After the initial implementation of a pacemaker in the 1950s, implanted cardiac devices have become the mainstay therapy for life-threatening arrhythmias and severe congestive heart failure (1). Thanks to technological advancements, the devices become cheaper and smaller, now improving the lives of millions of patients (2). As physicians who serve in an acute setting, we started to take care of patients with implanted cardiac devices on a daily basis. Therefore, we must know how to manage implanted cardiac devices-related emergencies.
The three most common implanted cardiac devices are pacemakers (PMs), implantable cardioverter-defibrillators (ICDs), and left ventricular assist devices (LVADs). PMs generate rhythmic electrical stimuli and consequent heart contractions when the intrinsic electrical activity is below a threshold. ICDs recognize and treat ventricular tachyarrhythmias electrically. Newer generation ICDs also function as pacemakers (3). While the PMs and ICDs mainly support the cardiac electrical function, LVADs support the mechanical function of the heart.
Pacemaker related emergencies are divided into two broad groups as complications of implantation and device malfunction. In this post (part 1), we will summarize complications of implantation.
Complications of Implantation
Although modern technology and technique have significantly decreased the complication rates., we as acute care providers still must be aware of the perioperative complications related to pacemaker implantation. Relatively common complications include pocket, lead-related, thromboembolic, mechanical complications, and pacemaker syndrome (1,4).
Hematomas are formed by perioperative arterial and venous bleeding and can spread tracking the pacemaker leads (5). Palpable hematomas require surgical evacuation as needle aspiration is ineffective, poses pacemaker damaging risk, and does not reveal the underlying source (6). Hematomas increase infection risk.
The infections of pocket or leads can occur, mostly due to cutaneous flora, namely, Staphylococcus aureus and Staphylococcus epidermidis (4). The presence of foreign bodies and hematomas contribute to the infectious process (4). Local infections may progress to lung infections, sepsis, skin erosion, and wound dehiscence. The clinical picture may vary from local inflammation and fluctuation to vague systemic complaints and even to sepsis/septic shock without origin (1, 5). Therefore, a clinician should always suspect pacemaker and lead-related infections as a source in patients with a pacemaker. In the ED, after taking blood cultures, intravenous wide-spectrum antibiotics should be started. Pocket cultures should be obtained under fluoroscopy (4). Pocket infections generally necessitate long admissions with IV antibiotics therapy and removal of the pacemaker (7).
Lead-related complications include lead malposition, dislodgment, fracture, and damage to the insulation, all of which cause various malfunctions (8, 9). Among them, lead malposition and dislodgement have some additional clinical implications.
Lead malposition refers to when a lead is inadvertently placed into the left ventricle (9). Lead may land in the left ventricle through a natural orifice of intracardiac variants and defects (atrial-septum defect, patent foramen ovale, sinus venosus defect, malpositioned coronary sinus or its tributaries) or perforation of the intraventricular septum (9). Also, the operator may erroneously place the lead through the subclavian artery and aortic valve.
Lead malposition significantly increases thromboembolic event risk, including transient ischemic attack and stroke (9). Even though there are rare nonpathological right bundle branch block causes, in the acute care setting, if pacing rhythm is right bundle branch block, especially in a patient, whose previous rhythm is known to be left bundle branch block, lead malposition should be suspected (9, 10). A chest X-ray shows the lead position.
Leads can be dislodged from the endocardial interface, mostly, days or months after implantation (11). In dual-chamber pacemakers, atrial leads get more frequently dislodged than the ventricular leads (11). Such dislodgement produces various rhythm problems due to malfunctions. Additionally, two lead dislodgement-related syndrome is defined below:
- Lead displacement dysrhythmia refers to when free-floating ventricular leads cause episodes of malignant arrhythmias (12). When a lead is dislodged from the endocardial interface, the patient’s pacemaker dependency determines the symptoms (11). While pacemaker-dependent patients experience episodes of bradycardia- and ventricular tachyarrhythmia-related symptoms, if the native rhythm is favorable, lead dislodgement may stay unknown until malignant arrhythmia episode. Additionally, hiccups may occur due to vagal pacing (11).
- Macrodislocation lead-dysfunctioning syndromes include Twiddler’s syndrome (coiling of the pacemaker leads due to rotation of the pacemaker generator on its long axis), Reel syndrome (coiling of the pacemaker leads around the pacemaker generator due to rotation of the pacemaker generator on its transverse axis) and Rachet syndrome (13). For further information, please check links 13 – 14.
The presence of leads in the venous system may cause thrombosis in axillary, subclavian, innominate, and upper arm veins or the superior vena cava up to varying degrees (4). Extensive collateralization masks symptoms. The most common symptoms include swelling and pain of the arm on the lead insertion side (5). However, pacemaker induced thrombosis may even lead to superior vena cava syndrome (5). Standard diagnostic and therapeutic measures apply.
Pacemaker and leads implantation may cause many mechanical complications, including tricuspid regurgitation, pneumothorax, hemothorax, air embolism, pericarditis, cardiac tamponade, and perforation (1, 7). All entities have distinct clinical courses and treatments. However, acute care providers should keep in mind all these differential diagnoses when a patient with a pacemaker presents with chest pain and shortness of breath.
It refers to when a patient’s symptoms progressively worsen after pacemaker implantation due to loss of AV synchrony and subsequent reduced cardiac output (15). These symptoms include fatigue, exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea, orthostatic hypotension, presyncope, and syncope (16). The syndrome is more frequent in patients with single-chamber ventricular pacing systems; however, it also occurs in patients with dual-chamber systems. If the patient has a single-chamber device, the treatment is upgrading the pacemaker to a dual-chamber system. If the patient has a dual-chamber device, the pacemaker programming should be adjusted (17).
References and Further Reading
- Cabrera, D., & Decker, W.W. (2013). Management of Emergencies Related to Implanted Cardiac Devices. In: J.G. Adams, E.D. Barton, J.L. Collings, P.M.C. DeBlieux, M.A. Gisondi, E.S. Nadel (Eds.), Emergency Medicine: Clinical Essentials (2nd ed., pp. 547-557). Philadelphia: Elsevier.
- Birnie, D., Williams, K., Guo, A., Mielniczuk, L., Davis, D., Lemery, R., … & Tang, A. (2006). Reasons for escalating pacemaker implants. The American journal of cardiology, 98(1), 93-97.
- Beyerbach, D. M. (2019). Pacemakers and Implantable Cardioverter-Defibrillators. Retrieved October 20, 2019 from https://emedicine.medscape.com/article/162245-overview.
- Niemann, J. T. & Squire, B. Implantable cardiac devices. (2014). In: J. A. Marx, R. S. Hockberger, R. M. Walls (Eds.), Rosen’s emergency medicine: Concepts and clinical practice (8th ed., pp. 1064-1074). Philadelphia: Elsevier.
- McMullan, J., Valento, M., Attari, M., & Venkat, A. (2007). Care of the pacemaker/implantable cardioverter defibrillator patient in the ED. The American Journal of Emergency Medicine, 25(7), 812-822.
- Trohman, R. G., Kim, M. H., & Pinski, S. L. (2004). Cardiac pacing: the state of the art. The Lancet, 364(9446), 1701-1719.
- Mulpuru, S. K., Madhavan, M., McLeod, C. J., Cha, Y. M., & Friedman, P. A. (2017). Cardiac pacemakers: function, troubleshooting, and management: part 1 of a 2-part series. Journal of the American College of Cardiology, 69(2), 189-210.
- Aguilera, A. L., Volokhina, Y. V., & Fisher, K. L. (2011). Radiography of cardiac conduction devices: a comprehensive review. Radiographics, 31(6), 1669-1682.
- Ohlow, M. A., Roos, M., Lauer, B., Von Korn, H., & Geller, J. C. (2015). Incidence, predictors, and outcome of inadvertent malposition of transvenous pacing or defibrillation lead in the left heart. Ep Europace, 18(7), 1049-1054.
- Erdogan, O., & Aksu, F. (2007). Right bundle branch block pattern during right ventricular permanent pacing: Is it safe or not?. Indian pacing and electrophysiology journal, 7(3), 187.
- Fuertes, B., Toquero, J., Arroyo-Espliguero, R., & Lozano, I. F. (2003). Pacemaker lead displacement: mechanisms and management. Indian pacing and electrophysiology journal, 3(4), 231.
- Burns, E. (2019). Pacemaker Malfunction. Retrieved October 20, 2019 from https://litfl.com/pacemaker-malfunction-ecg-library/
- Alvarez-Acosta, L., Garrido, R. R., Farrais-Villalba, M., & Afonso, J. H. (2014). Reel syndrome: a rare cause of pacemaker malfunction. British Medical Journal Case Reports, 2014, bcr2014204545.
- Munawar, M., Munawar, D. L., Basalamah, F., & Pambudi, J. (2011). Reel syndrome: A variant form of Twiddler’s syndrome. journal of arrhythmia, 27(4), 338-342.
- Prinzen, F. W., Vernooy, K., Lumens, J., Auricchio, A.(2017). Physiology of Cardiac Pacing and Resynchronization. In: K. A. Ellenbogen, B. L. Wilkoff, G. N. Kay, C. Lau, A. Auricchio. (Eds.), Clinical Cardiac Pacing, Defibrillation and Resynchronization Therapy (5th Ed., pp. 213-248). Philadelphia: Elsevier.
- Gillis, A. M. (2017). Pacing for Sinus Node Disease. In: K. A. Ellenbogen, B. L. Wilkoff, G. N. Kay, C. Lau, A. Auricchio. (Eds.), Clinical Cardiac Pacing, Defibrillation and Resynchronization Therapy (5th Ed., pp. 375-398). Philadelphia: Elsevier.
- Stephenson, E. A. & Davis, A. M. (2009). Electrophysiology, Pacing, and Devices. In: R. H. Anderson, E. J. Baker, D. Penny, A. N. Redington, M. L. Rigby, G. Wernovsky (Eds.), Paediatric Cardiology (3rd Ed., pp. 379-413). Philadelphia: Churchill Livingstone.