Arrhythmias

Brief overview of the ECG diagnosis of arrhythmias

See also ACC/AHA/ESC Guidelines for the Management of Patients with Atrial Fibrillation

1.     P wave = depolarization of the atria.
QRS = depolarization of the ventricle.
T wave = repolarization of the ventricle.

2.     Cardiac muscle cells depolarize with a positive wave of depolarization, then repolarize to a negative charge intracellularly.

3.     Skin “leads” or electrodes have a positive and negative end.

4.     A positive wave form (QRS mainly above the baseline) results from the wave of depolarization moving towards the positive end of the lead. A negative waveform (QRS mainly below the baseline) is when a wave of depolarization is moving away from the positive electrode (towards the negative end of the lead).

5.     ECG paper has 1 millimeter small squares – so height and depth of wave is measured in millimeters.

10 mm = 1.0 mVolt

6.     Horizontal axis is time.
.04 seconds for 1 mm (1 small box).
.2 seconds for 1 large box = 5 small boxes = 5 x .04 seconds.

Figure 1:
Positive QRS in Lead I. Negative QRS in Lead aVR.
R wave = 7-8 mm high in Lead I. QRS wave = .06 seconds long in Lead I.

7.     Lead nomenclature.

Limb Leads	Chest Leads	Rhythm Strip
I, II, III aVR, aVF, aVL	V1 – V6	Located on the bottom of the ECG printout. Selected to give the best relationship of the P wave to the QRS.

8.    

 

9.    
Figure 2: A normal ECG and rhythm strip.

10.                       ECG interpretation: look at five areas, in order, on each ECG.

Rate

Rhythm (Intervals)

Axis

Hypertrophy

Infarct

 

Rate

Rate is cycles or beats per minute.

Normal rate for the SA node 60-100.

<60 bradycardia

>100 tachycardia

SA node is the usual pacemaker, other potential pacemakers (if SA node fails) are atrial pacemakers with inherent rates of 60-80, AV node (rate 40-60), or ventricular pacer (rate 20-40). In certain pathologic conditions ectopic (out of place) pacemakers can go much faster at rates 150-250 cycles/minute. There are three methods of calculating rate:

1.     Most Common Method:
(Most rates can be calculated this way). Find an R wave on a heavy line (large box) count off “300, 150, 100, 75, 60, 50” for each large box you land on until you reach the next R wave. Estimate the rate if the second R wave doesn’t fall on a heavy black line.

Rate calculation

Memorize the number sequence:

300, 150, 100, 75, 60, 50

 Figure 4: Common Method.

2.     Mathematical method:
Use this method if there is a regular bradycardia, i.e. – rate < 50. If the distance between the two R waves is too long to use the common method, use the approach: 300/[# large boxes between two R waves].

Figure 5: Count number of large boxes between first and second R waves=7.5. 300/7.5 large boxes = rate 40.

3.     Six-second method:
Count off 30 large boxes = 6 seconds (remember 1 large box = 0.2 seconds, so 30 large boxes = 6 seconds). Then, count the number of R-R intervals in six seconds and multiply by 10. This is the number of beats per minute. This is most useful if you have an irregular rhythm (like atrial fibrillation) when you want to know an average rate.

Figure 6: Count 30 large boxes, starting from the first R wave. There are 8 R-R intervals within 30 boxes. Multiply 8 x 10 = Rate 80.

Rhythm (to include intervals)

We will focus on the basic “core” of rhythms and measured “intervals” (PR, QRS, QT). Rhythms are often the most challenging aspect of ECG’s. You will see most rhythms several times over the next few years of your training, and you will eventually recognize them at a glance.

Now for some basics – “arrhythmia” means abnormal rhythm.

The normal conduction pathway is: SA node –> AV node –> Bundle of HIS –> Bundle Branches.

Arrhythmia can be understood by realizing the existence of ectopic (out of place) foci (pacemakers) and understanding the normal conduction pathway of the heart. Very simply put, if the beat originates in the atria or AV node (supraventricular) the QRS is usually narrow (normal), because it comes from above along the normal pathway.

Figure 6a: QRS is narrow (normal).

If the beat is ventricular in origin, the QRS is wide and bizarre because it doesn’t come down the normal pathway.

Figure 6b: QRS is wide.

Aberrancy is an exception to this rule – here it does actually follow the normal pathway (atria – AV node – ventricle) but for some reason the pathway is refractory to the beat and you get a wide QRS.

A reasonable way to group arrhythmias is in four general groups. Let us briefly review these four groups, then we will develop some common sense principles for evaluating rhythm (to include intervals).

Group 1 Irregular rhythms.

(main clue is QRS is not spaced evenly apart anywhere, total irregularity of the beat).

A) Sinus arrhythmia.

P waves and P-R intervals are all identical because they originate from the sinus node. Sinus rate may vary normally a bit (increase with inspiration, decrease with expiration), but if the rate varies a lot, this term is used.

Figure 7: Sinus arrhythmia: P waves are identical.

B) Wandering atrial pacemaker.

Pacemaker discharges from different atrial locations – the clue here is the P waves are of varying shape and differing PR intervals. PR interval is measured from the beginning of the the Pwave to the beginning of the QRS – if the atrial pacemaker location varies it will take different lengths of time to get to the ventricle – resulting in different PR intervals. If the rate of the wandering atrial pacemaker is >100 it is descriptively called multifocal atrial tachycardia.

Figure 8: Multifocal atrial tachycardia.

C) Atrial fibrillation.

You will frequently see this arrhythmia. There are no P waves, only irregular or wavy baseline. The QRSs are irregularly spaced, therefore it is included under irregular rhythms.

Figure 9: Atrial fibrillation.

 

Group 2 Escape (late) beats
and premature (early) beats.

The bottom line for Group 2 arrhythmias is that the rhythm is fairly regular – then you will notice an early or late beat; try to figure out whether that beat is a premature atrial contraction, premature ventricular contraction, etc.

A) Escape beats.

The usual pacemaker fails, so a slower pacemaker fires at its inherent rate.

Atrial escape

Different appearing and late P wave.

Figure 10: Atrial Escape Rhythm. Note differing appearance of the P waves for Sinus Rhythm vs. Atrial Escape Rhythm.

Junctional escape

No P wave, normal QRS if not aberrant.

Figure 11: Note all beats are junctional escape.

Ventricular escape

No P, wide, bizarre QRS.

Figure 12: Ventricular escape.

B) Premature Beats.

An ectopic pacemaker fires early before the next scheduled beat.

Premature atrial contraction

“PAC”, early and differently shaped P wave, narrow QRS.

Figure 13: Premature Atrial Contractiooted by arrow.

Premature junctional

No P, normal QRS if not aberrant.

Figure 14: Note the two early, narrow beats at the arrow. These are probably PJCs.

Premature ventricular contraction

No P, wide bizarre QRS. PVCs that occur three (3) or more in a row (ventricular tachycardia), multifocal PVCs (different shapes), or PVCs that land on a previous T wave (R on T phenomenon) can be dangerous ion a patient with underlying heart disease.

Figure 15: Note: Every fourth beat is a PVC (beginning with the second beat).

Group 3 Rapid ectopic (out of place) rhythms.

Ectopic rate nomenclature:

[150-250]	Paroxysmal tachycardia
[250-350]	Flutter
[350+]	Fibrillation

So, the descriptives paroxysmal tachycardia, flutter, and fibrillation refer to the “rates” of the arrhythmia, e.g. – it could be atrial fibrillation (wavy baseline refers to the atria going >350 bpm.), or ventricular fibrillation (with the ventricle not contracting in a coordinated fashion resulting in only an erratic line that isn’t possible to count).

Figure 16: Paroxysmal supraventricular tachycardia: note accelerated rate and narrow QRS complexes.

Figure 17: Ventricular tachycardia: note fast rate and wide bizarre QRS.

Figure 18: Ventricular fibrillation: erratic and wavy baseline.

Group 4 Atrioventricular heart blocks.

(occur in three (3) degrees, like skin burns; third degree is the worst).

1st degree

PR interval > 0.2 seconds (1 large box), each P is followed by a QRS. PR interval is measured from the beginning of the P wave to the beginning of the QRS.

Figure 19: The PR interval is approximately 0.28 seconds.

2nd degree block – type 1

Also called “Wenkebach”. PR interval gets progressively longer each beat until finally a QRS is “dropped” (missing).

Figure 20: Note the increasing PR interval before the QRS is dropped, then the cycle is repeated.

2nd degree block – type 2

Also called “Mobitz II”. Look out! A more serious conduction problem than Type 1. PR intervals are constant and a QRS is “dropped” intermittently.

Figure 21: Note the dropped QRS after the second and sixth P wave in lead II (the rhythm strip).

3rd degree block

The atrial rate is independent of the ventricular rate (P wave and QRS march out separately. The clue here is no relationship at all of the P-R intervals). The P-R interval is constantly changing, the QRS is usually wide and bizarre because it is ventricular origin.

Figure 22: Note the P waves and QRS waves are independent of each other.

 

Intervals

An interval is a portion of the baseline and at least one wave. We measure an interval on the horizontal axis in seconds. The PR, QRS, and QT are the intervals which should be routinely scanned on each ECG. For measuring intervals, look at the widest form in any lead.

Figure 23: Intervals.

1.     PR interval (beginning of P wave to the beginning of the next QRS). Normally, < .2 seconds or one large box. If it is > .2 seconds, it is a first degree block. (Note: this concept was introduced under blocks).

Figure 24: Note the prolonged PR interval (.28 seconds), especially at the second beat.

2.     QRS interval (beginning of Q to the end of the S wave) should be < .12 seconds (< 3 small boxes). If QRS is > .12, check for bundle branch block.

A QRS > .12 and RR (2 peaks or R waves in QRS) occurring in the right chest leads (V1-V2) indicates a right bundle branch block.

Figure 25: RBBB.

If QRS is > .12 and RR occurs in the left chest leads (V5-V6), this indicates a left bundle branch block.

Figure 26: LBBB.

3.     QT interval (beginning of QRS to end of T wave) should be less than half of the preceding RR interval – this varies with the rate. For normal rates, QT < .4 seconds (2 large boxes). “QT prolongation” (too long) can lead to a refractory form of ventricular tachycardia called torsades de pointes.

Figure 27: The QT interval is greater than half the preceding RR interval. Look at lead I.

Rhythm Guidelines

1. Check the bottom of the rhythm strip for regularity, i.e. – is it completely regular, mostly regular with a few extra beats, or totally irregular?

2. Check for a P wave before each QRS, QRS after each P.

3. Check RR interval (for AV blocks) and QRS interval (for bundle branch blocks). Check for prolonged QT.

4. Continue to recognize “patterns” such as atrial fibrillation, PVCs, PACs, escape beats, ventricular tachycardia, paroxysmal atrial tachycardia, AV blocks and bundle branch blocks.

 

Fasicular Blocks

Fasicular blocks are blocks of part of the left bundle, either the posterior or anterior division:

Figure 28: Divisions of the bundles.

Anterior fasicular block – the most common.

You will see left axis deviation (-30 to -90) and a small Q wave in lead I and an S in lead III (Q1S3). The QRS will be slightly prolonged (0.1 – 0.12 sec).

Figure 29: Anterior fasicular block.

Posterior fasicular block – less common.

You will see right axis deviation, an S in lead I and an Q in lead III (S1Q3). The QRS will be slightly prolonged (0.1 – 0.12 sec).

Figure 30: Posterior fasicular block.

Bifasicular block.

This means two (2) of the three (3) fascicles (in diagram) are blocked. The most important example is a right bundle branch block and a left anterior fascicular block. Watch out for this. Only one fascicle is left for conduction, and if that fasicle is intermittently blocked, the dangerous Mobitz 2 is set up!

Figure 31: Right bundle branch block and left anterior fascicular block.

“Fasicular Blocks” may seem a bit complicated – simply remember that axis deviation is the clue. In your differential, consider posterior fasicular blocks with right axis deviation and consider anterior fasicular blocks with left axis deviation. Fascicular blocks cause axis deviations, like infarcts and hypertrophy. If you see a left or right axis deviation, first look for infarct or hypertrophy. If neither are present, the remaining diagnosis of fasicular block is usually correct. Review differential diagnosis of right and left axis deviation.

 

 

SYSTEMATIC INTERPRETATION GUIDELINES for Electrocardiograms
RATE
Rate calculation
Common method: 300-150-100-75-60-50
Mathematical method: 300/# large boxes between R waves
Six-second method: # R-R intervals x10
RHYTHM
Rhythm Guidelines:
1. Check the bottom rhythm strip for regularity, i.e. – regular, regularly irregular, and irregularly irregular.
2. Check for a P wave before each QRS, QRS after each P.
3. Check PR interval (for AV blocks) and QRS (for bundle branch blocks). Check for prolonged QT.
4. Recognize “patterns” such as atrial fibrillation, PVC’s, PAC’s, escape beats, ventricular tachycardia, paroxysmal atrial tachycardia, AV blocks and bundle branch blocks.
AXIS

	Lead I	Lead aVF
1. Normal axis (0 to +90 degrees)	Positive	Positive
2. Left axis deviation (-30 to -90) Also check lead II. To be true left axis deviation, it should also be down in lead II.	Positive	Negative
3. Right axis deviation (+90 to +180)	Negative	Positive
4. Indeterminate axis (-90 to -180)	Negative	Negative

Left axis deviation differential: LVH, left anterior fasicular block, inferior wall MI.
Right axis deviation differential: RVH, left posterior fascicular block, lateral wall MI.
HYPERTROPHY
1. LVH — left ventricular hypertrophy = S wave in V1 or V2 + R wave in V5 or V6 > 35mm or aVL R wave > 12mm.
2. RVH — right ventricular hypertrophy = R wave > S wave in V1 and gets progressively smaller to left V1-V6 (normally, R wave increases from V1-V6).
3. Atrial hypertrophy (leads II and V1)
Right atrial hypertrophy — Peaked P wave in lead II > 2.5 mm in amplitude. V1 has increase in the initial positive direction.
Left atrial hypertrophy — Notched wide (> 3mm) P wave in II. V1 has increase in the terminal negative direction.
INFARCT

Ischemia	Represented by symmetrical T wave inversion (upside down). Look in leads I, II, V2-V6.
Injury	Acute damage — look for elevated ST segments.
Infarct	“Pathologic” Q waves. To be significant, a Q wave must be at least one small square wide or one-third the entire QRS height.

Certain leads represent certain areas of the left ventricle:

V1-V2	anteroseptal wall	II, III, aVF	inferior wall
V3-V4	anterior wall	I, aVL	lateral wall
V5-V6	anterolateral wall	V1-V2	posterior wall (reciprocal)

 

Supraventricular Tachycardia

 

A 28-year-old woman suddenly has rapid palpitations accompanied by chest pain and dizziness while playing her cello. She is brought to an emergency department. She has a faint regular pulse of 190 beats per minute. Her blood pressure is 82/54 mm Hg. Cardiovascular examination reveals no signs of heart failure. An electrocardiogram shows a regular tachycardia with a narrow QRS complex and no apparent P waves. How should her case be managed?

The Clinical Problem

The term “supraventricular tachycardia” refers to paroxysmal tachyarrhythmias, which require atrial or atrioventricular nodal tissue, or both, for their initiation and maintenance. The incidence of supraventricular tachycardia is about 35 cases per 100,000 persons per year, and the prevalence is about 2.25 per 1000 (excluding atrial fibrillation, atrial flutter, and multifocal atrial tachycardia, which are not covered in this review).¹ Supraventricular tachycardias are often recurrent, occasionally persistent, and a frequent cause of visits to emergency rooms and primary care physicians.

Common symptoms of supraventricular tachycardia include palpitations, anxiety, light-headedness, chest pain, pounding in the neck and chest, and dyspnea. Syncope is uncommon, but some patients have serious psychological distress. Polyuria can occur in prolonged episodes, mainly owing to the release of atrial natriuretic factor.²

Most types of tachycardia have a reentry mechanism (Figure 1), and they are classified according to the location of the reentry circuit (Figure 2). Approximately 60 percent of cases are due to an atrioventricular nodal reentry circuit, and about 30 percent are due to an atrioventricular reentry circuit mediated by an accessory pathway — a short muscle bundle that directly connects the atria and ventricles.³ Atrial tachycardia comprises about 10 percent of cases and often has a focal origin.⁴ However, paroxysmal or persistent atrial tachycardia occurring long after cardiac surgery that involved a large atrial incision is usually caused by an intraatrial reentry.⁵ Sinus-node reentrant tachycardia, inappropriate sinus tachycardia, ectopic junctional tachycardia, and nonparoxysmal junctional tachycardia are rare.³

Figure 1. Mechanism of Reentry.

An impulse (Panel A, arrows), initiated normally in the sinus node, passes through two pathways — for example, the atrioventricular nodal connection and an accessory pathway. A premature atrial impulse (Panel B) occurs and reaches the accessory pathway when it is still refractory but conduction can occur in the atrioventricular node. The impulse takes sufficient time to circulate through the atrioventricular node and across the ventricle to allow the accessory pathway to recover its excitability and conduct the impulse back to the atrium (Panel C). The wave front reenters the atrioventricular node, continually encounters excitable tissue, and is perpetuated as a reentry circuit.

Figure 2. Main Mechanisms and Typical Electrocardiographic Recordings of Supraventricular Tachycardia.

In patients with atrioventricular (AV) nodal reentrant tachycardia (Panels A and B), the atrioventricular node is functionally divided into two pathways that form the reentrant circuit. In the majority of patients, during this type of tachycardia, antegrade conduction to the ventricle occurs over the slow pathway and retrograde conduction over the fast pathway. The activation of atria and ventricles is synchronous so that the retrograde P wave is buried in the QRS complex, or it may be visible soon after the QRS complex (as pseudo r’ in V1 or pseudo s in the inferior leads). Orthodromic AV reentrant tachycardia (Panels A and B) is the most frequent arrhythmia in patients who have an accessory pathway, with antegrade conduction through the AV node, activation of the ventricles, and retrograde conduction through the accessory pathway. Typically, there is a short RP interval, but a long RP interval may be associated with slow-conducting accessory pathways. With the use of adenosine or vagal maneuvers (Panel C), tachycardia often terminates with a retrograde P wave. In the approximately 70 percent of patients with this type of tachycardia who have an obvious accessory pathway, preexcitation may be seen in the ensuing beats; however, it is absent in the approximately 30 percent of patients with a concealed accessory pathway. In antidromic AV reentrant tachycardia (Panels A and B), the activation wave front travels in the opposite direction. On electrocardiography, it is impossible to distinguish antidromic AV reentrant tachycardia from ventricular tachycardia. Atrial tachycardias (Panels A and B) typically have a focal origin (star), and different mechanisms might be involved (reentry within several millimeters, automaticity, and triggered activity). RP intervals are typically long (longer than PR intervals), but this depends on the rate of tachycardia and properties of AV conduction. The PR interval can be prolonged by the use of vagal maneuvers and adenosine (Panel C), which may also produce a transient AV block. A substantial proportion of focal atrial tachycardias are terminated with the use of adenosine. Atrial flutter with 2:1 AV conduction (Panels A and B) may resemble atrial tachycardia or another type of supraventricular tachycardia and can be revealed when vagal maneuvers or adenosine is used (Panel C).

 

Supraventricular tachycardias are not usually associated with structural heart disease, although there are exceptions (e.g., the presence of accessory pathways associated with hypertrophic cardiomyopathy or Ebstein’s anomaly and atrial tachycardias in patients with congenital or acquired heart disease). Reentry arrhythmias are usually induced by premature atrial or ventricular ectopic beats, and precipitating factors — such as excessive intake of caffeine, alcohol, or recreational drugs and hyperthyroidism — can increase the risk of recurrence.

Strategies and Evidence

General Evaluation of Patients

While considering the patient’s history, the clinician should assess the duration and frequency of episodes, the mode of onset, and possible triggers (including the intake of alcohol and caffeine or other drugs) as well as previous cardiac or other disease. These features are useful in distinguishing supraventricular tachycardia from other tachyarrhythmias (Table 1). Supraventricular tachycardias have a sudden onset and termination, in contrast to sinus tachycardias, which accelerate and decelerate gradually; however, some patients do not perceive the sudden onset of supraventricular tachycardia. It may be misdiagnosed as panic disorder.⁶

Physical examination during episodes may reveal the “frog sign” — prominent jugular venous A waves due to atrial contraction against the closed tricuspid valve.⁷ When sinus rhythm is restored, physical examination is usually normal, but a careful examination is warranted to rule out evidence of structural heart disease.

The usual presentation of supraventricular tachycardia on electrocardiography (ECG) is as a narrow-QRS-complex tachycardia (a QRS interval of less than 120 msec), but in some cases (less than 10 percent), wide-complex tachycardia is the manifestation of supraventricular tachycardia. After the restoration of sinus rhythm, the 12-lead ECG should be examined for the presence of delta waves, which indicate an accessory pathway (Figure 2C). However, evidence of preexcitation may be minimal or absent if the accessory pathway (e.g., a left lateral accessory pathway) is located far from the sinus node or if, as occurs in approximately 30 percent of patients, the accessory pathways are “concealed” (i.e., they support exclusively retrograde conduction from the ventricle to the atrium and do not cause preexcitation of the ventricle during sinus rhythm). In ambulatory patients with frequent episodes (two or more per month) of supraventricular tachycardia, ECG recordings or event recorders (which record arrhythmias for up to seven days) may be useful to document arrhythmias.

An echocardiogram should be considered to rule out structural heart disease, even though it is uncommon. Because electrolyte abnormalities and hyperthyroidism may contribute to supraventricular tachycardia, it is reasonable to check potassium and serum thyrotropin levels; however, the tests for these values appear to have a low yield.

Electrophysiological testing allows for identification of the mechanism of arrhythma, but this procedure is generally performed only if catheter ablation is considered. Table 2 summarizes conditions for which this testing is generally recommended.

Treatment

Short-Term Therapy

Figure 3 shows an algorithm for the management of acute supraventricular tachycardia. In rare cases, episodes of arrhythmia are so poorly tolerated that they require immediate electrical cardioversion. Most supraventricular tachycardias depend on the atrioventricular node for maintenance of the reentry circuit and can be interrupted by vagal maneuvers or pharmacologic agents that slow conduction through the atrioventricular node.

Figure 3. Algorithm for the Short-Term Management of Supraventricular Tachycardia (SVT).

If the diagnosis of SVT with aberration or SVT with preexcitation is not certain, tachycardia with a wide QRS complex must be considered as an unknown mechanism and treated as such. SVT with preexcitation can be the result of either antidromic atrioventricular reentry or, uncommonly, another type of SVT (e.g., atrial tachycardia) with an accessory pathway that is not critical for the maintenance of the arrhythmia. BBB denotes bundle-branch block, VT ventricular tachycardia, IV intravenous, and ECG electrocardiogram. Adapted from Blomstrom-Lundqvist et al.⁸

Vagal Maneuvers

Massage of the carotid sinus stimulates baroreceptors, which trigger a reflexive increase in the activity of the vagal nerve and sympathetic withdrawal, slowing conduction through the atrioventricular node. If the physical examination does not reveal a carotid bruit and there is no history suggesting carotid artery disease, pressure may be applied at the level of the cricoid cartilage for about five seconds with a firm circular movement. If the tachyarrhythmia persists, the procedure may be repeated on the opposite side. Other approaches to increasing vagal tone include having the patient perform a Valsalva maneuver or (primarily in children) apply an ice pack to the face.

A continuous 12-lead ECG recording of the episode should be obtained during vagal maneuvers, since the way in which arrhythmias end may provide clues to their mechanism (Figure 2).⁹

Adenosine

As with vagal maneuvers, treatment with intravenous adenosine has both diagnostic and therapeutic value. Data from randomized trials show that supraventricular tachycardia is terminated in 60 to 80 percent of patients treated with 6 mg of adenosine and in 90 to 95 percent of those treated with 12 mg.¹⁰ In patients with atrial tachycardias, adenosine causes a transient atrioventricular nodal block or interrupts the tachycardia (Table 3 and Figure 2).^10,11,12 ECG monitoring is required during the administration of adenosine, and resuscitation equipment should be available in the event that the rare complications of bronchospasm or ventricular fibrillation occur. Adenosine is contraindicated in heart-transplant recipients and should be used cautiously in patients with severe obstructive lung disease. Adenosine is also contraindicated in patients with tachycardia with a wide QRS complex (unless the diagnosis of supraventricular tachycardia with aberrancy is certain).

            Other Agents

If supraventricular tachycardia is refractory to adenosine or rapidly recurs, clinical experience indicates that the tachycardia can usually be terminated by the administration of intravenous verapamil or a beta-blocker.^11,13,14 As a next step, procainamide, ibutilide, propafenone, or flecainide can be given intravenously if the patient’s blood pressure is stable.¹⁵ However, sequential trials with different antiarrhythmic agents should be undertaken only after careful consideration of their possible negative hypotensive, bradycardic, and proarrhythmic effects. At any point, electrical cardioversion is an alternative, but this technique is generally considered in patients in hemodynamically stable condition only if atrioventricular nodal-blocking agents fail. Table 3 reviews medications used for acute supraventricular tachycardia. These agents are contraindicated in patients with severe hypotension, a history of heart block, or congestive heart failure.

Atrial fibrillation with rapid ventricular conduction can occur spontaneously in patients with the Wolff–Parkinson–White syndrome or during treatment for supraventricular tachycardia. Emergency-resuscitation equipment should be available, since the arrhythmia can degenerate into ventricular fibrillation if the accessory pathway has a short refractory period (250 msec or less).¹⁶ Treatment with an electrical shock is a safe option. If the patient’s condition is hemodynamically stable, procainamide, ibutilide, propafenone, or flecainide may be used; all have a rapid onset of action, lengthen antegrade refractoriness of the accessory pathway, and terminate atrial fibrillation in the majority of cases.¹⁵

            Wide-QRS-Complex Supraventricular Tachycardia

Supraventricular tachycardia presents infrequently as a wide-complex tachycardia, in which there is an associated bundle-branch block or conduction over an accessory pathway. Wide-QRS-complex, regular tachycardia should routinely be treated as ventricular tachycardia, unless the diagnosis of supraventricular tachycardia with aberrancy or of supraventricular tachycardia with preexcitation is certain. Adenosine and other atrioventricular-nodal–blocking agents are ineffective and potentially deleterious in patients with ventricular tachycardia.

Long-Term Management

The risk of recurrence after a single episode of supraventricular tachycardia is not well defined, and a single episode is not an indication for long-term therapy. For patients with recurrent episodes, options for long-term treatment include medication and ablation therapy. However, not all patients with recurrent supraventricular tachycardia need treatment. The severity of the symptoms and patient preferences should be considered in decision making. Referral to an electrophysiologist is warranted for the conditions listed in Table 2 and should be considered in other cases to assist in decisions regarding therapy.^17,18

Figure 4 shows a decision algorithm for the long-term care of patients with supraventricular tachycardia. In cases in which the precise mechanism of tachycardia is uncertain, management is based on the presence or absence of preexcitation on the baseline ECG (Table 3 and Figure 4).

The pharmacologic management of atrial tachycardias has not been well evaluated in controlled trials. Depending on the mechanism causing the arrhythmia, beta-blockers, calcium-channel blockers, and class I or class III antiarrhythmic drugs may reduce or eliminate symptoms.

            “Pill-in-the-Pocket” Approach

For patients with infrequent (i.e., no more than a few per year) but prolonged (i.e., lasting more than one to two hours) episodes of supraventricular tachycardia that are well tolerated hemodynamically, or for patients who have had only a single episode of supraventricular tachycardia, another option is to prescribe single-dose pharmacologic therapy (the “pill in the pocket”) to be taken wheeeded for an arrhythmic event. Drugs administered in this fashion include calcium-channel blockers (e.g., 40 to 160 mg of verapamil), exclusively for patients without preexcitation; various beta-blockers; flecainide (100 to 300 mg); and propafenone (150 to 450 mg). In one study, 80 percent of episodes of supraventricular tachycardia were interrupted within two hours with a combination of diltiazem and propanolol or with flecainide.²³

            Supraventricular Tachycardia with the Wolff–Parkinson–White Syndrome

Verapamil and digoxin are contraindicated in patients with the Wolff–Parkinson–White syndrome, unless the accessory pathway has been shown to have a long refractory period (300 msec or more), because these drugs may increase the risk of rapid ventricular response, causing ventricular fibrillation in patients with atrial fibrillation.^24,25 Although catheter ablation is considered the treatment of choice for these patients, both flecainide and propafenone are effective and have been approved by the Food and Drug Administration for the prevention of paroxysmal supraventricular tachycardias mediated by an accessory pathway (with or without antegrade conduction).^26,27,28

            Catheter Ablation

Since the early 1990s, catheter ablation (Figure 5) has increasingly been used in the management of supraventricular tachycardia on the basis of its observed efficacy and overall safety when performed at centers with experienced clinicians. Observational studies of catheter ablation of tachycardia mediated by an accessory pathway indicate that success rates exceed 95 percent and recurrence rates are less than 5 percent during the first few months after the procedure is performed. Late recurrences are the exception.^29,30,31 In cases in which the accessory pathway is close to a His bundle, the application of radiofrequency current can be complicated by atrioventricular block that requires pacemaker therapy. Data from observational studies suggest that in this situation, the use of cryothermal ablation is similarly effective and reduces the potential for atrioventricular block, although studies directly comparing these approaches are lacking.³² Other complications associated with accessory-pathway ablation, occurring in less than 2 to 3 percent of patients, include damage to an artery, bleeding, arteriovenous fistula, venous thrombosis, pulmonary embolism, myocardial perforation, valvular damage, systemic embolism (in the case of a left-sided accessory pathway), and rarely, death.^33,34

Figure 5. Catheter Ablation of Cardiac Arrhythmias.

One to four catheter electrodes are introduced into the cavities of the heart through femoral (or, alternatively, internal jugular or subclavian) venous access after local anesthesia is administered. Radiofrequency current — a low-voltage, high-frequency (500 kHz) form of electrical energy used for electrocautery in surgery — is delivered through a catheter electrode to create small lesions through thermal injury in the myocardial tissue, the conduction system, or both, which have been identified as critical for mediating the cardiac arrhythmia. In patients with arrhythmias mediated by an abnormal accessory pathway, the catheter is positioned so that it is in contact with the pathway, and the application of radiofrequency current blocks conduction over the accessory pathway within a few seconds. For left-sided accessory pathways, a retrograde approach through the femoral artery and the aortic valve can be used. Alternatively, a transseptal puncture can be performed to gain access to the left atrium. Cryothermal ablation is an effective approach in patients with atrioventricular (AV) nodal reentrant tachycardia or an accessory pathway close to a His bundle because of the reversibility of the initial effect and the negligible risk of AV block. Most ablation procedures take one to three hours. Catheter ablation of supraventricular tachycardia can be performed as a one-day outpatient procedure, or it may require overnight hospitalization. Treatment with aspirin is often recommended for several weeks after ablation that has been performed in the left side of the heart to reduce the potential risk of emboli. Patients need no special follow-up after the intervention.

In patients with atrioventricular nodal reentrant tachycardia, the atrioventricular nodal slow pathway is targeted by catheter ablation in the posteroseptal region of the tricuspid annulus.³⁵ Success rates are higher than 95 percent.^34,36 Serious complications are uncommon but include pulmonary embolism (in up to 0.2 percent of patients) and the development of atrioventricular block requiring pacemaker therapy (in up to 1 percent of patients).^33,34 Tachycardia recurs in 3 to 7 percent of patients.³⁶

Catheter ablation of focal atrial tachycardias has slightly lower success rates (about 85 percent) and higher recurrence rates (about 8 percent).^36,37 Procedural risks are slightly increased for the treatment of left atrial tachycardia, which requires a transseptal puncture. For reentrant atrial tachycardias, radiofrequency ablation has high success rates and is often used as first-line therapy.^37,38,39

Areas of Uncertainty

Limited data suggest that, as compared with antiarrhythmic therapy, catheter ablation improves the quality of life and is more cost effective in the long term.^40,41 However, there is a lack of large randomized trials with prolonged follow-up to guide the choice between radiofrequency ablation and medical therapy.

The appropriate treatment strategy for patients with asymptomatic preexcitation syndromes is controversial.^42,43,44 The incidence of sudden death due to rapid conduction of atrial fibrillation that leads to ventricular fibrillation is estimated at between 0.15 and 0.45 percent per patient-year.^45,46,47 Attempts to stratify the risk according to the use of noninvasive methods or invasive measurements of the refractory period of the accessory pathway have been advocated but may be misleading.^17,44,48 A task force of the American College of Cardiology, the American Heart Association, and the European Society of Cardiology concluded that the positive predictive value of invasive electrophysiologic testing is too low to justify its routine use in asymptomatic patients and that the decision to ablate accessory pathways in persons with high-risk occupations or those who engage in high-risk recreational activities should be made on an individual basis.⁸

Guidelines

Comprehensive guidelines for the management of supraventricular tachycardia were published by an expert committee of the American College of Cardiology, the American Heart Association, and the European Society of Cardiology.⁸ Doses of antiarrhythmic drugs and their adverse effects are discussed in these societies’ guidelines for the management of patients with atrial fibrillation.⁴⁹ The recommendations in this review are in general agreement with these guidelines. Generally, radiofrequency ablation is recommended as primary therapy for patients in whom the preexcitation syndrome or hemodynamic instability occurs during their arrhythmias. In other cases, patient preference is an important consideration in the selection of therapy.

Conclusions and Recommendations

For a patient such as the one described in the vignette, I would first try carotid sinus pressure or other vagal maneuvers, followed by intravenous adenosine if the maneuvers are ineffective.

For patients in whom supraventricular tachycardia recurs, preventive therapy is generally warranted if there are frequent, prolonged, or highly symptomatic episodes that cannot easily be terminated by the patient’s use of vagal maneuvers. If the tachycardia is associated with preexcitation or syncope, electrophysiological evaluation is warranted. In the absence of preexcitation or syncope, atrioventricular-node–blocking agents are usually recommended as first-line treatment, even though there is a lack of data from large trials to compare these drugs with other approaches to management. However, many patients may have adverse effects or find it inconvenient to take medication over the long term. For patients in whom recurrences are infrequent but prolonged, pill-in-the-pocket treatment (e.g., 100 to 200 mg of flecainide) at the onset of supraventricular tachycardia is a reasonable approach. Catheter ablation, when performed at a center with experienced clinicians, is appropriate for supraventricular tachycardia associated with preexcitation or hemodynamic instability or if antiarrhythmic drugs are not effective or are poorly tolerated. Catheter ablation may also be used as primary therapy in other cases if the patients, informed of the risks and benefits, prefer this approach.

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24. Sellers TD Jr, Bashore TM, Gallagher JJ. Digitalis in the pre-excitation syndrome: analysis during atrial fibrillation. Circulation 1977;56:260-267. [Free Full Text]

25. Glatter K, Yang Y, Chatterjee K, et al. Chemical cardioversion of atrial fibrillation or flutter with ibutilide in patients receiving amiodarone therapy. Circulation 2001;103:253-257. [Free Full Text]

26. Ludmer PL, McGowan NE, Antman EM, Friedman PL. Efficacy of propafenone in Wolff-Parkinson-White syndrome: electrophysiologic findings and long-term follow-up. J Am Coll Cardiol 1987;9:1357-1363. [Abstract]

27. Kim SS, Lal R, Ruffy R. Treatment of paroxysmal reentrant supraventricular tachycardia with flecainide acetate. Am J Cardiol 1986;58:80-85. [CrossRef][ISI][Medline]

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29. Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med 1991;324:1605-1611. [Abstract]

30. Kuck KH, Schluter M, Geiger M, Siebels J, Duckeck W. Radiofrequency current catheter ablation of accessory atrioventricular pathways. Lancet 1991;337:1557-1561. [CrossRef][ISI][Medline]

31. Calkins H, Sousa J, el-Atassi R, et al. Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardias during a single electrophysiologic test. N Engl J Med 1991;324:1612-1618. [Abstract]

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35. Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med 1992;327:313-318. [Abstract]

36. Kay GN, Epstein AE, Dailey SM, Plumb VJ. Role of radiofrequency ablation in the management of supraventricular arrhythmias: experience in 760 consecutive patients. J Cardiovasc Electrophysiol 1993;4:371-389. [ISI][Medline]

37. Lesh MD, Van Hare GF, Epstein LM, et al. Radiofrequency catheter ablation of atrial arrhythmias: results and mechanisms. Circulation 1994;89:1074-1089. [Free Full Text]

38. Natale A, Newby KH, Pisano E, et al. Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter. J Am Coll Cardiol 2000;35:1898-1904. [Free Full Text]

39. Cosio FG, Lopez-Gil M, Goicolea A, Arribas F, Barroso JL. Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol 1993;71:705-709. [CrossRef][ISI][Medline]

40. Bathina MN, Mickelsen S, Brooks C, Jaramillo J, Hepton T, Kusumoto FM. Radiofrequency catheter ablation versus medical therapy for initial treatment of supraventricular tachycardia and its impact on quality of life and healthcare costs. Am J Cardiol 1998;82:589-593. [CrossRef][ISI][Medline]

41. Lau CP, Tai YT, Lee PW. The effects of radiofrequency ablation versus medical therapy on the quality-of-life and exercise capacity in patients with accessory pathway-mediated supraventricular tachycardia: a treatment comparison study. Pacing Clin Electrophysiol 1995;18:424-432. [ISI][Medline]

42. Klein GJ, Prystowsky EN, Yee R, Sharma AD, Laupacis A. Asymptomatic Wolff-Parkinson-White: should we intervene? Circulation 1989;80:1902-1905. [Free Full Text]

43. Lerman BB, Basson CT. High-risk patients with ventricular preexcitation — a pendulum in motion. N Engl J Med 2003;349:1787-1789. [Free Full Text]

44. Todd DM, Klein GJ, Krahn AD, Skanes AC, Yee R. Asymptomatic Wolff-Parkinson-White syndrome: is it time to revisit guidelines? J Am Coll Cardiol 2003;41:245-248. [Free Full Text]

45. Munger TM, Packer DL, Hammill SC, et al. A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953-1989. Circulation 1993;87:866-873. [Free Full Text]

46. Pappone C, Santinelli V, Rosanio S, et al. Usefulness of invasive electrophysiologic testing to stratify the risk of arrhythmic events in asymptomatic patients with Wolff-Parkinson-White pattern: results from a large prospective long-term follow-up study. J Am Coll Cardiol 2003;41:239-244. [Free Full Text]

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49. Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients with Atrial Fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology. Circulation 2001;104:2118-2150. [Free Full Text]

Approach to wide complex tachycardias

The correct diagnosis of a wide complex tachycardia (WCT)—QRS duration > 120 ms—remains a challenge despite numerous established criteria for the differentiation of ventricular from supraventricular tachycardia (SVT) with aberrant conduction. Making the correct diagnosis is important for the acute as well as long term management of patients with WCT. The objective of the present review is to discuss the major causes as well as clinical and electrophysiologic criteria of WCT in patients without structural heart disease.

Table 1  Causes of wide complex tachycardias (WCTs) in patients without structural heart disease

Monomorphic configuration Supraventricular tachycardia (SVT) • Bundle branch block (figs 1, 2) – functional (RBBB more often than LBBB) – pre-existing – rate related • Antidromic (i.e. retrograde conduction over AV node; figs 3, 4) • Non-specific conduction delay – class I or class III antiarrhythmic drugs – electrolyte imbalance Ventricular tachycardia (VT) • LBBB, inferior axis (fig 7): idiopathic right ventricular VT • RBBB, superior axis (fig 8): idiopathic left ventricular VT • Pacemaker mediated VT Polymorphic configuration Supraventricular tachycardia • Atrial fibrillation with pre-excitation (fig 3) Ventricular tachycardia • Torsade de pointes (long QT syndrome) (fig 9) • Brugada syndrome • Catecholaminergic polymorphic VT (fig 10) • Short QT syndrome   All WCTs should be treated as if the rhythm was VT until proven otherwise. AV, atrioventricular; LBBB, left bundle branch block; RBBB, right bundle branch block.

 

Broad categories of WCTs include ventricular tachycardia (VT), SVT with abnormal intraventricular conduction, and ventricular paced rhythms. A lack of underlying structural heart disease does neither exclude a VT nor imply a benign prognosis. However, if a patient has had similar episodes during previous years, SVT is more likely than VT. Termination of a tachycardia by the Valsalva manoeuvre or adenosine injection also suggests a supraventricular origin, although some VT can also be terminated by these manoeuvres (for example, fascicular VT).

A WCT in a patient who is alert and haemodynamically stable is not necessarily of supraventricular origin. The clinical presentation depends on the haemodynamic consequences it produces. These depend partly on tachycardia rate, the degree of myocardial dysfunction, the circumstances and suddenness of initiation, and autonomic factors. Physical examination in a patient presenting with WCT may indicate haemodynamic distress (low blood pressure, heart failure or cardiogenic shock). When cardiac output and blood pressure are maintained and/or when the tachycardia is short lived, the arrhythmia may present as palpitations, breathlessness or just discomfort.

WIDE COMPLEX SUPRAVENTRICULAR TACHYCARDIAS

Intraventricular conduction delay can result from heart rate changes, as well as from fixed pathological lesions in the conduction system. In patients with pre-existing or “fixed” (present during the normal baseline rhythm) bundle branch block (BBB), any SVT results in a broad complex tachycardia. However, rate related and/or “functional” (present only during tachycardia) BBB may also result in WCT. Functional aberration results from sudden increases in cycle length when parts of the His-Purkinje system are partially or wholly inexcitable. Functional right bundle branch block (RBBB) occurs more frequently than functional left bundle branch block (LBBB) because of the longer refractoriness of the former.¹ Sometimes, discrete variations in cycle length change a broad to a narrow complex tachycardia and thereby facilitate the correct diagnosis (fig 1). A sudden short long cycle length variation lengthens the refractoriness of the His-Purkinje system and an abrupt long-to-short cycle length change shortens the refractoriness of the His-Purkinje system refractoriness.² Functional BBB may persist for several successive impulses because the bundle branch that is blocked antegradely may be activated transseptally via its contralateral counterpart, a process known as linking phenomenon.³ As the duration of the refractory period is a function of the immediately preceding cycle length (the longer this cycle length, the longer the subsequent refractory period), abrupt cycle length variations (that is, long-to-short or short-to-long) predispose to the occurrence of functional BBB—for example, in atrial fibrillation, which is known as Ashman phenomenon⁴

ELECTROCARDIOGRAPHIC CLUES IN DIFFERENTIAL DIAGNOSIS: SVT VERSUS VT

QRS criteria for differential diagnosis in broad complex tachycardia: ventricular tachycardia (VT) versus supraventricular tachycardia (SVT) with left (LBBB) or right (RBBB) bundle branch block.

 

In general, if an ECG showing a WCT does not look like aberration, it is most likely a VT If there is any doubt about the origin of a WCT, the patient should be treated as if the rhythm was VT. The absence of an RS complex in any precordial lead or an interval of the R wave onset to the S wave nadir of more than 100 ms strongly suggest a VT.⁶ In addition, the following ECG criteria have been suggested to distinguish between VT and SVT with aberration

• QRS complex duration—VT is the probable diagnosis when the QRS duration with RBBB is greater than 140 ms, and greater than 160 ms with LBBB morphology.⁷

• QRS axis—A frontal axis between –90° to ±180° cannot be achieved by any combination of bundle branch block and therefore suggests VT. Thus, predominantly negative QRS complexes in leads I, II, and III are a useful criterion for identifying a VT.

• Concordant negative ECG patterns in the precordial leads—If all precordial leads are predominantly negative, a VT is the likely diagnosis. If all precordial leads are predominantly positive, the differential diagnosis is an antidromic tachycardia using a left sided accessory pathway or a VT.

• QRS morphologies in V1 and V6—In an RBBB pattern, a monophasic R wave, a broad (> 30 ms) R, or a qR in V1 strongly suggest VT. A monophasic R wave, or an S greater than an R in V6, also suggest VT. In the presence of an LBBB pattern, a broad R wave (usually greater than 30 ms) and/or a slow descent to the S wave nadir in V1 and a Q in V6 point towards a VT.

Atrioventricular dissociation
This is one of the most useful criteria for distinguishing VT from SVT. It occurs in 20–50% of VT and almost never in SVT. Atrioventricular dissociation may be diagnosed by a changeable pulse pressure, irregular canon A waves in the jugular veins and a variable first heart sound. It often demands long 12 lead ECG recordings and careful ECG analysis. In addition, about 30% of VTs have 1:1 retrograde conduction. In the presence of AV dissociation, one may also observe fusion beats which may result from the fusion of a P wave conducted to the ventricles.

The 12 lead ECG during VT can be helpful in providing an approximation of the site of origin. In general, VT that have an LBBB-like morphology in V1 have an exit in the right ventricle or the interventricular septum. A QRS axis that is directed superiorly generally indicates an exit in the inferior wall; an axis directed inferiorly indicates an exit in the anterior (superior) wall. In V2 to V4, dominant R waves usually indicate an exit near the base of the ventricle. In idiopathic right ventricular outflow tract tachycardia (RVOT-VT), the QRS duration during VT is usually > 140 ms if it originates from the free wall of the RVOT, and < 140 ms if the arrhythmia originates from the septal site of the RVOT. Furthermore, the precordial R wave transition in RVOT-VT usually occurs in leads V2 through V4 and becomes earlier as the site of origin advances more superiorly along the septum. An R wave transition in lead V2 suggests a site of origin immediately inferior to the pulmonic valve or the left ventricular outflow tract.

REFERENCES

 

1. Myerburg RJ, Stewart JW, Hoffman BF. Electrophysiological properties of the canine peripheral A-V conducting system. Circ Res 1970;26:361–78.[Abstract/Free Full Text]

2. Denker S, Shenasa M, Gilbert CJ, et al. Effects of abrupt changes in cycle length on refractoriness of the His-Purkinje system in man. Circulation 1983;67:60–8.[Abstract/Free Full Text]

3. Wellens HJ, Durrer D. Supraventricular tachycardia with left aberrant conduction due to retrograde invasion into the left bundle branch. Circulation 1968;38:474–9.[Abstract/Free Full Text]

4. Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am Heart J 1947;34:366.[CrossRef]

5. Klein GJ, Bashore TM, Sellers TD, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med 1979;301:1080–5.
   Large series on patients with Wolff-Parkinson-White syndrome and a history of sudden cardiac death that demonstrated that patients are most susceptible to ventricular fibrillation if they have a history of atrial fibrillation or reciprocating tachycardia, demonstrate rapid conduction over an accessory pathway, or have multiple pathways.[Abstract]

6. Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649–59.
   Original paper that reports on the absence of an RS complex in all precordial leads as an easily recognisable and highly specific predictor for the diagnosis of ventricular tachycardia.[Abstract/Free Full Text]

7. Akhtar M, Shenasa M, Jazayeri M, et al. Wide QRS complex tachycardia. Reappraisal of a common clinical problem. Ann Intern Med 1988;109:905–12.[Medline]

 

Heart Blocks

 

 Atrioventricular Heart Blocks

1st degree

PR interval > 0.2 seconds (1 large box), each P is followed by a QRS. PR interval is measured from the beginning of the P wave to the beginning of the QRS.

Figure: The PR interval is approximately 0.28 seconds.

Definition: 1AVB is a rhythm in which the electrical impulse which leaves the SA node and travels through the atria, AV node, Bundle of His to purkininjie fibers is slowed down and takes longer thaormal to arrive at its destination. The normal PR interval is 0.12- 0.20 seconds. A 1AVBT is greater than 0.20 seconds. The cause ranges from coronary heart disease, inferior wall MI’s, hyperkalemia, congenital abnormalities, and medications such as quinidine, digitalis, beta blockers, and calcium channel blockers.

  Rate: The atrial rate or P waves can vary to any rate. The ventricular rate can also vary. There must be a 1:1 conduction of the P waves to the QRS waves. Rhythm: Atrial and ventricular rates are usually regular, but they may also be irregular. P Wave: Usually normally shaped and occurring with a 1:1 ration with the QRS. PR interval: greater than0.20 seconds. QRS Complex: Withiormal limits or may have a bundle branch block. ST Segment: Withiormal limits for the intrinsic rhythm. T Wave: Withiormal size and configuration.

 

2nd degree block – type 1

Also called “Wenkebach”. PR interval gets progressively longer each beat until finally a QRS is “dropped” (missing).

Figure: Note the increasing PR interval before the QRS is dropped, then the cycle is repeated.

2nd degree block – type 2

Also called “Mobitz II”. Look out! A more serious conduction problem than Type 1. PR intervals are constant and a QRS is “dropped” intermittently.

Figure: Note the dropped QRS after the second and sixth P wave in lead II (the rhythm strip).

3rd degree block

The atrial rate is independent of the ventricular rate (P wave and QRS march out separately. The clue here is no relationship at all of the P-R intervals). The P-R interval is constantly changing, the QRS is usually wide and bizarre because it is ventricular origin.

Figure: Note the P waves and QRS waves are independent of each other.

Definition: Second degree AV block is also known as Second Degree Type I, Mobitz I, or Wenckelbach. This arrhythmia is characterized by a progressive delay of the conduction at the AV node, until the conduction is completely blocked. This occurs because the impulse arrives during the absolute refractory period, resulting in an absence of conduction, and no QRS. The next P wave occurs and the cycle begins again. Possible causes are acute inferior wall myocardial infraction, digitalis, beta blockers, calcium channel blockers, rheumatic fever, myocarditis, or excessive vagal tone.

  Rate is ususaly 60-100 beats per minute. Atrial rhythm is regular. Ventricular rhythm is irregular. P Wave configuration is normal. PR interval gets longer with each beat until QRS complex is dropped. QRS complex is normal, but is dropped periodically. ST Segment and T Wave are normal in configuration.

Mobitz II is characterized by 2-4 P waves before each QRS. The PR pf the conducted P wave will be constant for each QRS. It is usually associated with acute anterior or anteroseptal myocardial infarction. Other causes are cardiomyopathy, rheumatic heart disease, coronary artery disease, digitalis, beta blockers, and calcium channel blockers. Mobitz II has the potential of progressing into a third degree heart block or ventricular standstill

Ventricular rate will depend on the number of impulses conducted through the AV node, and will be less than the atrial rate. Rhythm: Atrial and ventricular rate is irregular. P Wave: Present in two, three or four to one conduction with the QRS. PR Interval: Constant for each P wave proir to the QRS. QRS: May be within normal limits for the intrinsic rhythm. ST Segment: Normal in size and configuration.

A third degree atrial ventricular block is also know as a complete heart block artrioventricular block of 3degree AV block. It is a problem with electrical conduction. All electrical conduction from the atria are blocked at the AV junction, therefore, the atria and the ventricles beat independently from each other. This arrhythmia is dangerous because it significantly decreases cardiac output, and could lead to asystole. Possible causes: acute inferior and anterior myocardic infraction, coronary heart disease, excessive vagal tone, myocarditis, endocarditis, age, edema from heart surgery, and meditation toxicity from digitalis, beta blockers, calcium channel blockers

 Atrial rate faster than ventricular rate. Rhythm: Regular, but there is normal configuration. PR Interval: There is no relationship between P waves and QRS complexes. QRS Complex: Variates depending on the intrinsic rhythm. ST Segment and T Wave: Normal configurations

 

Intervals

Longitudinal Heart Blocks

An interval is a portion of the baseline and at least one wave. We measure an interval on the horizontal axis in seconds. The PR, QRS, and QT are the intervals which should be routinely scanned on each ECG. For measuring intervals, look at the widest form in any lead.

 

Figure: Intervals.

4.     PR interval (beginning of P wave to the beginning of the next QRS). Normally, < .2 seconds or one large box. If it is > .2 seconds, it is a first degree block. (Note: this concept was introduced under blocks).

Figure: Note the prolonged PR interval (.28 seconds), especially at the second beat.

5.     QRS interval (beginning of Q to the end of the S wave) should be < .12 seconds (< 3 small boxes). If QRS is > .12, check for bundle branch block.

The QRS complex represents the amount of time required to depolarize the ventricles. A normal QRS is 0.08-0.12 seconds in length. A length greater than 0.12 seconds is considered a BBB. This means that there may be a block in one of the bundle branches, or the electrical impulse was conducted through an abnormal conduction pathway. This can occur in any rhythm. The causes range from normal to pericarditis, myocarditis, congested heart failure and congenital heart disease.

 Rate: Atrial and ventricular rate can vary depending on the specific rhythm involved. Any rhythm can have BBB. The P Wave depends on the intrinsic rhythm involved. The QRS is the determining factor and it must be greater than 0.12 seconds.

A QRS > .12 and RR (2 peaks or R waves in QRS) occurring in the right chest leads (V1-V2) indicates a right bundle branch block.

Figure: RBBB.

If QRS is > .12 and RR occurs in the left chest leads (V5-V6), this indicates a left bundle branch block.

Figure: LBBB.

6.     QT interval (beginning of QRS to end of T wave) should be less than half of the preceding RR interval – this varies with the rate. For normal rates, QT < .4 seconds (2 large boxes). “QT prolongation” (too long) can lead to a refractory form of ventricular tachycardia called torsades de pointes.

Figure: The QT interval is greater than half the preceding RR interval. Look at lead I.

 

Fasicular Blocks

Fasicular blocks are blocks of part of the left bundle, either the posterior or anterior division:

Figure: Divisions of the bundles.

Anterior fasicular block – the most common.

You will see left axis deviation (-30 to -90) and a small Q wave in lead I and an S in lead III (Q1S3). The QRS will be slightly prolonged (0.1 – 0.12 sec).

Figure: Anterior fasicular block.

Posterior fasicular block – less common.

You will see right axis deviation, an S in lead I and an Q in lead III (S1Q3). The QRS will be slightly prolonged (0.1 – 0.12 sec).

Figure: Posterior fasicular block.

Bifasicular block.

This means two (2) of the three (3) fascicles (in diagram) are blocked. The most important example is a right bundle branch block and a left anterior fascicular block. Watch out for this. Only one fascicle is left for conduction, and if that fasicle is intermittently blocked, the dangerous Mobitz 2 is set up!

Figure: Right bundle branch block and left anterior fascicular block.

“Fasicular Blocks” may seem a bit complicated – simply remember that axis deviation is the clue. In your differential, consider posterior fasicular blocks with right axis deviation and consider anterior fasicular blocks with left axis deviation. Fascicular blocks cause axis deviations, like infarcts and hypertrophy. If you see a left or right axis deviation, first look for infarct or hypertrophy. If neither are present, the remaining diagnosis of fasicular block is usually correct. Review differential diagnosis of right and left axis deviation.

MANAGEMENT OF SYMPTOMATIC BRADYCARDIA

CARDIAC PACING

Permanent cardiac pacing remains the only effective treatment for chronic, symptomatic bradycardia. In recent years, the role of implantable pacing devices has expanded substantially. At the beginning of the 21st century, exciting developments in technology seem to happen at an exponential rate. Major advances have extended the use of pacing beyond the arrhythmia horizon. Such developments include dual-chamber pacers, rate-response algorithms, improved functionality of implantable cardioverter defibrillators, combinations of sensors for optimum physiological response, and advances in lead placement and extraction. Cardiac pacing is poised to help millions of patients worldwide to live better electrically. We review pacing studies of sick-sinus syndrome, neurocardiogenic syncope, hypertrophic obstructive cardiomyopathy, and cardiac resynchronisation therapy, which are common or controversial indications for cardiac pacing. We also look at the benefits and complications of implantation in specific arrhythmias, suitability of different pacing modes, and the role of permanent pacing in the management of patients with heart failure.

Introduction

Permanent cardiac pacing is one of the most important medical innovations of the 20th century. Although originally designed for management of Stokes-Adams attacks (in patients with complete heart block), sick-sinus syndrome is now the most common indication for permanent pacemaker implantation. In the USA, sinus-node dysfunction is probably the primary indication for pacemaker implantation in over 50% of patients. Cardiac pacing remains the only effective long-term treatment for symptomatic bradycardia.

Recent technical advances in cardiac pacing have included dual-chamber devices, rate-response algorithms, and progressive refinement of antibradycardia-pacing function in implantable cardioverter defibrillators (ICDs). Indications have expanded beyond symptomatic bradycardia, and now include neurocardiogenic syncope, hypertrophic obstructive cardiomyopathy, and cardiac resynchronisation therapy (CRT, biventricular pacing) for congestive heart failure. The role of atrial pacing in the prevention of atrial fibrillation is being explored.

Pacing modes

The generic pacemaker code of the North American Society of Pacing and Electrophysiology and the British Pacing and Electrophysiology Group is used to describe various pacing modes. The first letter denotes the chamber or chambers that are paced (A=atrial, V=ventricular, D=dual [atrial and ventricular]). The second letter describes which chambers detect (sense) electrical signals. The third letter represents the response to sensed events (I=inhibition, T=triggering, D=dual [inhibition and triggering]). A fourth letter, R, denotes activation of rate-response features. The most commonly used pacing modes are: AAI(R) single-chamber atrial pacing without (or with) rate response, VVI(R) single-chamber ventricular pacing without (or with) rate response, and DDD(R) dual-chamber pacing without (or with) rate response. In the latest version of the code, a fifth position denotes the chamber or chambers in which multisite pacing is delivered.

Single-chamber right atrial pacing might be adequate for patients with sinus-node dysfunction and intact atrioventricular conduction. The disadvantage of this pacing modality is that atrioventricular block develops in 0·6–5·0% of patients with sick-sinus syndrome every year. Atrial pacing would be inadequate for this type of acquired (natural or ablation-induced) atrioventricular block. To upgrade to a dual-chamber pacing system is often more complicated (venous thrombosis/fibrosis, pocket fibrosis) and might entail more morbidity than a de novo dual-chamber implant. In patients with sinus-node dysfunction, the presence of bundle-branch block at implantation is a better predictor of subsequent atrioventricular block than the atrial rate (Wenckebach cycle length), where Mobitz type I atrioventricular block occurs.

Single-chamber right ventricular pacing can be associated with symptoms of pacemaker syndrome. During VVI pacing, this syndrome is most common in patients with normal (or near normal) left ventricular function and intact retrograde ventriculoatrial conduction.

Dual-chamber pacemakers that are programmed correctly assure maintenance of atrioventricular synchrony. Based on pacemaker programming and the intrinsic rhythm, patients with dual-chamber devices can show complete inhibition, atrial pacing with intact atrioventricular conduction, ventricular tracking of a sensed atrial rhythm (P-synchronous ventricular pacing), or atrioventricular sequential pacing (figure 1).

Figure 1. ECG patterns of dual-chamber devices 
(A) Complete inhibition (sinus rhythm is present with intact atrioventricular conduction). (B) Atrial pacing with intact atrioventricular conduction. (C) Ventricular tracking of a sensed atrial rhythm (P-synchronous ventricular pacing). (D) Atrioventricular sequential pacing. (E) Single-chamber right ventricular pacing. Arrows point to smaller deflections occurring at a slower rate, which might represent P waves or baseline artifact. AS=sensed intrinsic atrial rhythm. VS=sensed intrinsic ventricular rhythm. AP=paced atrial rhythm. VP=paced ventricular rhythm.

 

Loss of atrioventricular synchrony might reduce resting cardiac output by 20–30%.Retrograde ventriculoatrial conduction might also cause a negative atrial kick, and could result in atrial distention and an autonomically mediated vasodepressor response. Atrial contraction against closed atrioventricular valves results in systemic and pulmonary venous regurgitation and congestion, which might precipitate heart failure.

Symptoms of pacemaker syndrome include headache, disturbed mentation, neck pulsations, dyspnoea, chest discomfort, heightened cardiac awareness (transition from spontaneous to paced beats), fatigue, lethargy, exercise intolerance, and postural hypotension (lightheadedness, near-syncope, syncope).

Dual-chamber pacing is traditionally accomplished by lead placement in the right atrial appendage and right ventricular apex. Development of active fixation technology has allowed lead placement at various sites within the right heart chambers. Pacing in the right atrial septum seems to be antiarrhythmic. Haemodynamics can be improved by pacing in the right ventricular outflow tract; however, in short-term randomised studies, clinical benefits from outflow tract versus apical pacing have not been shown.

In VDD pacing, the atrium is sensed but not paced, which is useful for patients with atrioventricular block and intact sinus nodal function. The main advantage of VDD pacing is atrioventricular synchrony with a single lead (incorporation of tip electrodes for ventricular sensing and pacing plus floating atrial electrodes for P wave sensing). However, there has been concern that long-term stability of atrial sensing is not as reliable as in DDD systems and about VDD function under real-life conditions (atrial sensing might be variable). During atrial undersensing, a VDD system functions as a VVI system. Several recent studies suggest these concerns are not completely justified. Investigators have shown maintenance of atrioventricular synchrony during exercise. Another series of 13 children and 24 adults followed up for a mean of 3·5 years showed atrial electrogram stability and effective atrial sensing. Present technology does not allow reliable atrial pacing via floating electrodes. This accomplishment could become feasible in the future.

 

Clinical benefits of physiological (AAI or dual-chamber) pacing

Despite the apparent advantages of physiological pacing, recommendations that favoured dual-chamber over single-chamber ventricular pacing in patients with sick-sinus syndrome or atrioventricular block were mainly based on observational data and expert opinion, until recently. A retrospective study of patients with sick-sinus syndrome showed that development of chronic atrial fibrillation and stroke was strongly determined by clinical variables and secondarily by ventricular pacing modality.18 In some instances, atrial fibrillation might be promoted by ventricular pacing. Data from the same patient population revealed inconclusive mortality results, and showed that ventricular pacing did not increase the frequency of progressive or new onset heart failure compared with physiological pacing.

Andersen and associates published the first randomised study comparing pacemaker modes in patients with sick-sinus syndrome. By contrast with the studies noted earlier, patients assigned to atrial pacing had lower rates of atrial fibrillation, heart failure, thromboembolic events, and cardiovascular and total mortality than did ventricularly-paced patients. In the Pacemaker Selection in the Elderly (PASE) study, very little benefit in quality of life from dual-chamber pacing was shown in elderly patients. However, patients with sick-sinus syndrome (but not atrioventricular block) had improvement in quality of life and higher functional status with dual-chamber pacing. Ellenbogen and colleagues reviewed several variables at pacemaker implantation in patients from the PASE trial who were randomly assigned to the VVIR mode. Significant decreases in systolic blood pressure during ventricular pacing at implantation, β-blocker use at the time of randomisation, and non-ischaemic cardiomyopathy were the only variables that predicted crossover to DDDR pacing in the Cox multivariate regression model.

In the Canadian Trial of Physiologic Pacing (CTOPP), physiological pacing (AAI or DDD) provided little benefit over ventricular pacing in prevention of stroke or cardiovascular death. Further analysis of this large study showed that physiological pacing significantly reduced the frequency of chronic atrial fibrillation. Patients assigned to physiological pacing had a 27% relative risk reduction for development of chronic atrial fibrillation compared with those assigned to ventricular pacing. The yearly event rate for cardiovascular death or stroke rose steadily with decreased intrinsic heart rate in the ventricular pacing group. There was no event rate change in the physiologically-paced group, suggesting a benefit for pacemaker-dependent patients. The Mode Selection Trial in sinus-node dysfunction (MOST) showed no difference between dual-chamber and ventricular pacing in all-cause mortality or non-fatal strokes. In the Atrial Dynamic Overdrive Pacing Trial (ADOPT), patients with bradycardia-tachycardia syndrome who were randomly assigned to DDDR with atrial dynamic overdrive pacing had a significantly higher frequency of atrial pacing than those in the DDDR pacing alone group (table 1).

 

Table 1. Pacing trials for sick-sinus syndrome

In the UK Pacing and Cardiovascular Events study dual-chamber pacing did not reduce all-cause mortality compared with single-chamber ventricular pacing (fixed or adaptive) in patients over age 70 years with high-grade atrioventricular block. Secondary endpoint data also showed no difference in stroke or transient ischaemic attack, heart failure, and myocardial infarction. Analyses of quality of life, exercise tolerance, and other secondary endpoint data are pending.

These studies consistently showed a decreased frequency of atrial fibrillation with atrial-based pacing in patients with sinus-node dysfunction (table 1). The findings suggest that some time might be needed to see potential biological (remodelling) effects of right atrial pacing for atrial fibrillation prevention. Contrary to all expectations, a reduction in stroke, heart failure, and mortality has not been consistently shown. High crossover rates (from single-chamber ventricular to dual-chamber pacing) seen in MOST and PASE might have limited the value of data assessed by an intention-to-treat analysis.

Rate-responsive pacing

Inadequate rate response to exercise (chronotropic incompetence) could be a sign of sick-sinus syndrome. The syndrome might also be precipitated by drugs (eg, β blockers) used in the management of coronary disease or heart failure. Rate-responsive (adaptive) pacing uses sensors to detect physical or physiological indices and mimic the rate response of the normal sinus node. A rate-control algorithm affects the overall rate-adaptive characteristics of the pacing system. Although some features of rate-adaptive pacing are automatic, physicians need to programme one or more variables to achieve the clinically desired rate response. Benefits of rate-adaptive pacing for patients with chronotropic incompetence (eg, sick-sinus syndrome or atrial fibrillation with advanced heart block) are well established. Many sensors have been developed to modulate pacing rate (according to metabolic needs) and correct chronotropic incompetence. Activity, minute-ventilation, QT-interval, and stroke-volume sensors are commercially available in the USA and Europe.

The large number of sensors in clinical or investigational pacemakers suggests that none is ideal. Characteristics of an ideal sensor include: compatibility with standard pacing leads, rapid response, proportionality to workload, sensitivity to non-exercise physiological stimuli (eg, emotional stress, postural changes, meals, fever), and specificity to physiological stimuli. Among commonly used sensors, activity sensors have the fastest response, but have poor proportionality (eg, faster rates when going downstairs than upstairs), and specificity (eg, inappropriately fast rates when riding over a bumpy road). Minute ventilation and QT-interval pacemakers have good proportionality but slow speed of response. Only QT-interval systems respond to emotional stress. Processing of raw sensor data by refined algorithms reduces but does not eliminate these limitations. Sensor strengths and limitations are summarised in table 2.

 

Table 2. Sensor strengths and limitations

 

Sensors using special lead technology might be unreliable and difficult to implant. Sensors in the pulse generator are more dependable and only require conventional implant techniques. Hence, commonly used clinical devices use accelerometers, activity, QT-interval, and minute-ventilation sensors.

In AAI and VVI models, single-chamber pacing takes place when the sensed atrial or ventricular rate falls below a programmed lower rate limit. When rate response is activated, a sensor-driven rate is recorded. If the sensor-driven rate exceeds both the intrinsic rate and the lower rate limit, rate-adaptive pacing occurs. A programmed maximum sensor rate determines the fastest pacing that can occur.

In dual-chamber devices programmed in the DDDR mode, rate adaptation might result from ventricular tracking of the atrial rhythm or be sensor driven (atrial or atrioventricular sequential pacing). Maximum ventricular tracking and sensor rates can be programmed separately. If a fast atrial rate during exercise is assumed to be more likely to represent sinus tachycardia than a fast atrial rate at rest, a maximum sensor rate (that is programmed faster than the maximum ventricular tracking rate) helps provide faster ventricular rates during exertion and limits the ability to track atrial tachyarrhythmias. Dual-chamber devices also allow rate-responsive atrioventricular delays to be programmed (which simulates normal shortening of the PR interval).

Rate-response features could be adapted to individual patients. For instance, activity sensors can be programmed to various thresholds (high, medium, low), which can trigger rate-responsive pacing. The slope of acceleration and deceleration of pacing rate might also be programmed. Recently, different sensors have been combined to provide a more physiological response to exercise. Sensor combination aims to improve the speed of rate response, proportionality to workload, sensitivity to changes induced by exercise-related and non-exercise-related requirements, and specificity in rate adaptation.

Combinations of sensors, which exploit strengths and counteract weaknesses of individual sensors, are a logical step toward optimisation of rate-responsive pacing. Clinically available combinations include activity/minute ventilation, accelerometer/minute ventilation, and activity/QT sensors. Combinations have included a fast reacting activity sensor with a more proportional and specific metabolic sensor. Initial dual-sensor systems needed time-consuming tailoring of the individual sensors and their interactions for every patient. Present systems allow for the automated tailoring of rate response, via self-learning rate-response algorithms (Vitatron, Arnhem, the Netherlands), or programming of a target rate histogram on the basis of the patient’s activity level and frequency of exercise (Medtronic, Minneapolis, MN, USA).

Benefits of rate-adaptive pacing are difficult to gauge in the usual pacemaker recipient. Most patients already have a quality of life similar to that of age-matched controls. VVIR pacing seems to be better than VVI pacing in terms of symptoms. In one study, DDD pacing offered a better quality of life in all patient subgroups than did dual-sensor VVIR pacing. There is little evidence to support a major clinical difference between sensors and their combinations. Cowell and colleagues reported evidence (in one patient) of potential benefit of a dual-sensor compared with a single sensor.

Rate modulation is available in almost all modern pulse generators. In the USA, rate modulation and atrioventricular synchrony are given to pacemaker recipients whenever possible. Many sophisticated rate-adaptive features are poorly understood by clinicians and not well programmed. We believe that rate response is highly beneficial on occasion, although automated features are rarely an adequate substitute for careful physician input.

Sensors using special lead technology might be unreliable and difficult to implant. Sensors in the pulse generator are more dependable and only require conventional implant techniques. Hence, commonly used clinical devices use accelerometers, activity, QT-interval, and minute-ventilation sensors.

In AAI and VVI models, single-chamber pacing takes place when the sensed atrial or ventricular rate falls below a programmed lower rate limit. When rate response is activated, a sensor-driven rate is recorded. If the sensor-driven rate exceeds both the intrinsic rate and the lower rate limit, rate-adaptive pacing occurs. A programmed maximum sensor rate determines the fastest pacing that can occur.

In dual-chamber devices programmed in the DDDR mode, rate adaptation might result from ventricular tracking of the atrial rhythm or be sensor driven (atrial or atrioventricular sequential pacing). Maximum ventricular tracking and sensor rates can be programmed separately. If a fast atrial rate during exercise is assumed to be more likely to represent sinus tachycardia than a fast atrial rate at rest, a maximum sensor rate (that is programmed faster than the maximum ventricular tracking rate) helps provide faster ventricular rates during exertion and limits the ability to track atrial tachyarrhythmias. Dual-chamber devices also allow rate-responsive atrioventricular delays to be programmed (which simulates normal shortening of the PR interval).

Rate-response features could be adapted to individual patients. For instance, activity sensors can be programmed to various thresholds (high, medium, low), which can trigger rate-responsive pacing. The slope of acceleration and deceleration of pacing rate might also be programmed. Recently, different sensors have been combined to provide a more physiological response to exercise. Sensor combination aims to improve the speed of rate response, proportionality to workload, sensitivity to changes induced by exercise-related and non-exercise-related requirements, and specificity in rate adaptation.

Combinations of sensors, which exploit strengths and counteract weaknesses of individual sensors, are a logical step toward optimisation of rate-responsive pacing. Clinically available combinations include activity/minute ventilation, accelerometer/minute ventilation, and activity/QT sensors. Combinations have included a fast reacting activity sensor with a more proportional and specific metabolic sensor. Initial dual-sensor systems needed time-consuming tailoring of the individual sensors and their interactions for every patient. Present systems allow for the automated tailoring of rate response, via self-learning rate-response algorithms (Vitatron, Arnhem, the Netherlands), or programming of a target rate histogram on the basis of the patient’s activity level and frequency of exercise (Medtronic, Minneapolis, MN, USA).

Benefits of rate-adaptive pacing are difficult to gauge in the usual pacemaker recipient. Most patients already have a quality of life similar to that of age-matched controls. VVIR pacing seems to be better than VVI pacing in terms of symptoms. In one study, DDD pacing offered a better quality of life in all patient subgroups than did dual-sensor VVIR pacing. There is little evidence to support a major clinical difference between sensors and their combinations. Cowell and colleagues reported evidence (in one patient) of potential benefit of a dual-sensor compared with a single sensor.

Rate modulation is available in almost all modern pulse generators. In the USA, rate modulation and atrioventricular synchrony are given to pacemaker recipients whenever possible. Many sophisticated rate-adaptive features are poorly understood by clinicians and not well programmed. We believe that rate response is highly beneficial on occasion, although automated features are rarely an adequate substitute for careful physician input.

Permanent bradycardia pacing via implantable cardiac defibrillators

Previously, 15–20% of ICD recipients needed separate pacemakers. Strict criteria for dual-chamber pacing are present in 11–29% of recipients. This percentage seems certain to rise as biventricular pacing for heart failure becomes increasingly common. Present ICDs capable of dual-chamber and triple-chamber, rate-responsive pacing provide state-of-the-art treatment. Shortcomings in early-generation devices have been corrected. However, addition of full-featured pacing is technically complex, and the final product is not merely the sum of a DDDR or DDDRV pacemaker and a tiered-therapy ICD. A tiered-therapy ICD includes antitachycardia pacing, cardioversion, and defibrillation capabilities. Emphasis on safe and reliable defibrillation can result in suboptimum pacemaker function.

If present and future trials expand indications for prophylactic defibrillator implantation, a large number of patients needing pacemakers for bradycardia or heart failure might instead receive (at least in the most developed countries) an ICD.39,40 Cost considerations aside, substituting ICDs would have a profound effect on how cardiac rhythm management devices are designed, marketed, implanted, and followed up. Panel 1 shows the limitations of ICDs as pacemakers.

Panel 1: Limitations of ICD pacing function

 

·        Increased incidence of hardware and software design problems

·        Uncertain long-term reliability of presently available defibrillation leads (compared with standard pacing leads)

·        Increased current drain that reduces device longevity

·        Heightened susceptibility to oversensing of endogenous (eg, diaphragmatic myopotentials) or exogenous (eg, electromagnetic interference) signals

·        Pacing at rapid rates might delay or prevent detection of ventricular tachyarrhythmias

·        Complicated pacing algorithms could result in inappropriate detection of ventricular tachyarrythmias by ICDs

Frequent right ventricular pacing could be detrimental to ICD patients without indications for antibradycardia pacing. In the Dual chamber and VVI Implantable Defibrillator (DAVID) trial,41 dual-chamber ICDs were programmed VVI 40 beats per minute or DDDR with a lower rate limit of 70 beats per minute. 1-year survival free of the composite endpoint (time to death or first admission for heart failure) was 89·3% in the VVI-40 group compared with 73·3% for the DDDR-70 group (p < 0·03). Although the VVI-40 group had less congestive heart failure and death than did the DDDR-70 group, these differences for these individual endpoints were not significant. Nearly 60% of ventricular beats were paced in the DDDR-70 group compared with 1% in the VVI-40 patients. Andersen and colleagues22 noted an improvement in cardiovascular and total mortality with AAI pacing. Dual-chamber pacing has not shown similar benefits.23,25,29,31 Data from MOST42 suggested that increased admission for heart failure was not associated with pacing mode, but with a prevalence of right ventricular pacing exceeding 40%. DAVID investigators suggested that right ventricular pacing (and the resultant left ventricular conduction delay) increases heart failure by creating ventricular desynchronisation.41

From the DAVID trial, single-chamber ICDs seem to be the device of choice. However, many ICD recipients will develop sinus-node dysfunction and atrial tachyarrhythmias. The diagnostic and therapeutic features of dual-chamber devices would be more suitable for these patients. Instead, the message from the DAVID trial should be that, when a dual-chamber ICD is chosen, the programming of a long atrioventricular delay (to reduce or avoid right ventricular pacing) should be considered for patients with intact atrioventricular conduction and narrow QRS complexes.

Pacing to terminate ventricular tachyarrhythmias

Antitachycardia pacing might terminate, accelerate, or have no effect on ventricular tachycardia. Because acceleration can turn a haemodynamically stable tachyarrhythmia into lethal ventricular fibrillation, this treatment requires backup defibrillation capabilities via an ICD. ICD treatment aims to prevent syncope and sudden death with minimum shock delivery. Antitachycardia pacing has traditionally been used to treat monomorphic ventricular tachycardias with rates up to 200 beats per minute. Only re-entrant monomorphic ventricular tachycardia (usually associated with clinically significant structural heart disease) can be ended by antitachycardia pacing. Ventricular tachycardia rates exceeding 200 beats per minute might be more likely to be accelerated by antitachycardia pacing and deteriorate into ventricular fibrillation. Adjuvant antiarrhythmic treatment might slow ventricular tachycardia rates and help with pace termination.43 Various pacing techniques can be used or combined to find a regimen that works consistently without arrhythmia acceleration (figure 2).

Figure 2. Antitachycardia pacing for ventricular tachycardia

(A) Ventricular tachycardia at cycle lengths of 310–20 ms (188–94 beats/minute). (B) Simulated ventricular tachycardia (courtesy of Medtronic) with cycle lengths of 330–70 ms (162–82 beats/minute). (C) Ventricular tachycardia at cycle lengths of 340–50 ms (rate 171–76 beats/minute). EGM1 Vtip to Vring=intracardiac ventricular electrogram recorded from pacing electrodes. EGM2=intracardiac ventricular electrogram recorded from high voltage (shock electrodes). TS=tachycardia sensing. TD=tachycardia detection. TP=tachycardia pacing. VS=sensing of intrinsic ventricular rhythm. V-V interval=ventricular cycle length (ms).

Antitachycardia pacing requires pacing faster than each tachycardia. Figure 2A shows burst pacing at 290 ms (fixed rate of 207 beats per minute), which terminates ventricular tachycardia. In scanning burst pacing (figure 2B), successive bursts are paced at fixed and faster rates. The second attempt ends another ventricular tachycardia. More aggressive ramp pacing (rate increase or cycle length decrement between beats) is required to terminate the tachyarrhythmia in figure 2C.

Termination success rates of 80% or more can be achieved in heart disease. Termination rates of induced ventricular tachycardia with biventricular or right ventricular antitachycardia pacing are much the same. Careful programming can result in acceleration rates as low as 1%. Almost all slow ventricular tachycardia episodes are pace terminable. However, in some patients antitachycardia pacing is unsuccessful and low-energy shocks are effective. Both treatments have comparable success, failure, and acceleration rates. Almost all patients describe shocks of 1 J or more as uncomfortable. By contrast, effective and painless pacing can be achieved with μJ and is therefore more tolerable and less energy-consuming than cardioversion. Additionally, appropriately delivered pacing is unlikely to result in atrial proarrhythmia.

Antitachycardia pacing treatment might be guided by electrophysiological test results or chosen empirically. New data suggest that ventricular tachycardia faster than 200 beats per minute can respond to empirical antitachycardia pacing.46

Pacing to prevent ventricular tachyarrhythmias

Algorithms that prevent ventricular tachyarrhythmias use continuous or intermittent (rate smoothing or stabilisation) pacing (with ventricular capture) to suppress triggering of ectopic beats, prevent re-entry, decrease dispersion of refractoriness, and eliminate pauses that might induce tachyarrhythmia. Various pacing techniques have been thought to prevent ventricular tachyarrhythmias; most are not very effective. In the acquired long-QT syndrome, torsades de pointes is invariably preceded by pauses or bradycardia.

We reviewed publications of acquired torsades de pointes in patients with permanent pacing. Studies providing documentation of tachycardia onset and pacemaker programming were included in our analysis, and events occurring less than 1 month after atrioventricular nodal ablation were excluded. 18 cases were identified. No patients developed the tachyarrhythmia with an effective pacing rate of more than 70 beats per minute. Programmed lower rates of up to 70 beats per minute were not protective. At programmed lower rates of over 70 beats per minute, torsades de pointes occurred only by programmable pause-promoting features or oversensing. Whether rate-smoothing algorithms can prevent the condition when the baseline rate is programmed to less than 70 beats per minute remains to be seen. Viskin and colleagues reported most pauses leading to torsade de pointes were unequivocally longer than the preceding basic cycle length (ventricular rate). The shortest culprit pause was 760 ms. They recommended pacing at a cycle length of 750 ms (ventricular rate of 80 beats per minute). We agree that this is reasonable. A detailed review of pacing in the long-QT syndrome has been published.

Acute and chronic congestive heart failure contribute to the need for tachyarrhythmia treatment in ICD recipients. Although small trials (93 patients in total) have shown that biventricular pacing treatment diminished ventricular arrhythmias, these results were not confirmed in larger trials.

Pacing for neurally-mediated syncope

Case history, physical examination, and a 12-lead electrocardiogram (ECG) are most important in the assessment of a patient with syncope. With these investigations, the diagnosis can be ascertained or suspected in 40% of patients. Although echocardiography is commonly requested, little evidence supports its use if the physical examination and ECG are normal. Myocardial ischaemia rarely causes syncope, and stress testing is low yield unless there is a high index of suspicion (ie, angina pectoris). Holter monitoring is also low yield. If another diagnosis is not established or suspected, patients without evidence of structural heart disease are generally referred for assessment of neurally-mediated syncope (carotid sinus massage, head-up tilt table testing [HUT]). Those with structural heart disease or known cardiac arrhythmias are usually referred for electrophysiological testing.

Benefit from pacing in patients with severe symptoms or unexplained falls and evidence of cardioinhibitory carotid sinus hypersensitivity has been recorded. Carotid hypersensitivity is common in elderly patients with unexplained falls. Although empiric pacing is generally used, whether bradycardia causes these episodes is uncertain. The Syncope and Falls in the Elderly—Pacing and Carotid Sinus evaluation (SAFE-PACE) randomly selected patients to clinical observation or pacemaker implantation. After follow-up, paced patients had a lower incidence of recurrent falls than did controls. A second study (SAFE-PACE 2) is an ongoing multicentre trial in which similar patients are randomly assigned to permanent pacing or an implantable loop recorder. Table 3 summarises the pacing trials for carotid sinus hypersensitivity.

 

Table 3. Pacing trials for carotid sinus hypersensitivity

The role of permanent pacing in management of neurocardiogenic (vasovagal) syncope remains controversial. A predominant cardioinhibitory (bradycardic <40 beats per minute or asystolic) response during HUT testing has been proposed as a means to identify patients with neurocardiogenic syncope who may respond to permanent pacing.

Maloney and colleagues described a patient who had 73 s of asystole provoked by HUT. After the investigators acknowledged that vasovagal spells were usually benign, they defined long episodes (that could alter lifestyle or threaten health) of cardiac standstill during vasovagal spells as malignant vasovagal syncope. Even with a dual-chamber pacemaker, the patient had severe symptomatic hypotension on repeat HUT. Maloney and co-workers recommended permanent dual-chamber pacing as adjuvant treatment for such patients. Sra and colleagues subsequently assessed 22 patients with bradycardia (or asystole) and hypotension provoked by HUT. Temporary pacing did not prevent a substantial decline in mean arterial pressure during repeat HUT. During long-term follow-up (median 16 months), of 19 patients treated with drugs alone, 18 did not have presyncope or syncope. Sra and co-workers concluded that drug treatment was often effective for prevention of cardioinhibitory neurocardiogenic syncope, whereas permanent pacing was not. Baron-Esquivias and colleagues reported a study including 1322 patients and concluded that neither pacing nor drug treatment affected the outcome of patients with tilt-induced asystole. They also concluded that the patients’ clinical course was affected mainly by the frequency of pretreatment events.

Two new pacing modalities—search hysteresis and rate-drop response—could be more effective than conventional pacing. Search hysteresis allows the patient’s heart rate to fall to a low value before pacing begins at a much faster rate. When search hysteresis is turned on, the escape interval automatically continues for an extra cycle to allow spontaneous sinus rhythm to resume. In rate-drop response, a substantial drop in spontaneous rate triggers rapid pacing (90–100 beats per minute) for a programmable period. In the Vasovagal Syncope International study, dual-chamber permanent pacing with search hysteresis was compared with no treatment. During follow-up, syncope occurred significantly more often in untreated patients than in those with permanent pacing.

Two controlled studies compared permanent pacing with drug treatment in patients with vasovagal syncope. In the North American Vasovagal Pacemaker Study (VPS), a large treatment effect for permanent pacing with rate-drop response versus medical treatment resulted in the study finishing early: a greatly reduced risk of syncope was seen in paced patients. Syncope Diagnosis and Treatment compared dual-chamber permanent pacing (with rate-drop response) with atenolol treatment in patients with recurrent vasovagal syncope. This study was also ended early after an interim analysis showed significant benefit from permanent pacing. Rate-drop response seems to be more effective than search hysteresis. New syncope sensors such as monitoring QT interval, right ventricular pressure, and other indicators of contractility are under investigation.

Results of the second Vasovagal Pacemaker Study (VPS II) were not as encouraging as the first VPS: cumulative risk of recurrent syncope did not differ significantly in patients with dual-chamber pacemakers with either ODO (control group, not actively pacing) or DDD (with rate-drop response). Because of a lower than expected event rate in the control group, the study lacked sufficient statistical power to prove that pacemaker treatment prevents recurrent vasovagal syncope. This unexpectedly low event rate could represent a placebo effect that resulted from device implantation in the control group. Flevari and associates recently compared the effects of propranolol, nadolol, and placebo in 30 patients with recurrent vasovagal syncope and positive HUTs. All three treatments significantly reduced spontaneous presyncope and syncope, although no differences in recurrence rates were seen between treatment arms. The vasovagal syncope and pacing trial (SYNPACE) randomised 29 patients to pacemaker on versus pacemaker off modes and was unable to show a benefit from active pacing in prevention of recurrence in patients with severe recurrent tilt-induced syncope.

We believe that neurocardiogenic syncope is generally a benign condition and can usually be managed without permanent pacing. Pure or predominantly vasodepressor episodes do not need pacing. At present, we believe that dual-chamber pacing should be regarded as an adjunctive treatment for patients with frequent and severe cardioinhibitory spells, especially for those who are drug refractory or intolerant or have asystole exceeding 5 s that can be shown clinically or during HUT.

Pacing in hypertrophic obstructive cardiomyopathy

Dual-chamber pacing has been proposed as an alternative to septal myotomy-myectomy for patients with hypertrophic obstructive cardiomyopathy (that is refractory to drug treatment). DDD pacing is used because patients with the condition often cannot tolerate loss of atrioventricular synchrony. Placement of the right ventricular electrode at the apex pre-excites the right-sided septum. Reduced inward septal motion (during systole) augments left ventricular outflow tract diameter and diminishes obstruction, which allows further systolic emptying.

Appropriate timing of the atrioventricular interval is essential for effective pacing. The programmed delay must be less than the native PR interval (to ensure full ventricular capture), but long enough to allow adequate atrial contribution to ventricular filling (to avoid falls in cardiac output and systemic blood pressure). Paced, sensed, and rate-adaptive atrioventricular delays help to maintain optimum atrioventricular intervals during daily activities. Correctly programmed dual-chamber pacing results in a 30–60% acute reduction in the left ventricular outflow tract gradient without systemic compromise.

Several investigations have been undertaken to assess the clinical benefits of pacing in hypertrophic obstructive cardiomyopathy (table 4). These studies have generated much controversy. Some investigators have suggested that responders tend to be older and more symptomatic thaon-responders. The balance between gradient reduction and impaired diastolic relaxation during ventricular pacing might determine clinical response. Pacing might be more favourable in patients with slight (or well compensated) diastolic dysfunction. Attempts to objectively assess functional capacity could be frustrated by the intrinsic heterogeneity of disease in hypertrophic obstructive cardiomyopathy. Much attention has been drawn to the consistent placebo effect noted in randomised pacing trials.72

Table 4. Summary of hypertrophic obstructive cardiomyopathy studies

 

Surgery is still regarded as the gold standard intervention for medically refractory hypertrophic obstructive cardiomyopathy. Patients should be aware that percutaneous transluminal septal myocardial ablation (PTSMA) is a treatment option. These procedures are associated with a risk of atrioventricular block, which needs subsequent permanent pacing. Permanent dual-chamber pacing might be considered in patients who are not candidates for surgery or PTSMA. Pacing might also be a reasonable adjunct for patients who use drugs that greatly impair their native conduction system.

Pacing to palliate, prevent, and interrupt atrial fibrillation

Complete atrioventricular junction ablation and permanent pacing was introduced in 1982 as an alternative treatment for patients with medically refractory supraventricular tachycardia. When radio-frequency currents were used as the energy source for ablation, this technique became a popular and effective method for palliative treatment of atrial fibrillation with a rapid ventricular response. In atrioventricular nodal modification, radio-frequency current is used to reduce ventricular rates. Energy is initially delivered to the posterior atrioventricular nodal imputs (near the ostium of the coronary sinus) and, if needed, gradually applied anteriorly (toward the compact atrioventricular node and bundle of His) until the desired effect is achieved. Attempts to modify the atrioventricular node have been successful in achieving long-term rate control in over 70% of patients. Inadvertent high-grade atrioventricular block (that needs permanent pacing) is seen in 10–20% of patients. Both nodal ablative techniques substantially improve symptoms, left ventricular function, and quality of life. However, complete atrioventricular junction ablation had a significantly greater effect on frequency of major symptoms and quality of life than did node modification.

Use of these palliative techniques has waned, as curative procedures (ie, pulmonary vein isolation and left atrial ablation) continue to develop. Atrioventricular junction ablation and permanent pacing might still be useful in elderly patients with clinically significant underlying structural heart disease, and those with persistent or chronic atrial fibrillation.

Atrial pacing has been investigated for prevention (and reduced frequency) of atrial fibrillation. Theoretical explanations are: (1) prevention of bradycardia-induced dispersion of refractoriness, which reduces the likelihood for re-entry; (2) overdrive suppression of spontaneous atrial ectopy that could trigger atrial fibrillation; and (3) change in atrial excitation patterns and prevention of intra-atrial re-entry, in response to premature atrial beats. As previously noted, the benefit of atrial-based pacing (compared with ventricular-based pacing) in reduction of atrial fibrillation (over time) in patients with sick-sinus syndrome has been well established in several randomised studies.

Clinical data have suggested that right atrial pacing is less effective for atrial fibrillation prevention in patients with right atrial conduction delays or increased dispersion of refractoriness. Site-specific pacing from the atrial septum or Bachmann’s bundle could shorten atrial conduction time and help to prevent atrial fibrillation.

Intra-atrial conduction delay can be diagnosed in the presence of P waves longer than 120 ms. Right atrial pacing could produce delayed left atrial activation with a suboptimum left-sided atrioventricular conduction time, which could result in left atrial mechanical systole close to, or simultaneous with, left ventricular systole. Loss of the atrial contribution to left ventricular filling could be haemodynamically deleterious. Simultaneous biatrial pacing (right atrium and proximal or distal coronary sinus), manifested by normalisation of P-wave configuration and duration, improves haemodynamics.

Multisite atrial pacing has been investigated for prevention of atrial flutter and fibrillation. Some investigators have combined high right atrial and distal coronary sinus pacing. Saksena and co-workers paced the right atrium and the coronary sinus ostium. In another small study, no difference was recorded in atrial fibrillation frequency or duration between right atrial and dual-site atrial pacing. Long-term results of multisite atrial pacing in heterogeneous atrial fibrillation populations have not been uniformly favourable. Benefits of dual-site pacing over right atrial pacing seem to be, at best, modest and clinical enthusiasm for this technique has waned.

The value of atrial pacing to prevent atrial fibrillation in patients without bradycardia remains controversial. Trials have been small and undertaken in individuals with frequent, drug-refractory atrial fibrillation and in populations in which effective treatments are difficult to find. In the Atrial Pacing Peri-Ablation for Prevention of Atrial Fibrillation study, the investigators concluded that in patients with drug–refractory, paroxysmal fibrillation who were candidates for ablation, right atrial pacing did not prevent atrial fibrillation. In a subsequent randomised crossover comparison of DDDR and VDD pacing modalities in patients with paroxysmal atrial fibrillation, the time to first recurrence did not differ between groups and the atrial fibrillation burden (h/day) increased significantly over time in both. In the New Indications for Pacing Prevention of Atrial Fibrillation study, although time to first recurrence was extended by dual-site pacing compared with high right atrial pacing in conjunction with a consistent atrial-pacing algorithm, total atrial fibrillation burden was much the same in the two groups.

New pacemaker pulse generators will include antitachycardia pacing modalities. Studies in patients receiving dual-chamber ICDs show that atrial tachyarrhythmias are common. Antitachycardia or high-frequency burst pacing could end two-thirds of these episodes. Whether these episodes indicate true pace termination will need further investigation. Although we are skeptical that atrial fibrillation can be reliably pace-terminated, arrhythmias that trigger atrial fibriallation (such as atrial flutter or tachycardia) can be readily pace-terminated.

Pacing for heart failure

Two small studies have suggested that DDD pacing with a short atrioventricular delay might benefit patients with dilated cardiomyopathy and a prolonged baseline PR interval. CRT refers to pacing techniques that alter the degree of atrial or ventricular electromechanical asynchrony in patients with major conduction disorders, and is usually done by pacing more than one atrial or ventricular site (biatrial or biventricular pacing, respectively). Bifocal pacing refers to two sites in the same anatomic cardiac chamber (ie, right ventricular apex and outflow tract). CRT can also be achieved by pacing from an atypical site (such as single-site left ventricular pacing). The Pacing Therapies in Congestive Heart Failure II study group showed that left ventricular pacing significantly improved exercise tolerance in patients with left ventricular systolic dysfunction, chronic heart failure, and a QRS duration of more than 150 ms. At least 20–30% of class III and IV chronic heart failure patients have major left ventricular conduction disorders that make them potential candidates for ventricular CRT.

Ventricular CRT has had far greater effect on improvement of heart failure than biatrial pacing has had on atrial fibrillation. Several studies have shown beneficial effects from biventricular or left ventricular pacing in patients with severe left ventricular systolic dysfunction and major left-sided intraventricular conduction disorders, such as complete left bundle-branch block. These conduction delays result in inefficient left ventricular contraction, shortened diastole (or overlap of systole and diastole), and worsened functional mitral regurgitation. CRT improves the sequence of left ventricular contraction and reduces functional mitral regurgitation. By contrast to inotropic agents, this treatment reduces myocardial oxygen consumption.

Atrioventricular optimisation might be needed to ensure continuous ventricular pacing. Patients with chronic atrial fibrillation might respond to biventricular pacing. Atrioventricular junction ablation might be needed to maintain pacemaker-controlled ventricular depolarisation. Biventricular pacing is technically complex. Until recently, CRT was accomplished with modified use of conventional hardware. The left ventricular lead is usually placed over the epicardial left ventricular surface via a tributary of the coronary sinus. Lateral and posterolateral cardiac veins seem to provide the best haemodynamic benefit (figure 3, figure 4), but could result in diaphragmatic (phrenic nerve) stimulation. Access to these lateral veins might be limited by variation in anatomy.

Figure 3. Diagrammatic presentation of heart showing positions for coronary venous lead placement

Figure 4. Chest radiographs showing lead placements

(A) Posteroanterior and (B) lateral chest radiographs showing tip of a left ventricular lead (arrows) in a tributary of the middle cardiac vein. Despite proximity of the lead to the left hemidiaphragm, phrenic nerve stimulation did not take place. The right ventricular lead points anteriorly toward the rib cage.

Success rates of implantation are dependent on experience, and experienced implanters achieve initial success in about 90% of patients. Median time for implantation has been reported to be 2·7 h. Lead dislodgment occurs in 5–10% of cases. Other potential complications include: increased left ventricular pacing thresholds, cardiac sinus dissection, cardiac tamponade, and various sensing problems. As mentioned earlier, cardiac venous anatomy is more variable than coronary artery anatomy. Leads and lead delivery systems likewise vary in length, shape, and stiffness. We caow choose from an increasing variety of catheters, sheaths, guidewires, and leads, to assist left ventricular epicardial pacing. Recent addition of leads designed specifically for cardiac venous pacing (including models that can be advanced over wires used for percutaneous transluminal coronary angioplasty) helps to reduce procedure times and increase success rates. Some older biventricular pacing ICDs might sense every conducted QRS twice, because ventricular activation is detected at different times by the right and left ventricular leads. Iewer devices, detection of tachyarrhythmias based on right ventricular sensing prevents the triggering of inappropriate shocks related to sequential ventricular sensing.

In several trials, CRT has improved 6-min walking distance, quality of life score, left ventricular ejection fraction, functional class, exercise time, and peak oxygen consumption.

The less impressive results from the CONTAK CD study might relate to less stringent QRS duration and New York Heart Association (NYHA) functional class requirements. The US Food and Drug Administration felt that the CONTAK CD studydid not fully establish the effectiveness of CRT as a treatment for heart failure. In the Focused Confirmatory Study, 127 patients with class III or IV heart failure received the CONTAK CD system. In about half the patients, only the defibrillator component was turned on. In the other half, both defibrillator and CRT components were turned on. These results established the effectiveness of CRT for heart failure. Additional supporting evidence showed reduced left ventricular intracavitary dimensions and improved left ventricular ejection fraction in patients on CRT. In the InSync ICD trial, patients given CRT had significantly improved quality of life, NYHA functional class, peak VO2 (oxygen consumption), exercise duration, left ventricular intracavitary dimensions, and ejection fraction.

In a meta-analysis of four controlled CRT studies (Multisite Stimulation in Cardiomyopathy trial [MUSTIC], CONTAK CD, InSync ICD [MIRACLE ICD], and MIRACLE; 1634 patients) CRT significantly reduced death from progressive heart failure and admission for heart failure, at follow-up. Total mortality was reduced by 23%, although this was not significant. In a meta-analysis, nine CRT trials were analysed for efficacy. All-cause mortality was significantly reduced by 21%. This result was largely driven by a reduction in progressive heart failure. A non-significant increase in sudden cardiac death was noted. A metaregression showed no difference in all-cause mortality benefit between CRT patients an CRT-D patients. Data from the Comparison of Medical Therapy, Pacing, and Defibrillation in Chronic Heart Failure trial (companion) were not included in the metaregression. The companion trial was stopped prematurely because of the significant benefit of CRT and CRT defibrillators (CRT-D) in the combined primary endpoint of all-cause mortality and admission. The investigators recorded a non-significant 24% relative reduction in all-cause mortality with CRT alone. However, a significant relative reduction in all-cause mortality with CRT-D was reported.

The MIRACLE ICD trial showed that at 6 months, patients assigned to CRT-D had a greater improvement in quality of life and functional class than controls. Treadmill exercise duration increased in the CRT-D group and decreased in the control group. No significant changes in left ventricular size or function, survival, or rates of admission were noted. Proarrhythmia was not seen and arrhythmia termination was likewise not impaired.

Which patients are the best candidates for CRT? Presently, those with drug-refractory NYHA class III or IV congestive heart failure, left ventricular ejection fraction up to 35%, left ventricular end-diastolic diameter equal to or more than 55 mm, and a major left-sided conduction delay (QRS duration ≥130 ms) seem to be reasonable candidates to offer biventricular pacing. The underlying rhythm should be sinus or atrial fibrillation with a ventricular response slow enough to allow continuous biventricular stimulation and capture. We believe that CRT is rapidly becoming invaluable in the management of severe heart failure. We almost always offer CRT-D rather than CRT alone. Although some researchers maintain that the benefits of CRT and CRT-D are similar, we have seen CRT reduce the burdensome multidrug treatment that looms as a crisis during management of patients with heart failure. The most striking examples include elimination of the need for intermittent inotropic infusions.

Because right ventricular pacing might lead to ventricular asynchrony, patients who are dependent on ventricular pacing are candidates for biventricular pacing. Preliminary data from a subanalysis of the biventricular pacing after ablate compared with right ventricular study (PAVE) suggests that CRT might benefit patients with left ventricular ejection fractions of 35% or less and chronic atrial fibrillation who undergo ablation of the atrioventricular junction. Controversy exists over whether patients with right bundle-branch block should be candidates for CRT. Few with this condition have been included in clinical trials. Some cardiac electrophysiologists believe that the type of bundle-branch block does not predict clinical response and advocate biventricular pacing for advanced heart failure and any QRS duration of 130 ms or longer. Others have suggested that there might be a benefit in patients with right bundle-branch block accompanied by a substantial concomitant left-sided intraventricular conduction delay (assessed by echocardiography).

We cautiously offer biventricular pacing to patients with right bundle-branch block after counselling them that the benefits for their patient group are uncertain. Achilli and co-workers have shown that CRT might be helpful in patients with severe heart failure and narrow and incomplete left bundle-branch block QRS complexes who show echocardiographic evidence of intraventricular and interventricular asynchrony. Larger studies will be needed to confirm these preliminary results. A recent analysis of CRT cost-effectiveness suggested that CRT should not be considered in patients with comorbidities that are likely to reduce life expectancy. Table 5 summarises some of the data from CRT studies.

Table 5. Summary of CRT studies

Percutaneous lead extraction

Advances in cardiac pacing have spurred the use of percutaneous techniques for permanent lead extraction. Formal methods for transvenous extraction of permanent pacing leads have been available since 1988. Although new methods are still being developed, currently available techniques are generally safe and very effective.

All lead extractions need some degree of direct traction (pulling). Simple direct traction on the proximal portion of the lead might be sufficient to remove newly implanted leads. Some evidence has shown that infected leads respond to direct traction alone more often. The tensile strength of fibrous lead encapsulation increases over time. Passive fixation leads are generally more difficult to remove than active fixation leads. Traction alone is often ineffective and unsafe in leads implanted for more than 4–6 months. A variety of locking stylets (inserted into the proximal conductor coil and bound to its tip at the distal pacing electrode) has greatly simplified the application of direct traction.

Most operators begin with a superior vena caval (subclavian) approach and switch to an inferior vena caval (transfemoral) approach if needed. The ability to use snares and basket catheters makes the inferior venal caval approach more versatile than the superior approach. A transfemoral approach is recommended when a subclavian insertion site is grossly infected and when leads are broken or free-floating.

Many sheath systems are available for extraction. Sheaths provide counterpressure (forward movement to break adhesions) as they are advanced, and countertraction (opposition to movement of the myocardial wall) as the extractor pulls to remove the lead. The Pacemaker Lead Extraction with the Excimer Sheath trial showed that excimer laser sheaths (which vaporise fibrous adhesions) improved the effectiveness of lead extraction and reduced procedure time. Complete lead removal was achieved in 94% of patients with laser sheaths compared with 64% of those using conventional telescoping non-laser sheaths. In a more recent study, extraction of 2561 pacing and defibrillator leads was attempted with three sizes of laser sheaths. Complete removal took place in 90% of leads, 3% were partially removed, and the remaining 7% were failures. Multivariate analysis showed that implant duration was the only preoperative independent predictor of failure; female sex was the only multivariate predictor of complications.128 Indications for lead extraction are evolving. We believe that decisions on lead removal should be guided by parallel hierarchies that assess procedural timing (emergent, urgent, elective) and the risk benefit ratio (ie, whether extraction is mandatory, necessary, or discretionary; panel 2). Success is inversely related to duration of implantation and patient age.

Panel 2: Assessment of risk benefit ratios for lead removal

Mandatory

 

•Life-threatening condition, leads must be removed

 

•Indications include septicaemia (endocarditis), migration (causing emboli, arrhythmia, or perforation), device interference (ie, abandoned ICD lead), and occlusion of all usable vessels

 

Necessary

 

•Great potential for morbidity or mortality, leads should be removed

 

•Indications include pocket infection, chronic draining sinus, erosion, potential device interference, venous thrombosis, and lead replacement (extract and reimplant via thrombosed vein)

 

Discretionary

 

•Lead removal is optional

 

•Indications include pain, malignant disease, and replacement of leads abandoned for less than 3–4 years (not advisable to remove non-infected leads that have been implanted for more than 8–10 years)

 

Major complications of lead extraction can be expected in up to 2% of patients, and happen more often during an operator’s early experience. These problems include low cardiac output, lead breakage, pulmonary embolism, lead migration (consequences depend on size and ultimate destination of the debris), avulsion of veins or myocardial tissue, venous or myocardial tears (resulting in haemothorax, cardiac tamponade, or death), and failure to remove an infected lead. The US extraction database enrolled 4090 patients between January, 1994, and December, 1997. Major complications took place in 1·6% of patients (0·2% mortality rate). The 109 women who underwent removal of three or more leads had a 7·3% major complication rate.

Complications of permanent pacing

Expanding indications and the relative ease of percutaneous implantation have fuelled enthusiasm for permanent pacing devices. However, complications vary in clinical significance (and patient effect) from benign to life-threatening. An acute pacemaker implant might be associated with a complication rate of 4–5%.Incidence of acute complications is related to operator experience. In MOST, the incidence of late complications was 2·7%. Some investigators believe this incidence correlates with the number of leads implanted, but this opinion is debatable. However, the direct correlation between procedure duration and the patient’s risk for system infection is generally accepted.

Complications related to venous access include pneumothorax, haemothorax, and air embolism. In MOST, the incidence of pneumothorax was 1·5%. Risk of pneumothorax is associated with the experience of the implanter, plus the number and difficulty of subclavian punctures. This risk can be eliminated by the cephalic vein cutdown technique. Pneumothorax is often small, asymptomatic, and noted incidentally on follow-up chest radiography; however, tension pneumothorax should always be part of the differential diagnosis when hypotension or pulseless electrical activity ensues during an implantation. Haemothorax results from trauma to the great vessels. Arterial puncture must be promptly recognised and treated with manual compression. Arterial cannulation (with a sheath or lead) can be avoided by advancing a guide wire to the inferior vena cava before any introducer insertion. Patients are surprisingly tolerant of air emboli. The air is filtered, absorbed in the lungs, and treatment is generally not needed. However, large emboli can result in respiratory distress, oxygen desaturation, and hypotension. Treatment with 100% oxygen, inotropic agents, or aspiration of the embolus from the right heart might be needed.

Lead-related complications include perforation, dislodgment, diaphragmatic stimulation, and malposition.132 Perforation can involve the great vessels, right atrium, or right ventricle. Most perforations do not result in major sequelae. Cardiac tamponade, usually the result of chamber perforation, is the most ominous implant complication and should be suspected whenever hypotension occurs. The diagnosis is supported by enlargement of the cardiac silhouette and weak contractions, and can be confirmed by emergent 2D echocardiography. Definitive treatment via emergent pericardiocentesis should not be delayed. Surgical intervention might be needed if the bleeding persists and pericardial fluid reaccumulates. Trauma to the great vessels is more common with lead extraction than implantation and might result in direct bleeding into the mediastinum, which is an indication for emergent open chest surgery. Lead dislodgment takes place in 2·5% of implants, usually in the first 24–48 h postimplant. If the patient is not dependent on pacing in that chamber, a different pacing mode could be reprogrammed to manage dislodgement. Definitive correctioeeds lead repositioning or replacement.

Diaphragmatic stimulation results from phrenic nerve stimulation. Right atrial leads can stimulate the right phrenic nerve, whereas right and left (cardiac venous leads) ventricular leads stimulate the left phrenic nerve and left hemidiaphragm. Screening for this complication by pacing at maximum outputs is a requisite part of correct implantation procedure.

Presence of an atrial or ventricular septal defect can allow passage of a lead to the left heart. Passage into the left heart is more common with ventricular leads. Confirmation of lead position by use of a left anterior oblique fluoroscopic projection of equal to or more than 40° should identify this problem during implantation. A lateral chest radiograph usually provides definitive diagnosis (figure 5). A paced right bundle-branch block configuration on surface ECG might result from left ventricular pacing. However, this configuration can be present in up to 8% of patients with properly placed right ventricular leads. Coman and Trohman have developed an algorithm to distinguish right versus left ventricular lead positions when pacing produces a right bundle-branch block configuration.

 

Figure 5. Lateral chest radiograph of lead passing through atrial septum

This ventricular lead points posteriorly and its tip is in the left ventricular endocardium. The lead passed through a patent foramen ovale, the left atrium, and the mitral valve into the left ventricle. This abnormal position is emphasised by comparison with figure 4B in which the right ventricular lead points anteriorly and the left ventricular epicardial lead points posteriorly.

 

Pocket-related complications include haematoma, wound pain, pocket erosion, and infection. Haematomas are usually managed conservatively. Evacuation is required in 1–2% of implants. Risk of bleeding is increased in anticoagulated patients, especially in those receiving heparin. Simple analgesics usually control wound pain. Pain that initially improves and then recurs or is temporally remote from the implant suggests infection.

The frequency of pacemaker implant infection ranges from 1–19%. We believe that laboratory or surgical-suite infection rates greater than 7–8% suggest (potentially correctable) contamination or technical problems that need thorough investigation. Manifestations of pacemaker infection range from mild local pain and erythema to life-threatening septicaemia. Early infection tends to be more clinically evident than the often indolent course of late infection. In one large series of patients with infected implantable antiarrhythmic devices,137 the most common pathogens were coagulase-negative staphylococci (68%), Staphylococcus aureus (24%), and gram-negative enteric bacilli (17%). 16 of 123 (13%) infected patients had polymicrobial infections. When infection is strongly suspected, the entire system should be regarded as contaminated. The treatment of choice is complete system removal (pulse generator explant plus transvenous lead extraction), and antimicrobial therapy. Reimplantation should be undertaken at a different site. Morbidity due to persistent infection (ie, when infected leads are not removed) can be as high as 66%. Erosion is associated with a high risk of infection and complete extraction of the device-lead system is likewise advised.

Delayed complications of permanent pacing leads include venous thrombosis, exit block, insulation failure, and conductor fracture. Late lead damage might be reduced by use of axillary or cephalic venous access. Symptomatic venous thrombosis takes place in up to 5% of patients. Treatments depend on the site and symptoms associated with thrombosis, and vary from heparin (followed by warfarin) or thrombolysis to angioplasty or open surgery. Exit block manifests as increased pacing thresholds. Insulation failure results in decreased lead impedance. Conduction fracture manifests as increased lead impedance. Definitive treatment for these complications is lead replacement.

We postulated that the design of bipolar coaxial leads from modern endocardial pacemakers might be susceptible to a high failure rate. We analysed the long-term survival of bipolar coaxial leads and unipolar leads implanted at the Cleveland Clinic, OH, USA. At 5 years, the cumulative survival was 98·6% for both types. However, at 10 years, the survival of bipolar coaxial leads was only 92·4% compared with 98·6% of unipolar leads. Silicone lead insulation has proved to be reliable for over 30 years. To improve handling, polyurethane (low coefficient of friction) was used for bipolar leads, but failed to show satisfactory insulation. Pacing failure in bipolar systems with polyurethane-insulated leads can be frequent and might result in oversensing or failure to capture, or both. Failure is often due to chemical degradation (via oxidation) causing breakage in the inner insulation. In one series, overall lead failure occurred more often in the polyurethane group than in the silicone group. Most lead failures took place in the first 36 months after implantation.

Most modern pulse generators have an expected longevity of 5–9 years. Unexpected pulse generator (electrical) failure is rare. Many problems discovered iew models can be corrected by software upgrades. Lead-related problems (increased thresholds, decreased impedance) resulting in increased current drain are the most common causes of premature battery depletion. Stepwise changes in pacing or magnet pacing rates, changes in pacing mode, pulse-width stretching, and telemetered battery voltages or impedances are clinical indicators used to measure the time for elective generator replacement and battery end-of-life.144 Lithium-iodine batteries used in current pulse generators are not rechargeable and surgical replacement of the entire generator is needed.

 

 

 

SYSTEMATIC INTERPRETATION GUIDELINES for Electrocardiograms
RATE
Rate calculation
Common method: 300-150-100-75-60-50
Mathematical method: 300/# large boxes between R waves
Six-second method: # R-R intervals x10
RHYTHM
Rhythm Guidelines:
1. Check the bottom rhythm strip for regularity, i.e. – regular, regularly irregular, and irregularly irregular.
2. Check for a P wave before each QRS, QRS after each P.
3. Check PR interval (for AV blocks) and QRS (for bundle branch blocks). Check for prolonged QT.
4. Recognize “patterns” such as atrial fibrillation, PVC’s, PAC’s, escape beats, ventricular tachycardia, paroxysmal atrial tachycardia, AV blocks and bundle branch blocks.

AXIS

Left axis deviation differential: LVH, left anterior fasicular block, inferior wall MI.
Right axis deviation differential: RVH, left posterior fascicular block, lateral wall MI.

HYPERTROPHY
1. LVH — left ventricular hypertrophy = S wave in V1 or V2 + R wave in V5 or V6 > 35mm or aVL R wave > 12mm.
2. RVH — right ventricular hypertrophy = R wave > S wave in V1 and gets progressively smaller to left V1-V6 (normally, R wave increases from V1-V6).
3. Atrial hypertrophy (leads II and V1)
Right atrial hypertrophy — Peaked P wave in lead II > 2.5 mm in amplitude. V1 has increase in the initial positive direction.
Left atrial hypertrophy — Notched wide (> 3mm) P wave in II. V1 has increase in the terminal negative direction.

INFARCT

Certain leads represent certain areas of the left ventricle:

 

 

References.

A – Basic:

1.                                    Davidson’s Principles and practice of medicine (21^st revised ed.) / by Colledge N.R., Walker B.R., and Ralston S.H., eds. – Churchill Livingstone, 2010. – 1376 p.

2.                                    Harrison’s principles of internal medicine (18^th edition) / by Longo D.L., Kasper D.L., Jameson J.L. et al. (eds.). – McGraw-Hill Professional, 2012. – 4012 p.

3.                                    The Merck Manual of Diagnosis and Therapy (nineteenth Edition)/ Robert Berkow, Andrew J. Fletcher and others. – published by Merck Research Laboratories, 2011.

4.                                    Web -sites:

a.       http://emedicine.medscape.com/

b.      http://meded.ucsd.edu/clinicalmed/introduction.htm

 

B – Additional:

1.      Lawrence M. Tierney, Jr. et al: Current Medical Diagnosis and treatment 2000, Lange Medical Books, McGraw-Hill, Health Professions Division, 2000.

2. Braunwald’s Heart Disease: a textbook of cardiovascular medicine (9^th ed.) / by Bonow R.O., Mann D.L., and Zipes D.P., and Libby P. eds. – Saunders, 2012. – 2048 p.

3. Braunwald’s Heart Disease: review and assessment (9^th ed.) / Lilly L.S., editor. – Saunders, 2012. – 320 p.

4. Cardiology Intensive Board Review. Question Book (2^nd ed.) / by Cho L., Griffin B.P., Topol E.J., eds. – Lippincott Williams & Wilkins, 2009. – 385 p.

5. Cleveland Clinic Cardiology Board Review / Griffin B.P., Kapadia S.R., Rimmerman C.M., eds. – Lippincott Williams & Wilkins, 2012. – 952 p.

6. Hurst’s the Heart (13^th ed.) / by Fuster V., Walsh R.A., Harrington R., eds. – McGraw-Hill, 2010. – 2500 p.

7. Oxford Handbook of Cardiology (2^nd ed.) / by Ramrakha P., Hill J., eds. – Oxford University Press, 2012. – 851 p.