Pacemaker and AICD management in the Emergency Department

Authors: Elizabeth Hall, MD (EM Resident Physician, New York Methodist Hospital) and Hilary Fairbrother, MD/MPH (Assistant Professor of EM / Attending Physician, NYU / Bellevue) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit, EM Resident Physician at SAUSHEC, USAF)


With the aging population and advances in the technological treatment of dysrhythmias and heart failure, a vast number of people are receiving automated implantable cardiac devices (AICDs). In the United States, an estimated 370,000 people receive AICDs annually, and this number is anticipated to grow significantly (1). AICDs come in various models from standard single chamber pacemakers, biventricular pacemakers, to implantable cardioverter defibrillators (ICDs). As emergency physicians, it is essential to have a sophisticated understanding of the various devices and associated malfunctions in order to effectively care for these patients.


At a basic level, a pacemaker is comprised of a generator (including hardware and battery) and the leads. A pulse is created by the generator, it travels down the leads, and then depolarizes the surrounding myocardium. Atrial leads are usually placed in the right atrial appendage, whereas right ventricular leads can be placed in the right ventricular apex, right ventricular outflow tract, or inter-ventricular septum (2). Left ventricular leads travel through the coronary sinus and lay on the posterior or lateral walls of the left ventricle.

Pacemakers typically function to pace the heart, while AICDs  are able to perform cardioversion, defibrillation, and pacing.

The pacemaker code system is comprised of 5 letters to identify the type and function of the pacemaker. The first three letters are the most important: the first letter indicates the lead location; the second determines the chamber(s) being sensed; and third identifies the response of the pacemaker to a sensed pulse. The codes for the first two letters include (A) atrium, (V) ventricle, (D) both chambers, and (O) none. The third letter codes include (T) triggered, (I) inhibited, (D) triggered and inhibited, and (O) none. For example, a common pacer encountered in the emergency department is a DDD, meaning both chambers are being paced, sensed, and will respond to sensing. The 4th letter represents the pacers ability for rate modulation and ability to connect with external telemetry. Lastly, the 5th letter, added in 2002, indicates that multi-site pacing is present in each chamber (2). Many patients will have their device manufacturer card with them; however, if identification is an issue, an over-penetrated chest x-ray can provide the desired information.

Indications for cardiac devices are provided by the American Heart Association with their most recent update in 2013 (3). Sinus node dysfunction is the most frequent etiology for pacemaker placement; however, cardiac resynchronization therapy (CRT) as a therapy for heart failure is becoming increasingly prevalent. Research has demonstrated that CRT, which involves pacing of both right and left ventricles, ultimately improves morbidity and mortality outcomes for those with NYHA Class II, III, and IV heart failure (4,5). Other indications include acquired atrioventricular block, chronic bifascicular or trifascicular block, and syndromes associated with sudden cardiac death, such as Brugada syndrome, hypertrophic cardiomyopathy, WPW, and prolonged QT syndromes (6).


Immediate goals in evaluating patients in the emergency department should include identification of the type of pacemaker, review the indication for placement, and date of implantation and revisions. This information will be necessary to perform device interrogation. Additionally, the patient should be asked about symptoms associated with device failure, such as light-headedness, palpitations, syncope, racing heart, extra-cardiac muscular twitching, and shocks delivered. A thorough history should include a list of current medications, with specific attention to those that can cause electrolyte disturbances, especially hyperkalemia, or change pacer-sensing thresholds. If implantation was recent, physical exam should focus on erythema, edema, or tenderness surrounding the site as infection or hematoma is a possible complication. A 12-lead EKG, chest X-ray, and laboratory tests to identify possible electrolyte abnormalities are usually indicated in the evaluation of patients with cardiac-related symptoms.

Early Complications

Early complications that present in the first 6 weeks post-implantation generally relate to the surgical procedure itself, venous access, lead positioning, or lead displacement (7). Immediate post- surgical complications include pneumohemothorax, bleeding, venous thrombosis, air embolism, and hematoma. Any apparent dyspnea in patients who underwent recent AICD implantation should receive a chest x-ray to assess for hemothorax and pneumothorax. Venous thrombosis typically presents with pain and swelling of the ipsilateral extremities and is more frequently found in the subclavian or brachiocephalic veins. If edema is noted to the face, neck, and upper trunk, superior vena cava syndrome should be considered. Doppler ultrasound, CT, or venogram can be used to make the diagnosis and immediate anticoagulation should be initiated. Pocket hematoma is a common complication, as dissection of the fascial plane during pocket creation can lead to venous and arterial bleeding. This is especially prevalent in those anti-coagulated with clopidogrel or heparin. Most hematomas do not require treatment; however, if the surrounding area is large and tense, surgical evacuation and hemostasis may be required and can be indentified via ultrasound (2).

Infection is a possible complication as with all surgical procedures and is more frequent in patients who are immunocompromised (diabetes or cancer) or those on steroids or anticoagulation (7). Although most infections are isolated to the pocket itself, it can progress to septicemia requiring long-term intravenous antibiotics and eventual device removal. Lead infection is more worrisome as thrombus or vegetation can form from typical skin flora (Staphylococcus aureus and Staphylococcus epidermidis). Cardiac device infective endocarditis (CDIE), although quite serious, is relatively rare with an occurrence rate of 0.4% (8). Echocardiogram, transesophageal ultrasound, and blood cultures will generally be involved in establishing this diagnosis with a prolonged antibiotic course and likely device removal.

Lead displacement occurs in 2.4% of implantations and usually occurs in the first 4-6 weeks after implantation (7). Suspicion should be raised if patients present with recurrence of bradycardia and associated symptoms such as weakness and fatigue. Under-sensing or failure to capture secondary to lead displacement can be detected on EKG and device interrogation. On EKG, changes in axis deviation or a change from a LBBB to a RBBB pattern are suggestive of lead dislodgment. Lead migration near the diaphragm or phrenic nerve can result in diaphragmatic twitching or chronic singultus (hiccups). Echocardiogram confirms the diagnosis of lead displacement and may result in the need for temporary transcutaneous or transvenous pacing in the ED with eventual permanent lead replacement. A rare but serious device implantation complication is cardiac perforation resulting in pericardial effusion, cardiac tamponade, and hemodynamic instability (9). Once again, an echocardiogram will establish this diagnosis.

Twiddler syndrome is a patient induced form of lead dislodgment caused by compulsive manipulation of the pacemaker generator (9). The leads become coiled around the generator which can be diagnosed on chest x-ray. Treatment includes use of Woven Dacron pouches or sub-pectoral implantation that prevent device migration (9,10).

Late Complications

Late complications are relatively rare due to major improvements in device technology. The most frequent complication is battery malfunction (2). Overall, device malfunctions occur at a rate of 4.6 per 1000 pacemakers and 20.7 per 1000 ICDs (2). Patients may present with symptoms related to pacemaker failure such as palpitations, light-headedness, fatigue, or syncope.

A primary component in initial evaluation of those with pacemakers and ICDs is obtaining an EKG. Device failure evaluated from an EKG perspective can be divided into three main categories: failure to capture, failure to pace, and failure to sense.

Failure to capture is when a pacemaker sends an impulse without myocardial depolarization. If impulse delivery is provided while the myocardium is in a refractory state, depolarization will not occur. Additionally, failure to capture can be secondary to a pathological disturbance such as heart disease, electrolyte abnormalities, or medications.

Failure to pace, conversely, is when the pacemaker device does not provide a stimulus to the heart. Patients with this issue often present with heart rates below the lower limit designated by their device and the absence of pacemaker artifact on EKG (6). Pacemaker over-sensing is the most common cause of failure to pace. Lead fracture can be the result of blunt trauma, most often from sports-related injuries, falls, and motor vehicle accidents. Over-sensing can also be caused by device misinterpretation of myopotentials from the surrounding muscle near the heart such as the pectoralis, diaphragm, and rectus abdominis muscles. Additionally, retrograde P waves, T waves, or other post- depolarization electrical activity can be inappropriately sensed by pacemaker devices as a normal potential, thus inappropriately eliminating the need for the pacer to send an impulse.

Lastly, failure to sense is when the pacemaker does not recognize a myocardial depolarization wave after it travels up the lead wire. Devices are normally designed to have refractory periods following intrinsic depolarizations to prevent over-sensing. However, prolonged refractory periods or “blanking” may result in the failure of a pacer to sense a normal myocardial depolarization. Prolonged refractory periods can be secondary to changes in patient’s intrinsic EKG complex (i.e. a new bundle branch block), and thus cause functional undersensing. A pathologic etiology for failure to sense is most commonly due to lead fracture or insulation defects.

Other causes of late complications include battery depletion, and therefore patients should be asked about date of device implantation and last battery change (11). One method to determine if the battery is low is to place a magnet over the generator. If the magnet rate is slower by more than 10% of the preset rate, then battery depletion is the likely source.

Pacemaker mediated tachycardia (PMT) is a re-entry arrhythmia in which the pacemaker itself becomes part of the circuit (6,12). It is generally initiated by a premature ventricular contraction; however, it can occur spontaneously and results in a rapid, wide complex tachycardia. The rate will not exceed the upper limit programed on the device but may nonetheless result in uncomfortable symptoms for patients. Placement of a magnet over the pacemaker will interrupt sensing, breaking the circuit and tachycardia. When this occurs, the pacemaker will perform at its pre-set rate. As part of the evaluation with PMT, device interrogation will be essential in order to determine if programming adjustments should be made.

Patients with ICDs who receive a single shock without the presence of cardiac-related symptoms do not need immediate electrophysiology referral. These patients can be observed in the ED and referred within the week. However, if patients received multiple shocks or have cardiac-like symptoms such as dyspnea, chest pain, or weakness, a more thorough workup should be initiated to search for underlying etiologies. The patient should be placed on a cardiac monitor in the ED until the device can be interrogated. Three or more appropriate shocks in a 24 hour period is termed an “electrical storm,” and patients should be evaluated for electrolyte abnormalities, acute coronary syndrome, and medication side effects. (2,12). Electrical storm can be treated with anti-arrhythmics such as amiodarone, beta-blockers, and propofol and will require hospital admission.

Acute Myocardial Infarction

Electrocardiograms (EKGs) with a left bundle branch block (LBBB) pattern, typical for most paced rhythms, make the diagnosis of acute myocardial infarction (AMI) challenging. The Sgarbossa criteria (sensitivity of 20% and specificity of 98%) or modified Sgarbossa criteria (sensitivity of 90% and specificity of 90%) can be applied to identify AMI in those with AICDs (13,14).

The original criteria are:

~ ST elevation ≥ 1 mm in a lead with upward (concordant) QRS complex = 5 points

~ ST depression ≥1 mm in lead V1, V2, or V3 = 3 points

~ ST elevation ≥5 mm in a lead with downward (discordant) QRS complex = 2 points

Modified Sgarbossa criteria is applied to the 3rd rule and states that ST discordance of the QRS complex in leads V1-V4 as noted by a ST/S ratio of ≥0.25 and at least 2 mm of ST elevation is significant (15).

Causes of Pacemaker malfunction Evaluation Treatment
Battery Depletion  EKG, Device interrogation Battery replacement
Medications/Electrolyte Abnormality HPI, EKG, electrolytes Correct electrolyte abnormality or medication adjustment
Lead fracture/dislodgement CXR, EKG or device interrogation Repositioning or replacement
Pocket Hematoma Physical Exam Reassurance or surgical evacuation
Pocket Infection Physical Exam, CBC Antibiotics; if severe possible temporary removal
Venous Thrombosis Ultrasound/venography Anticoagulation or surgery
Pneumothorax/hemothorax CXR/ultrasound Conservative or chest tube
Endocarditis Echo, TEE, blood cultures Antibiotics; possible replacement

Table 1. Evaluation and treatment of various pacemaker malfunction etiologies.


In patients with pacemakers or ICDs who are hemodynamically unstable, the immediate priority is to restore their hemodynamic status. In device failure, patients may need to be transcutaneously paced, especially those patients who revert back to 3rd degree AV block or Mobitz type II block. Alternatively, atropine can be effective in patients with bradycardia. In those with arrhythmias or those with pacemaker-mediated tachycardia, placing a magnet over the device will immediately terminate these rhythms, and patients will have heart rates as determined by the device’s reset rate. Cardioversion and defibrillation can be performed as needed and pacer pads should be placed in the anterior-posterior orientation at least 8 cm away from the device (2). In those that are hemodynamically stable, a thorough work-up includes EKG, electrolytes, CXR, and device interrogation which should occur in the ED. Cardiology consultation will ultimately need to be arranged for most pacemaker malfunctions, with  likely hospital admission.

A Clinical Approach in the Evaluation of Patients with Possible Pacemaker Malfunction

AICD Workup

References / Further Reading:

  1. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics – 2014 update: a report from the American Heart Association. Circulation. 2014; 129 (3): e28-e292. (executive summary)
  2. Martindale J, deSouza IS, et al. Managing Pacemaker-Related Complications and Malfunctions in the Emergency Department. Emergency Medicine Practice. Sept. 2014; 16 (9).
  3. Epstein AE, DiMarco JP, Ellenbogen KA, et al. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for devise-based therapy of cardiac rhythm abnormalities: a report for the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013; 61 (3): e6-e75. (guidelines).
  4. Linde C, Abraham WT, Gold et al. Randomized trial of cardiac resynchronization in mildly symptomatic heart failure patients and in asymptomatic patients with left ventricular dysfunction and previous heart failure symptoms. J Am Coll Cardiol. 2008;52 (23): 1834-1843.
  5. Bristow MR, Saxon LA, Boehmer J, et al. Cardia-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med. 2004; 350 (21): 2140-2150.
  6. Ammirati F, Colivicchi F, Santini M, et al. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope: a multicenter, randomized, controlled trial. Circulation 2001; 104 (1): 52-57.
  7. Lam CW. Permanent cardiac pacemaker: an emergency perspective. Hong Kong Journal of Emergency Medicine. 2001; 8 (3): 168-175.
  8. Osmonov D, Ozcan KS, Erdinler I, et al. Cardiac device-related endocarditis: 31-years’ experience. J Cardiol. 2013; 61 (2): 175-180.
  9. Ellenbogen KA, Hellkamp AS, Wilkoff BL, et al. Complications arising after implantation of DDD pacemakers: the MOST experience. Am J Cardiol. 2003; 92 (6): 740-741.
  10. Newland GM, Janz TG. Pacemaker-twiddle’s syndrome: A rare cause of lead displacement and pacemaker malfunction. Ann Emerg Med, 1994; 23: 136-38.
  11. Brady WJ, Truwit JD. Critical Decisions in Emergency & Acute Care Electrocardiography.2009. Wiley Blackwell.
  12. Maisel WH, Moynahan M, Zuckerman BD, et al. Pacemaker and ICD generator malfunctions: analysis of Food and Drug Administrations annual reports. JAMA. 2006; 295 (16): 1901-1906
  13. Smith, SW, Dodd, KW, Henry TD, Dvorak, DM, Pearce LA (2012). Diagnosis of ST- Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block with the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Annals of Emergency Medicine. 60 (6): 766-776.
  14. Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, Califf RM, and Wagner GS. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med. 1996. Feb 22; 334(8) 481-7.
  15. Klimczak A, Wranicz JK, Cygankiewicz I, Chudzik M, Goch JH, and Baranoski R. Electrocardiographic diagnosis of acute coronary syndromes in patients with left bundle branch block or paced rhythm. Cardiol J 2007;14(2) 207-13.

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