Pacemakers… In a RUSH

Goal of This Blog

Pacemakers are becoming increasingly common as our population ages, and are seen more and more in the emergency department. The goal of this post is to summarize common pacemaker settings, the 5-letter nomenclature of pacemakers, indications for pacemaker placement, pacemaker components, common pacemaker complications (majority of blog), and lastly the management of pacemakers in the ED (including applying a magnet).  …And as always, the blog ends with some medical history

Background

  • Modern pacemakers essentially have two functions:  1) To sense and 2) To pace.
  • Sensing:  pacemakers can either sense the atria or ventricle (or both) for intrinsic cardiac function.
  • Pacing:  If the pacemaker does not sense an adequate atrial or ventricular depolarization for a selected time interval, then the pacemaker will “fire”, thus, providing the needed electrical stimulus to cause cardiac depolarization
    • If the pacemaker does sense an adequate atrial or ventricular depolarization, then it will allow the intrinsic heart to function without interruption (in short, the pacemaker will inhibit itself)

Common Pacemaker Settings and Default Settings

Pacemakers can come in a variety of types and settings (think of all the 3 letter combinations you could make below). Luckily, however, most modern pacemakers come in two main settings (VVI and DDD)
VVI
  • VVI implies that the ventricle is being paced and sensed. Furthermore, the pacemaker will inhibit itself in response to intrinsic ventricular depolarization
  • VVI is more commonly used in elderly/inactive patients
  • A CXR that shows only a single lead in the right ventricle often implies VVI mode. (However, it can also be seen in multiple lead pacemakers as well)
  • If the pacemaker is firing, the EKG will show a pacer spike prior to the QRS complex which will result in the appearance of a LBBB (formation of RBBB signifies lead displacement)
  • It is also possible to see the appearance of “fusion beats” which occur when intrinsic ventricular depolarization begins at the same time as the pacemaker discharge. This is often seen in intermittent heart block, when the pacemaker is intermittently firing.
    Fusion Beats
    Each beat is preceded by a pacer spike. The complexes marked “P” have normal paced LBBB morphology. The complexes marked “F” have varying QRS morphology as the intrinsic and paced ventricular depolarization occur together

DDD

  • I think this description of DDD from Canadiem.org explains it the best: “[DDD] is the wonderkid of pacemakers. It can pace and sense both the atria and ventricle. So if you have a normal P and QRS it just sits back and relaxes. If your P is normal but your QRS is lazy it will kick in to pace the ventricle. If your P is slow but always followed by a normal QRS it will pace the atria but not the ventricle. Finally, if both the atria and ventricle are slow it will pace them both consecutively.”
  • CXR will show an atrial lead and a ventricular lead
  • The EKG may have a variable appearance depending on the intrinsic underlying cardiac function as noted above. For instance:
    • The EKG can appear “normal”—atria and ventricles are depolarizing on their own
    • There can be an atrial pacer spike with a normal narrow QRS that follows as seen in sick sinus syndrome (implies abnormal SA node with intact AV circuitry)
      DDD pacing in sick sinus syndrome
      Atrial Pacer Spike Followed By Normal Narrow Intrinsic QRS Complex
    • There can be normal intrinsic P Waves with a paced wide QRS as seen in complete heart block (implies normal SA node but abnormal AV circuitry)
      Intrinsic P wave followed by paced QRS wave
      Normal Intrinsic P Wave Followed By Paced QRS Complex
    • Or there can be dual pacing of the atria and ventricle with corresponding pacer spikes to each
      Atrial and Ventricle Pacer Spikes
      Atria and Ventricle Pacer Spikes
    • Also of note, the above issues can be intermittent so an EKG can show complexes with intrinsic function as well as paced complexes
      Intermittent DDD Pacing
      1st Circle: Atrial paced – 2nd Circle: normal P and QRS – 3rd Circle: both atrial and ventricle Paced – 4th Circle: normal intrinsic P with paced QRS

VOO/DOO

  • The vast major of pacemakers are set to VVI or DDD. If a magnet is applied, it will revert the pacemaker to its default settings. VVI typically becomes VOO, while DDD becomes DOO.
  • These are called Fixed-Rate Settings
  • VOO:  results in a paced ventricular depolarization at a constant rate (often near 70 bpm) regardless of the patient’s own heart rate or rhythm. Therefore, it will compete with the intrinsic function of the heart. Due to this, fusion beats are not uncommon. Also, if pacer spikes occur during the refractory period, then it will not produce a QRS
    • There is a small risk that the pacer spike can fall during the “Vulnerable period” resulting in Ventricular Fibrillation
  • DOO:  same concept as VOO except it will pace an atrial as well as ventricular beat. Again it does so at a fixed-rate despite the patient’s own heart rate or rhythm.

Overview of 5 Letter Code System

Although the above settings are the most common, it is still important to have a basic understanding of the 5 letter code system so that we are prepared for any situation.
  • Letter 1:  chamber paced:  (A)—atria, (V)—ventricle, or (D)—both chambers
  • Letter 2:  chamber sensed:  (A)—atria, (V)—ventricle, or (D)—both chambers
  • Letter 3:  response to pacemaker sensing: (I)—inhibited, (D)—both chambers inhibited. (T)—triggered (however, no longer seen in modern pacemakers)
  • Letter 4:  refers to rate modulation. This indicates method pacemaker uses to modulate rate in response to physiologic demand (e.g. increasing heart rate during exercise, etc.)
  • Letter 5 (added in 2002):  indicates the presence of multi-site pacing in each chamber
Settings for Pacemaker
Source: RebelEM

Pacemaker EKG

  • The pacing spikes may be difficult to see in all leads. There are many reasons for this, but the type of pacemaker greatly affects this
    • Epicardially placed leads result in smaller pacing spikes than endocardially placed leads
    • Bipolar leads produce smaller pacer spikes than unipolar pacer spikes
  • Intrinsic QRS complexes are typically narrow while paced QRS complexes are wide with LBBB morphology.

Pacemaker Indications

  • Sinus node dysfunction (most common cause)
  • 3rd degree or advanced 2nd degree (Mobitz type II) AV Block
  • Symptomatic bradycardia
  • Atrial fibrillation with slow ventricular response

Components of the Pacemaker 

  • Pulse Generator (lithium battery)
  • Electronic circuitry
  • Leads
    • Number of Leads
      • Single lead–endocardial lead positioned in contact with right ventricle
      • Dual Lead–endocardial lead positioned in contact with right atrium and right ventricle
    • Type of Lead
      • Unipolar Configuration:  not compatible with ICD systems and is prone to oversensing of depolarization. Since is of small diameter, less prone to fractures. Consists of negative electrode within the heart and positive electrode within the pulse generator. Due to the distance between the two electrodes, unipolar leads are relatively more prone to oversensing as “outside electrical impulses” can be mistaken for cardiac electrical impulses
        • Pacer spikes are larger  (>20 mm in amplitude on EKG) due to distance between electrodes
      • Bipolar Configuration:  compatible with ICD systems but are larger and relatively more prone to lead fractures. Oversensing is rarely a problem (as the electrodes are closer together so that outside potentials do not get confused as depolarizations). Consists of positive (proximal) electrodes separated by 1 cm negative (distal) electrode both located within the heart.
        • Pacer spikes are smaller (<5 mm amplitude on EKG)

Common Pacemaker Complications

Background of Pacemaker Complications

—  The vast majority of pacemaker complications occur soon after its placement, often within weeks to months. Most often these issues are discovered on routine postoperative pacemaker interrogations.
—  Furthermore, the symptoms that suggest pacemaker malfunctions are often similar to the symptoms that prompted the placement of the pacemaker in the first place (e.g. syncope, pre-syncope, orthostatic hypotension, lightheadedness, dyspnea, or palpitations)
—  There are several ways to divide pacemaker problems, and they differ within resources. Below is a combination of a few of the methods, and I think it helps organize the differential. They are discussed in more detail in a corresponding order as below

1. Pacemaker Box Complications
2. Rate is Too Fast
3. Rate is Too Slow
4. Uncommon problems (But Fun to Talk About)
5. STEMI in paced rhythms
 

1. Pacemaker Box Complications

These are issues that occur relatively soon after placement of a pacemaker including infection, hematoma, thrombophlebitis, and pacemaker syndrome
Infection
  • Pocket Infection (2%)
  • Bacteremia (1%)
    • 20-25% of pts have positive blood cultures. Staph aureus and Staph epidermidis are identified in ~60-70% of cases
  • Endocarditis as a complication of the above should also be considered as infections like to spread contiguously
  • Tx:
    • Vancomycin until culture results
    • Often requires replacement of pacemaker system after appropriate control of infection via antibiotics
Hematoma 
  • May mimic presentation of wound or pocket infection
  • Tx:  Needle aspiration of the pocket. This should be done under fluoroscopy by cardiothoracic team to minimize risk of damaging the pulse generator
Thrombophlebitis
  • Presents as pain, swelling, venous engorgement of the ipsilateral arm (most commonly left). Pain in the ipsilateral arm should prompt the consideration of thrombophlebitis. The incidence of venous obstruction seen on imaging ranges from 30-50%. However, due to the creation of collateral vessels, only ~0.5-3.5% of pts develop above symptoms
  • Tx:  anticoagulation

Pacemaker Syndrome

  • This occurs from the loss of AV synchrony and the presence of ventriculoatrial conduction. This is most commonly seen in VVI pacing with intact sinus node function, which results in the atria contracting against a closed tricuspid and mitral valve. This “contractile asynchrony” results in backloading of atrial contents and loss of atrial “kick”
  • This results in symptoms similar to CHF:  syncope/presyncope, orthostatic hypotension, exercise intolerance, generalized weakness, palpitations, chest fullness, uncomfortable pulsations in the neck or abdomen, cough, RUQ pain (hepatic congestion).
  • Pt may present shortly after pacemaker placement complaining that initial symptoms that prompted pacemaker are now worse
  • Of note, this is a diagnosis of exclusion. Full work-up including pacemaker interrogation should be performed prior to making this diagnosis.
  • Tx:  ~20% of pts reports symptoms suggestive of pacemaker syndrome. In most instances, symptoms are mild and patients adapt to them. However, 6% of patients may experience severe symptoms. If symptoms are severe, pacemaker settings can be adjusted. If necessary, pacemaker can be replaced with a dual chamber pacemaker which creates better atria and ventricular synchrony as supplies both P and QRS depolarizations.

 2.  Is the Rate Too Fast

Tachycardia in the setting of a pacemaker can be normal physiology vs. atrial arrhythmias. However, it can also be from a “malfunctioning pacemaker,” which should be of consideration. Of note, this tachycardia will not exceed the upper heart rate limit set in the pacemaker settings.

Normal Response to Intrinsic Fast Heart Rate
  • The pacemaker should adapt to physiologic needs, therefore, normal causes of tachycardia (infection, hypovolemia, PE) should be considered.
Atrial Arrhythmias 
  • Atrial Flutter, Afib with RVR, SVT can cause tachycardia as the P waves will be sensed by the pacemaker leading to tachycardia

Pacemaker-Mediated Tachycardia (PMT)

  • This is a type of reentry tachycardia—ventricular depolarization (e.g. PVCs) conducts retrograde into the atria leading the atrial lead to detect activity as incoming P wave resulting in ventricular depolarization (“vicious cycle” develops). Note, that since the pacemaker has a set upper rate limit, the heart rate will not exceed this upper limit.
  • Tx:  block AV to stop reentry tachycardia (adenosine, BB, CCB). Can always apply magnet if unstable. Vagal maneuvers
    • It can also spontaneously self resolve
    • Most modern pacemakers have a feature that will help recognize this issue and self-terminate the loop. It is called the “PMT Function”–it works by prolonging the refractory interval between V and A
      Pacemaker-Mediated-Tachycardia-LITFL-765x436
      Pacemaker-Mediated Tachycardia

Sensor-Induced Tachycardia

  • Pacemaker is designed to respond to physiologic stress by increasing heart rate (i.e. during exercise, hypercapnia, tachypnea)
  • The pacemaker can react to stimuli not intended to increase heart rate (vibrations, electrocautery during surgery, intense muscle contractions) causing pacemaker to fire at higher rates. Again, this should not exceed the upper heart rate limit set by the pacemaker.
  • Tx:  apply a magnet or decrease upper limit of pacemaker

3.  Is the Rate Too Slow (aka Output Failure)

The pacemaker was placed to prevent bradycardia. If bradycardia is present, then this indicates the pacemaker is not functioning appropriately. This is commonly caused by failure to capture or failure to pace.
Failure to Capture Overview

Failure to capture can be divided into two broad categories. The first category is that the pacemaker is malfunctioning completely, and therefore, there will be no pacer spikes present at all. The second category is that the interface between the lead electrode and the endocardium has changed. This produces an EKG where the pacer spikes are present, however, they are not reaching the needed threshold to result in P or QRS depolarization.

Failure to Capture (Complete Malfunctioning with No Pacer Spikes)
  • No pacer spikes often implies a hardware problem (lead disconnection from pulse generator, lead fracture, battery depletion, or a severely displaced lead)
  • Of note, lead fractures are relatively uncommon nowadays due to the durability of the lead coating. If it does occur, it is often at predictable locations (e.g. site of attachment to pulse generator or at abrupt angulations).
  • Severe lead displacement can also result in lack of pacer spikes. It is discussed below as the lead is more commonly displaced only a few millimeters resulting in failure to capture. It can also result in intermittent capture and pacing if it is “floating” in the pulmonary vasculature as discussed below.
Failure to Capture (Pacer Spikes Present But No Resultant P/QRS depolarizations)
  • Exit Block
    • Exit Block typically results in presence of pacer spikes but no resultant P or QRS depolarization. This is caused from injury or process that affects the endocardium at site of pacer electrode.
    • Most often this is from an MI that causes injury at this electrode site causing scarring that prohibits conduction of the pacer spike
    • It can also be caused by systemic electrolyte abnormalities (e.g. hyperkalemia) that suppress endocardium reaction to the pacer spike
    • Rarely, it can be caused by drugs that suppress cardiac activity (e.g. Class III anti-arrhythmic drugs such as amiodarone)
  • Displaced Lead
    • This is the most common cause of failure to capture. It most often occurs within the first month of pacemaker insertion.
    • Micro-dislodgment:  describes small displacement of the lead that is too small to be seen on CXR. However, the small displacement reduces the lead’s contact with the endocardium resulting in an increased threshold for capture (results in presence of pacer spikes but no resultant P/QRS waves).
    • Macro-Dislogment:  describes larger displacement that can be seen on CXR. This can result in two possibilities
      • Most commonly this results in catheter tip “floating” in pulmonary outflow tract, which allows for intermittent contact with the endocardium. Therefore, will see the presence of intermittent paced complexes as well as loss of some pacer spikes. This leads to a dynamic and changing QRS morphology on EKG
      • If very severe dislodgment, then will see complete lack of pacer spikes as discussed above.
Failure to Pace

This occurs from inappropriate sensing (oversensing or undersensing).
Remember that oversensing=less pacing spikes. Undersensing=more pacing spikes

  • Undersensing
    • Undersensing occurs when the pacemaker fails to detect spontaneous intrinsic depolarizations. This results in asynchronous pacing. Atrial or ventricular pacing spikes arise regardless of P waves or QRS complex

      Undersensing
      Pacer spikes occur at fixed rate as pacemaker is not appropriately sensing P and QRS waves.
    • As you can see, the pacemaker is not appropriately sensing the underlying rhythm, therefore, it is firing in attempt to pace the strip. However, since the pacer spikes are occurring during refractory period, it is not resulting in a paced complex
      • Pacer spikes within QRS and T waves are indicative of undersensing
    • Undersensing can be complete or intermittent so it is possible to see some paced complexes depending on when the pacer spike appears in the EKG rhythm
    • Undersensing can result from a change in pacemaker settings (e.g. the sensitivity threshold is increased so that a larger amplitude is needed to result in sensing by the pacemaker)
    • More commonly it results from right ventricular infarction or progressive fibrosis that accompanies several of the cardiomyopathies—these changes in the endocardium result in a decrease in the intracardiac amplitude which may not be sensed by the pacemaker
      • Note that we also discussed these as causes of failure to capture. Damage to the endocardium can cause both a sensing and capturing issue, and it is possible for these to occur concurrently.
  •  Oversensing
    • These are events that cause the pacemaker to think the heart has intrinsic depolarizations when it really does not. Therefore, the pacemaker does not fire when it should.
    • This is rare. It is caused by the pacemaker detecting “electrical activity” that is non-cardiac in origin. This may lead to intermittent/irregular pacing or a complete absence of pacemaker function
    • Myopotentials from the pectoralis major can cause this.
    • More common in unipolar lead system
    • Can also be caused by Large T waves that are confused for QRS complexes

4.  Uncommon Problems But Fun to Talk About

Runaway Pacemaker
  • More of a historical footnote that occurred in older generation pacemakers resulting from low battery voltage
  • Pacemaker delivers runs of pacing spikes in excess of 2000 bpm. On EKG, it looks similar to VFib
runaway pacemaker
Runaway Pacemaker
Twiddler’s Syndrome
  • Dysfunction of pacemaker resulting from patient manipulation of the pulse generator (accidentally or purposely). Can result in diaphragmatic or brachial plexus pacing (e.g. arm twitching)
  • This is a specific form of displaced lead
Battery Depletion
  • Although discussed as an etiology above. This should be relatively rare with the newer lithium batteries as they are not prone to sudden power failure. Instead, they should have issues with gradual battery depletion which should cause a low battery alarm over months to years before complete depletion.

 5.  STEMI in Paced Rhythm 

Although not specifically a pacemaker malfunction, identifying STEMI in pacemakers can be difficult
Sgarbossa Criteria Utility in Pacemakers
  • Sgarbossa criteria was initially developed from the GUSTO-1 trial. Less than 0.1% of these patients had a ventricular paced rhythm.
  • The best evidence I could find was a retrospective study in 2010 that examined 57 patients (not a great sample size) with ventricular paced rhythms who were formally diagnosed with MI
    • Essentially, it did not find great utility in using the Sgarbossa criteria.
    • It did find
      • discordant STE >5 mm to be the most useful criteria (specificity 99%, sensitivity 10%)
      • No pts had concordant STE >1 mm
      • STD >1 mm in leads V1-V3 (specificity 81%, sensitivity 19%)
  • Takeaway:  Sgarbossa’s criteria may be able to point you towards MI, however, it by no means rules it out. Therefore, if you are worried for MI based on history and/or have an EKG that is dynamic or changed from previous EKGs (pacemaker patients should have several), then it is likely a good idea to involve cardiology early

Pacemaker Management In The Emergency Department

Labs and Imaging

  • Luckily, the work-up for pacemaker related symptoms is the same for any patient with palpitations, chest pain, or SOB (CBC, BMP, +/- Magnesium, CXR, troponin, EKG). However, it should also always include pacemaker interrogation as well.
  • CXR
    • requires AP and lateral views to determine correct location of pacer wires
    • Although there are algorithms to determine correct position based on these views alone, it is much easier to compare to lead placement on previous CXRs
    • Requires over penetration of CXR if want to see model of pacemaker
Applying a Magnet
  • Magnet is useful in any unstable tachycardic patients with pacemaker
  • Magnet causes closure of a “reed switch” within the pacemaker circuitry which converts the pacemaker to an asynchronous or fixed rate-rate pacing mode (VOO or DOO depending on the type of pacemaker discussed above).
    • VOO:  ventricle is paced.
    • DOO:  both the atria and ventricle are paced.
    • Once the magnet is removed, the reed switch will revert back causing the pacemaker to resume its regular programmed settings. If PMT, then should stop the tachycardia as magnet eliminates the reentry tachycardia.
  • Note that if there is a co-associated ICD, the magnet will also deactivate the ICD, as long as the magnet is in place
Performing CPR
  • No changes
Applying Pacer Pads
  • Apply pacer pads in anterior-posterior orientation, often at least 8 cm away from the device so that its circuitry is not augmented.
Post-Arrest
  • CXR should be performed post-arrest (as in all patients). Although rare, special consideration should be taken to note if the pacing leads were displaced during chest compression.
  • Immediate return of pacing (capture) may not occur after resuscitation and/or defibrillation–this is a result of global ischemia and increased pacing threshold (Exit Block), and often not an indication of pacemaker malfunction. This may require temporary transcutaneous pacing if capture or pacing cannot be resumed.

Main Takeaways

  • Know the settings of VVI and DDD as these are the most common
  • Pts often carry a pacemaker card which should list the reason the pacemaker was placed as well as the pacer settings
  • The vast majority of pacemaker complications occur within the first few weeks or months of pacemaker implantation
  • Pacemaker complications/malfunctions can fall into several categories including
    • Pacemaker Box Complications (infection, hematoma, thrombophlebitis, pacemaker syndrome)
    • Rate is Too Fast (Normal response, Atrial Arrhythmias, Pacemaker-Mediated Tachycardia, Sensor-Induced Tachycardia)
    • Rate is Too Slow (failure to capture, failure to pace)
    • Uncommon problems (Twiddler’s syndrome, Runaway Pacemaker, Battery Depletion)
    • STEMI in paced rhythm:  Sgarbossa can point you in the right direction; however, does not rule out. A changed or dynamic EKG in the right history is concerning.

History of Implanted Pacemakers

The first implanted pacemaker surgery was performed in Sweden in 1958. The idea of an implanted pacemaker was developed by a surgeon name Ake Senning and a physician inventor named Rune Elmqvist. The patient was a 43-year old engineer named Arne Larsson (pictured below) who suffered from complete heart block as well as Stokes-Adams attacks that required multiple resuscitations per day. His wife learned of the experimental work of Senning and Elmqvist through press reports, and pleaded with the physicians to perform this operation on her husband despite the lack of adequate testing. Senning was later quoted as saying, “In the 1950s we did not have any liability problems. The patients and relatives were happy if the patient survived.”
Arne Larson.jpg
Arne Larson

As most good stories go, the operation was a success with adequate pacing of his heart. This success was short-lived, however, as the patient had to be taken back to the OR to replace the circuitry as it quickly malfunctioned a few hours after the initial operation. This set up the patient, Arne Larsson, for a common phenomenon throughout his life as he required re-implantation of a total of 5 lead systems and 22 pulse generators during his lifetime

In 1969, the first lithium battery implantable pacemaker was produced, which led to the more modern era of pacemakers. It also meant that Arne Larson did not require as many pacemaker revisions as before.

Interestingly, the patient, Arne Larsson, out survived both scientists living to the ripe age of 86 yoa, passing in 2001 from unrelated melanoma. The scientists, Ake Senning and Rune Elmqvist, lived long lives as well passing at age 84 in 2000 and age 90 in 1996, respectively.

Bonus Pacemaker History–How did we find out that we could externally pace the heart? It’s crazy.

In 1882, a 46-year-old female, named Catharina Serafin, from Upper Silesia in Prussia developed a thoracic mass. She visited a surgeon by the name of Hugo Von Ziemssen who excised the mass as well as the left anterior chest wall, thus, exposing her heart which could be seen under a thin layer of skin. Von Ziemssen (I’m assuming out of pure curiosity) applied external electrical current to this area, and noted that he could change her heart rate at will via the electrical current. Ever the scientist, he documented his findings via 1882-based Instagram techniques (seen below). This was the first demonstration that we could externally pace the heart.
Thoracic Wall PatientPatient's Paced Rhythm.jpg
                      Catharina Serafin Along Side The First Paced Rhythm

Resources

  1. RebelEM (Link)
  2. CanadiEM (Link 1Link 2)
  3. LITFL (Link 1Link 2)
  4. Aquilina O. A brief history of cardiac pacing. Images in Paediatric Cardiology. 2006;8(2):17-81. (Link)
  5. Rosen’s (Marx, J. A., & Rosen, P. (2014). Rosen’s emergency medicine: Concepts and clinical practice (8th ed.). Philadelphia, PA: Elsevier/Saunders.)

Leave a Reply