Ventricular Undersensing Pvc Av Delay

Ineffective Pacing

Figure 7.1. Pacing stimuli present with intermittent failure to capture. The large unipolar stimuli are readily identified. The gentle downslope following the ineffective pacing stimulus is an RC decay curve. The pause is due to appropriate sensing of a native QRS, which is virtually isoelectric in this lead. RC = resistance capacitance.

Figure 7.1. Pacing stimuli present with intermittent failure to capture. The large unipolar stimuli are readily identified. The gentle downslope following the ineffective pacing stimulus is an RC decay curve. The pause is due to appropriate sensing of a native QRS, which is virtually isoelectric in this lead. RC = resistance capacitance.

Anodal Stimulation Recognizing Iegm

Figure 7.2. Evaluation of the atrial capture threshold while monitoring the surface ECG (top tracing), telemetered event markers and intervals, the atrial electrogram (middle tracing) and the ventricular electrogram (bottom tracing). Capture is present at 1.00 volts and 0.4 milliseconds. This is visible on both the surface ECG and the atrial EGM (arrows). With loss of capture at 0.75 volts, there is the loss of the large complex on the atrial EGM and a loss of the visible P wave on the surface ECG. The atrial output is bipolar resulting in a diminutive stimulus artifact that is virtually invisible on the surface ECG. Effective blanking on the intracardiac atrial EGM prevents distortion of the EGM.

Figure 7.2. Evaluation of the atrial capture threshold while monitoring the surface ECG (top tracing), telemetered event markers and intervals, the atrial electrogram (middle tracing) and the ventricular electrogram (bottom tracing). Capture is present at 1.00 volts and 0.4 milliseconds. This is visible on both the surface ECG and the atrial EGM (arrows). With loss of capture at 0.75 volts, there is the loss of the large complex on the atrial EGM and a loss of the visible P wave on the surface ECG. The atrial output is bipolar resulting in a diminutive stimulus artifact that is virtually invisible on the surface ECG. Effective blanking on the intracardiac atrial EGM prevents distortion of the EGM.

results in a uniform, relatively large "pacing artifact" generated by the ECG machine itself. This precludes differentiation of unipolar from bipolar pacing. Even nonpacemaker signals may be displayed as a pacing stimulus with these recording systems.

The differential diagnosis of stimuli present with failure to capture is relatively limited (Table 7.1). A likely etiology can often be established simply by knowing when the problem was encountered with respect to lead implantation. If the loss of capture occurred within hours or days of the implant, the most likely explanation is lead dislodgment. Loss of capture occurring weeks to months after implantation is most likely to be due to high capture thresholds resulting from the lead maturation process although this is less likely in the past decade due to the routine use of steroid-eluting electrodes. If this problem occurs many months to years after implantation, it is usually due to a mechanical or structural problem with the lead (such as damaged insulation or a conductor fracture) or due to an abnormality in the myocardium itself. During this time, it is also appropriate to consider extracardiac causes such as metabolic abnormalities or pharmacologic agents. Failure to program an adequate output safety margin may result in loss of capture due to physiologic variations in the capture threshold. Latency from the pacing stimulus to the onset of the P wave or QRS complex may simulate loss of capture. Eventually, the battery will deplete such that the actual output, despite its programmed value, will fall below the capture threshold, resulting in loss of capture.

Lead Dislodgment: Accompanying the loss of capture with an acute lead dis-lodgment, there may be changes in the morphology of capture beats, in the

Table 7.1. Differential Diagnosis of Pacing Stimuli Present—Persistent or Intermittent Loss of Capture

Etiology

ECG*

Chest Radiograph* Impedance Threshold Management

Lead dislodgment

• Early: unstable position

• Late: Twiddler's syndrome Lead maturation

• Early: inflammatory response

• Late: progressive fibrosis Late high thresholds

• Progressive fibrosis

Myocardial infarction

• Cardiomyopathy

• Metabolic/drugs

• Damaged lead or tissue interface

Insulation failure

Conductor failure

• Lead fracture

• Loose set-screw Battery depletion Functional noncapture

• Pseudomalfunction

Abnormal Abnormal or Normal Normal Elevated

Normal Normal

Normal Normal

Normal Elevated

Normal Elevated

Reposition lead

Increase output, trial of steroids, or reposition

Increase output, correct cause, or replace lead

Normal* Normal or conductor Decreased abnormality

Normal§ Abnormal Increased

Normal Normal

Normal Normal

Normal Normal

Elevated Elevated

Elevated""

Normal

Reprogram to unipolar, replace lead

Reprogram to unipolar (lead fracture), replace lead, reoperate for set screw

Replace pulse generator Decrease rate, decrease refractory period(s), or increase sensitivity

* In ECG column, normal refers to a stable morphology of the evoked potential; abnormal refers to a change in the morphology of the evoked potential.

^ In the chest radiograph column, normal refers to stable lead position and no obvious deformity of the conductor coil; abnormal refers to a change in lead position or a deformity of the conductor coil. The insulation is radiolucent and will not be visualized on the x-ray.

* The ECG with an insulation failure involving a unipolar lead will show a decrease in the amplitude of the pacing stimulus. An insulation failure involving the outer insulation of a bipolar lead will show an increase in the amplitude of the pacing stimulus. Failure of the internal insulation of a coaxial bipolar lead will show a decrease in stimulus amplitude. This presupposes that all recordings are made with an analog ECG machine.

§ The ECG with an intermittent conductor fracture may show a varying amplitude pacing stimulus if recorded with an analog ECG machine. See Table 7.3 for a total conductor fracture.

11 Pacing threshold is increased as measured through the depleted generator but is normal through the PSA.

Source: Modified from Levine PA. Pacing system malfunction: Evaluation and management. In: Podrid PJ, Kowey PR, eds. Cardiac Arrhythmia: Mechanisms, Diagnosis, and Management. Philadelphia: Williams & Wilkins, © 1995. By permission of Williams & Wilkins.

dipole of the pacing stimulus, and/or in the lead position identified on a repeat chest radiograph. It is important to obtain the follow-up chest radiograph in an identical projection to that used for the baseline study. Even so, small "micro-dislodgments" of the lead tip may compromise the electrode contact with the myocardium but not be discernible with radiography. Despite some early reports in the literature to the contrary, neither partial lead dislodgment nor a simple rise in capture threshold due to tissue reaction at the electrode-myocardial interface will result in a significant change in stimulation impedance.4

A change in the morphology of the capture beat is often a clue to lead dislodgment, but this is the case only when fusion with the native QRS complex is absent. Fusion can also occur in the atrium. The morphologic changes in the paced P wave when combined with the native atrial depolarization are more difficult to identify because of the smaller size of the atrial complex. In biven-tricular systems, one has to be concerned with the position of two ventricular leads—one in the right ventricle and the other stimulating the left ventricle.

Correction of a lead dislodgment requires surgical intervention to reposition the lead. Before this is done, the reason for the dislodgment should be investigated. Careful attention should be directed to the original chest radiograph, and an adequate heel on the intracardiac portion of the lead should be sought at the time of lead implantation. Either too little or too much will predispose to dislodgment.9 One should also review the recorded electrograms from the initial implant, looking for a 2 to 3mV current of injury pattern ("ST-segment" elevation). The absence of this degree of current of injury has been correlated with an increased incidence of lead dislodgment; the implication is that the electrode is not making good endocardial contact. An examination of the anchoring sleeve for adequate fixation should be done at the time of reoperation.10

One should observe several precautions at the time of lead repositioning. When repositioning a dislodged lead, a thrombus may have developed around the lead tip, encasing the passive-fixation tines or fins or active-fixation helix, effectively preventing the lead from being adequately secured at the repeat pro-cedure.Thus, once the lead is thought to be in a good position, the patient should be instructed to take as deep a breath as possible and to cough vigorously so that the electrical and mechanical stability of the lead may be assessed. If the dislodgment is due to Twiddler's syndrome, the most common cause of a late lead dislodgment, the portion of the lead within the pocket should be carefully inspected. If damage to the conductor coil or insulation is noted, the lead should not be reused. If a dislodgment occurs and the reason is not sufficiently apparent that it could be corrected at the second procedure, it would be prudent to remove the dislodged lead and replace it with an active fixation lead. One needs to be aware that use of an active fixation lead does not guarantee chronic stability—dislodgments have been reported years after implantation.911

High Thresholds; Lead Maturation: When the electrode is first inserted, it is making intimate contact with the endocardium. The presence of foreign mate rial and the pressure of the lead-electrode system against the myocardium induce an inflammatory reaction at the electrode-myocardial interface. This local trauma is responsible for the current of injury pattern on the acute EGM recording. Due to the inflammatory reaction, the electrode is physically displaced from the excitable myocardium. This process increases the capture threshold. In addition, it attenuates the electrogram amplitude and slew rate to compromise sensing. With time, the inflammatory reaction subsides, leaving a thin capsule of fibrous tissue between the electrode and active myocardium. As the distance between the electrode and active myocardium is reduced, the capture and sensing thresholds improve.

Sometimes the inflammatory reaction at the electrode-myocardial interface is excessive, causing the capture threshold to rise above the output of the pace-maker.11-14 This has been termed exit block. If exit block is the reason for loss of capture, there will be no change in the morphology of any capture beats, nor will there be a change in the radiographic position of the lead. Exit block can occur even with steroid-eluting leads and excellent acute capture thresholds; however, if the implanting physician accepts an electrode position with a high threshold (i.e., greater than 1.5 V), there may be an increased likelihood of exit block due to less "reserve" for the threshold to rise. The literature reports the incidence of exit block of less than 5%.11

Early experience with systemic steroids to limit acute threshold rises led to the development of the steroid-eluting electrode, which has been effective in attenuating the inflammatory reaction and its associated early rise in capture and sensing thresholds.15-20 Isolated cases of massive threshold rises have also been encountered with the steroid-eluting leads, although the incidence is probably lower than with non-steroid-eluting leads.21,22 Acute management of high thresholds, with or without loss of capture, requires increasing the output of the pacemaker. If this is not feasible, one needs to determine the status of the native underlying rhythm. If it is stable and adequate to physiologically support the patient, one might simply wait for the threshold to fall or try a course of high dose systemic steroids. If the underlying rhythm is not stable, one will need to insert a temporary pacemaker lead and consider an urgent intervention to reposition or replace the lead.

If thresholds increase during the early postimplantation period and one elects to use systemic steroids in an attempt to reverse the phenomenon, a regimen of 60 mg of prednisone per day, often administered in divided doses, has been found effective in approximately 50% of patients. In the pediatric population, the dose is 1 mg/kg. Capture thresholds are repeated 4 to 5 days after the initiation of steroids. If there is no change or if there is a further increase in capture thresholds, the steroids are considered ineffective and are simply discontinued. If the threshold, however, has decreased by at least two programming steps (pulse width and/or pulse amplitude), it is likely that the steroids are effective. The steroids are then continued for a month, with biweekly monitoring of capture thresholds. At the end of the month, a slow but progressive tapering schedule is initiated that continues for a minimum of 2 months.

High Thresholds; Chronic Lead: High capture thresholds may develop at any time. Those that are not associated with the acute lead maturation process are not likely to respond to steroids. When this problem is encountered, one should evaluate the patient for transient etiologies, including electrolyte and acid-base abnormalities such as hyperkalemia and acidemia.15-17,23-26 Also included are pharmacologic agents such as the antiarrhythmic drugs; the 1C agents such as flecainide have developed a particularly poor reputation.27-30 If a transient cause is identified and it can be corrected, the problem can be managed with a transient increase in output or by use of temporary pacing until the situation has resolved.

Permanent late rises in capture thresholds may also occur with progressive myocardial fibrosis, a primary myopathic process, or myocardial infarction.31 If the output programmability of the device is not sufficient to overcome these causes, placement of a new lead will be required. Given that the lead is not infected, explantation is not mandatory.32

One must be very cautious about invoking the diagnosis of a high threshold due to a primary myocardial process in the absence of a change in the morphology of the intrinsic P wave or QRS complex. With a stable native complex on the surface ECG, a more likely explanation is a primary problem developing with the lead itself. If the malfunction were due to a mechanical abnormality developing in the lead, one would expect to see a change in the telemetered or invasively measured stimulation impedance, although this may not always be the case. Normal telemetry values may occur in the presence of an intermittent problem if the lead was functioning properly at the time of the measurements. When the lead impedance is abnormal, a very low impedance value (commonly less than 200 ohms) reflects a failure of the insulation, most commonly the inner insulation in a coaxial bipolar lead. A very high lead impedance (greater than 2000 to 3000 ohms) is consistent with a complete conductor fracture (open circuit). Measurement-to-measurement changes in telemetered lead impedance that are still within the normal range are totally consistent with normal lead function. Changes up to 300 ohms may still be compatible with normal lead function.33 Further, a change in the measured impedance in the absence of a clinical malfunction, such as a massive rise in capture threshold, noncapture, or a sensing problem, may be a telemetry error. Although this might warrant closer follow-up assessment, an isolated abnormality of a telemetry measurement does not mandate operative intervention.

Lead Insulation Defects: An insulation defect may develop from the intrinsic design and/or a manufacturing limitation as was the case with an early series of 80A polyurethane insulated leads. Most insulation problems, however, are due to extrinsic forces applied to the lead either at or following implant that physically damage the lead. In part, this problem is a direct result of the request by the medical community for thinner leads, both unipolar and bipolar. One method of reducing the lead's diameter is to reduce the thickness of the insulating material. In-line bipolar coaxial leads are the least forgiving of extrinsic stresses for this very reason. Insulation defects have occurred with both silicone rubber and polyurethane insulation material.34 Industry continues to evaluate new materials having the relative benefits of both polyurethane and silicone rubber while minimizing some of their weaknesses.

Extrinsic stress applied to the lead can result in damage to the insulation and/or a conductor fracture. There are three common mechanical stresses on the lead. The first is the suture sleeve, in which an excessively tight ligature is used to anchor the lead to the underlying fascia. If one sees a visible distortion of the conductor coil either at implant or on a follow-up chest radiograph, the ligature around the suture sleeve and lead is too tight.35 Although this was originally considered a benign observation, late adverse consequences associated with this area of stress have recently been appreciated.34 The second source of stress on the lead is the point where the lead traverses the plane between the clavicle and first rib on its way to the subclavian vein.36,37 The normal motion of the arm causes the space between the clavicle and first rib to widen and narrow, much like the jaws of pliers. This is exacerbated if the course of the lead traverses the costoclavicular ligament or the subclavius muscle in its path to the subclavian vein. The lead located in this position can be repeatedly crushed, pinched, pulled or stretched, resulting in a deformation of the conductor coils, which in turn will predispose to either an insulation failure and/or conductor fracture occurring months to years after implantation (Fig. 7.3). This has been termed the medial subclavicular musculotendinous complex and is an increasingly recognized cause of malfunction of both standard pacing and defibrillator leads. A recent recommendation has been to access the axillary or cephalic vein rather than the subclavian vein to avoid both the acute and late complications associated with the implant procedure.38,39

A third mechanism involves abrasion of the external insulation. This may occur between overlapping coils of the same or contiguous leads or between the housing of the pulse generator and the lead coiled behind it.

Manifestations of a lead insulation defect are determined, in part, by the location of the defect.40 In unipolar leads or a defect associated with the proximal conductor of a bipolar lead, there may be extracardiac muscle stimulation due to the electrical current leaking from the defect. Muscle stimulation in the area of a unipolar pacemaker may also be due to an upside-down pacemaker with the anode or indifferent electrode making direct contact with the underlying muscle. The author is also aware of several cases in which the insulating material applied to the pulse generator was damaged, thus allowing for local muscle stimulation with a totally normal lead.

Another manifestation of a lead insulation defect includes changes in the amplitude of the pacing stimulus, although this is difficult to evaluate given the differences in pacemaker stimulus reproduction between different ECG machines. This is best identified with an analog ECG recording system. In a unipolar system, there is a shorter path between the exposed conductor and the pulse generator, resulting in attenuation of the pacemaker stimulus amplitude. When the breach involves the outer insulation covering the anodal conductor

Xray Pacemaker Header Set Screw Loose

Figure 7.3. Lead fracture diagnosed on chest x-ray. Three years after dual chamber pacemaker implant for sick sinus syndrome this patient was found to have complete loss of ventricular capture and bipolar lead impedance of greater than 2000ohms. There is a clear fracture of the lead just before it enters the subclavian vein. The fracture may have been due to the subclavian access that passes the lead through the costoclavicular ligament apparatus. There is a slight deformity of the atrial lead at this position suggesting compressive force on this lead as well.

Figure 7.3. Lead fracture diagnosed on chest x-ray. Three years after dual chamber pacemaker implant for sick sinus syndrome this patient was found to have complete loss of ventricular capture and bipolar lead impedance of greater than 2000ohms. There is a clear fracture of the lead just before it enters the subclavian vein. The fracture may have been due to the subclavian access that passes the lead through the costoclavicular ligament apparatus. There is a slight deformity of the atrial lead at this position suggesting compressive force on this lead as well.

of a bipolar lead, there will then be two pathways for current flow. This will result in a larger "unipolarized" stimulus on the ECG. If the insulation is breached between the distal and proximal conductors of a bipolar lead, the current flow will be short-circuited and little or none of it will ever reach the active electrodes. In this case, the already small bipolar stimulus amplitude will be further attenuated. In any case the shunting of current through the insulation defect and away from the myocardium can result in higher capture thresholds.

Sometimes an intermittent problem is identified on a Holter monitor or is suspected on the basis of symptoms, but when the patient is evaluated in the office, the system is functioning properly. This is particularly likely if the insulation defect occurs between the proximal and distal conductor of a bipolar lead.

When the patient is lying quietly on the examination table, the normal elastic recoil of the conductor coils may separate the two wires even if the insulation between them has been breached. To reveal the problem different maneuvers can be performed while monitoring the ECG, telemetered lead impedance, event markers, and/or electrograms (Fig. 7.4). One technique that is particularly effective in identifying a problem resulting from a ligature that is too tight mode: ODD Rate: 45 ppm A-V Delay: 125 msec

( ECG/IEGm PARAMETERS

Surface EGG- On

Shin Gain- 1.0 mu/diu

Intracardiac EGm-V IEGR1 UNI

Intracardiac Gain- 10 mu/diu

Chart Speed- 25.0 mm/sec

Ddd Pacing Rhythams With Pvc

Figure 7.4. Repeated ventricular oversensing with resultant inhibition was demonstrated in this dual bipolar DDD pacing system. Measured data telemetry reported a ventricular lead impedance of less than 250ohms; the baseline had been 645ohms. Telemetry of the ventricular electrogram while simultaneously recording a surface ECG demonstrates non-physiologic large electrical transients (arrows) occurring at a time when the pacemaker is being inhibited, indicating that the pacemaker is sensing these signals. The ventricular sensitivity had been reduced in an attempt to minimize this oversensing problem. However, the nonphysiologic transients were approximately 20mV, larger than the least sensitive setting of the pacemaker, and the oversensing continued. However, the reduced sensitivity resulted in undersensing of the native R waves, resulting in competition. The nonphysiologic electrical transients were treated as PVCs by the pacemaker and activated the PVC algorithm, extending the refractory period and resulting in intermittent functional atrial undersensing.

Figure 7.4. Repeated ventricular oversensing with resultant inhibition was demonstrated in this dual bipolar DDD pacing system. Measured data telemetry reported a ventricular lead impedance of less than 250ohms; the baseline had been 645ohms. Telemetry of the ventricular electrogram while simultaneously recording a surface ECG demonstrates non-physiologic large electrical transients (arrows) occurring at a time when the pacemaker is being inhibited, indicating that the pacemaker is sensing these signals. The ventricular sensitivity had been reduced in an attempt to minimize this oversensing problem. However, the nonphysiologic transients were approximately 20mV, larger than the least sensitive setting of the pacemaker, and the oversensing continued. However, the reduced sensitivity resulted in undersensing of the native R waves, resulting in competition. The nonphysiologic electrical transients were treated as PVCs by the pacemaker and activated the PVC algorithm, extending the refractory period and resulting in intermittent functional atrial undersensing.

around the anchoring sleeve is for the examiner to trace the course of the subcutaneous portion of the lead with his or her fingers while applying pressure at each point. If there is an insulation defect, the two conductor coils will be pushed together, unmasking the problem. Extending the ipsilateral arm as high as possible, as in reaching toward the ceiling or placing the arm behind the back and rotating the shoulder backward, may unmask a problem caused by the medial subclavian-muscular complex.

Obtaining a chest radiograph may reveal a problem, although the insulation defect alone will not be seen because the insulating material is radiolucent. One might see a deformity of the conductor coil (Fig. 7.5) allowing one to infer the diagnosis when these observations are combined with the clinical and telemetry data. However, a radiographic abnormality in the absence of independent corroboration of a system malfunction would be insufficient grounds to recommend an operative intervention.

Open Circuit: The most common cause of an open circuit is a conductor fracture. The second, but more embarrassing, cause is a failure to adequately tighten the set-screw in the terminal pin connector block of the pulse generator (Fig. 7.6).

Loose Set Screw Pacemaker Ray

Figure 7.5. In-line bipolar coaxial lead with an indentation (arrow) created by a tight ligature around the lead. This has been called a pseudofracture and was previously considered to be of little clinical consequence. It has since been learned that the excessively tight ligature predisposes to both conductor fractures and insulation defects.

Figure 7.5. In-line bipolar coaxial lead with an indentation (arrow) created by a tight ligature around the lead. This has been called a pseudofracture and was previously considered to be of little clinical consequence. It has since been learned that the excessively tight ligature predisposes to both conductor fractures and insulation defects.

Coductor Fracture

Figure 7.6. Chest radiograph demonstrating displacement of the terminal pin out of the head of a pacemaker. For the atrial lead entering the top of the header (bottom of the figure) the terminal pin is seen extending beyond the header posts for both the ring and tip electrodes (heavy arrow). The ventricular lead, however, does not reach to the header post for the tip electrode (thin arrow). The ventricular lead impedance was unmeasur-able. In addition, pseudofractures are seen in both leads due to constriction of the insulation by the tying sleeves (arrowheads).

Figure 7.6. Chest radiograph demonstrating displacement of the terminal pin out of the head of a pacemaker. For the atrial lead entering the top of the header (bottom of the figure) the terminal pin is seen extending beyond the header posts for both the ring and tip electrodes (heavy arrow). The ventricular lead, however, does not reach to the header post for the tip electrode (thin arrow). The ventricular lead impedance was unmeasur-able. In addition, pseudofractures are seen in both leads due to constriction of the insulation by the tying sleeves (arrowheads).

There are two common clinical manifestations of an open circuit. With a total open circuit, no energy will traverse the gap between the two portions of the lead and there will be an absence of pacing artifacts on the ECG and loss of capture. This is included in the class of malfunction associated with an absent pacing stimulus. If the two ends of the conductor are making any contact at all, the resistance to current flow will be increased to attenuate the amount of current and energy reaching the heart, but a stimulus will be present. If the effective energy reaching the heart is subthreshold, there will be loss of capture. Although a physical break in the conductor is the most common cause of an open circuit and usually does not manifest until months to years after implantation, there are two circumstances when an open circuit can occur at the time of implantation. One is a failure to tighten the set-screw allowing the lead to pull out of the set-screw connector block (see Fig. 7.6). The other involves a small unipolar pacemaker used as a replacement for a larger model pacemaker. If there is air trapped within the pocket, this may serve as an insulator separating the indifferent electrode on the case of the pacemaker from the patient's

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Responses

  • awate
    What does a pacemaker lead fracture look like on xray?
    6 years ago

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