrhythmic

agents, which appear to depress conduction in the fast pathway, may be tried if other drugs fail.

DC cardioversion: Consider DC cardioversion before digitalis or a beta blocker is

administered.

Radiofrequency catheter ablation: Should be considered early in the management of patients

with symptomatic recurrent episodes of AV node reentry.

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PSVT Due to Accessory Pathways (The Wolff-Parkinson-White Syndrome)

Preexcited AV Node-Dependent Tachycardias

Preexcitation Syndrome

ELECTROCARDIOGRAPHIC RECOGNITION: Three basic features typify the ECG

abnormalities of patients with the usual form of WPW syndrome caused by an AV connection:

(1) P-R interval less than 120 msec during sinus rhythm;

(2) QRS complex duration exceeding 120 msec with a slurred, slowly rising onset of the QRS

in some leads (delta wave) and usually a normal terminal QRS portion; and

(3) Secondary ST-T wave changes that are generally directed opposite to the major delta and

QRS vectors.

The most common tachycardia is characterized by a normal QRS, by ventricular rates of

150 to 250 beats/min and by sudden onset and termination.

The prognosis is excellent in patients without tachycardia or an associated cardiac

anomaly. For most patients with recurrent tachycardia the prognosis is good but sudden death

occurs rarely.

Termination of the acute episode of reciprocating (using accessory pathway) tachycardia

should be approached as for AV nodal reentry. After vagal maneuvers, adenosine followed by

verapamil is the initial treatment of choice. In many patients, particularly those with a very

rapid ventricular response, electrical cardioversion is the initial treatment of choice.

Oral administration of two drugs, such as quinidine and propranolol or procainamide and

verapamil, to decrease conduction capabilities in both limbs of the reentrant circuit, can be

beneficial. Class IC drugs and amiodarone, which prolong refractoriness in both the accessory

pathway and the AV node, can be effective.

ELECTRICAL ABLATION: Ablation of the accessory pathway is advisable for:

- patients with frequent symptomatic arrhythmias that are not fully controlled by drugs, or

- With rapid AV conduction over the accessory pathway during atrial flutter or fibrillation and

in whom significant slowing of the ventricular response during tachycardia cannot be

obtained by drug therapy.

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Atrial Fibrillation

The arrhythmia is characterized by wavelets propagating in different directions and

causing disorganized atrial depolarizations without effective atrial contraction. Electrical

activity of the atrium can be detected on ECG as small irregular baseline undulations, called f

waves, at a rate of 350 to 600 beats/min. The ventricular response is grossly irregular (irregular

irregularity) and is usually between 100 and 160 beats/min.

It is a common arrhythmia, occurring in 5 – 10 % of individuals over 65 years of age. It

also occurs in a paroxysmal form in younger patients.

The hemodynamic consequences of atrial fibrillation are due to two factors:

(1) The loss of atrial systole may impair ventricular function in the noncompliant ventricle

[e.g., aortic stenosis, left ventricular hypertrophy (LVH)] or the dilated ventricle with

systolic dysfunction, and

(2) A rapid ventricular rate will encroach upon the diastolic filling period of the left ventricle

and the diastolic flow time of the coronary arteries.

(3) The risk of embolism and stroke is a long-term concern of special importance. Atrial

fibrillation may occur in paroxysmal, persistent, and chronic patterns.

Clinical expression of atrial fibrillation:

Definition Duration

- Paroxysmal Minutes/hours

- Short-lasting Seconds --<1 hour

- Long-lasting >1 hour; -- < 48 hours

- Persistent Two days -- weeks

- Permanent (Chronic) Months / years

Table: Causes of atrial fibrillation

With structural heart disease

- Rheumatic mitral valve disease

- Ischemic heart disease

- Hypertension

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- Cardiomyopathy: Dilated, Hypertrophic

- Atrial septal defect, - Constrictive pericarditis, Myocarditis

Without structural heart disease

- Alcohol

- Thyrotoxicosis

- Acute pericarditis

- Pulmonary embolism

- Sick sinus syndrome, Lone atrial fibrillation

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FIG 6. ECG tracings from AV node-dependent and AV node-independent tachycardias.

Panel A shows a narrow ORS complex tachycardia with a 1 : 1 AV relationship in a

patient with an AV nodal reentrant tachycardia. Panel B shows classic atrial flutter

persisting despite 2:1 AV block. Negative retrograde P waves are seen in ECG leads 11,

Ill, and aVF. ECG indicates electrocardiogram; and AV, atrioventricular.

FIG 7. General scheme to select antiarrhythmic drug therapy for the prevention of atrial

fibrillation. See text for details. HPB, hypertension; CHF, congestive heart failure; CAD,

coronary artery disease; CR, controlled release; AF, atrial fibrillation.

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FIG 8. Protocol for the ACUTE (Assessment of Cardioversion Using Transesophageal

Echocardiography) study. Patients with atrial fibrillation were randomised to the

conventional approach or to the TEE-guided group. LA, left atrial; LAA, left atrial

appendage.

Clinical picture

Onset and offset are sudden in paroxysmal cases.

Symptoms: Paroxysmal AF produces symptoms similar to those of supraventricular

tachycardia. Established AF (persisting for more than two weeks) is better tolerated than the

paroxysmal variety. Congestive heart failure may occur if the attack is prolonged, the

ventricular rate is very rapid, or the underlying heart disease is severe.

Signs:

1- Arterial pulse:

a- Rate is usually 100-150/min. Slower rates may be encountered in old age and in patients

receiving digitalis or beta-blockers.

b- Rhythm shows marked (irregular) irregularity. c- Force is irregular. d- Pulsus deficit:

The radial pulse rate is less than the cardiac rate counted at the apex beat. This is due to

inability of the week ventricular contractions following short diastolic periods to open

the aortic valve.

2- Neck veins show systolic expansion; no “a” waves are seen.

3- Auscultation reveals varying intensity of S1.

4- Exercise increases the pulse irregularity and deficit.

Electrocardiogram: The P waves are replaced by irregular f waves. The QRS complexes are

normal in shape but irregularly spaced.

Complications of Atrial Fibrillation:

1- Atrial thrombosis due to stagnation of blood in the fibrillating atria. The formed thrombi

may embolize in the systemic and pulmonary circulations. Thrombi in left auricle may

embolise to brain causing stroke or transient cerebral ischemic attacks; may embolize to retinal

artery causing sudden blindness in this eye; or embolize to other systems. Right auricular

thrombi will embolize to the lungs causing pulmonary infarctions.

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2- Heart failure due to loss of the atrial contribution to contractility and the cardiac output. 3-

Tachycardia induced cardiomyopathy. 4- Complications of treatment as bleeding from marevan

Treatment of Atrial Fibrillation

Pharmacologic Management of Patients with Recurrent Persistent or Permanent AF:

- Recurrent Persistent AF:

A) Minimal or no symptoms: Anticoagulation and rate control as needed.

B) Disabling symptoms in AF:

1- Anticoagulation and rate control

2- Antiarrhythmic drug therapy

3- Electrical cardioversion as needed, continue anticoagulation as needed and therapy to

maintain sinus rhythm

- Permanent AF: Anticoagulation and rate control as needed.

Antiarrhythmic Drug Therapy to Maintain Sinus Rhythm in Patients with Recurrent

Paroxysmal or Persistent AF:

A) No or minimal heart disease:

1- Flecainide, propafenone, sotalol

2- Amiodarone, dofetilide

3- Disopyramide, procainamide, quinidine

4- Consider non-pharmacological options.

B) Heart disease present:

a- Heart failure: Amiodarone, dofetilide

b- Coronary artery disease:

1- Sotalol

2- Amiodarone, dofetilide

3- Disopyramide, procainamide, quinidine

C) Hypertension: With

1- With LVH (septum greater than or equal to 1.4 cm): Amiodarone

2- Without this degree of LVH: - Flecainide, propafenone.

- Amiodarone, dofetilide, sotalol

- Disopyramide, procainamide. quinidine

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Recommended Doses of Drugs Proven Effective for Pharmacologic Cardioversion of AF

(Rhythm Control):

Drug Route of Admin. And Dosage

Amiodarone Oral: 1.2 to 1.8 g /day then 200 to 400 mg /d maintenance.

IV: 1.2 g /d IV continuous or in divided doses, then 200 to

400 mg /d maintenance

Dofetilide Oral: Creatinine clearance > 60 ml/min: 500 mcg BID

Flecainide Oral 200 to 300 mg

IV: 1.5 to 3 mg /kg over 10 to 20 min

Ibutilide IV: 1 mg over 10 min; repeat 1m when necessary

Propafenone

(Rytmonorm)

Oral: 450 to 600 mg

IV: 1.5 to 2 mg per kg over 10 to 20 min

Sotalol

(Betacor)

Tablet 80 mg give up to 3 tablets per day

Quinidine Oral: 0.75 to 1.5 g in divided doses over 6 to 12 h usually

with a rate-slowing drug.

Recommendations for Use of Orally Administered Pharmacological Agents for Heart

Rate Control in Patients with AF (Rate Control):

Drug Loading dose Maintenance dose

Digoxin 0.25 mg PO each 2h;

up to 1.5 mg

0.125 to 0.375 mg daily

Diltiazem NA 120 to 360 mg daily in divided doses

Metoprolol* NA 25 to 100 BID

Propranolol NA 80 to 360 mg daily in divided doses

Verapamil NA 120 to 360 mg daily in divided doses

Amiodarone 600 mg/d for 1 wk

400 mg/d for 4 to 6 wk

200 or 100 mg daily

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* Other beta-blockers could be used in appropriate doses

Two other drugs not mentioned here: Dronedarone and Vernakalant.

TABLE: ANTICOAGULATION OF PATIENTS WITH ATRIAL FIBRILLATION

Indications

Rheumatic mitral valve disease with recurrent or chronic atrial fibrillation.

Dilated cardiomyopathy with recurrent persistent or chronic atrial fibrillation.

Prosthetic valves.

Prior to (>3 weeks) elective cardioversion of persistent or chronic atrial fibrillation, and

also for 3 weeks after cardioversion (because of atrial stunning).

Coronary heart disease or hypertensive heart disease with recurrent persistent or chronic

atrial fibrillation

Atrial fibrillation in thyrotoxicosis (while awaiting long-term control; elective

cardioversion)

Chronic or persistent lone atrial fibrillation, age >60 years

Controversial; or limited data

Coronary or hypertensive heart disease with normal left atrial size, after first episode of

paroxysmal atrial fibrillation

Elective cardioversion of atrial fibrillation of short duration (2-3 days) with normal left

atrial size

Chronic or persistent lone atrial fibrillation, age <60 years

Not indicated

Lone atrial fibrillation, short paroxysms (<48 h)

Most clinical settings associated with short paroxysms (minutes to hours)

Relative contraindications

Difficulty controlling prothrombin times

Dementia

Malignancies, especially associated with bleeding risk

Prior major bleeding events

Uncontrolled hypertension

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Question: Give the causes of atrial fibrillation, clinical consequences, and different lines of

management.

TREATMENT OF CARDIAC ARRHYTHMIAS WITH CATHETER ABLATIVE

TECHNIQUES

Over the past several years various techniques have been introduced using catheter

ablative procedures for patients with cardiac arrhythmias. Radiofrequency ablation destroys

tissue by controlled heat production and avoids the need for general anesthesia since pain is

minimal. Presently, catheter ablation is used to treat patients with four major tachyarrhythmias:

atrial flutter/fibrillation, AV nodal reentry, AV reentry and ventricular tachycardia.

VENTRICULAR TACHYCARDIA

SPECIFIC FORMS OF VENTRICULAR TACHYCARDIA

Duration: Salvo (3-5 impulses)

Nonsustained VT: (6 impulses, up to 29 seconds)

Sustained VT: (>30 seconds)

ELECTROCARDIOGRAPHIC RECOGNITION. Ventricular tachycardia arises distal to

the bifurcation of the His bundle, in the specialized conduction system, in ventricular muscle,

or in combinations of both tissue types. The electrocardiographic diagnosis of ventricular

tachycardia is suggested by the occurrence of a series of three or more bizarrely shaped

premature ventricular complexes whose duration exceeds 120 msec, with the ST-T pointing

opposite to the major QRS deflection.

Depending on the particular type of ventricular tachycardia, the rates range from 70 to

250 beats/min, and the onset can be paroxysmal (sudden) or nonparoxysmal. QRS contours

during the ventricular tachycardia can be unchanging (Uniform, monomorphic), can vary

randomly (multiform, polymorphic), vary in more or less repetitive manner (Torsade de

points), vary in alternate complexes (bi-directional ventricular tachycardia), or vary in a stable

but changing contour (i.e., right bundle branch contour changing to left bundle branch contour).

Ventricular tachycardia can be sustained, defined arbitrarily as lasting longer than 30 sec or

requiring termination because of hemodynamic collapse, or nonsustained (Unsustained), when

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it stops spontaneously in less than 30 sec. Most commonly, very premature stimulation is

required to initiate ventricular tachycardia electrically.

CLINICAL FEATURES. Symptoms occurring during ventricular tachycardia depend on

the ventricular rate, duration of tachycardia, the presence and extent of the underlying heart

disease, and peripheral vascular disease.

Management: Termination of Sustained Ventricular Tachycardia: Ventricular tachycardia that

does not cause hemodynamic decompensation can be treated medically to achieve acute

termination by administering intravenous lidocaine or procainamide, followed by an infusion

of the successful drug. If the arrhythmia does not respond to medical therapy, electrical DC

cardioversion can be employed. Ventricular tachycardia that precipitates hypotension, shock,

angina, or congestive heart failure or symptoms of cerebral hypoperfusion should be treated

promptly with DC cardioversion. Very low energies can terminate ventricular tachycardia,

beginning with a synchronized shock of 10 to 50 watt-seconds. Digitalis-induced ventricular

tachycardia is best treated pharmacologically. After conversion of the arrhythmia to a normal

rhythm, it is essential to institute measures to prevent a recurrence.

A search for reversible conditions contributing to the initiation and maintenance of

ventricular tachycardia should be made and the conditions corrected if possible.

Prevention of Recurrences: This is generally more difficult than is terminating the acute

episode, and there is no "right" drug to choose. Although amiodarone is very effective, side

effects limit its use.

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Fig 9. Ventricular rhythm disturbances. A, Idioventricular rhythm. B, Multiple ventricular

premature complexes (arrows). C, Monomorphic ventricular tachycardia at a rate of 200

beats/min. The QRS complex is wide and p waves are seen to occasionally alter the QRS

morphology (arrows), reflecting AV dissociation. D, Polymorphic ventricular tachycardia

(torsade de pointes). (Note: the rhythm strip is at half the usual speed). There is QT

prolongation and several complexes occur at the peak of the preceding T waves (arrows)

with resultant induction of a wide-complex tachycardia that appears to rotate around the

base line. E, Ventricular fibrillation.

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Fig 10. Electrocardiographic characteristics of right ventricular dysplasia. A: A

ventricular tachycardia having a left bundle-branch block QRS morphology and a left axis

deviation. B: The electrocardiogram during sinus rhythm in the same patient. Note the inverted

T waves across the anterior chest leads.

.

Fig 11. Typical characteristics of Torsade des Pointes.

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Specific Types of Ventricular Tachycardia

Torsade de Pointes

ELECTROCARDIOGRAPHIC RECOGNITION. The term "torsades de pointes" refers

to a ventricular tachycardia characterized by QRS complexes of changing amplitude that

appear to twist around the isoelectric line and occur at rates of 200 to 250/min.

More recent data suggest that early afterdepolarizations may be responsible for both the

long Q-T and the torsades de pointes.

CLINICAL FEATURES. While many predisposing factors have been cited, the most

common are congenital, severe bradycardia, potassium depletion, and use of class IA and some

IC drugs. Clinical features depend on whether the torsades de pointes are due to the acquired or

congenital (idiopathic) long Q-T syndrome.

In all patients with torsades de pointes, administration of class IA, possibly some class IC,

and some class II antiarrhythmic agents can increase the abnormal Q-T interval and worsen the

arrhythmia. Class IB drugs can be tried.

CONGENITAL LONG QT INTERVAL SYNDROME

The congenital long QT interval syndrome, which is present persistently from childhood,

is characterized by the presence of long QT intervals and/or prominent U waves on the

standard 12-lead ECG. The affected patients are prone to episodes of torsade de pointes, which

may cause transient light-headedness or syncope or sudden cardiac death. Arrhythmias may

occur at rest, under emotional stress, or with exercise.

The two general patterns of the syndrome are the Romano-Ward syndrome, which has

an autosomal dominant inheritance pattern, and the Jervell-Lange-Nielson syndrome, which

has an autosomal recessive inheritance pattern and is associated with congenital deafness.

Drugs that block the sodium channel, such as mexiletine, have been suggested as a

possible pharmacologic therapy for this specific variant of the syndrome.

ACQUIRED LONG QT INTERVAL SYNDROME

The most common causes for acquired long QT interval syndromes are the antiarrhythmic

drugs, classically quinidine but also other class IA agents and class III agents. Bradycardia,

hypokalemia, and hypomagnesemia contribute to the risk. The class III drugs, particularly

sotalol, prolong the QT interval in a dose-dependent pattern.

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There is a growing list of other drugs that may prolong the QT interval, and establish

susceptibility to torsade de pointes. These include the phenothiazines, certain antibiotics,

pentamidine, cocaine, and terfenadine, among others.

MANAGEMENT OF CONGENITAL LONG QT INTERVAL SYNDROME

Long-term therapy includes B-adrenergic blockade. Placement of an ICD should be

considered for patients with resistant arrhythmias.

MANAGEMENT OF ACQUIRED LONG QT INTERVAL SYNDROME

Treatment is directed at the underlying cause(s), with careful attention to electrolyte and

metabolic disturbances and to identifying and reversing or removing iatrogenic factors.

Intravenous magnesium sulfate is often effective, especially when torsades de pointes are due

to quinidine. Lidocaine also may be beneficial, as may other class IB drugs. These drugs tend

to shorten the QT interval in normal myocardium.

CARDIOVERSION AND DEFIBRILLATION

Differences between cardioversion and defibrillation:

Cardioversion Defibrillation

Elective Emergency

Synchronized Non-synchronized

For AF, A. flutter, SVT, VT For V. fibrillation

50, 100, 150, 200 Joules Start by 200 Joules

Need sedative first Patient is unconscious

VENTRICULAR FLUTTER AND FIBRILLATION

MANAGEMENT. Immediate nonsynchronized DC electrical shock using 200 to 360 joules is

mandatory treatment for ventricular fibrillation and for ventricular flutter that has caused loss

of consciousness. Cardiopulmonary resuscitation is employed only until defibrillation

equipment is ready. Time should not be wasted with cardiopulmonary resuscitation maneuvers

if electrical defibrillation can be done promptly. Defibrillation requires fewer joules if done

early.

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The Implantable Cardioverter Defibrillator (ICD)

TABLE: GUIDELINES FOR ICD IMPLANTATION

1. ICD indicated

A. Cardiac arrest not due to acute ischemia or infarction or reversible causes

B. Documented sustained VT with hemodynamic compromise

C. Syncope of unknown origin in structural heart disease patients with inducible sustained VT.

D. Cardiomyopathy ischemic or non-ischemic with ejection fraction 30% or lower (MADIT II

results)

II. ICD may be indicated in highly symptomatic long QT interval despite optimal medical

therapy.

AV HEART BLOCK

Heart block is a disturbance of impulse conduction that can be permanent or transient,

owing to anatomical or functional impairment.

The conduction disturbance is classified by severity in three categories.

During first degree heart block, conduction time is prolonged but all impulses are

conducted (P-R interval > 0.2 sec.). Second degree heart block occurs in three forms: Mobitz

type I (Wenckebach) and type II; and persistent 2:1 block. Type I heart block is characterized

by a progressive lengthening of the conduction time until an impulse is not conducted. Type II

heart block denotes occasional (Mobitz II) or repetitive sudden block of conduction of an

impulse without prior measurable lengthening of conduction time. When no impulses are

conducted, complete or third degree block is present.

COMPLETE AV BLOCK

ELECTROCARDIOGRAPHIC RECOGNITION: Complete AV block occurs when no

atrial activity conducts to the ventricles and therefore the atria and ventricles are controlled by

independent pacemakers. Thus, complete AV block is one type of complete AV dissociation.

The atrial pacemaker can be sinus or ectopic (tachycardia, flutter, or fibrillation). The

ventricular focus is usually located just below the region of block, which can be above or

below the His bundle bifurcation. Sites of ventricular pacemaker activity that are in, or closer

25

to the His bundle appear to be more stable and may produce a faster escape rate than those

located more distally in the ventricular conduction system. The ventricular rate of acquired

complete heart block is less than 40 beats/min but may be faster in congenital complete AV

block. The ventricular rhythm, usually regular, can vary owing to premature ventricular

complexes, or a shift in the pacemaker site.

CLINICAL FEATURES. Complete AV block can result from block at the level of the

AV node (usually congenital), within the bundle of His, or distal to it in the Purkinje system

(usually acquired). Block proximal to the His bundle generally exhibits normal QRS complexes

and rates of 40-60 beats/min because the escape focus that controls the ventricle arises in or

near the His bundle.

Unusual forms such as paroxysmal AV block or AV block following a period of rapid

ventricular rate can occur. Paroxysmal AV block in some instances can be due to hyper-

responsiveness of the AV node to vagotonic reflexes. Surgery, electrolyte disturbances,

endocarditis, tumors, Chagas' disease, rheumatoid nodules, calcific aortic stenosis, myxedema,

polymyositis, infiltrative processes (such as amyloid, sarcoid, or scleroderma). In the adult,

drug toxicity, coronary disease, and degenerative processes appear to be the most common

causes of AV heart block.

MANAGEMENT: Drugs cannot be relied on to increase the heart rate for more than

several hours to several days in patients with symptomatic heart block without producing

significant side effects. Therefore, temporary or permanent pacemaker insertion is indicated in

patients with symptomatic bradyarrhythmias. Vagolytic agents such as atropine (novatropine

15 drops every 8 hours) are useful for patients who have AV nodal disturbances, while

catecholamines such as isoproterenol (Allupent syrup 5 ml every 8 hours) can be used

transiently to treat patients who have heart block at any site. Isoproterenol should be used with

extreme caution or not at all in patients who have acute myocardial infarction. The use of

transcutaneous pacing is preferable.

26

Fig 12. Heart block. A, First degree atrioventricular (AV) block; the PR interval is prolonged.

B, Second-degree AV block, type 1 (Wenckebach). There is progressive PR prolongation

preceding a nonconducted P wave (arrows). C, Second degree AV block, type 11.

Nonconducted P waves are seen (arrows) in the absence of progressive PR prolongation.

D, Third degree (complete) AV block with AV dissociation and a narrow-complex (AV

nodal) escape rhythm. (Reproduced from Cecil Essentials of Medicine).

Antiarrhythmic Drugs

Class Mode of

Action

Drugs Indication Dose Side Effects

Class

IA

Reduces

rate of

entry of

sodium

into the

cell

Quinidine

(Quinidine)

For

supraventricular

and ventricular

arrhythmias

including

conversion of

AF or A flutter,

SVT, VT

600 –

1000

mg/day

Marked

prolongation of

QT interval, risk

of Torsade de

pointes.

Quinidine

syncope,

quinidine

induced sudden

27

death. Diarrhea,

vomiting

Procainamid

e

(Pronestyl)

Is effective

against

supraventricular

and ventricular

arrhythmias

2-6

mg/min

IV. 350-

1000 mg

q 6 h PO

SLE like

syndrome,

prolonged QT,

nausea, rash,

myalgia,

Disopyrami

de

(Norpace)

Is effective

against

supraventricular

and ventricular

arrhythmias

100-400

mg q 8 h

Worsening of

heart failure,

anticholinergic

actions as urine

retention, dry

mouth. Avoid in

pts with

glaucoma

Class

IB

Lidocaine

(Zylocain)

Ventricular

arrhythmias only

1-4

mg/min

IV (50-

150 mg

IV

loading

dose)

Confusion,

convulsions

Mexiletine

(Mexitil)

Ventricular

arrhythmias only

150-300

mg q 6-8

h

Confusion,

tremor,

bradycardia,

hypotension

Class

IC

Flecainide

(Tambocor)

Is very effective

for ventricular

and

supraventricular

tachycardias

100-200

mg q 12 h

PO

Aggravation of

arrhythmia

(proarrhythmia),

negative

inotropic effect,

depression of

sinus node

Propafenone

(Rytmonor

m)

Has a rule in

treatment of

many types of

arrhythmias

including

supraventricular

arrhythmias

150-300

mg q 8-12

h

Negative

inotropic effect

28

Class

II

Beta

adrenerg

ic

blockers

e.g.

Propranolol

(Inderal),

Atenolol,

Bisoprolol,

Carvedilol

For premature

beats atrial and

ventricular, for

torsade de

pointes,

10-200

mg q 8 h

PO

Bradycardia,

hypotension,

heart failure,

intermittent

claudication,

worsening of

asthma,

impotence

Class

III

Prolong

action

potential

duration

Amiodarone

(Cordarone)

Life-threatening

ventricular

arrhythmias,

conversion and

slowing of atrial

fibrillation,

AVNRT,

tachycardias

associated with

WPWs

200-400

mg q 6-8

h

Corneal deposits,

photosensitivity,

skin

pigmentation,

thyroid

disturbances

(hypo &

hyperfunction),

alveolitis, liver

enzyme elevation

Sotalol

(Betacor)

Effective in

supraventricular

and ventricular

arrhythmias

80-160

mg x 2-3

PO

Torsade de

pointes,

bronchospasm in

asthmatic

patients

Ibutilide

(Covert)

FDA approved

for rapid

conversion of

recent AF & A

flutter

1 mg over

10 min IV

Torsade de

pointes

Dofetilide

(Tikosyn)

Approved for

oral therapy of

AF & flutter

0.1 – 0.5

mg q 12 h

PO

Torsade de

pointes

Dronedaron

e (Multaq)

For prevention

of recurrence of

AF (for

maintenance of

sinus rhythm)

400 mg

/tab twice

daily

Contraindicated

for Heart Failure

Class III, IV

Class

IV

Calcium

antagoni

sts

Verapamil

(Isoptin)

Diltiazem

Slow the

ventricular rate

in AF or flutter,

treat and prevent

AVNRT

0.1 Mg/kg

IV 40-160

mg q 6-8

h PO

60-120

mg q 6-8

h PO

Constipation,

edema of LL,

negative

inotropic effect

Uncla Activate Adenosine Is very effective 6-18 mg Contraindicated

29

ssified s K+

channels

(Adenocore) for the acute

conversion of

paroxysmal SVT

IV rapidly in sick sinus s.,

or 2nd

or 3rd˚

heart block.

Antidote is

theophylline

Enhance

s central

and

peripher

al vagal

tone

Digoxin

(Lanoxin,

Cardixin)

Slow ventricular

rate in AF,

flutter

0.5 – 1

mg IV or

0.125 –

0.25 mg

/d PO

Bradycardias and

tachycardias

(atrial,

junctional, vent.

tachycardia),

nausea, vomiting

Sudden Cardiac Death

Definition

Natural death due to cardiac causes, within one hour of the onset of acute symptoms in a person

with known or unknown cardiac disease, but the time and mode of death are unexpected .’

Common Causes of SCD

CAD (80 %)

DCM (10 %)

Other CM: HCM, RVCM (ARVD).

Myocarditis.

Non atherosclerotic CAD: Anomalies, M Bridge

Congenital HD: F4, TGA, AS, PS

Valvular HD: AS, AR, MVP, MS, …

Primary Electrical Abnormalities:

LQTS, Brugada S., CPVT, IMVT, IVF, WPW, Bradyarrhythmias.

Congenital Arrhythmogenic Syndromes

With structural heart disease:

- Right ventricular dysplasia

- Hypertrophic cardiomyopathy

- Dilated cardiomyopathy

- Significant mitral valve prolapse

30

- Anomalous coronary artery

With no or minimal structural heart disease

- Long QT syndrome

- Brugada syndrome

- Wolff Parkinson White syndrome

- Idiopathic ventricular tachyarrhythmias

- Short QT, catecholaminergic VT

- Congenital complete heart block

Clinical syndromes treated with ICD implantation (Implantable Cardioverter Defibrillator)

- Ejection fraction below 35%, ischemic or no ischemic cardiomyopathy.

Cardiac arrest survivors.

VT not hemodynamically well-tolerated

Idiopathic cardiomyopathy/syncope or VT

Hypertrophic cardiomyopathy/syncope or VT

RV dysplasia

Long QT syndrome

Brugada syndrome