67. Pacemakers – Managing and Troubleshooting- Clinical Scenarios

Jessica G.Y. Luc, MD, Christopher C. Cheung, MD, Jamil Bashir, MD

Concept

• Overview of the cardiac conduction system
• Epicardial pacing
• Transvenous pacing
• Transcutaneous pacing
• Pacing modes
• Pacemaker troubleshooting
• Potential questions / scenarios

Cardiac Conduction System

Normal cardiac activity originates at the sinoatrial (SA) node, located in the superior right atrium and near the junction with the superior vena cava. Cells in the SA node has intrinsic automaticity to generate a spontaneous action potential, resulting in a cyclical depolarization and repolarization and forming the basis of intrinsic cardiac electrical activity. Following depolarization, the electrical impulse spreads across both atria, arriving at the atrioventricular (AV) node. The AV node, located within the triangle of Koch (delineated by coronary sinus, tendon of Todaro, and tricuspid valve septal leaflet), serves as an important “gatekeeper” regulating depolarization of the ventricle. Following depolarization of the AV node, the electrical impulse enters the His-Purkinje system to depolarize the ventricles. The His-Purkinje network branches into the left and right bundle branches, allowing for rapid synchronized conduction of the electrical impulse down to ventricular muscle.

Disease can occur at any point along the cardiac conduction system. Typically, pathology associated with the SA node can result in sinus node dysfunction or commonly termed “sick sinus syndrome,” leading to resulting sinus bradycardia or pauses. Pathology in atrial tissue can result in ectopic atrial beats (i.e. premature atrial complexes), atrial flutter and fibrillation. Prior instrumentation of the atrium may lead to scar formation, providing the substrate for re-entry for atrial flutter. Pathology at the level of the AV node can result in the non-conduction of atrial or sinus impulses to the His-Purkinje system, commonly resulting in progressive conduction block. Pathology in the infra-Hisian conduction system manifests as intraventricular conduction block, or right or left bundle branch block, frequently associated with cardiomyopathy and leading to dyssynchronous contraction of the ventricle. Disease in ventricular myocardium, frequently arising from progressive cardiomyopathies or infarction, can result in scar formation and re-entry circuits and forming the substrate for ventricular arrhythmias.

Options for Pacing/Pacemaker Implantation

A. Epicardial Pacing

Pacing Wire Insertion

Temporary epicardial pacing wires are often utilized to allow temporary pacing after cardiac surgery to treat temporary rhythm disturbances. Depending on surgeon preference, some prefer not to place pacing wires in patients with no evidence of bradycardia or heart block immediately after cardiopulmonary bypass to avoid bleeding complications. However, if a patient is bradycardic, has low cardiac output, heart block or has undergone valvular surgery, a minimum of ventricular wires should be considered. Epicardial wires are manufactured with a small needle on one end. This is used to embed the wire in the myocardium, after which the needle is cut off. Some wires are coiled to assist fixation; others can be clipped or loosely sutured in place. A larger straight needle on the other end of the wire is used to penetrate the body wall, bringing the wire to the surface. The lead should be sufficiently well anchored in the myocardium to avoid premature dislodgement, while still allowing eventual removal by gentle traction.

Epicardial wires can be placed on the epicardium prior to closing the chest during open heart surgery. Atrial wires are placed on the right atrium typically away from the SA node.  Ventricular wires can be placed anywhere on the right ventricle.  Most surgeons seek out exposed muscle for best threshold and sensing and place them just under the epicardium. The wires should be tested intraoperatively to confirm capture and threshold while there is still an opportunity for repositioning. Both sets of wires are then brought out to the skin by passing them directly lateral to the xiphisternum, taking care to not traverse the plane of the sternum to avoid entrapment upon sternal closure, and are then sutured and secured in place.

Temporary Pacing Wire Removal

When the patient is no longer bradycardic or has evidence of conduction system disease, usually by postoperative day 3, temporary epicardial pacing wires can be removed. It is safest to be done during daytime hours in case of bleeding complications. Patients who are anticoagulated should have their INR<2.0 and heparin should be discontinued for three hours prior to pacing wire removal. Platelet counts should be above 100,000 and the patient should not hypertensive.  The patient should be in a recumbent position.

Vitals should be taken prior to wire removal. The wires are mobilized from the skin edge and with gentle traction, the wires can be pulled out smoothly one at a time. If resistance is encountered upon attempt to remove the wires, the wires can be pulled taut and cut flush to the skin. Following pacing wire removal, the patient should remain on telemetry, in bed in a recumbent position with vitals taken every 15 minutes to monitor for hypotension for 45 minutes. If hypotension or arrhythmias develop, one should retain a low index for suspicion of tamponade and appropriate measures taken.

B. Permanent Epicardial Pacemaker Leads

Permanent epicardial pacemaker leads can also be implanted in patients with an expected pacemaker requirement, such as those with known underlying conduction disease or a prior indication for permanent pacemaker. In addition, patients with severe cardiomyopathy requiring cardiac resynchronization pacing may also benefit from synchronized pacing of the left ventricle. In such cases, pacemaker leads can be implanted transvenously (in the coronary sinus) or through an epicardial approach. The ideal place for the left ventricular lead is basal, just anterior and inferior to the left atrial appendage where there is visible muscle between the obtuse marginal artery branches. Furthermore, permanent epicardial leads would be the desired option for patients with complicated vascular access (e.g. venous thrombosis, congenital anatomical variations, prosthetic tricuspid valve, prior failed transvenous pacing implantations) or active bloodstream infection in which the placement of transvenous leads may be contraindicated. Steroid eluting bipolar button leads have the best long-term outcomes.

C. Transvenous pacing

Most patients who require temporary or permanent pacing will receive transvenous pacing, either through the insertion of a temporary pacing wire or implantation of permanent pacemaker leads. Further, some Swan-Ganz catheters have a port for a pacing wire.  Risk factors for requiring permanent pacing after cardiac surgery include age, preoperative bundle branch block and conduction system disease, valvular surgery, prolonged cardiopulmonary bypass, transcatheter aortic valve implantation and suboptimal intraoperative myocardial protection.

Temporary transvenous pacing wires

Temporary transvenous pacing wires are typically inserted at the bedside in patients requiring urgent ventricular pacing due to bradycardia or ventricular pauses. The temporary pacing wires are typically advanced through a single lumen sheath in the internal jugular vein or femoral veins and directed towards the right ventricle. It is important to insert a sheath that is large enough to fit the pacing wire, but not too large as it will result in bleeding around the wire itself. Transvenous pacing wires can be both rigid tip (inserted under fluoroscopic guidance) or balloon-tip (fluoroscopic guidance not necessary).

When using the balloon-tip pacing wire, it is common to test the balloon prior to insertion. Once the balloon is deflated, it can be connected to the pacing box and the balloon tip advanced into the single-lumen sheath. Once the balloon tip is sufficiently within the body (past the end of the sheath, approximately 10 cm), the balloon can be re-inflated and locked. The catheter should be carefully advanced while observing cardiac telemetry for demonstration of ventricular capture. It is common to see pacing spikes on telemetry, but the absence of ventricular capture, demonstrate that the pacing wire is not in the correct position.

As the balloon is gradually advanced, ventricular capture will become evident on cardiac telemetry. At this point, the balloon can be deflated, and the ventricular capture threshold checked. Positioning of the temporary pacing wire should also be evaluated by chest radiography. Fluoroscopy can be used to facilitate any temporary pacemaker insertion if necessary.

Permanent transvenous pacemaker

Permanent transvenous pacemakers are the most common cardiac devices implanted in patients requiring long-term pacing support. Pacemaker leads are typically inserted in the cephalic vein using a cut-down approach which has literature proven lowest complication rate and best lead longevity, or in the axillary or subclavian veins through needle puncture and fluoroscopic guidance (Seldinger technique). Access can be performed on either the left or right side. Once the vein is cannulated, the pacemaker leads can be advanced (typically through a sheath in the case of the axillary or subclavian vein access) into the superior vena cava and into the heart.

Permanent pacemaker leads can be advanced and fixated into atrial and ventricular tissue, and into the coronary sinus for cardiac resynchronization devices. Permanent pacemaker leads typically use an active fixation mechanism with a screw-in tip.  Passive fixation leads are used less frequently than active fixation leads due to the greater ease of site selection, ease of extraction and position stability. Once in position, the pacemaker leads are tested to ensure appropriate capture thresholds, sensed atrial/ventricular amplitudes, and lead impedances. The pacemaker leads are then carefully sutured into place without dislodging or pulling back the pacemaker lead. Finally, the pacemaker leads are connected to the device and placed in the pocket and closed. Ensuring that the lead is very securely fixed at the exit site will prevent dislodgement.

Intra-operative and post-operative complications of permanent pacemaker implantation include:

1. Pneumothorax
2. Arterial injury
3. Acute pocket hematoma
4. Pericardial effusion
5. Tricuspid leaflet dysfunction/valve regurgitation associated with pacemaker lead
6. Venous thrombosis +/- superior vena cava syndrome
7. Cardiac implantable electronic device infection (can present with sepsis, endocarditis, pocket infection, lead erosion)

D. Transcutaneous pacing

Transcutaneous pacing is frequently considered in situations when patients are asystolic or significant bradycardic resulting in cardiac arrest. Transcutaneous pacing pads connected to the pacing/defibrillation system are applied to the patient, typically in the anterior/precordial and lateral/apical positions. The pacing rate and output is dialed into the pacing system. Transcutaneous pacing should be avoided in conscious patients, as transcutaneous stimulation can be associated with significant discomfort.

3. Pacing Modes

Pacing settings are classified using the Heart Rhythm Society / British Pacing and Electrophysiology Group Generic Code (the NBG Code) as follows:

I	II	III	IV	V
Chamber paced	Chamber sensed	Response to sensing	Rate modulation	Multisite pacing
O = none	O = none	O = none	O = none	O = none
A = atrium	A = atrium	T = triggered	R = rate modulation	A = atrium
V = ventricle	V = ventricle	I = inhibited		V = ventricle
D = dual (atrial and ventricular)	D = dual (atrial and ventricular)	D = dual (triggered and inhibited)		D = dual (atrial and ventricular)

Pacing modes:

I	II	III	Description	Indication
A	O	O	Asynchronous atrial pacing	Sinus bradycardia
A	A	I	Demand atrial pacing	Sinus bradycardia, junctional bradycardia
V	O	O	Asynchronous ventricular pacing	No ventricular rhythm, cautery
V	V	I	Demand ventricular pacing	Heart block
D	O	O	Asynchronous dual pacing	No ventricular rhythm, cautery
D	V	I	AV sequential, ventricular demand pacing	Suitable for most bradyarrhythmias
D	D	D	AV sequential, dual chamber demand	Heart block
D	D	DR	AV sequential, dual chamber demand with rate responsiveness	Combination sinus node dysfunction and heart block

Typical pacemaker settings:

Atrial and ventricular output	10-20mA
PR interval / AV delay	150 ms (20-300 ms) or ‘auto’, determined by rate
Lower rate limit (‘rate’)	40 (backup); 60-100 (pacing)
Atrial overdrive stimulation	Up to 500 ppm
Atrial sensitivity	0.5 mV (0.4-1.2mV)
Ventricular sensitivity	2.5 mV (0.8-5mV)
Post-ventricular atrial refractory period	250 ms or ‘auto’, determined by rate

Figure 1: Simplified decision tree approach to setting the pacing mode

Pacing Definitions

1. Sensitivity = minimum amplitude that the pacemaker is able to sense. A lower number corresponds to a greater sensitivity. For example, if the pacemaker senses or “sees” an electrical impulse of 5 mV, but the sensitivity is set at 6 mV, it will not “detect” the impulse. The sensitivity will need to be lowered to detect the electrical impulse.
   • To check sensitivity in temporary epicardial or transvenous pacing boxes:
     1. Set pacemaker rate below the patients’ native rate
     2. Place in VVI, AAI or DDD modes (i.e. intrinsic cardiac activity should inhibit the pacemaker)
     3. Slowly increase sensitivity threshold until the sense indicator stops flashing
     4. Check that pacing is occurring asynchronously in the chamber being tested
2. Pacing threshold = minimum output required for pacing capture. A higher number corresponds to a higher capture threshold. For example, if the pacemaker paces with an output of 1 mA but is unable to capture the ventricle, the pacing threshold is higher than 1 mA, and the pacing output will need to be increased until ventricular capture is demonstrated.
   • To check pacing threshold in temporary epicardial or transvenous pacing boxes:
     1. Gradually decrease the output until there is no longer pacing capture. Before doing so, ensure that the patient is not dependent.
     2. Following loss of capture (simultaneously evident on cardiac telemetry), increase the pacing output back to the capture threshold. Typically, the pacing output is set at approximately 2-5 times the capture threshold to ensure reliable capture.

The above steps can be performed with pacing boxes connected to temporary epicardial and transvenous pacing wires. Evaluating sensitivity and capture threshold in permanent pacemakers requires the use of a programmer.

Pacemaker Troubleshooting

For all issues with pacing, one should see and assess the patient to ensure hemodynamic stability. A systematic approach is essential and can include the following:

1. Review rhythm strip and 12 lead ECG
2. Check integrity of circuit (start at patient -> pacing box): lead placement, polarity, integrity, tightly connected to correct port of pacing box (atrial/ventricular), battery, settings
3. Check mode
4. Check rate
5. Check capture threshold (find threshold and double it for safety)
6. Check sensitivity (normal = 2-5mV) – changes with position
7. Fixes: change patient position, reverse bipolar pacing leads, convert to unipolar pacing, replace pacing equipment, try high-output pacer or return to operating room for reinsertion of epicardial wires or transvenous pacemaker implantation
8. Back up plan in emergency: transcutaneous or transvenous pacing, atropine, adrenaline, isoprenaline, ephedrine, correction of electrolytes or underlying metabolic issues such as severe acidosis

Common Issues with Pacing/Pacemakers

The following is a summary of common issues and potential complications that may arise with the use of temporary epicardial pacing wires:

A. Failure to pace

Failure to pace occurs when there is no electrical output at the pacing wire tip when the pacing mode set requires output. Failure to pace is distinguished from failure to capture by the absence of pacing spikes in ECG at a heart rate less than the minimum heart rate set on the pacemaker.

Differential: (from easiest to hardest to fix)

• Pacing output may be too low -> correct by turning up the pacing output
• Leads or contacts faulty -> check all connections yourself, swap pacing wires between ports, change pacing cable
• Box battery may be low -> check box battery and if necessary, change batteries
• Pacing wires not in contact with myocardium
• Pacing wires short-circuiting

Treatment if patient hemodynamically unstable:

• External pacing pads
• Insert transvenous pacing wires

B. Failure to capture

Failure to capture is when there is electrical output at the pacemaker wire tips, as confirmed by visible pacing spikes on ECG, which fail to cause a depolarization and cardiac contraction. Failure of cardiac contraction can be confirmed by an absent cardiac impulse on arterial pressure waveform or pulse oximeter waveform.

Differential

• Pacing output may be too low -> correct by turning up the pacing output
• Pacing wires have been dislodged or in contact with area of high threshold -> try to reposition or change pacing wires
  • Differential for increased threshold:
    1. Myocardial ischemia
    2. Electrolyte imbalance (e.g., hyperkalemic, acidosis)
    3. Post defibrillation
    4. Medications (e.g., beta blockers, calcium channel blockers, antiarrhythmics)

Treatment if patient hemodynamically unstable:

• External pacing pads (transcutaneous pacing), or;
• Insert transvenous pacing wires

C. High threshold

A high threshold occurs when a high amount of energy is required to achieve myocardial capture. In temporary pacing wires, this can be a result of lead dislodgement and may raise concern of further dislodgement or failure to capture. In permanent pacemakers, this can also be a sign of lead dislodgement (and associated complications), lead integrity (i.e. lead fracture), and may also influence battery life if the threshold remains persistently high.

Differential:

• Pacing wire dislodgement or in contact with an area of scar or high threshold
• Metabolic and pharmacologic considerations (i.e. myocardial ischemia, electrolyte imbalance, post-defibrillation, medications)
• Hematoma
• Edema
• Scarring

Treatment:

• Consider transvenous wires if threshold >10mA in a pacing-dependent patient

D. Oversensing

Oversensing occurs when the pacemaker “senses” too much- for example, if the pacemaker senses T waves, or double-counts the QRS complex, this can result in inappropriate inhibition of pacing. This is particularly relevant in pacemaker dependent patients, as it can lead to excessive bradycardia or pauses.

Treatment:

• Increase sensing threshold
• Change modes

E. Diaphragmatic pacing

Differential:

• Proximity of phrenic nerve with lead.
• Incorrectly positioned lead (cardiac vein, myocardial perforation, migration)
• High stimulation amplitude

Treatment:

• Reduce output
• Use ventricular pacing (rather than atrial pacing), given that atrial wires are often closer to the phrenic nerve.
• Reposition of pacing wires

F. Retained wire

Generally temporary epicardial pacing wires can be removed postoperatively with gentle traction. However, if resistance to traction occurs, the pacing wire can be cut flush with the skin so that the residual wire retracts into the tissue.

Complications with retained epicardial pacing wires include:

• Localized cutaneous abscess or fistula
• Distant migration of the temporary epicardial pacing wires
• Infective endocarditis (theoretical risk)
• Contraindication to MRI

G. Pericardial effusion or tamponade after transvenous pacing wire/pacemaker insertion

The development of a pericardial effusion or tamponade after transvenous pacing wire/pacemaker insertion can occur if there is perforation secondary to the pacing wire. This can occur in either the right atrium or right ventricle, as both are thin-walled structures.

Clinical findings:

• Chest discomfort, shortness of breath or evidence of pericarditis
• Progressive hypotension and tachycardia
• Elevated jugular venous pressure and pulsus paradoxus
• Muffled heart sounds and pericardial rub

Diagnosis:

• Physical signs
• Chest x-ray: enlarged cardiac silhouette
• Echocardiography: pericardial fluid with right ventricular diastolic collapse
• CT scan of the chest with contrast (if patient is hemodynamically stable): examine for lead positioning and contrast extravasation which would suggest of lead perforation
• Pacemaker interrogation: if pacemaker functions well, it is unlikely that the lead has perforated

Treatment:

Importantly, the pacing wire/pacemaker lead should not be immediately removed, as it may be “plugging the hole” and preventing further development of a pericardial effusion or tamponade. It should be removed under close observation, typically in the surgical OR.

1. IV access, telemetry, monitors (blood pressure, heart rate, oxygen saturation)
2. Volume resuscitation
3. Aspiration / Drainage: Pericardiocentesis, correcting coagulation and await 3-4 days for the hole to scar down and thrombose. Following this, lead repositioning should then be attempted.  

H. Pericardial effusion or Tamponade after temporary epicardial pacing wire removal

Clinical findings:

• Progressive hypotension and tachycardia
• Elevated jugular venous pressure and pulsus paradoxus
• Muffled heart sounds and pericardial rub
• Decreased urine output

Diagnosis:

• Physical signs
• Chest x-ray: enlarged cardiac silhouette
• Echocardiography: pericardial fluid with right ventricular diastolic collapse

Treatment:

• IV access, telemetry, monitors (blood pressure, heart rate, oxygen saturation)
• Volume resuscitation
• Aspiration / Drainage: Pericardiocentesis, subxiphoid pericardial window or urgent resternotomy

7. Potential questions / scenarios

What is the difference between an intrinsic left bundle branch block and a paced rhythm?

The major difference is that the QRS will almost always be negative in V5-V6 with a paced rhythm.

What does it mean if my patient develops a new right bundle branch block during pacing after implantation of a permanent transvenous pacemaker?

A typical paced QRS morphology from a right ventricular lead resembles a left bundle-branch block morphology (with minor differences). However, the finding of a right bundle branch block morphology, or tall R-wave in V1, suggests left-sided pacing. This can occur if the right ventricular lead is advanced inadvertently into the coronary sinus, or the right ventricular lead is advanced through a patent foramen ovale / atrial septal defect into the left ventricle. Pacing wires in the coronary sinus are typically used for cardiac resynchronization pacing but should not be used routinely as a surrogate for right ventricular pacing, as the wire itself may dislodge and have important implications for pacemaker-dependent patients (sudden loss of capture). Pacing wires in the left ventricle due to a patent foramen ovale / atrial septal defect will also substantially increase the risk for stroke or systemic embolism. In both cases, the pacing wire will capture the left ventricle and should be repositioned.

What is the effect of paced rhythms on an ECG’s ability to detect an acute myocardial infarction?

As with an intrinsic left bundle branch block, ventricular pacing results in depolarization and repolarization abnormalities that can confound the ECG’s ability to detect an acute myocardial infarction. The Sgarbossa criteria is frequently referenced as a method to identify an acute myocardial infarction in patients with intrinsic left bundle branch block. Although the Sgarbossa criteria was not validated with paced QRS morphologies, it is sometimes extrapolated to patients with paced QRS morphologies. However, the Sgarbossa criteria itself is specific but not sensitive for acute myocardial infarction with concordant ST elevation >1mm having the highest specificity for acute myocardial infarction in paced rhythms. However, the absence of these findings does not rule out an acute myocardial infarction.

Postoperative patient from cardiac surgery with cardiac arrest. A code blue is called. What do you do?

Ensure adequate IV access. Assess the rhythm. The Society of Thoracic Surgeons protocol for resuscitation of patients who arrest after cardiac surgery should be followed if the patient is <10 days after surgery. For patients beyond day 10, the protocol should still be followed but a senior clinician should decide whether resternotomy is indicated. Briefly, for the following scenarios:

1. Ventricular fibrillation or tachycardia -> DC shock x 3 should be attempted after which basic life support should be initiated and amiodarone 300mg should be given by central venous line. The team should prepare for emergency resternotomy and continue CPR with single DC shock every 2 minutes until resternotomy.
2. Asystole or severe bradycardia -> if pacing wires available, external pacing should be attempted. If external pacing fails, the team should continue CPR until emergency resternotomy.
3. Pulseless electrical activity -> if the patient is paced, turn off pacing to exclude underlying ventricular fibrillation. If ventricular fibrillation, resort to ventricular fibrillation pathway. If pulseless electrical activity, the team should continue CPR until emergency resternotomy.

During this time, epinephrine should not be given unless a senior physician advises for it. If an intra-aortic balloon pump is in place, change it to pressure trigger. Examine for reversible causes for cardiac arrest including hypovolemia, hypoxia, acidosis, hypo-/hyperkalemia, hypothermia, tension pneumothorax, cardiac tamponade, pulmonary thrombosis, coronary thrombosis and toxins as per Advanced Cardiovascular Life Support algorithm.

You are called to see a patient post-permanent transvenous pacemaker insertion with a pericardial effusion with concern for ventricular lead perforation. What do you do? 

Go and assess the patient. If patient is hemodynamically unstable, bedside echocardiogram can demonstrate tamponade physiology and the patient should undergo urgent pericardiocentesis or be taken immediately to the operating room. If the patient is hemodynamically stable, one should obtain a 12-lead ECG and chest x-ray to evaluate for changes in lead position. A CT scan of the chest with contrast may also be helpful when looking for lead migration or perforation with contrast extravasation. If the echocardiogram does not demonstrate tamponade physiology and the pacemaker interrogation demonstrates that the pacemaker is functioning well, then the pericardial effusion is likely due to microperforation during lead insertion and can be treated conservatively if not large.  

If the patient is pacing dependent and electrocautery will be used, this can result in inappropriate inhibition of the pacemaker due to sensing of the noise from the electrocautery. Inappropriate inhibition can result in excessive bradycardia or pauses, particularly in pacemaker-dependent patients. In such cases, the pacemaker can be programmed to AOO, VOO or DOO depending on whether there is an intact atrioventricular conduction. This should be re-evaluated or re-programmed as soon as electrocautery is not needed. Another option is to place a magnet over the generator for the pacemaker- a magnet will cause the pacemaker to default to an asynchronous mode (e.g. VOO or DOO).

Utilization of bipolar cautery is preferred with short duration cautery bursts <5s allowing for >5s between bursts when using monopolar electrocautery is recommended. In addition, the electrosurgical receiving plate should be positioned so that the current pathway does not pass through or near the pacemaker. Backup equipment for urgent transcutaneous pacing, defibrillation or cardioversion should be prepared. These steps would be especially important if the surgical site is above the hip.

Do patients with permanent transvenous pacemakers or epicardial leads require endocarditis antibiotic prophylaxis for procedures?

Patients with pacemakers or defibrillators are considered negligible risk and do not require endocarditis antibiotic prophylaxis prior to procedures.

My patient has a permanent transvenous pacemaker and requires an MRI. What do I do?

The concern with MRI is that the induced currents during imaging can lead to risk of arrhythmia induction, capture threshold changes, lead dislodgement and device damage. If the patient is pacemaker dependent and the pacemaker is MRI conditional, it means that the specific MRI environment with the device with specified conditions of use does not pose a known hazard. However, many devices have an “MRI-mode” that should be turned on prior to undergoing the MRI, and most devices should be checked before and after the MRI is performed to ensure of no unanticipated programming changes.

Patients with non-MRI compatible devices include those with device/lead manufacturer mismatch, or those with simply non-compatible devices. In rare circumstances, these patients can also undergo MRI with close monitoring and a collaborative effort with radiologists. Finally, MRI is contraindicated in patients with a new pacemaker implantation (within 4-6 weeks) as this may cause dislodgement of the leads, even in MRI compatible devices. In such cases, the MRI is typically deferred until after the waiting/recovery period. However, if there are any concerns, an appropriate consultation should be obtained to determine if imaging would be reasonable.

Suggested Readings

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2. Reade MC. Temporary epicardial pacing after cardiac surgery: a practical review Part 2: Selection of epicardial pacing modes and troubleshooting. doi:10.1111/j.1365-2044.2007.04951.x
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