AUTHORS
Kathleen McMahon, DO, Attending Physician, St. Luke’s University Health Network, Bethlehem, PA
Guhan Rammohan, MD, FACEP, Emergency Medicine Faculty, St. Luke’s Hospital, Bethlehem, PA
PEER REVIEWER
Larissa I. Velez, MD, Associate Dean for Graduate Medical Education, Professor and Vice Chair for Education, Michael P. Wainscott Professorship in Emergency Medicine, Department of Emergency Medicine, UT Southwestern Medical Center, Dallas, TX
Case Presentation
A 67-year-old male patient with past medical history significant for sick sinus syndrome, hypertension, and hyperlipidemia presents to the emergency department (ED) for fever, fatigue, and shortness of breath. He underwent permanent pacemaker placement six months prior to presentation. On examination, the patient is noted to have a heart rate of 130 beats per minute, blood pressure of 100/60 mmHg, 26 respirations per minute, and a temperature of 39.5° C. Auscultation of the heart reveals a new systolic ejection murmur over the precordium. A non-blanching macular rash is noted on his hands, particularly the palmar aspect. During his ED evaluation, he is found to have bilateral nodular opacities throughout both lungs on chest X-ray and an electrocardiogram (ECG) remarkable for sinus tachycardia without any morphologic abnormalities or pacer spikes. Laboratory studies are remarkable for a white blood cell count of 25 × 103/uL, hemoglobin 8 g/dL, and creatinine 2.0 mg/dL. The patient ultimately is admitted to the hospital for sepsis and treated with aggressive intravenous (IV) fluid hydration and broad-spectrum antibiotics.
During his hospitalization, he undergoes a formal echocardiogram that reveals a large vegetation on his tricuspid valve. He is suspected to have endocarditis related to his recent pacemaker placement and undergoes transvenous lead extraction to remove the nidus for infection. An hour after the procedure, he is noted to have new, acute focal neurologic deficits, including weakness of the right arm, a right-sided lower facial droop, and dysarthria. The patient undergoes an emergent non-contrast computed tomography (CT) of the head and CT arteriography of the head and neck that demonstrates an acute occlusion of the left middle cerebral artery. The patient then undergoes endovascular clot retrieval and is admitted to the intensive care unit (ICU) for stroke-oriented intensive care while continuing antibiotics for endocarditis. The patient progresses through a prolonged hospitalization and course of antibiotics. He ultimately is discharged from the hospital with minor residual neurologic deficits and with plans to undergo insertion of a new pacemaker after completing outpatient IV antibiotics.
Introduction
Cardiac implantable electronic devices (CIEDs) are commonly encountered when caring for ED patients. An estimated 3% to 8% of patients with CIEDs may face complications, some life-threatening, during the lifespan of their device.1 In the immediate post-procedure period, in-hospital complications may even be as high as 16%, depending on the particular device used.1 The risk of complications is greater for those undergoing re-intervention procedures, such as replacement of the device or battery change.1 Given their prevalence in the population, knowledge of potential complications associated with CIEDs is critical for ED providers.
The term CIED encompasses both permanent pacemakers (PPMs) and implanted cardiac defibrillators (ICDs). PPMs primarily are used in the treatment of symptomatic bradycardia and advanced heart blocks.2 They also may be indicated in some cases of heart failure, congenital long QT syndrome, Brugada syndrome, and hypertrophic cardiomyopathy.3 More than 200,000 PPMs are implanted in the United States annually, a number that is expected to rise in the coming years.4
Transvenous pacemakers are temporary devices inserted through central venous access for stabilization of patients with severe bradycardia or advanced heart block. These will not be discussed in this review.
Pacemaker Structure
The two primary functions of pacemakers are sensing the heart’s electrical activity and providing an electrical stimulus to depolarize the myocardium.3,5 Structurally, they consist of an electrical generator and intracardiac leads, the latter of which also act as sensors of intrinsic cardiac electrical activity.3,5 PPMs may be single- or dual-chamber devices. Single-chamber devices most often have a lead placed into the right ventricle or right atrium, whereas dual-chamber pacemakers usually have leads in both the right atrium and right ventricle.6 Single-chamber devices are chosen more often for patients with significant comorbidities or who require pacing infrequently. The basic structure of a pacemaker has changed little over the last several decades, although development in leadless and battery-less pacemakers is ongoing.4
A pacemaker has several settings that regulate its activity, some more relevant to an ED provider than others. The upper and lower rate limits provide parameters for device activity based on the patient’s heart rate, preventing a pacemaker from pacing at too low or high of a rate, respectively.5 The maximum tracking rate is the highest rate of atrial depolarization that a dual-chamber pacemaker can sense to appropriately pace the ventricles.5 The amount of time after an atrial contraction that a pacemaker will initiate ventricular contraction in the absence of intrinsic activity is known as the sensed atrioventricular (AV) delay. Similarly, if no ventricular contraction occurs in the setting of atrial pacing, one will be initiated by the device after a specified amount of time called the paced AV delay. The programmed refractory period after a ventricular contraction after which the device will not trigger another ventricular response despite atrial activity is known as the post-ventricular atrial refractory period.5 When interpreting an ECG with a paced rhythm, the ECG is characterized by pacer spikes that may be noted prior to atrial contraction, ventricular contraction, or both. (See Figure 1.)
Figure 1. Normal Pacemaker Electrocardiogram |
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Used with permission from: lifeinthefastlane.com |
Pacemaker Modes
Pacemaker modes are described as a code that denotes the locations of sensing and pacing as well as response and adaptiveness of the myocardium to pacing.3 Modes are listed most commonly as a combination of three or four letters. The first letter indicates the chamber being paced (A for atrium, V for ventricle, D for dual, O for none or off). The second letter indicates the location of sensing (A, V, D, or O). The third letter corresponds to the type of response to pacing signals (I for inhibiting, T for triggering, D, or O). The fourth letter, when present, denotes rate adaptiveness, which can be either R for rate adaptiveness capable or O for none. (See Table 1.) Rate adaptive features are used for patients who are unable to independently increase their heart rate in response to physical activity or metabolic demand due to structural or electrical pathology.3
Table 1. Pacemaker Modes |
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Position |
I |
II |
III |
IV |
Category |
Chambers paced |
Chambers sensed |
Response to sensing |
Programmability rate modulation |
Letters |
O - None A - Atrium V - Ventricle D - Dual (A&V) |
O - None A - Atrium V - Ventricle D - Dual (A&V) |
O - None T - Triggered I - Inhibited D - Dual (T&I) |
O - None P - Simple M - Multi C - Communicating R - Rate modulation |
Reprinted with permission from: Bernstein AD, Daubert JC, Fletcher RD, et al. The revised NASPE/BPEG generic code for antibradycardia, adaptive-rate, and multisite pacing. Pacing and Clinical Electrophysiology 2002;25:260-264. |
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Single-chamber device modes include VOO, VVI, AOO, and AAI. Dual-chamber modes are divided into tracking and non-tracking modes depending on whether atrial activity is tracked by the device. DDD and VDD are tracking modes; DDI and DOO are non-tracking modes.3
The device’s mode can be discovered through characteristic ECG patterns or device interrogation if not already known through the patient’s device identification card or medical records. The choice of mode depends on the patent’s underlying indication for a permanent pacemaker, intrinsic atrial and AV nodal activity, and other patient comorbidities.
Epidemiology of Permanent Pacemaker Complications
There are numerous mechanical and functional complications associated with pacemaker placement procedures and the device itself. Studies have reported an in-hospital mortality rate of up to 0.9% to 1.3% for patients undergoing initial pacemaker placement.1,7 Around 13% of patients overall are readmitted within the first several months following the procedure; however, this is most commonly due to congestive heart failure exacerbation, which may be related to a patient’s underlying comorbidities rather than the device.7
Certain epidemiologic factors are associated with a higher risk of complications, especially in the peri-procedural time period and in the six months following the procedure.1 Age older than 80 years, placement of a single-chamber ventricular pacemaker (which is more likely than dual-chamber devices to be placed in sicker patients), and patients with a low body mass index (BMI) have higher mortality rates during this early period.1 Lower BMI also is associated with a higher risk for pneumothorax and hematoma at the implantation site.1 Women have a higher incidence of complications overall compared to men, and of pneumothorax and cardiac perforation.1,8
The incidence of complications also is related to the volume of pacemakers implanted at a given center and to the experience of the proceduralist.9 Patients undergoing PPM placement in a facility that performs fewer than 750 procedures per year, or by a proceduralist who performs fewer than 50 procedures per year, are at higher overall risk for complications.1 A higher risk of complications also is seen when patients undergo CIED placement emergently.1
Pacemaker complications may be temporally categorized into peri-procedural, short-term, and long-term. Significant peri-procedural complications include cardiac perforation, lead malpositioning, vascular injury, and pneumothorax. Within the first several months after the procedure, lead dislodgement, hematoma formation, and infection can occur. Long-term complications include lead fracture or other lead malfunction (> 50% of long-term complications), battery depletion, infection, and mechanical complications associated with repeat procedure.9 Pacemaker malfunction and functional complications may occur at any time.
Mechanical and Procedure-Related Complications
Pneumothorax
Ipsilateral pneumothorax complicates approximately 0.5% to 1.0% of permanent pacemaker placements and typically occurs when a needle is used for cannulation of the subclavian vein and inadvertently punctures the pleura.8,10 It is more common in women, patients with BMI < 20, in those with chronic obstructive pulmonary disease, in those with previous procedures or radiation to the area, and in those with corticosteroid treatment.8 The clinical presentation is similar to that of any other pneumothorax, with shortness of breath, chest pain, hypoxia, and decreased or absent breath sounds.8 Diagnosis is guided by physical exam and imaging in the form of chest X-ray or point-of-care ultrasound noting an absence of lung sliding. Management requires chest tube insertion in many cases. An isolated pneumothorax with less than 10% of the pleural space involved can potentially be managed supportively without chest tube placement.10 Rare cases of associated contralateral pneumothorax and even pneumopericardium have been reported.10 The use of ultrasound during subclavian vein cannulation may decrease the risk for pneumothorax formation.8
Cardiac Perforation
The risk of cardiac perforation, especially that of the right atrium, occurs in 1% to 2% of procedures using screw-in leads.8 Use of atrial screw-in leads, abnormal right atrium anatomy, and lateral location of lead implantation are associated with an increased risk of right atrium perforation. Ventricular leads are less likely to cause perforation because of the thicker wall of the ventricle compared to the atrium.8 When the ventricle is involved, the right ventricular apex is the more common site for perforation to occur.11 Cardiac perforation is more common in women; patients older than 80 years of age; patients on chronic steroid therapy; and patients with chronic obstructive pulmonary disease (COPD), dilated or ischemic cardiomyopathy, or abnormal cardiac anatomy.8 It also is more common in lead revision procedures.8,11 It also may be more common when magnetic resonance imaging (MRI)-compatible leads are implanted, because of their relatively larger size and greater stiffness.10
The presentation of symptomatic cardiac perforation typically occurs within the first month; however, onset may range from within the first 24 hours (acute) to many months after the procedure (chronic).8,11 Signs and symptoms range from chest pain and shortness of breath to those of cardiac tamponade and sudden cardiovascular collapse requiring emergent pericardiocentesis.11 Echocardiography aids in diagnosis.11
Patients without symptoms are sometimes managed expectantly with close observation in conjunction with electrophysiology and cardiovascular surgery consultations. Others advocate for lead extraction and repositioning, with other surgical interventions as needed, in both symptomatic and asymptomatic patients.8 A prophylactic pericardial drain often is placed at this time.8 A small, isolated pericardial effusion may occur in 10% of patients after PPM insertion and is suspected to be due to cardiac wall perforation. These typically resolve spontaneously.8
Thrombosis/VTE/Upper Extremity DVT
Pacemaker leads frequently contribute to clot formation, stasis of blood flow, and stenosis of vessels in the venous system.12,13 Even so, many patients remain asymptomatic.12 Mild venous stenosis occurs in almost 20% of patients, moderate stenosis in 20%, and total occlusion may occur in up to another 22% of patients.12 Vessels on the left side of the thorax and left upper extremity are more frequently and severely involved.12 The subclavian and brachiocephalic veins are affected most frequently, but superior vena cava involvement (SVC) and SVC syndrome may occur.12,14
Treatment of vessel stenosis and thrombosis may involve transvenous lead extraction (TLE) or venoplasty for severe cases, such as for those who develop SVC syndrome.12,14,15 Venography can be used to determine the feasibility and methods for future CIED reimplantation.12 This is especially important in patients who may need central venous access (such as a port or central line) or an arteriovenous (AV) fistula in the future.12 A history of SVC syndrome, if resolved, is not a contraindication to future CIED placement.15
Bleeding: Pocket Hematomas and Anticoagulation
Bleeding following PPM placement may occur and is of particular concern given that many candidates for pacemaker insertion are taking anticoagulation or antiplatelet agents for comorbid conditions.16 Locally, a hematoma in the pacemaker pocket may form. Deeper bleeding and bleeding at the venous puncture site also may occur. The decision whether to continue anticoagulant and antiplatelet medication in patients undergoing non-emergent PPM placement may be individualized based on a patient’s comorbidities and other risk factors for bleeding.17 While studies suggest that continuing systemic anticoagulation with warfarin and direct oral anticoagulant medications may not significantly increase the risk for pocket hematomas, simultaneous antiplatelet administration and other combined anticoagulant and antiplatelet therapies may increase the risk.16,17 Novel oral anticoagulants are not associated with an increased risk for pocket hematoma development.16
Treatment of pocket hematomas usually is expectant, since attempts at aspiration or other methods of drainage may either worsen the hematoma or introduce infection.4 In some cases, aspiration, excision, or other surgical intervention is required. The need for surgical intervention corresponds with hematoma size, failure of conservative management, and presence of underlying infection.4 Changes in pacemaker pockets and use of compression devices have been employed to decrease the risk of developing a pocket hematoma.
Infection
Both superficial and deep infections may complicate PPM placement. The most commonly implicated pathogens are Staphylcoccus aureus (including methicillin-resistant species, known as MRSA) and Staphylococcus epidermidis.18 The risk of infection is approximately 0.5% to 1.0% within the first year following pacemaker implantation, somewhat lower than that associated with ICD placement.2 About 25% of infections occur within days to weeks of placement, while 42% are noted to occur greater than one year after the procedure.2
Superficial infections associated with the surgical site and pacemaker pocket are relatively less severe than deeper infections but still are associated with significant morbidity. Local infections are the most common type of CIED-associated infections and often can be diagnosed clinically based on physical exam by noting local redness, swelling, and warmth.2,19 Swelling that develops after the initial postoperative period is particularly concerning for infection.2 Native skin flora are implicated most commonly, although anaerobic and gram-negative bacteria and even fungi may be involved.2 Wound swabs should be obtained to identify culprit organisms but may be sterile in up to 15% of cases.2 The mortality rate associated with superficial CIED infections ranges from 2% to 5%.2
Superficial infection not involving device leads, and which occurs within 30 days of device placement, may be treated with seven to 10 days of antibiotics with an 80% success rate. Antibiotic choice should be based on coverage for skin flora with consideration of local resistance patterns.2 MRSA coverage should be considered as well.
Deep infections may be difficult to diagnose, since some present only with fever and positive blood cultures, with no local abnormalities on physical examination.19 Superficial and pocket infections may lead to systemic infection involving the leads and heart valves, or may result in bacteremia.2,19 More rarely, bacteremia from another source may cause secondary infection of CIED leads that acts as a persistent focus of infection due to biofilm formation.2 Deep CIED-associated infections are associated with an overall 5% to 15% mortality rate.
Endocarditis can result in severe systemic infection and morbidity. It is associated with an in-hospital mortality rate of 6% to 15% and one-year mortality rate of 12% to 23%.2 While the tricuspid valve is involved most frequently, the left side of the heart is involved in 10% to 15% of cases.2 Echocardiography and blood cultures should be obtained as in other cases of endocarditis. Inflammatory markers, including C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), are not elevated in all cases.2 Procalcitonin is only 60% sensitive and 82% specific for CIED-associated endocarditis and cannot be relied upon to screen for or exclude the diagnosis.2 Septic shock ensues in up to 10% of patients.2
Positive blood cultures obtained for purposes other than suspected CIED infection present a diagnostic and treatment dilemma, since not all of these patients have involvement of the CIED.19 CIED leads can be seeded with bacteria from the bloodstream from a remote site of infection.19 Blood cultures positive for Staphylococcus aureus are associated with CIED infection in 45% of cases, and these patients warrant echocardiography and further testing to exclude endocarditis.2 In other scenarios, further workup should be undertaken on a case-by-case basis. In cases of suspected deep or systemic CIED-associated infection but negative workup, a positron emission tomography (PET) scan may be performed.2
Patients with suspected deep and systemic PPM-associated infection should be admitted and started on broad-spectrum antibiotics. CIED extraction often is required. Transvenous extraction usually is favored over surgical explantation in cases of CIED infection.2,20 Without device removal, patients face a nearly 40% mortality rate within one year, whereas those whose devices are removed have a mortality rate half as high.2 Cases with delayed explantation also are associated with a higher mortality rate than those with immediate device removal.2 Temporary pacing may be done via a percutaneously inserted right ventricular lead as a bridge to new PPM insertion in patients requiring interim pacing.2
Unfortunately, the decision to remove a PPM due to associated infection is not always straightforward because of risks associated with the procedure. Large valvular vegetations may embolize during lead extraction and, in the setting of a patent foramen ovale (PFO), cause stroke.25 Larger vegetations also are more likely to require open heart surgery for lead extraction to effectively eradicate infection.20 Future CIED replacement procedures also are associated with a higher risk of complications than primary procedures, which must be taken into account when considering treatment strategies.1,2
Post Cardiac Injury Syndrome and Pericarditis
While more well defined as a complication of myocardial injury from ischemia, trauma, or surgery, post cardiac injury syndrome (PCIS) rarely may occur after CIED placement.21 It is an immune-mediated inflammatory condition that may present with fever, pericarditis, and pleural effusions composed of lymphocyte predominant exudates.21 The incidence of pericarditis is increased when active atrial fixation leads and screw-in atrial leads are used.22 Onset typically is days to weeks following the procedure.21
Diagnosis is based on history, physical exam, laboratory testing, ECG, and imaging in the form of radiography and echocardiography. It is considered a diagnosis of exclusion. Awareness of the condition and a high index of suspicion are key to diagnosis, since its presentation may be subtle or nonspecific. Patients with pericarditis may present with chest pain, fatigue, or shortness of breath. A cardiac friction rub may be auscultated. Pleural or pericardial effusions may present with shortness of breath or hypoxia. An ECG with patterns consistent with pericarditis may be noted, and new-onset atrial fibrillation may occur. Erythrocyte sedimentation rates may be elevated.
Treatment involves anti-inflammatory agents and steroids. Large, symptomatic pleural or pericardial effusions may require drainage. Treatment and disposition decisions should be made in conjunction with cardiology and/or electrophysiology. Despite treatment, recurrence rates may be as high as 10% to 15%, although data in the setting of CIED-associated PCIS are lacking because of its rare occurrence.21
Pleural Effusions
More common than PCIS, pleural effusions may arise in patients with permanent pacemakers without optimal device settings.23 Any pacemaker activity that prevents synchrony between the atria and ventricles or otherwise decreases cardiac output may lead to pleural effusions through similar physiologic mechanisms as in heart failure. These effusions often are diagnosed late because of their rarity in this setting and also because of their nonspecific presentation.23 One study noted a delay of about four months from PPM insertion to pleural effusion identification.23 Patients with pleural effusions caused by PPM dysfunction are treated with settings adjustment and repeated thoracenteses as needed for symptom control.23
Twiddler’s Syndrome
Pacemaker leads may become dislodged or other pacemaker components may become damaged in patients who manipulate the pacemaker in their chest wall. This is known as Twiddler’s syndrome. Pacemaker dysfunction may occur, with hemodynamically significant consequences. It may be diagnosed based on a history of contributing behaviors. Chest X-ray may demonstrate lead displacement or abnormal position of the device in the chest wall or lead discontinuity. Damage to the device may result in failure to pace and cardiovascular compromise from reduced cardiac output. This syndrome is noted to have a high recurrence rate, and efforts to reduce repeat events include placing anchoring sutures in the pectoralis fascia or reinserting the device in an antimicrobial pouch to enhance stability. One small case series noted a significant reduction in recurrent events when an antimicrobial pouch was used.24
Stroke Caused by TLE
Transvenous extraction of pacemaker leads (TLE) is associated with several complications, with stroke being one of the most devastating. Lead removal may contribute to clot formation and may dislodge preexisting clots that may embolize to the brain. Systemic infection and deep infection associated with the device itself are leading indications for pacemaker lead extraction, and lead extraction may cause embolization of septic vegetations. In a cohort of patients who underwent TLE in the setting of CIED infection, 1.9% of the 774 included patients had a stroke; approximately half of these strokes occurred after the procedure. The presence of a PFO increases the risk of paradoxical embolization of septic clot to the brain. The presence of PFO also is independently associated with stroke risk in all patients undergoing TLE.25
Functional and Electrical Complications
Electromagnetic Interference (Imaging, LVADs, Procedures, etc.)
Electromagnetic interference (EMI) from various electronic devices may disrupt pacemaker function. Left ventricular assist devices (LVADs), deep brain stimulators, spinal cord stimulators, electrocautery tools, radiation treatments, endoscopy, and bronchoscopy are iatrogenic sources of EMI that may disrupt pacemaker function.5,26 Extracorporeal shock wave lithotripsy may damage components of certain PPMs containing piezoelectric crystals.5 Significant interference is more common in devices that respond to minute ventilation.27 Pacemaker settings may be altered inadvertently or output may be inhibited altogether upon exposure to EMI, and these may or may not be reversible with reprogramming.5,26 Awareness of sources of EMI can help prevent device dysfunction. Management should be undertaken in conjunction with cardiology and electrophysiology.
Magnetic Resonance Imaging Concerns
The magnetic field generated for MRI also may disrupt PPM function. Changes in pacing output, mode programming, current generation and passage through leads, and damage to wiring may result.5 Patients with newer, MRI-conditional devices may be able to undergo an MRI uneventfully, since these devices are constructed with materials that can withstand exposure to a strong electromagnetic field.5 It is prudent to investigate whether a patient’s PPM is MRI-conditional prior to such imaging to avoid pacemaker malfunction. Consultation with an electrophysiologist is warranted when MRI compatibility is in doubt.
Pacemaker-Related (Mediated) Tachycardia
A re-entry arrhythmia that may occur in patients with dual-chamber pacemakers with atrial sensing (DDD or VDD modes) is dubbed pacemaker-mediated tachycardia (PMT). It may occur in 30% to 80% of patients with permanent pacemakers. Similar to antidromic AV nodal re-entry tachycardia (AVRT), the device acts as a pathologic accessory pathway limb that results in an endless re-entry loop tachycardia.28 Retrograde ventriculo-atrial (VA) conduction triggered by various stimuli can trigger this re-entry loop. The resulting elevated heart rate is due to a loss of AV nodal rate control.28 Subsequent signals traveling from the ventricles to the atria through a pathologic retrograde conduction pathway may then be sensed by the pacemaker as an endogenous atrial depolarization, triggering the pacemaker to pace the ventricles at an inappropriately high rate.27 The pacemaker itself acts as an antegrade limb of the re-entry pathway that bypasses normal AV node regulation of ventricular stimulation.5 In unusual cases, interventricular interaction between leads of a combined PPM-ICD may lead to PMT.27 PMT is less common in patients with newer-generation pacemakers, which have pre-programmed algorithms to minimize its onset.5
Common triggers include premature ventricular contractions (PVCs), premature atrial contractions (PACs), loss of atrial capture or sensing, long AV delays, and certain changes to pacemaker modes.5,27,28 Any condition causing temporal separation of the P wave and QRS complex on an ECG may trigger PMT in a patient with an existing VA conduction pathway.27
Certain patients are at a higher risk for PMT. Many patients with sick sinus syndrome and, to a lesser extent, those with preexisting AV nodal block may already have retrograde VA conduction pathways, which increases the risk for PMT. Overall, 6% of patients with pacemakers develop PMT, but the prevalence is about 20% in patients with preexisting retrograde conduction pathways.27
Diagnosis is made largely based on history and ECG. The ECG typically has a regular, often wide-complex tachycardia with pacer spikes. (See Figure 2.) Less commonly, the rhythm may be irregular, due to changes in the circuit or refractory periods in the antegrade or retrograde limbs, or due to activity of the pacemaker.27 The number of P waves typically equals the maximum tracking rate of the pacemaker but also may be lower.27 The exact rate varies based on pacemaker settings and conduction pathway characteristics.27 In cases in which an upper rate limit or maximum tracking rate is programmed into the device, atrial or VA signals that exceed these limits on ventricular pacing may result in a Wenckebach pattern on ECG.5
Resolution of PMT may occur via several mechanisms. The PMT may terminate spontaneously if the conduction system becomes fatigued or by endogenous electrical aberrancies, such as another PVC.27 Carotid sinus massage may be attempted.27 Verapamil or beta-blockers also may be administered to disrupt VA conduction.27 Short-term management of PMT may be achieved by placing a magnet over the device, thus preventing pacemaker sensing and reverting the device to asynchronous mode.5,27 For long-term management, the device must be reprogrammed by electrophysiology.6
Figure 2. Pacemaker-Mediated Tachycardia Electrocardiogram |
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Used with permission from: lifeinthefastlane.com |
Undersensing and Oversensing
Undersensing describes a pacemaker failing to sense intrinsic cardiac activity and then provide pacing support synchronous with endogenous electrical activity.5 Pacemaker spikes will be seen on ECG without a proceeding QRS complex and there may be more than one pacemaker spike per QRS complex.5 (See Figure 3.) Undersensing may occur when a pacemaker’s threshold setting is too high, when leads are displaced or fractured, or when the endogenous myocardial voltage is insufficient to trigger a properly programmed pacemaker.5 Electrolyte abnormalities also may contribute.5 Treatment is targeted toward the underlying cause.
Figure 3. Ventricular Undersensing and Oversensing |
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Top: Ventricular undersensing. Bottom: Ventricular oversensing. Reprinted with permission from: Texas Heart Institute Journal. Safavi-Naeini P, Saeed M. Pacemaker troubleshooting: Common clinical scenarios. Tex Heart Inst J 2016;43:415-418. |
Conversely, a pacemaker that is oversensing detects inappropriate electrical signals, which prevents appropriate pacemaker stimulation of the myocardium. Any electrical impulse that reaches a certain strength may be sensed by the pacemaker as an endogenous cardiac impulse, which then inhibits response to appropriate native depolarizations.5 Electromagnetic interference and lead malfunction are sources of exogenous electrical stimuli.5 Sometimes endogenous electrical activity, such as T waves, are the culprit. An ECG shows fewer pacing spikes than would be anticipated based on a pacemaker’s settings.5 (See Figure 3.) Treatment of the underlying cause should resolve the issue.
Both undersensing and oversensing require pacemaker reprogramming, in addition to standard protocols for a patient with a symptomatic or unstable arrhythmia. Symptomatic and unstable patients should be admitted.
Other Pacemaker-Associated Arrhythmias
In some cases of rapid atrial electrical discharges, such as in atrial fibrillation, atrial flutter, and other atrial tachycardias, a pacemaker may pace at an inappropriately high rate. This occurs most often in devices without an active mode switch option.27 Devices with unipolar leads are more likely than other leads to sense myopotentials from adjacent muscle groups and pace inappropriately.27 Depending on muscle activity and pacemaker settings, this also may lead to tachycardia.27 Device reprogramming and treatment of the underlying causes should occur in these circumstances.
Failure to Capture
If an impulse generated by the pacemaker fails to appropriately depolarize the myocardium, it is described as failure to capture. Lead fracture or dislodgement may cause failure to capture. Other causes include fibrosis at the lead implantation site, certain antiarrhythmic drugs, hyperkalemia, and acidemia, all of which increase myocardial depolarization thresholds.5 On ECG, the absence of an appropriate P wave or QRS complex (depending on the paced chamber) after the pacer spike is diagnostic. (See Figure 4.) Treatment involves addressing the underlying cause when feasible.
Figure 4. Failure to Capture Electrocardiogram |
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Used with permission from: lifeinthefastlane.com |
Output Failure
Output failure describes the failure of a pacemaker to generate an electrical impulse when a patient’s heart rate is below the lower rate limit, which would normally trigger the device to begin pacing.5 Lead fracture, generator or battery failure, oversensing, and crosstalk inhibition are potential causes of output failure.5 The ECG shows an absence of pacer spikes in a patient with bradycardia.5 Treatment is for the underlying malfunction.
Crosstalk Inhibition
In the setting of a dual-chamber pacemaker, a ventricle may sense electrical discharge from a lead in another chamber as a native depolarization, causing inhibition of pacing in the ventricle.5 This results in inappropriately decreased ventricular depolarization and decreased cardiac output. ECG shows fewer pacer spikes than would be expected. Pacemakers may be programmed with ventricular safety pacing (SP) that prevents this phenomenon.5
Runaway Pacemaker
Runaway pacemaker occurs when the pacemaker paces the ventricles much more frequently than its programmed rate. It is uncommon in modern devices.27 It typically occurs as a pacemaker battery nears the end of its lifespan, but it may result from software errors or with damage to the pacemaker components.5,27 The morphology of runaway pacemaker on ECG is that of captured beats alternating with non-captured, high-rate spikes.5
Pacemaker Syndrome
Pacemaker syndrome may occur as frequently as in 20% to 80% of patients with PPMs, depending on the pacemaker mode.28,29 It occurs when a mistimed atrial contraction occurs against a closed AV valve or atrial contraction occurring soon after that of the ventricle, which causes an increase in venous pressure. Loss of the atrial kick contributes to decreased cardiac output.29 It typically occurs in patients with single-chamber VVI pacing, since pacing only the ventricle may lead to poor coordination between the atrium and ventricle that results in decreased cardiac output.29 Desynchrony of the ventricles themselves also may occur that leads to decreased cardiac output through mistimed contraction of the interventricular septum and the rest of the left ventricular wall.29 Ultimately, overload of the pulmonary circulation ensues.
Pacemaker syndrome is considered a diagnosis of exclusion. Physical stigmata of heart failure, such as peripheral edema, shortness of breath, and exercise intolerance, may be noted.29 Pacemaker spikes with capture but without concordance between P waves and QRS complexes may be seen on ECG.29 On chest X-ray, a single chamber pacemaker with a single lead in the right ventricle will be seen.29
Treatment of heart failure symptoms may be achieved with standard therapies for other causes of heart failure.29 Replacement of a single-chamber pacemaker with dual-chamber pacemaker with DDD or VDD mode is advised for patients in sinus rhythm, when applicable.29,30 Upgrading to a device with cardiac resynchronization capabilities is recommended for those patients with low ejection fraction (EF).29 Continued single-chamber pacing may be an option for those patients who are only intermittently paced by the device, since these devices carry a lower risk of developing significant symptoms associated with pacemaker syndrome.30
Pacemaker-Induced Cardiomyopathy
Impaired left ventricular function in the setting of right ventricle (RV) pacing can cause pacemaker-induced cardiomyopathy (PICM).31 It may occur in single-chamber and dual-chamber devices. It occurs most often within the first year of insertion.32 Ventricular desynchrony over time triggers remodeling of the myocardium, leading to a decrease in cardiac output. Clinical manifestations are those associated with left-sided heart failure, including pulmonary and peripheral edema, orthopnea, shortness of breath, pleural effusions, and hypoxia. Formal diagnosis is based on a decrease in left ventricular ejection fraction (LVEF) of greater than 10% of baseline; ECG evidence of pacing being performed at least 20% of the time; and exclusion of other causes of decreased LVEF. Early recognition is important to prevent further irreversible cardiac remodeling.32 Admission and electrophysiology consult is recommended. Treatment is through device reprogramming or replacement with a biventricular pacer that prevents ventricular desynchrony.
Difficulty with ECG Interpretation
Pacemaker activity may produce characteristic “spikes” on ECGs representing pacemaker electrical stimulus followed by unusual morphology in the QRS and ST segments and T waves representing myocardial depolarization and repolarization. The exact morphology depends on factors such as the frequency of pacing, capture of myocardium, and location of the pacemaker sensors and leads.
ECG interpretation in patients with pacemakers may be challenging, particularly in detecting abnormalities associated with myocardial ischemia and infarction. ECG changes resulting from ventricular pacemaker activity may complicate the diagnosis of myocardial infarction based on ECG features.33 Some have suggested that the Sgarbossa criteria may be applied to ventricularly paced ECGs. ST segment elevation
> 5 mm discordant from the QRS complex, one of the Sgarbossa criteria, may have relatively high specificity, although low sensitivity, for myocardial infarction on ventricularly paced ECGs. However, the Sgarbossa criteria in whole are not sufficiently sensitive or specific in these patients.33
Leadless Pacemakers
Leadless pacemakers (LPMs) lack the traditional implanted leads and instead are placed percutaneously using a femoral approach and stimulate the myocardium. Most are single-chamber pacemakers that pace only the RV, although newer devices with biventricular pacing capability have been tested.34,35 They are growing in popularity and may be encountered in ED patients.
LPMs are associated with different relative risks of similar complications as traditional pacemakers. Major complications associated with placement of LPMs include bleeding at the access site, cardiac perforation, and infection.34-36 A rate of early bleeding, pericardial effusions, and cardiac perforation may be higher for LPMs, but some suggest that this is due to the learning curve associated with performing a new procedure.34 In a Japanese population in which LPMs are placed frequently, a study found that time from placement to discharge and time of the procedure itself were actually shorter in these patients. Despite increased early complications, leadless pacemakers tend to have a lower rate of complications overall.37,38
Effect of Magnets
Commercially available magnets placed over a permanent pacemaker will revert the device to asynchronous mode, which prevents the device from sensing electrical impulses that may inhibit artificial pacing from the device. This may be clinically useful in cases of EMI that prevents proper sensing of intrinsic electrical activity, or lack thereof, that the device requires to function appropriately.39 Other indications include PMT and crosstalk phenomena. Magnets do not cause the device to cease functioning completely.
If a pacemaker battery is depleted or nearly depleted, placement of a magnet over the device may not cause any ECG or clinical changes.39 Magnet application also may be unsuccessful in patients with large body habitus or in whom the position of the device is too far from the magnetic field on the surface of the body to disrupt pacemaker functioning.39 Removal of the magnet from over the device typically reverts the device back to its previous settings.
Permanent Pacemaker Considerations in the Critically Ill
Abnormal heart rhythms that may be contributing to decompensation in a critically ill patient may benefit from device reprogramming. Artificially increasing a patient’s heart rate via overdrive pacing may help a patient with severe shock or those at risk for torsades de pointes.28
Standard advanced cardiac life support procedures, including electrical cardioversion and defibrillation, can and should be performed in patients with CIEDs.28 Chest compressions should be performed according to standard cardiac arrest algorithms. To minimize the risk of malfunction or device damage, pads should be placed 8 cm to 12 cm away from the generator and in the anteroposterior (AP) configuration.28
Conclusion
Given the prevalence of CIEDs in ED populations, it is critical to be aware of the relative risk and variety of complications related to these devices so that proper workup and treatment can be initiated. Awareness of new developments in pacemaker technology also is beneficial, since they may be associated with a different array of complications.
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Given the prevalence of cardiac implantable electronic devices in emergency department populations, it is critical to be aware of the relative risk and variety of complications related to these devices so that proper workup and treatment can be initiated.
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