Tài liệu Indications for Pacing pptx

Types of heart block can be more accurately assessed with a His bundle study, discussed in the section, “His-Purkinje System.” The Cardiac Electrical System Automaticity All of the e

Authors: Moses, H Weston; Mullin, James C.

Title: A Practical Guide to Cardiac Pacing, 6th Edition

Copyright ©2007 Lippincott Williams & Wilkins

> Table of Contents > 1 - Indications for Pacing

1 Indications for Pacing

Indications For Permanent Pacemaker Therapy

Any physician implanting pacemakers must be familiar with the American College of

Cardiology/American Heart Association/North American Society Pacing Electrophysiology (now termed the Heart Rhythm Society) Guidelines that are published intermittently in their various journals Only a brief summary of basic concepts is discussed here

Symptoms of a slow heart rate may include syncope, dizziness, and transient confusion Less commonly, a chronically slow heart rate can lead to fatigue, dyspnea, poor exercise ability, and rarely, frank congestive heart failure All of these clinical manifestations are more

commonly caused by other etiologies The decision to place a pacemaker must be based on an understanding of the indications for pacing, as well as knowledge of anatomy and physiology, put in context of the individual patient For instance, syncope is clinically most often due to “neurocardiogenic syncope”—a sudden drop in blood pressure and/or heart rate that leads to fainting The young healthy person who has had a single episode of fainting at the sight of blood does not need pacemaker implantation even if transient asystole were to

accompany the event Transient asystole in an elderly person with sick sinus syndrome could cause serious injury due to syncope with collapse

The tools to evaluate the patient are the history and physical, the EKG, and the monitoring rhythm strip, ideally a rhythm strip taken during the symptomatic episode (although this is often not possible) Twenty-four-hour ambulatory monitoring can be useful in patients with daily symptoms Usually, a more productive approach is to use an event monitor in an attempt

to capture a rhythm during symptoms over a period of time, typically 4 weeks An

implantable loop recorder, which is placed beneath the skin, can monitor for tachy- or

bradyarrhythmias for many months

Electrophysiologic testing for bradyarrhythmias due to sick sinus syndrome is currently suboptimal Pacing the atrium in the area of the sinus node and checking the length of time it takes for the sinus node to recover is not a

P.2

particularly sensitive or specific test for sick sinus syndrome Types of heart block can be more accurately assessed with a His bundle study, discussed in the section, “His-Purkinje System.”

The Cardiac Electrical System

Automaticity

All of the electrically active cells of the heart have an inherent automaticity, meaning that with time they will gradually depolarize and then “fire.” The sinus node is a small collection of cells in the upper portion of the right atrium near the insertion of the superior vena cava This is the normal pacemaker of the heart, the top of the hierarchy A typical heart rate would be 70 beats per minute (bpm) in a healthy person The sinus rate responds to various physiologic events and increases in rate with exercise, fever, emotional stress, or other factors and decreases in rate with rest or increased vagal tone The majority of these changes are mediated by the sympathetic and the vagal system

The cells of the atrial myocardium, excluding the sinus node, are not particularly good

pacemakers themselves Occasionally there can be areas in the atrium that can become

automatic or fire early leading to an atrial premature contraction or an atrial tachycardia

A slow sinus heart rate can allow the AV node to fire and pace the heart with a junctional rhythm This tends to be a very steady rhythm often at a rate of about 40 or 50 bpm Even if the sinus node were surgically removed, the junctional rhythm would take over in a normal person Digitalis toxicity, myocarditis, cardiac surgery, and ischemia can lead to a more rapid junctional rhythm called “nonparoxysmal junctional tachycardia.”

At the bottom of the hierarchy is the ventricle The ventricular escape rhythm in the setting of complete heart block is an ominous rhythm, usually at a very slow rate, perhaps in the 20s or 30s This rhythm is potentially lethal if it becomes too slow, mainly due to prolongation of the

QT interval resulting in polymorphic ventricular tachycardia

Sinus Node and Atrium

The sinus node itself is, physically, a relatively small group of cells and is not routinely recorded with electrophysiologic studies and standard intracardiac catheters The sinus node responds to various physiologic stimuli, going slow or fast, as appropriate Rate-adaptive pacemakers try to reproduce this with varying degrees of success

The atrium conducts electricity from the sinus node down to the AV node This forms a P wave on the electrocardiogram The atria push blood into their respective left and right

ventricles improving cardiac output through the Frank–Starling mechanism (See Chapter 5, Fig 5-1) Maintaining

P.3

atrial–ventricular synchrony is an important goal with dual-chamber pacemakers The atria are the location of two of the most common pathologic rapid rhythms: atrial fibrillation and atrial flutter Sometimes with atrial fibrillation and flutter, rapid rhythms may alternate with episodes of bradycardia (bradycardia-tachycardia syndrome) Also, pharmacologic attempts to control a rapid ventricular response associated with atrial fibrillation and atrial flutter can lead

to episodes of inappropriately slow ventricular responses requiring a pacemaker

AV Node

The atria are separated from the ventricles by the two atrioventricular valves and the

supporting fibrous tissue (essentially acting as an “insulator” separating the upper and lower chambers) The only normal electrical pathway is through the AV node This can be viewed, teleologically, as the source of a brief delay in conducting the depolarization wave from its atria to the ventricles, which allows blood to be pumped from the atria into the

ventricles, for more efficient cardiac output Electrical conduction through the AV node is so slow and of such small amplitude that is does not show up on even intracardiac electrodes The AV node is responsive to vagal and sympathetic input A highly trained athlete can have asymptomatic episodes of intermittent block in the AV node due to high vagal activity as a normal variant The node itself, like all electrically conducting tissue, can become fibrotic and develop conduction block severe enough to require pacemaker therapy

His-Purkinje System

After electrical activity has been slowed in the AV node, it enters a very rapidly conducting set of specialized conducting tissue, the His-Purkinje system The bundle of His is the initial portion and is a fairly thick bundle of cells Its electrical activity routinely shows up on an appropriately done intracardiac electrophysiologic evaluation (but not on the surface ECG), as the His spike (Fig 1-1) Isolated heart block in this particular anatomic structure is relatively uncommon When it occurs it is categorized as infranodal block and is a potentially dangerous form of heart block The bundle of His almost immediately splits into components of the Purkinje system These are the left and right bundles The left bundle is divided into the left anterior and left posterior fascicles (thus the term trifascicular block for infranodal complete

heart block) This could be viewed, again teologically, as a rapidly conducting electrical system that spreads through the left and right ventricular myocardium to allow almost

simultaneous, synchronized, contraction of the ventricles (the newer approach of cardiac resynchronization therapy for congestive heart failure represents an effort to reproduce this effect) Disruption of these bundles is quite common and left bundle branch block

P.4

(LBBB) and right bundle branch block (RBBB) are routinely diagnosed on EKGs The

clinical significance of this block is dependent on the clinical scenario and can range from completely benign to pathologic as discussed below

Figure 1-1 His Bundle Recording

A: The normal His bundle recording demonstrates an A deflection corresponding to the P wave on the surface ECG The H deflection occurs during the isoelectric period between the P wave and the QRS complex and is due to activation of the Bundle of His The V deflection corresponds to the QRS complex B: Prolonged AH interval (>140 msec) block within the AV node C: Prolonged HV interval (>55 msec) block below the AV node

Nomenclature of AV Block

Mobitz type I block is characterized by gradual lengthening of the PR interval in sequential beats until there is a nonconducted P wave (Fig 1-2) One important way to identify this is to look for a difference in the PR interval of the beats preceding and following the dropped beat With Mobitz I second-degree AV block, the AV node has had time to recover after the

dropped beat and the PR interval will be shortest after the dropped beat, compared to all other

PR intervals This type of block usually occurs in the AV node and the native QRS complex is narrow, unless there is coincidental bundle branch block present The term Mobitz I block can

be a description of block in other parts of the conduction system For our purposes, we will assume the more common occurrence, block in the AV node

P.5

Figure 1-2 Nodal Versus Infranodal Heart Block

A statistically and clinically significant association between ECG pattern and the anatomic location of block is shown In general, block within the AV node is often benign (with some important exceptions), and block of second or third degree below the AV node has a more consistently poor prognosis The less common situation of Mobitz I second-degree AV block

in association with a wide QRS complex is not depicted in the figure This type of block can

be caused by nodal or infranodal block and may require investigation with electrophysiologic studies Rarely the Mobitz II second-degree AV block can occur with a narrow QRS complex due to block in the His-bundle itself, without associated BBB (SAN, sinoatrial node; AVN, atrioventricular node; RBB, right bundle branch; LPF, left posterior fascicle; LAF, left

anterior fascicle.)

Mobitz type II second-degree AV block is described as a dropped P wave, but with no

progressive lengthening of the PR interval before the dropped P wave and no difference in the

PR interval before or after the dropped beat (Fig 1-2) This type of block occurs almost exclusively in the His bundle or the Purkinje system Block in the isolated His bundle is quite rare If this did occur, then the subsequent QRS could be narrow The much more typical situation is block in the Purkinje system and this is usually associated with wide QRS

complex A logical way to view this is that it is unlikely that all three major branches of the Purkinje system (right bundle, left anterior fascicle, and left posterior fascicle) would conduct simultaneously and then block simultaneously Almost always two of the three fascicles are “broken” or not conducting, leading to a wide QRS complex and the third fascicle conducting intermittently

It is of note that patients with 2-to-1 block, ventricular conduction with every other P wave, cannot be categorized into Mobitz I or Mobitz II block simply because you cannot tell if there

is prolongation of the PR On the other

hand, a long rhythm strip will often locate consecutively conducted beats and clarify the type

of block

Third-degree AV block, also known as complete heart block, describes the failure of any depolarizations to pass from the atria through the AV node and His-Purkinje system to the ventricle The atria may beat regularly in response to the SA node (or the patient could be in atrial fibrillation) The ventricles beat independently in response to whatever intrinsic rhythm has taken over: the AV node, the His bundle (junctional rhythm), the Purkinje system, or cells

in the ventricle The escape rate below the AV node may be about 50 bpm with junctional rhythm (although this may be highly variable) or 0 to 40 bpm in the ventricle with a

ventricular escape rhythm Third-degree AV block is a potentially dangerous rhythm,

depending on the clinical setting For example, third-degree AV block can occur in the setting

of an acute inferior wall myocardial infarction (MI) with block in the AV node and an

adequate junctional rhythm This is virtually always a transient event If the heart rate is unduly slow, a temporary pacemaker is required There are clinical situations in which

observation is adequate with standby transcutaneous pacemaker and immediate availability of atropine to speed up conduction through the AV node, if required This would be a relatively benign form of third-degree AV block On the other hand, third-degree AV block due to chronic degenerative disease of the His-Purkinje system can lead to syncope or sudden

cardiac death

His Bundle Electrogram

Much of our understanding of the conduction anatomy of the heart has come from study of the intracardiac electrogram, often referred to as the His bundle electrogram Depolarization

of the AV node and the His bundle produces no deflection on the surface ECG; however, a closely spaced bipolar electrode can be positioned across the anterosuperior portion of the septal tricuspid valve leaflet, in close proximity to the His bundle A depolarization spike originating from the common His bundle can be recorded (refer to the H spike in Fig 1-1)

On the intracardiac ECG, atrial (A) depolarization precedes the H spike, and ventricular (V) depolarization follows the H spike The interval between the atrial and His depolarizations (AH interval) reflects conduction through the AV node The HV interval is the result of conduction in the Purkinje system between the His bundle and the ventricles Thus, AH interval prolongation indicates a conduction abnormality within the AV node (above the His bundle), and HV interval prolongation indicates an infranodal conduction abnormality in the Purkinje system (left and/or right bundle) A potential value of measuring the His bundle electrogram is to document an abnormally long HV interval An interval of greater than 100 msec, implies a significantly diseased Purkinje system that, in the presence of worrisome symptoms, may even warrant pacing Pacing the atrium rapidly with the development of infranodal block can also be an indication of a significantly diseased His-Purkinje system P.7

Indications for Pacemakers

Sick Sinus Syndrome

The sinus node itself may simply develop fibrosis and lose effectiveness, leading to

bradycardia If the heart rate is slow enough to cause symptoms and is not due to medication such as beta-blockers, verapamil, diltiazem, or other multiple drugs that may slow the heart rate, then pacemaker therapy is indicated Normally this would include pacing the atrium (and possibly having a ventricular lead in case heart block occurs later) in order to maintain atrio ventricular synchrony Some patients with sick sinus syndrome may require medications that slow the heart rate and this would also be an indication for pacemaker therapy The term

bradycardia-tachycardia syndrome applies to patients with rapid heart rates but who also have episodes of slow heart rate (this can occur even without medications that tend to slow the rapid rate) Such patients often require beta-blockers or calcium channel blockers, and the only way to control the bradycardia portion of the problem is with a pacemaker

Unfortunately, uncertain situations do occur If a patient has a heart rate less than 40 bpm and symptoms that may be related to the bradycardia, but are not clearcut, then there is

“circumstantial evidence” that this is due to the slow heart rate A pacemaker may be indicated, but clinical judgment is required No pacemaker is indicated if the heart rate is slow due to medications that can be stopped or exchanged for drugs that do not slow the heart rate, without risk to the patient Some patients may have symptoms that, on careful evaluation, are clearly not the result of a slow heart rate A slow heart rate by itself is not an indication for a pacemaker

Heart Block

Third-degree and advanced second-degree heart block, whether in the AV node or infranodal block, that is associated with slow heart rate and symptoms, episodes of asystole greater than

or equal to 3 sec, or “escape rates” less than 40 bpm even if the patient is asymptomatic, require a pacemaker If the patient has a tachyarrhythmia or other medical problem requiring drugs resulting in symptomatic bradycardia (usually beta-blockers, verapamil, or diltiazem),

he or she requires a pacemaker

An iatrogenic cause of AV block is catheter ablation of an AV junction The most typical scenario is a patient with atrial fibrillation with a rapid ventricular response that cannot be controlled with drugs, so therefore an ablation is done This leaves the patient with complete heart block and a pacemaker is always required in this situation

Some types of cardiac surgery can lead to complete heart block For instance, aortic valve replacement can lead to injury to the AV node or His bundle Some types of cardiac

congenital operations lead to complete heart block

P.8

Various forms of muscular dystrophy can be associated with heart block In some situations the unusual step is taken of placing a “prophylactic” pacemaker in these patients with minor conduction system disease, even in the absence of second- or third-degree heart block and symptoms These are rare indications for permanent pacing and decisions should be made

in consultation with a knowledgeable expert The “ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmic Devices” mentions specifically myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (limb-girdle), and peroneal muscular atrophy

Second-degree AV block leading to symptomatic bradycardia is an indication for a

pacemaker Typically, the more dangerous type of second-degree AV block is Mobitz type II second-degree AV block On the other hand, particularly in elderly patients, disease in the AV node with Wenckebach phenomenon (Mobitz type I second-degree AV block) can lead to symptomatic bradycardia and the need for pacing It is not always benign

Mobitz type II second-degree AV block usually is accompanied by a wide QRS complex implying that two of the three fascicles are nonfunctioning and the third fascicle is

intermittently blocked (the escape rhythm would then be a ventricular escape, if there is any escape rhythm at all) This is a strong indication for a pacemaker There are relatively rare instances of Mobitz II second-degree block with a narrow QRS complex (implying block in the His bundle itself) This is uncommon, but most cardiologists would place a pacemaker in that setting

Type I second-degree AV block can occur below the AV node and is a potential indication for pacing This is generally found only with electrophysiologic testing and is rarely encountered

or documented in routine practice

Pacing for first-degree AV block is extremely rare Occasionally a patient with prolonged first-degree AV block can have such a loss of AV synchrony that symptoms can occur,

particularly in the setting of LV dysfunction Mobitz I second-degree AV block could also lead to a similar clinical situation If such a patient is symptomatic, it is usually due to the mitral and tricuspid valves being open when ventricular contraction occurs, because of the long PR delay Pacing may be indicated in the neuromuscular disorders previously mentioned, even with just first-degree AV block, but expert consultation is recommended

Alternating bundle branch block (episodes of LBBB alternating with RBBB) is an indication for pacemaker therapy One of the recurrent themes we discuss is that infranodal block is a potentially dangerous type of block and the presence of alternating LBBB and RBBB implies that the entire Purkinje system is at risk

A rare indication for pacing is an incidental finding on an electrophysiologic study (perhaps for a ventricular arrhythmia) of a very prolonged HV interval of greater than or equal to 100 msec, even in an asymptomatic person Data on this are limited, but it does imply severe infranodal block with risk for syncope or even sudden death and pacing may be indicated Also, in a similar

P.9

scenario, atrial pacing leading to induced infra-His block that is not physiologic could be an indication for a pacemaker This, of course, is purely in the province of the

electrophysiologist and guidelines should always be followed

A fairly common scenario that has been studied fairly well is the setting of fascicular block with first-degree AV block, but without symptoms; for example, LBBB or RBBB and a left hemiblock and first-degree AV block without symptoms Intuitively, one may think that patient would be at risk for syncope, but studies indicate that the risk is so low that when it occurs, it usually presents with transient reversible symptoms rather than sudden death It is not considered an indication for pacing and not even for an electrophysiologic study, in the absence of symptoms

Pacing in Hypersensitive Carotid Sinus Syndrome

The carotid sinus in the neck, when stimulated with brief massage, can slow heart rate and lower the blood pressure, is a normal response Marked slowing of the heart rate with asystole

of greater than 3 sec can occasionally be an indication for pacing, only if associated with recurrent syncope, associated with neck manipulation (placing a neck tie, turning neck to back

up car) This is a relatively uncommon indication for pacing If it becomes a common source

of pacemaker implantation at one institution, then perhaps careful review of the criteria being used to implant the pacemaker is warranted Occasionally a patient may have recurrent

syncope and a hypersensitive carotid inhibitory response, but the two cannot be clearly

connected This is a less strong indication for pacing

Pacing in Neurocardiogenic Syncope

Neurocardiogenic syncope refers to a triggering of a neural reflex that causes a usually brief episode of hypotension with components of both bradycardia and peripheral vasodilation Another term for this is vasovagal syncope Head-up tilt testing is the only available

diagnostic study for this Generally this is not required and the diagnosis is made on the basis

of the history alone Usually a prodrome of symptoms such as nausea, diaphoresis, or gradual onset of lightheadedness occurs It can be triggered by pain, stress, prolonged standing, and sometimes patients present with this after sitting in a stiff wooden pew at church When this is studied, for example, at the time of a tilt table test, it is noted that some people have profound asystole and in others the heart rhythm remains fairly appropriate, but there is sudden drop in

blood pressure More commonly there is a combination of the two components It is apparent that patients who develop a profoundly slow heart rate can be paced with the hope that this will ameliorate the symptoms of recurrent neurocardiogenic syncope

Unfortunately, the degree of benefit is variable and inconsistent Although pacing can keep the heart rate at a reasonable level, the drop in blood pressure

P.10

due to vasodilation is not treated with a pacemaker and is in many, or perhaps most, patients the most difficult component to control Special pacemaker algorithms have been used to sense an abrupt slowing of the heart rate and then pace at a fairly rapid rate, for a brief period

of time Further work is ongoing in this area, but in general a patient would be considered for pacemaker implantation only if there is a significant documentation of bradycardia in the setting of recurrent neurocardiogenic syncope that could not be treated with avoidance

behavior to minimize symptoms through lifestyle changes

Dilated Cardiomyopathy

One of the original uses of pacing in a dilated cardiomyopathy was an attempt to maintain ideal AV interval in a patient with a weak heart to optimize the Frank-Starling effect This was an isolated indication for pacing and has virtually disappeared as an indication now that more effective therapies are available

A breakthrough in pacing has revolutionized the treatment of cardiomyopathy in patients with dyssynchronous LV contractility (usually with a wide QRS complex) We are using the term synchrony somewhat differently here than in “atrioventricular synchrony,” and we are concentrating on the synchronization of the walls of the left ventricle If a patient with a dilated cardiomyopathy has LBBB, for example (dyssynchrony can also occur without a classic left bundle), then the septum may contract at a slightly different time than the lateral wall (this is described in Chapter 7, Fig 7-1) Basically, one pacemaker lead is paced to the right ventricle and a separate lead is placed through the coronary sinus and down a vein on the lateral wall of the left ventricle By firing the pacemaker and causing both portions of the heart to contract at the same time, the efficiency of LV contractility can be significantly improved Note that we are referring to synchronizing the contractility of the left ventricle (not necessarily synchronizing the left and right ventricles or the atria and the ventricles) This has been well demonstrated to improve symptoms in patients who have congestive heart failure with dyssynchrony and has proven to be a very valuable tool in therapy Note that it is

an unusual use of pacemakers to treat LV dyssynchrony and not to treat an underlying

bradycardia Almost all of these patients also meet criteria for placement of a prophylactic ICD

The majority of patients will improve clinically with this approach, but some patients do not Some programmable features of the pacemaker can help with the nonresponders, but there will be some patients who simply do not improve Optimization of the AV interval remains very important in these patients and considerable research has been dedicated to the ideal AV interval The AV intervals should not be so long that the pacemaker capture does not occur and the native conduction through the AV node takes over, since the main goal of this therapy

is to pace two sides of the left ventricle simultaneously Too short a PR interval could result in inefficient filling of the left ventricle, however, and the

P.11

ideal AV interval will vary depending on the patient's clinical situation This form of pacing is discussed further in Chapter 7

Special Situations

Pacing for Tachycardia

There is an entity referred to as “pause-dependent” ventricular tachycardia This can occur after a pause and is often associated with a long QT interval; a pacemaker can be used

to treat that rare type of ventricular tachycardia

A more rapid-paced heart rhythm will physiologically shorten the QT interval in patients with congenital long QT syndrome at high risk for syncope or sudden death This is often used in combination with beta-blocker therapy to lower morbidity/mortality

Numerous efforts have been made to pace the atrium at a reasonable rate to reduce episodes

of atrial fibrillation The hope is that a regularly paced atrium will lead to less dispersion of the refractory period In other words, a regular rate may, in theory, reduce the opportunities for atrial fibrillation or flutter to occur Unfortunately, these efforts have had mixed success, particularly in the treatment of atrial fibrillation There are some case reports of benefit and some specialized pacemakers have algorithms designed to optimize the pacing of the atrium

to reduce episodes of atrial fibrillation, but this is not a routine indication for a pacemaker If

it is done, it should be by a center with electrophysiologic expertise and in a rational manner Pacemaker therapy is being investigated for prevention of atrial fibrillation, including pacing

at different areas in the right atrium or pacing the left and right atria simultaneously

Children and Adolescents

Children, adolescents, and patients with congenital heart disease may have various degrees of heart block that require pacing The principles are fairly similar to the ones already described, but they need to be adjusted for children For instance, if there is congential third-degree AV block in an infant, then a ventricular rate of less than 50 to 55 bpm becomes ominous Some types of congential surgery will cause transient heart block that may resolve with time, but with persistence after at least 7 days, permanent pacing may be required

Bradycardia-tachycardia syndrome may be a factor Long QT syndrome may require pacing, particularly if there is pause-dependent ventricular tachycardia Multiple types of complex situations can arise and the assistance of a pediatric cardiologist is necessary

Heart Transplant

After heart transplant, symptomatic bradyarrhythmias may occur and ultimately require pacing The transplant procedure “denervates” the heart and

P.12

the heart rate becomes dependent on circulating catecholamines A rate-responsive pacemaker may normalize the heart's response to activity

Pacing for Hypertrophic Obstructive Cardiomyopathy

Initial hopes to lower the gradient in a patient with a left ventricular outflow tract obstruction due to asymmetric septal hypertrophy (ASH) or “hypertrophic obstructive

cardiomyopathy” (another common abbreviation is IHSS, idiopathic hypertrophic

subaortic stenosis) have unfortunately been somewhat disappointing The main indication for

a pacemaker would be for sinus node dysfunction or AV block, as noted earlier, and this is uncommon

Some therapies for hypertrophic obstructive cardiomyopathy do, however, lead to a need for a pacemaker, as discussed later in this chapter Surgical myectomy, which removes part of the septum to physically remove some of the obstruction, can lead to damage in the AV node, leading to heart block A percutaneous approach has been developed with injection of alcohol into septal perforator branches off the left anterior descending coronary artery to cause a “controlled myocardial infarction” and thus shrink the septal size This can lead to damage with the His-Purkinje system in the ventricular septum, and can lead to significant heart block and the need for long-term pacemaker therapy (although this is only in a modest percentage of patients who are treated with alcohol septal ablation)

Pacing Post Myocardial Infarct

Third-degree AV block after an acute anterior wall MI is an indication for pacing Infranodal

AV block with associated bundle branch block, which occurs with an anterior wall MI and is persistent, may be a rare instance requiring prophylactic permanent pacing An

electrophysiologic study may be required to evaluate this These are now rare long-term sequela of a MI in the age of reperfusion therapy Heart block due to an acute inferior wall MI

is in the AV node (due to ischemia and/or vagal effect) and is virtually always reversible over time Permanent pacing is almost never required

A Concern

Until recently it was often thought that pacing in the right ventricular apex, the most common area paced, was innocuous Evidence now shows that consistent pacing in the right ventricular apex has some deleterious effects on LV function The most convincing evidence

documenting this is from a large study of patients with dual-chamber ICDs In patients who had no indication for ventricular pacing, if the right ventricle was consistently paced, there was evidence of deleterious effects in terms of heart failure and possibly even increased mortality Therefore, current practice is to avoid consistent pacing of the right ventricular apex in this setting unless it is necessary The mechanism of this unfortunate effect is not totally understood; one reasonable theory is that

P.13

chronic stimulation from the right ventricular apex leads to congestive heart failure due to chronic ventricular desynchronization This finding suggests that a patient with sick sinus syndrome who could be paced from the atrium or the ventricle would benefit from consistent atrial pacing rather than ventricular pacing (as discussed later in the book, AAI pacing versus VVI pacing) Alternative pacing sites in the right ventricle are being investigated, for

example, pacing from the right ventricular outflow tract instead of from the right ventricular apex

The Importance of Guidelines

This is a very brief summary, in an effort to make somewhat intuitive the indications for cardiac pacing The appropriate guidelines as outlined by the American College of

Cardiology/American Heart Association Arrhythmia Society must be understood and

followed in the appropriate clinical setting This is such an important document that it is footnoted at the end of this chapter and also at the end of the text It should also be noted that this, like all of medicine, is a dynamic area of knowledge and is updated regularly The Web site address is included as a reference also

Indications For Temporary Pacemaker Therapy

Atrial Ventricular Block with Myocardial Infarction

Inferior Myocardial Infarction

The inferior wall MI occurs with occlusion of the artery supplying the inferior wall of the left ventricle (Fig 1-3), which most often is the right coronary artery, but can also occur when a dominant left circumflex coronary artery gives off the posterior descending artery (PDA) AV block with an inferior wall MI may be due to ischemia of the AV node, but it is also possible that vagal stimulation due to the infarction (on the diaphragm) can lead to heart block Block

in the AV node can lead to first-degree AV block If it leads to second-degree AV block, it is virtually always Mobitz I second-degree AV block If third-degree AV block occurs, the escape rhythm is typically at the junction and is often adequate to maintain a reasonable blood pressure Block in the AV node usually responds to atropine or theophylline therapy When escape rhythms do occur with third-degree AV block, the QRS is usually narrow (unless there

is coincidental bundle branch block present) Third-degree AV block does not always require

a pacemaker since the escape rhythm is often adequate; however, if advanced heart block occurs then atropine can be kept at the bedside and sometimes a temporary pacemaker is necessary Permanent pacemaker therapy is rarely required in this setting and almost always